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Essential MCU regulator (EMRE) in the Mitochondrial Calcium Uniporter (MCU) Complex

Reviewer and Curator: Larry H. Bernstein, MD, FCAP 

 

UPDSTED on 9/22/2018

 

J Biol Chem. 2016 Dec 2;291(49):25505-25515. Epub 2016 Oct 28.

CRISPR/Cas9-mediated endogenous C-terminal Tagging of Trypanosoma cruzi Genes Reveals the Acidocalcisome Localization of the Inositol 1,4,5-Trisphosphate Receptor.

Lander N1Chiurillo MA2Storey M3Vercesi AE2Docampo R4,3.

https://www.ncbi.nlm.nih.gov/pubmed/27793988

 

The article that follows establishes the essential role that the mitochondria have in calcium-uptake that requires a calcium-binding protein, MICU1 and MICU2  mitochondrial uptake proteins,  the pore forming subunit mitochondrial uniporter (MCU), and occurs through a selective calcium channel MCU regulator in the inner membrane – EMRE, not previously characterized.  This is the case in neural transmission as well as in cardiac contraction.

EMRE Is an Essential Component of the Mitochondrial Calcium Uniporter Complex

Y Sancak1,2, AL Markhard1, T Kitami1,2,*, E Kovács-Bogdán1, et al.

1Department of Molecular Biology, Massachusetts General Hospital, Department of Systems Biology, Harvard Medical School, Boston, MA
2Broad Institute of MIT and Harvard, Cambridge, MA
3Howard Hughes Medical Institute, Department of Cardiology, Children’s Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA
Science 13 Dec 2013; 342 (6164): 1379-1382
http://dx.doi.org/10.1126/science.1242993

ABSTRACT

The mitochondrial uniporter is a highly selective calcium channel in the organelle’s inner membrane. Its molecular components include the EF-hand–containing

  • calcium-binding proteins
  • mitochondrial calcium uptake 1 (MICU1) and MICU2 and
  • the pore-forming subunit mitochondrial calcium uniporter (MCU).

We sought to achieve a full molecular characterization of the uniporter holocomplex (uniplex). Quantitative mass spectrometry of affinity-purified uniplex recovered

  • MICU1 and MICU2,
  • MCU and its paralog MCUb, and
  • essential MCU regulator (EMRE), a previously uncharacterized protein.

EMRE is a 10-kilodalton, metazoan-specific protein with a single transmembrane domain. In its absence,

  • uniporter channel activity was lost
  • despite intact MCU expression and oligomerization.

EMRE was required for the interaction of MCU with MICU1 and MICU2. Hence,

  • EMRE is essential for in vivo uniporter currentand additionally, 
  • bridges the calcium-sensing role of MICU1 and MICU2 with the calcium-conducting role of MCU.
EDITOR’S SUMMARY

EMRE Emerges

L. Bryan Ray
Sci. Signal. 17 Dec 2013: 6(306), p. ec310.  [DOI: 10.1126/scisignal.2005002]

Concentrations of calcium within mitochondria are tightly regulated and modulate physiological mitochondrial functions,

including control of metabolism and cell death.

Sancak et al. complete the molecular characterization of the mitochondrial calcium uniporter (MCU), the multicomponent channel that allows concentration of calcium within the organelle.

They identified a small protein termed “essential MCU regulator”—or EMRE—which was required for calcium transport activity of the fully assembled uniporter.

Heart Rate Variability (HRV) as a Tool

Reporter and Curator: Larry H. Bernstein, MD, FCAP

The article that follows expands on the discussions about exercise, walking or running, and burning calories, an adjunct to good nutrition.  It elucidates how monitoring of performance in physical conditioning is done by monitoring the heart rate variability.  The fact is that outside of concussion injuries that may take a toll in time, or even cause a subdural hematoma, there are “silent” events that are related to sudden death.  These are serious cardiovascular events.

Heart Rate Variability (HRV) as a Tool for Diagnostic and Monitoring Performance in Sport and Physical Activities

Journal of Exercise Physiology  Jun 2013; 15(3):103-131.  ISSN 1097-9751

B Makivic, M Djordjevic, MS Willis

1Center for Sport Science and University Sport, University of Vienna, Vienna, Austria, 2Faculty of Sport and Physical Education, Belgrade, Serbia, 3McAllister Heart Institute, University of North Carolina, Medical Biomolecular Research Building, Chapel Hill, NC.

The dynamic autonomic responses during exercise can be measured

  • to give actionable information for training
  • by analysis of the ECG to determine heart rate variability (HRV).

While application of HRV has been applied to

  • predict sudden cardiac death and diabetic neuropathy
  • in assessing disease progression,

recent studies have suggested that it may be applied to exercise training. In this review, we present

  • the rationale for measuring HRV.

We describe the

  • different variables used and
  • what they can tell us about the autonomic nervous system.

The use of HRV in detecting changes in exercise intensity is presented, along with evidence that

  • gender and age changes may affect autonomic HRV.

Lastly, we illustrate how

  • HRV measurements taken immediately post-exercise have proven to be useful
  • in measuring and monitoring training load to proscribe workouts and/or prevent over-training.

Despite the studies that

  • vary widely in their application to different training levels of athletes being tested and
  • HRV measures used,

the standardization of methodologies and results should help accelerate the use of HRV in sports training.
Key Words: Autonomic Nervous System; Overtraining; HRV

Promising Technique to keep Tumors from Spreading Developed by Cornell Researchers

Reporter: Aviva Lev-Ari, PhD, RN

Jan. 6, 2014

Metastatic cancer cells implode on protein contact

Lindsay France/University Photography
Professor Michael King, right, with students Elizabeth Wayne, left, and Michael Mitchell in the King laboratory.

By attaching a cancer-killer protein to white blood cells, Cornell biomedical engineers have demonstrated the annihilation of metastasizing cancer cells traveling throughout the bloodstream.

The study, “TRAIL-Coated Leukocytes that Kill Cancer Cells in the Circulation,” was published online the week of Jan. 6 in the journal Proceedings of the National Academy of Sciences.

<iframe src=’http://www.cornell.edu/video/metastatic-cancer-cells-implode-on-protein-contact/embed&#8217; width=’560′ height=’315′ frameborder=’0′>

“These circulating cancer cells are doomed,” said Michael King, Cornell professor of biomedical engineering and the study’s senior author. “About 90 percent of cancer deaths are related to metastases, but now we’ve found a way to dispatch an army of killer white blood cells that cause apoptosis – the cancer cell’s own death – obliterating them from the bloodstream. When surrounded by these guys, it becomes nearly impossible for the cancer cell to escape.”

Metastasis is the spread of a cancer cells to other parts of the body. Surgery and radiation are effective at treating primary tumors, but difficulty in detecting metastatic cancer cells has made treatment of the spreading cancer problematic, say the scientists.

King and his colleagues injected human blood samples, and later mice, with two proteins: E-selectin (an adhesive) and TRAIL (Tumor Necrosis Factor Related Apoptosis-Inducing Ligand). The TRAIL protein joined together with the E-selectin protein stick to leukocytes – white blood cells – ubiquitous in the bloodstream. When a cancer cell comes into contact with TRAIL, which becomes unavoidable in the chaotic blood flow, the cancer cell essentially kills itself.

“The mechanism is surprising and unexpected in that this repurposing of white blood cells in flowing blood is more effective than directly targeting the cancer cells with liposomes or soluble protein,” say the authors.

In the laboratory, King and his colleagues tested this concept’s efficacy. When treating cancer cells with the proteins in saline, they found a 60 percent success rate in killing the cancer cells. In normal laboratory conditions, the saline lacks white blood cells to serve as a carrier for the adhesive and killer proteins. Once the proteins were added to flowing blood, which models forces, mixing and other human-body conditions, however, the success rate in killing the cancer cells jumped to nearly 100 percent.

As this research is newly announced, King says animal trials will continue and he hopes that the research will proceed to human clinical trials sometime in the future.

In addition to King, the paper’s researchers include first author Michael Mitchell, a Cornell doctoral candidate in the field of biomedical engineering; Elizabeth C. Wayne, a Cornell doctoral student in the field of biomedical engineering; Kuldeepsinh Rana, a Cornell Ph.D. ’11; and Chris Schaffer, associate professor in biomedical engineering. The National Cancer Institute (Physical Sciences-Oncology program) of the National Institutes of Health, Bethesda, Md., funded the research through Cornell’s Center for the Microenvironment and Metastasis.

SOURCE

http://www.news.cornell.edu/stories/2014/01/metastatic-cancer-cells-implode-protein-contact

Look Out, Cancer Cells, Here Come ‘Sticky Balls’

By John Johnson,  Newser Staff
Posted Jan 7, 2014 2:12 PM CST
Stock image of a cancer cell.

(NEWSER) – It sounds ingenious: Cornell researchers have created roving proteins whose sole purpose is to destroy cancer cells in the bloodstream. If further tests hold up, this could offer a way to keep cancers from metastasizing, or spreading, reports the BBC, which uses the phrase “cancer-killing sticky balls” to describe what’s happening. When unleashed into the bloodstream, these sticky balls—made up partly of a cancer-attacking protein known as TRAIL—hitch a ride on white blood cells. When the white blood cells bump into a cancer cell on the move, the cancer cell is destroyed, explains the Cornell Chronicle.

“These circulating cancer cells are doomed,” says the lead author of the study in the journal Proceedings of the National Academy of Sciences. “About 90% of cancer deaths are related to metastases, but now we’ve found a way to dispatch an army of killer white blood cells that cause apoptosis—the cancer cell’s own death—obliterating them from the bloodstream. When surrounded by these guys, it becomes nearly impossible for the cancer cell to escape.” The results were “dramatic,” he says, though testing now needs to move beyond blood samples and mice.

SOURCE

http://www.newser.com/story/180300/look-out-cancer-cells-here-come-sticky-balls.html

Burden of Depressive Disorders

Reviewer and Curator: Larry H Bernstein, MD, FCAP

 

This article is an important contribution to the literature on depression, substantiation the cardiovascular burden of depression on cardiovascular disease.

Burden of Depressive Disorders by Country, Sex, Age, and Year:Findings from the Global Burden of Disease Study 2010

AJ Ferrar*,FJ Charlson,RE Norman,SB Patten, G Freedman, CJL.Murray,T Vos

1Universityof Queensland, School of Population Health,Herston, Queensland, Au
2Queensland Centre for Mental Health Research, Wacol, Queensland, Au
3University of Queensland, Queensland Children’s Medical Research Institute,Herston,Queensland, Au
4Universityof Calgary, Department of Community Health Sciences,Calgary, Alberta, Ca
5University of Washington,Institute for Health Metrics and Evaluation, Seattle, Wash

Abstract

Background

Depressive disorders were a leading cause of burden in the Global Burden of Disease (GBD) 1990 and 2000  studies. Here, we analyze the burden of depressive disorders in GBD 2010 and present severity proportions ,burden by country, region, age, sex, and year, as well as burden of depressive disorders as a risk factor fo rsuicide and ischemic heart disease.

Methods and Findings

Burden was calculated for major depressive disorder (MDD) and dysthymia. A systematic review of  epidemiological data was conducted. The data were pooled using a Bayesian meta-regression. Disability weights from population survey data

  • quantified the severity of health loss from depressive disorders.

These weights were used to calculate

  • years lived with disability (YLDs) and
  • disability adjusted life-years (DALYs).

Separate DALYs were estimated for

  • suicide and
  • ischemic heart disease

attributable to depressive disorders. Depressive disorders were the second leading cause of YLDs in 2010.

  • MDD accounted for 8.2% (5.9%–10.8%) of global YLDs and
  • dysthymia for 1.4% (0.9%–2.0%).

Depressive disorders were a leading cause of DALYs even though no mortality was attributed to them as the underlying cause.

  • MDD accounted for 2.5% (1.9%–3.2%) of global DALYs and
  • dysthymia for 0.5% (0.3%–0.6%).

There was more regional variation in burden for MDD than for dysthymia; with

  • higher estimates in females, and
  • adults of working age.

Whilst burden increased by 37.5% between 1990 and 2010, this was due to population growth and ageing. MDD explained

  • 16 million  suicide DALYs and
  • almost 4 million ischemic heart disease DALYs.

This attributable burden would increase the overall burden of depressive disorders from 3.0% (2.2%–3.8%) to 3.8% (3.0%–4.7%) of global DALYs.

Conclusions

GBD 2010 identified depressive disorders as a leading cause of burden. MDD was also a contributor of burden

  • allocated to suicide and ischemic heart disease.

These findings emphasize the importance of including depressive disorders as a public-health priority and

  • implementing cost-effective interventions to reduce its burden.

Please see later in the article for the Editors’ Summary.

Citation:Ferrari AJ, Charlson FJ, Norman RE, Patten SB, Freedman G,etal.(2013) Burden of Depressive Disorders by Country, Sex, Age, and Year: Findings from the Global Burden of Disease Study 2010. PLoS Med 10(11):e1001547. http://dx.doi.org/10.1371/journal.pmed.1001547

Abbreviations: CRA, comparative risk assessment; DALY, disability adjusted life years; DSM, Diagnostic and Statistical Manual of Mental Disorders; GBD, global burden of disease; ICD, International Classification of Diseases; MDD, major depressive disorder; MEPS, US Medical Expenditure Panel Survey; NESARC, US National Epidemiological Survey on Alcohol and Related Conditions 2000–2001 and 2004–2005; NSMHWB, Australian National Survey of Mental Health and Well being of Adults 1997; RR, relative risk; YLD, years lived with disability;YLL,years of life lost.

Figure1.YLDs by age and sex for MDD and dysthymia in 1990 and 2010.  http://dx.doi.org/10.1371/journal.pmed.1001547.g001

Figure1.YLDsbyageandsexforMDDanddysthymiain1990and2010.

Figure2.YLD rates (per100,000) by region for MDD and dysthymia in 1990 and 2010. 95%UI, 95% uncertainty interval; AP-HI, Asia Pacific, high income; As-C, Asia Central; AS-E, Asia East; AS-S, Asia South;A-SE, Asia Southeast; Aus, Australasia; Caribb, Caribbean; Eur-C, Europe Central; Eur-E, Europe Eastern; Eur-W, Europe Western; LA-An, LatinAmerica, Andean; LA-C, Latin America, Central; LA-Sth, LatinAmerica, Southern; LA-Trop, Latin America, Tropical; Nafr-ME, NorthAfrica/MiddleEast; Nam-HI, North America, high income; Oc, Oceania; SSA-C, Sub-Saharan Africa, Central; SSA-E, Sub-Saharan Africa, East; SSA-S, Sub-Saharan Africa Southern; SSA-W, Sub-Saharan Africa,West.  http://dx.doi.org/10.1371/journal.pmed.1001547.g002

Figure2. YLD rates (per100,000) by region for MDD and dysthymia in 1990 and 2010

Plot 1  age dtandardized YLD rates

Editors’ Summary

Background.

Depressive disorders are common mental disorders that occur in people of all ages across all world regions. Depression—an overwhelming feeling of sadness and hopelessness that can last for months or years—can make people feel that life is no longer worth living. People affected by depression lose interest in the activities they used to enjoy and can also be affected by physical symptoms such as disturbed sleep. Major depressive disorder (MDD, also known as clinical depression) is

  • an episodic disorder with a chronic (long-term) outcome and increased risk of death.

It involves at least one major depressive episode in which the affected individual experiences

  • a depressed mood almost all day, every day for at least 2 weeks.

Dysthymia is a milder, chronic form of depression that lasts for at least 2 years. People with dysthymia are often described as constantly unhappy. Both these subtypes of depression (and others such as that experienced in bipolar disorder) can be treated with antidepressant drugs and with talking therapies.

Why Was This Study Done? Depressive disorders were a  leading cause of disease burden in the 1990 and 2000 Global Burden of Disease (GBD) studies, collaborative scientific efforts that quantify the health loss attributable to

  • diseases and injuries in terms of disability adjusted life years (DALYs; one DALY represents the loss of a healthy year of life).

DALYs are calculated by adding together the years of life lived with a disability (YLD, a measure that includes a disability weight factor reflecting disease severity) and the years of life lost because of disorder-specific premature death. The GBD initiative aims

  • to provide data that can be used to improve public-health policy.

Thus, knowing that depressive disorders are a leading cause of disease burden worldwide has helped to prioritize depressive disorders in global public-health agendas. Here, the researchers analyze the burden of MDD and dysthymia in GBD 2010 by country, region, age, and sex, and

  • calculate the burden of suicide and ischemic heart disease attributable to depressive disorders (depression is a risk factor for suicide and ischemic heart disease).

GBD 2010 is broader in scope than previous GBD studies and quantifies the direct burden of 291 diseases and injuries and the  burden attributable to 67 risk factors across 187 countries.

What Did the Researchers Do and Find? The researchers collected data on

  • the prevalence, incidence, remission rates, and duration of MDD and dysthymia and on deaths caused by these disorders from published articles.

They pooled these data using a statistical method called Bayesian meta-regression and calculated YLDs for MDD  and dysthymia using disability weights collected in population surveys. MDD accounted for 8.2% of global YLDs in 2010, making it the second leading cause of YLDs. Dysthymia accounted for 1.4% of global YLDs. MDD and dysthymia were also leading causes of DALYs, accounting for 2.5% and 0.5% of global DALYs, respectively. The regional variation in the burden was greater for MDD than for dysthymia, the  burden of depressive disorders was higher in women than men, the largest proportion of YLDs from depressive  disorders occurred among adults of working age, and the  global burden of depressive disorders increased by 37.5%  between 1990 and 2010 because of population growth and ageing. Finally, MDD explained an additional 16 million  DALYs and 4 million DALYs when it was considered as a risk factor for suicide and ischemic heart disease, respectively.  This ‘‘attributable’’ burden increased the overall burden of depressive disorders to 3.8% of global DALYs.

What Do These Findings Mean? These findings update and extend the information available from GBD 1990 and  2000 on the global burden of depressive disorders. They confirm that

  • depressive disorders are a leading direct cause of the global disease burden and show that
  • MDD also contributes to the burden allocated to suicide and ischemic heart disease.

The estimates of the global burden of depressive disorders reported in GBD 2010 are likely to be more accurate than those in previous GBD studies but are  limited by factors such as the sparseness of data on depressive disorders from developing countries and, consequently,

  • the validity of the disability weights used to calculate YLDs.

Even so, these findings reinforce the importance of treating  depressive disorders as a public-health priority and

  • of implementing cost-effective interventions to reduce their  ubiquitous burden.

Additional Information. Please access these websites via  the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001547.

Registered Dietitian (RD) recommends 7 Brain Foods for Breakfast

Reporter: Aviva Lev-Ari, PhD, RN

Eating a healthy breakfast can jump start your brain and help boost your productivity and focus throughout the morning. Try incorporating these seven “brain foods” in your morning meal to give yourself a mental edge.

  • 1Eggs

    Choline, a B vitamin found in eggs, has been shown to play a role in brain function and memory. In a study of almost 1,400 men and women published in the American Journal of Clinical Nutrition, those who consumed foods with choline performed better on memory and verbal learning tests than other subjects.

    Eggs also provide high-quality protein, a nutrient that helps you concentrate by keeping your blood sugar stabilized and helping you feel fuller, longer. Whether you like your eggs scrambled, in an omelet, or hard-boiled, eggs are a rich source of nutrition to help keep your brain and body charged throughout the morning rush.

  • 2Grains

    iStock

    Grain products are important in the morning because our body converts the carbs to glucose, which is the brain’s preferred fuel. Whole and enriched grain foods also contain B vitamins, which are important for concentration and helping your brain to stay healthy over time. The general recommendation is to make half of your grains whole grains.

    Couple your grains with some protein for sustained energy and mental performance. A few quick and easy grain-protein combos to boost your brain power in the morning include toast with almond butter, oatmeal with berries and chia seeds, a toasted English muffin topped with a scrambled egg and slice of turkey bacon or a high-fiber fruit and nut muffin.

  • 3Grapes

    Studies indicate that consuming a variety of green, red and black grapes plays a role in improving our antioxidant defenses, which has ramifications for brain health. In preliminary studies, grapes seem to help protect brain health by counteracting oxidative stress and inflammation, or by targeting the actions of certain genes involved in age-related diseases of the brain. Try adding grapes to your morning parfait or smoothie, or enjoy a handful straight off the vine.

  • 4Blueberries

    iStock

    All berries are rich in tannins, which protect brain cells and may play a role in improving memory by promoting communication between brain cells. Specifically, blueberries are rich in antioxidants and other phytochemicals that have been linked to improvements in learning, thinking and memory, as well as possible reductions in neurodegenerative oxidative stress. For a smart start to your morning, add blueberries to your yogurt, oatmeal, smoothies or baked goods.

  • 5Almonds

    Almonds are an excellent source of vitamin E, providing 37 percent of your daily recommended intake in a one-ounce serving (about 23 almonds or a handful). A study published in the American Journal of Epidemiologysuggests that a good intake of vitamin E might help to prevent cognitive decline, particularly in the elderly.

    Almonds also provide a healthy combination of protein, fiber and healthful fats to help maintain your blood sugar levels, which can help you stay focused and energized. To start your day bright, go for an almond-rich muesli or slivered almonds in your yogurt or oatmeal.

  • 6Oats

    Oats contains iron, zinc, potassium and B vitamins, nutrients that help brain development and help the brain to function at full capacity. The fiber contained in oats will also help keep hunger at bay until your next meal.

    Studies show that children who ate oatmeal for breakfast scored up to 20 percent higher on tests than children who ate sugary cereal, likely due to the fact sugary-foods result in dips in blood sugar that affect memory and concentration. Whether you like your oatmeal topped with berries, nuts, cinnamon or sliced banana, a hearty bowl in the morning will help get your mental juices flowing.

  • 7Apples

    Apples are rich in quercetin, an antioxidant plant chemical that protects brain cells. According to researchers at Cornell University, quercetin defends your brain cells from free radical attacks, which can damage the outer lining of delicate neurons and eventually lead to cognitive decline. Grab an apple in the morning and be sure to eat it with the skin on, since the highest amount of quercetin is found in the skin.

Patricia Bannan is a Los Angeles-based registered dietitian specializing in nutrition and health communications.  She is the author of “Eat Right When Time Is Tight: 150 Slim-Down Strategies” and “No-Cook Food Fixes.” Visit her website athttp://www.patriciabannan.com/.

SOURCE

http://www.foxnews.com/health/2014/01/11/7-brain-foods-for-breakfast/

The Economics of Obesity – NBER Research Summary

Reporter: Aviva Lev-Ari, PhD, RN

Thirteen Facts About the Economics of Obesity

By   January 13, 2014

Coy is Bloomberg Businessweek‘s economics editor.

Every week seems to bring a new study about the economics of obesity, but it’s rare for a top scholar in the field to piece it all together for a general audience. John Cawley, who directs Cornell University’s Institute on Health Economics, Health Behaviors & Disparities, has done just that in the latest issue of the National Bureau of Economics Research Reporter. Here are 13 statements—some controversial—from his article, which draws on dozens of studies by himself and others:

1. About 2.8 million people a year die from excess weight worldwide.

2. Body mass index, which is based only on height and weight and ignores fat, misclassifies some muscular people as obese and some unmuscled people as not obese.

3. The black-white gap in obesity among women is only half as large if obesity is defined as a percentage of body fat rather than high BMI.

4. The rise in obesity began 10 to 20 years earlier if obesity is measured by skinfold thickness rather than BMI.

5. Obesity raises annual medical costs by $2,741 (in 2005 dollars).

6. Obesity accounted for about 21 percent of national health spending in 2005.

7. There is little evidence that income affects weight, but weight seems to affect income.

8. For white women, whose incomes are most affected, being 64 pounds heavier is associated with 9 percent lower wages. Some studies “suggest that discrimination plays an important role.”

9. Excess weight is now the primary reason that applicants to the military are rejected.

10. There is no evidence that increases in physical education requirements for school children have any impact on youth weight. It doesn’t even increase physical activity for high school boys.

11. It’s possible that for some young people, increased physical education increases muscle and decreases fat with little net effect on weight.

12. People who were offered financial rewards in a workplace weight-loss program didn’t lose more weight than a control group. Those with some of their own money at stake lost two pounds more than the controls.

13. There is “very little, if any, evidence” that over-the-counter weight-loss products are effective. Some are dangerous.

Cawley, who got his economics Ph.D. at the University of Chicago, edited the Oxford Handbook of the Social Science of Obesity, a book you probably didn’t know existed. According to the Reporter, Cawley (profile pic here) is married to a fellow Cornell economist, Rachel Dunifon, and “in his spare time, he enjoys watching hour-long TV dramas with his wife and trying not to cheer too [loudly] at his sons’ soccer games.”

SOURCE

http://www.businessweek.com/articles/2014-01-13/13-facts-about-the-economics-of-obesity

NBER Reporter 2013 Number 4: Research Summary

The Economics of Obesity

John Cawley *http://nber.org/reporter/2013number4/cawley.htmlDuring the past three decades in the United States, many indicators of population health such as life expectancy, the prevalence of smoking, and drug and alcohol use among youths improved significantly.1 In stark contrast to these trends, over same period the United States also experienced a doubling of the prevalence of obesity, which is defined as a body mass index (BMI) of greater than or equal to thirty, which corresponds to a weight of 221 pounds for someone six feet tall. As of 2009 to 2010, more than one-third of adult Americans are obese. 2 The United States is not alone; many countries worldwide have experienced a significant increase in obesity, and the World Health Organization estimates that 2.8 million people die each year as a result of excess weight.3

This has led to considerable debate about the causes and consequences of obesity and what can be done to prevent and treat it. Answering these questions is complicated because in many cases researchers cannot conduct randomized experiments: it would be unethical to experimentally manipulate individuals’ weight. For this reason the empirical methods of economics, particularly the attention to issues of selection and omitted variables, are especially useful for identifying causal effects.

My primary research interest is the economics of risky health behaviors, in particular the economics of obesity. In a series of studies, my co-authors and I have investigated the economic causes and consequences of obesity and evaluated policies and programs to improve diets and increase physical activity. This research summary provides an overview of several recent projects and findings. A broader review of the economics of risky health behaviors that I co-authored with Christopher Ruhm is also available.4

Measurement and Trends

An important limitation of BMI, the standard measure of fatness in epidemiology, is that it does not distinguish fat from lean mass: it simply measures weight for height. A study that I conducted with Richard Burkhauser 5 found that BMI, relative to more accurate measures of fatness such as percentage of body fat, misclassifies substantial percentages of individuals as obese and non-obese. BMI tends to be less accurate at classifying men (among whom there is more variation in muscularity) than women. The use of BMI also results in biased estimates of health disparities; the black-white gap in obesity among women is only half as large if one defines obesity using percentage of body fat rather than BMI. Moreover, the timing of the rise in obesity is sensitive to the measure of fatness used; Richard Burkhauser, Max Schmeiser and I find that if one uses skinfold thickness rather than BMI to define obesity then the rise in obesity becomes apparent 10 to 20 years earlier, which suggests that more gradual or long-run influences may be responsible. 6 It also suggests that the rise in BMI might have been detected earlier, and public health responses initiated sooner, if epidemiological surveillance had not relied so exclusively on BMI. Although many social science datasets continue to collect only self-reported weight and height, some innovative surveys such as the Health and Retirement Study (HRS) and the Household, Income and Labour Dynamics in Australia (HILDA) Survey are collecting additional measures of fatness such as waist circumference.

Economic Causes and Consequences of Obesity

Many theories have been advanced to explain the rise in obesity. To measure the extent to which income affects obesity, John Moran, Kosali Simon, and I exploit the natural experiment of the Social Security Benefits Notch.7 The Notch is the result of a legislative accident that created variation in retirement income that was large, unanticipated, and beyond the control of the individual, making it a suitable instrument. We estimate models of instrumental variables (IV) using data from the National Health Interview Survey and find little evidence that income affects weight. The small effects are precisely estimated: for a permanent $1,000 increase in Social Security income (in 2006 dollars) our confidence intervals rule out a change in weight of more than 1.4 pounds in either direction for men or women.

Understanding the consequences of obesity is important for evaluating calls for government intervention and for measuring the cost-effectiveness of treatment and prevention programs. One important potential consequence of obesity is higher medical care costs. Fat releases hormones that lead to insulin resistance and damage the cardiovascular system, with the result that obesity is associated with a wide variety of health conditions such as diabetes, heart disease, and cancer. Previous studies estimated the correlation of obesity with medical care costs, which is difficult to interpret because weight may be correlated with important unobserved factors (such as socioeconomic status) and there may be reverse causality (an expensive back injury may lead to weight gain). To estimate the causal effect of obesity on medical care costs, Chad Meyerhoefer and I exploit the heritable component of weight as a natural experiment. 8 The identifying assumption is that the similarity in weight of biological relatives is caused by genetics rather than shared environment, an assumption that is supported by a large number of studies in genetics. We estimate the IV model using data from the Medical Expenditure Panel Survey, and the results indicate that obesity raises medical costs by $2,741 per obese individual (in 2005 dollars). This is higher than the non-IV estimate because the IV method corrects for both the endogeneity of weight and reporting error in weight. Medical costs are much greater for those whose weight places them well above the threshold for obesity than for those who are only slightly obese. Thus obesity is a heterogeneous category, with much of the medical costs occurring among a small percentage of individuals with extremely high BMI. The results imply that obesity-attributable medical costs for non-institutionalized adults in the United States totaled $190.2 billion in 2005, or 20.6 percent of national health expenditures. These estimates suggest that the magnitude of the obesity-related externalities imposed through public and private health insurance is greater than previously appreciated, and that historically the cost-effectiveness of methods of preventing and treating obesity may have been underestimated.

Given the effect of obesity on health, one would expect obese individuals to experience worse labor market outcomes than non-obese individuals. To estimate the effect of weight on wages, I estimate models of instrumental variables that exploit the heritable component of weight as a natural experiment using data from the National Longitudinal Survey of Youth (NLSY) 1979 Cohort. 9 I find that weight lowers wages for white females: an increase in weight of two standard deviations (roughly 64 pounds) is associated with 9 percent lower wages. In general, the labor market consequences of obesity are greater for women than for men, and greater for white females than for other females. Based on the NLSY data, it is impossible to say whether the labor market consequences of obesity are the result of relatively worse health impairing productivity, or to employer discrimination, but other studies suggest that discrimination plays an important role.

Some occupations and industries are more affected by employee obesity than others. For the military, fitness is an important job requirement and thus rising obesity is a particular concern. Johanna Catherine Maclean and I examine data from the National Health and Nutrition Examination Surveys and find that the percentage of age-eligible civilians who exceed the U.S. Army’s weight-for-height requirements more than doubled for men and tripled for women between 1959 and 2008. 10 Excess weight is now the primary reason that applicants to the military are rejected, and a coalition of retired generals and admirals has called obesity a threat to military readiness.

Policies to Prevent or Reduce Obesity

There are a staggering number of policies and programs to prevent and reduce obesity, and an important contribution that economists can make is to evaluate these programs’ effectiveness. For example, the Centers for Disease Control, the American Academy of Pediatrics, and the Institute of Medicine have called for increases in physical education (PE) for school children, despite a lack of evidence that it has any impact on youth weight. To assess how PE affects youth physical activity and obesity, Chad Meyerhoefer, David Newhouse and I exploit variation across states in PE requirements. 11 To minimize the risks of policy endogeneity or unobserved heterogeneity biasing the results, we control for a host of state characteristics, such as the prevalence of adult obesity, the socioeconomic status of residents, and resources provided to public schools. Using data on high school students from the Youth Risk Behavior Surveillance System (YRBSS) we find that increasing PE requirements increases physical activity among girls (not boys) but has no detectable effect on weight.

To complement that study of high school students, Meyerhoefer, David Frisvold and I estimate the impact of PE on elementary school children using data from the Early Childhood Longitudinal Study, Kindergarten Cohort (ECLS-K)12 . The results of the IV model that exploits variation over states and time in PE requirements indicate that an additional 60 minutes per week spent in PE reduces the probability of obesity in fifth graders by 4.8 percentage points. There is no significant effect in earlier grades, which could be attributable to differences in PE curriculum, variation of the treatment effect with age, or to several states instituting large PE requirements before the fifth grade wave, increasing the power of the instrument. Taken together, the results suggest that increasing PE requirements increases physical activity and decreases the risk of obesity for certain subgroups, but not for all students. However, the limitations of BMI are relevant here. The YRBSS and ECLS-K datasets contain only height and weight, but no information about body composition. It is possible that increased PE requirements increase muscle mass and decrease fat mass, with little net effect on weight.

An innovative approach is to offer obese individuals financial rewards for weight loss. Insurance companies may face lower claims and employers may experience lower job absenteeism and higher productivity if their enrollees or employees lose weight; as a result, these organizations are increasingly seeking a win-win solution by offering overweight individuals financial rewards for weight loss. In addition, people with time-inconsistent preferences may be willing to put their own money at risk, hoping that loss aversion will provide them with incentives to lose weight in order to get the money back. To evaluate the effectiveness of these approaches, Joshua Price and I examine outcomes in a workplace wellness program that offers financial rewards and deposit contracts for employee weight loss. 13 Interesting features of this program include its large sample size (2,635 workers across 24 work sites) and long duration (one year). We find that attrition in this program is high: 42.9 percent dropped out by the end of the first quarter, and 68.0 percent by the end of the year-long program. We find modest results in the program. Those offered financial rewards for weight loss have no higher year-end weight loss than those in the control group, and those who make deposit contracts have year-end weight loss that is roughly two pounds greater than that of the control group after adjusting for attrition. An important next step is to determine the optimal structure of such programs, such as the most cost-effective size of financial reward, what should be rewarded (loss of pounds, loss of fat, increase in physical activity), the optimal number and timing of measurements of progress, whether group challenges can be designed to create beneficial peer effects, and how to avoid creating incentives for the use of unhealthy methods of weight loss.

Discouraged by failed attempts at weight loss through dieting and exercise, substantial percentages of Americans have taken over-the-counter (OTC) weight loss products. There is very little, if any, evidence suggesting that these products are effective, and some have potentially fatal side effects. Rosemary Avery, Matthew Eisenberg and I study the impact of exposure to advertising on the probability of consuming such products using data from the Simmons National Consumer Survey merged with data on magazine and television advertising. 14 We measure the extent to which advertisements are deceptive using detailed guidelines developed by the Federal Trade Commission for this specific market. To address the targeting of ads, we control for each magazine read and each television show watched, and we identify the effect of exposure to advertising using changes over time in the number of ads within individual magazines and shows. We find little evidence that advertising of OTC weight loss products expands the size of the market. Instead, advertising seems to be a way to battle for market share.

Future Directions

Given the scarcity and low quality of data on calories consumed and calories expended, it may never be possible to affirm with any degree of certainty the percentage of the rise in obesity attributable to specific factors. However, it will continue to be important to exploit natural experiments in order to determine the extent to which economic variables such as food prices, income, and technological change affect the risk of obesity, and to estimate the various economic consequences of obesity. Measuring the effectiveness, and calculating the cost-effectiveness, of anti-obesity programs and policies will help ensure that the public and private sectors get the biggest “bang for the buck” from their expenditures on obesity prevention and treatment.

* Cawley is a Research Associate in the NBER’s Programs on Health Economics and Health Care and a Professor in the Departments of Policy Analysis and Management, and Economics, at Cornell University, where he co-directs the Institute on Health Economics, Health Behaviors and Disparities.


1. See, for example, Centers for Disease Control, “Deaths: Final Data for 2007,” National Vital Statistics Reports, 58(19) (2010) pp. 1-17; L. D. Johnston, P. M. O’Malley, J. G. Bachman, and J. E. Schulenberg, Monitoring the Future: National Results on Adolescent Drug Use, Overview of Key Findings, 2010. Ann Arbor: Institute for Social Research, The University of Michigan, 2011.

2. K. M. Flegal, M. D. Carroll, B. K. Kit, and C. L. Ogden. “Prevalence of obesity and trends in the distribution of body mass index among U.S. adults, 1999–2010.” Journal of the American Medical Association, 307(5) (2012), pp. E1–E7.

3. World Health Organization, Global Status Report on Noncommunicable Diseases, 2010. Geneva: World Health Organization, 2011.

4. J. Cawley and C. Ruhm, “The Economics of Risky Health Behaviors.” NBER Working Paper No. 17081, May 2011, and published as chapter 3 in Handbook of Health Economics, Volume 2, T. G. McGuire, M. V. Pauly, and P. P. Barros, eds., New York: Elsevier, 2012, pp. 95-199.

5. J. Cawley and R.V. Burkhauser, “Beyond BMI: The Value of More Accurate Measures of Fatness and Obesity in Social Science Research,” NBER Working Paper No. 12291, June 2006, published in Journal of Health Economics, 27(2) (2008), pp. 519-29.

6. R. V. Burkhauser, J. Cawley, and M. Schmeiser, “Differences in the U.S. Trends in the Prevalence of Obesity Based on Body Mass Index and Skinfold Thickness,” NBER Working Paper No. 15005, May 2009, published in Economics and Human Biology, 7(3) (2009), pp. 307-18.

7. J. Cawley, J. R. Moran, and K. I. Simon, “The Impact of Income on the Weight of Elderly Americans,” NBER Working Paper No. 14104, June 2008, published in Health Economics, 19(8) (2010), pp. 979-93.

8. J. Cawley and C. Meyerhoefer, “The Medical Care Costs of Obesity: An Instrumental Variables Approach,” NBER Working Paper No. 16467, October 2010, published in the Journal of Health Economics, 31(1) (2012), pp. 219-30.

9. J. Cawley, “Body Weight and Women’s Labor Market Outcomes,” NBER Working Paper No. 7841, published as “The Impact of Obesity on Wages,” Journal of Human Resources, 39(2) (2004), pp. 451-74.

10. J. Cawley and J. C. Maclean, “Unfit for Service: The Implications of Rising Obesity for U.S. Military Recruitment,” NBER Working Paper No. 16408, September 2010, published in Health Economics, 21(11) (2012), pp. 1348-66.

11. J. Cawley, C. D. Meyerhoefer, and D. Newhouse, “The Impact of State Physical Education Requirements on Youth Physical Activity and Overweight,” NBER Working Paper No. 11411, June 2005, published in Health Economics, 16(12) (2007), pp. 1287-301.

12. J. Cawley, D. Frisvold, and C. Meyerhoefer, “The Impact of Physical Education on Obesity among Elementary School Children,” NBER Working Paper No. 18341, August 2012, published in the Journal of Health Economics, 32(4) (2013), pp. 743-55.

13. J. Cawley and J. A. Price, “Outcomes in a Program that Offers Financial Rewards for Weight Loss,” NBER Working Paper No. 14987, May 2009, and published as chapter 4 in Economic Aspects of Obesity, M. Grossman and N. Mocan eds., Chicago, IL: University of Chicago Press, 2011, pp. 91-126. See also J. Cawley and J. A. Price, “A Case Study of a Workplace Wellness Program That Offers Financial Incentives for Weight Loss.” Journal of Health Economics, 32(5) (2013), pp. 794-803.

14. J. Cawley, R. J. Avery, and M. Eisenberg, “The Effect of Deceptive Advertising on Consumption of the Advertised Good and its Substitutes: The Case of Over-the-Counter Weight Loss Products,” NBER Working Paper No. 18863, March 2013.

SOURCE

http://nber.org/reporter/2013number4/cawley.html

The Role of Medical Imaging in Personalized Medicine

Writer & reporter: Dror Nir, PhD

The future of personalized medicine comprise quantifiable diagnosis and tailored treatments; i.e. delivering the right treatment at the right time. To achieve standardized definition of what “right” means, the designated treatment location and lesion size are important factors. This is unrelated to whether the treatment is focused to a location or general. The role of medical imaging is and will continue to be vital in that respect: Patients’ stratification based on imaging biomarkers can help identify individuals suited for preventive intervention and can improve disease staging. In vivo visualization of loco-regional physiological, biochemical and biological processes using molecular imaging can detect diseases in pre-symptomatic phases or facilitate individualized drug delivery. Furthermore, as mentioned in most of my previous posts, imaging is essential to patient-tailored therapy planning, therapy monitoring, quantification of response-to-treatment and follow-up disease progression. Especially with the rise of companion diagnostics/theranostics (therapeutics & diagnostics), imaging and treatment will have to be synchronized in real-time to achieve the best control/guidance of the treatment.

It is worthwhile noting that the new RECIST 1.1 criteria (used in oncological therapy monitoring) have been expanded to include the use of PET (in addition to lymph-node evaluation).

pet

In previous posts I already discussed many examples concerning the use of medical imaging in personalized medicine: e.g. patients’ stratification; Imaging-biomarkers is Imaging-based tissue characterization, the future of imaging-biomarkers in diagnostic; Ultrasound-based Screening for Ovarian Cancer, imaging-based guided therapies; Minimally invasive image-guided therapy for inoperable hepatocellular carcinoma, treatment follow-up; the importance of spatially-localized and quantified image interpretation in cancer management, and imaging-based assessment of response to treatment; Causes and imaging features of false positives and false negatives on 18F-PET/CT in oncologic imaging

Browsing through our collaborative open-source initiative one can find many more articles and discussions on that matter; e.g. Tumor Imaging and Targeting: Predicting Tumor Response to Treatment: Where we stand?, In Search of Clarity on Prostate Cancer Screening, Post-Surgical Followup, and Prediction of Long Term Remission

In this post I would like to highlight the potential contribution of medical imaging to development of companion diagnostics. I do that through the story on co-development of Vintafolide (EC145) and etarfolatide (Endocyte/Merck). Etarfolatide is a folate-targeted molecular radiodiagnostic imaging agent that identifies tumors that overexpress the folate receptor. The folate receptor, a glycosylphosphatidylinositol anchored cell surface receptor, is overexpressed on the vast majority of cancer tissues, while its expression is limited in healthy tissues and organs. Folate receptors are highly expressed in epithelial, ovarian, cervical, breast, lung, kidney, colorectal, and brain tumors. When expressed in normal tissue, folate receptors are restricted to the lungs, kidneys, placenta, and choroid plexus. In these tissues, the receptors are limited to the apical surface of polarized epithelia. Folate, also known as pteroylglutamate, is a non-immunogenic water-soluble B vitamin that is critical to DNA synthesis, methylation, and repair (folate is used to synthesize thymine).

Vintafolide (EC145) delivers a very potent vinca chemotherapy directly to cancer cells by targeting the folate receptor expressed on cancer cells. Approximately 80-90 percent of ovarian and lung cancers express the receptor, as do many other types of cancer. Clinical data have shown that patients with metastases that are all positive for the folate receptor, identified by etarfolatide, benefited the most from the treatment with vintafolide, the corresponding folate-targeted small molecule drug conjugate.

Having both drug and imaging agent rely on folate receptors within the patients body Endocyte’s strategy was to develop the imaging agent and to use it to accelerate R&D and regulation. Endocyte and Merck entered into a partnership for vintafolide in April 2012. Under this partnership Merck was granted an exclusive license to develop, manufacture and commercialize vintafolide. Endocyte is responsible for conducting the PROCEED Phase 3 clinical study in women with platinum resistant ovarian cancer and the Phase 2b second line NSCLC (non-small cell lung cancer) study named TARGET. Merck is responsible for further clinical studies in additional indications. This Co-development of a diagnostic and therapeutic agent, was conducted according to the FDA guidance on personalized medicine and resulted with vintafolide gaining, already in 2012, status of orphan drug in EMA.

 

 The following is an extract from a post by Phillip H. Kuo, MD, PhD, associate professor of medical imaging, medicine, and biomedical engineering; section chief of nuclear medicine; and director of PET/CT at the University of Arizona Cancer Center.

 0213-figure-1

Figure 1 — Targeted Radioimaging Diagnostic and Small Molecule Drug Conjugate

Etarfolatide is comprised of the targeting ligand folic acid (yellow), which has a high folate receptor binding affinity, and a Technetium-99m–based radioimaging agent (turquoise). Etarfolatide identifies metastases that express the folate receptor protein in real time (A). The folic acid-targeting ligand is identical to that found on vintafolide, the corresponding therapeutic small molecule drug conjugate, which also contains a linker system (blue) and a potent chemotherapeutic drug (red) (B).

 

 vinta

Figure 2 — Whole-Body Scan With 111In-DTPA-Folate 

Diagnostic images of whole-body scans obtained following administration of the targeted radioimaging agent 111In-DTPA-folate, which is constructed with the same folic acid ligand as that engineered in etarfolatide. The healthy patient image on the left shows no folate receptor-positive abdominal tumor. Instead, only healthy kidneys (involved in excretion) are revealed. The patient on the right shows folate receptor-positive tumors in the abdomen and pelvis. Patients with metastases, identified with the companion imaging diagnostic etarfolatide as folate receptor-positive are most likely to respond to treatment with the corresponding small molecular drug conjugate vintafolide. Note: Vintafolide currently is being evaluated in a phase 3 clinical trial for platinum-resistant ovarian cancer and a phase 2 trial for non–small-cell lung cancer. Both studies also are using etarfolatide.

0213-figure-3

Figure 3 — Vintafolide’s Mechanism of Action

Folate is required for cell division, and rapidly dividing cancer cells often express folate receptors to capture enough folate to support rapid cell growth. Elevated expression of the folate receptor occurs in many human malignancies, especially when associated with aggressively growing cancers. The folate-targeted small molecule drug conjugate vintafolide binds to the folate receptor (A) and subsequently is internalized by a natural endocytosis process (B). Once inside the cell, vintafolide’s serum-stable linker selectively releases a potent vinca alkaloid compound (C) to arrest cell division and induce cell death.

Epilog

I think that those of you who reached this point in my post deserve a special bonus! So here it is: A medical-imaging initiative that is as ambitious and complex as the initiative to send humans into deep-space.

This is the The European Population Imaging Infrastructure initiative of the Dutch Federation of University Medical Centres (NFU) and the Erasmus University Medical Centre Rotterdam, Department of Radiology, chaired by Professor Gabriel P. Krestin. The NFU has made available initial funding for the development of this initiative.

The European Population Imaging Infrastructure closely cooperates with the European Biomedical Imaging Infrastructure Project EURO-BioImaging which is currently being developed.

The ultimate aim of the infrastructure is to help the development and implementation of strategies to prevent or effectively treat disease. It supports imaging in large, prospective epidemiological studies on the population level. Image specific markers of pre-symptomatic diseases can be used to investigate causes of pathological alterations and for the early identification of people at risk.

More information on this infrastructure and on the role of the European Population Imaging Infrastructure in this can be found in the Netherlands Roadmap for Large-Scale Research Facilities, the applicaton for funding of the Roadmap Large Scale Research Facilities Application form of the Roadmap EuroBioImaging, and on the Euro-BioImaging website.

Certainly, while making progress with this initiative, many lessons will be learned. I recommend to explore this site and Enjoy!

Cardiovascular Risk Reduction in Diabetes in Sub-Saharan Africa

Reporter and Curator: Larry H. Bernstein, MD, FCAP 

 

In the immediate preceding article we discussed the problem of small subsistence farming and dependence on crop, and milk as a main source of food. We discussed the dilemma of unavailability of adequate nutrition, that posed a dilemma.  Insects invade and destroy the vegetation.  That can be avoided by either of two choices, crop-treatment with pesticide or by GMO crops resistant to types of destruction, both having unaffordable costs that impose an austere challenge and abject poverty with marginal after sales gains, in no way comparable to farming in Iowa, Wisconsin, Minnesota, or California, U.S.  So the situation could be improved by the introduction of/or development of a practical genome-based synthetic tehnology that might be free of Western dominance, if there were the home-based universities and scientific research.
I also touched on the consequences of the malnutrition in that region because of a diet that imposes either marasmic or kwashiorkor-like feature, the distinction being made based on the body compartment related to loss of fat mass or the loss of lean body mass, the latter being more serious.

Cardiovascular Risk Reduction in Diabetes in Sub-Saharan Africa

The abstract of this discussion is directly taken from an article published in Clinical Medicine Insights: Cardiology; 2008: 2: 25-31,  Libertas Academica, ISSN(s):1178-1165.  Added to DOAJ: 2008-05-01
http://la-press.com/article.php?article_id=529

Cardiovascular Risk Reduction in Diabetes in Sub-Saharan Africa: What should the Priorities be in the Absence of Global Risk Evaluation Tools?

Subjects: Diseases of the circulatory (Cardiovascular) system, Specialties of internal medicine, Internal medicine, Medicine, Cardiovascular, Medicine (General), Health Sciences
Andre Pascal Kengne, Alfred Kongnyu Njamnshi, Jean Claude Mbanya

Keywords: diabetes mellitus, cardiovascular disease, risk factors, prevention, Sub-Saharan Africa

Background

The growing burden of type 2 diabetes in Sub-Saharan Africa (SSA) and related cardiovascular complications call for vigorous actions into prevention. Comprehensive cardiovascular risk evaluation is important for the success of such actions.

Methods

We have reviewed 3 currently existing sets of recommendations for cardiovascular prevention in diabetes in SSA. Distribution of major risk factors and patterns of reported cardiovascular outcomes are used to suggest orientations for cardiovascular prevention in diabetes in this region. Papers and reports published over the period 1990 to 2007 were used.

Results

Existing guidelines share some similarities, but also have areas of inconsistencies. They are generally adaptations of existing guidelines, focused more on individual risk factors, and are not usually backed-up by local evidence.

  • They all have a projection on blood pressure lowering.

This focus is supported by the high prevalence of hypertension among people with diabetes in SSA.

  • Blood pressure and tobacco smoking are the modifiable risk factors accessible to evaluation and interventions on a wide scale in SSA.

Appropriate blood pressure control will have a major impact on stroke (the commonest cardiovascular disease) through

  • a reduction of the cerebrovascular risk, and
  • to a lesser extent on coronary heart disease and
  • total deaths in diabetes in this region.

Conclusions

In the absence of global risk evaluation tools,

  • the use of blood pressure lowering as a primary focus of cardiovascular prevention strategies is relevant for SSA.

However, there is a need to set-up diabetes and stroke registers

  • to monitor outcomes and generate tools for accurate risk prediction and management in diabetes in this region.

Publications on Heart Failure by Prof. William Gregory Stevenson, M.D., BWH

Reporter: Aviva Lev-Ari, PhD, RN

 

Prof. William Gregory Stevenson, M.D.

Title Professor of Medicine
Institution Brigham and Women’s Hospital
Department Medicine
Address Brigham and Women’s Hospital Cardiovascular 75 Francis St Boston MA 02115
Phone 617/732-7535
Fax 617/732-7134
  1. Givertz MM, Teerlink JR, Albert NM, Westlake Canary CA, Collins SP, Colvin-Adams M, Ezekowitz JA, Fang JC, Hernandez AF, Katz SD, Krishnamani R, Stough WG, Walsh MN, Butler J, Carson PE, Dimarco JP, Hershberger RE, Rogers JG, Spertus JA, Stevenson WG, Sweitzer NK, Tang WH, Starling RC. Acute decompensated heart failure: update on new and emerging evidence and directions for future research. J Card Fail. 2013 Jun; 19(6):371-89.
    View in: PubMed
  2. Tokuda M, Kojodjojo P, Tung S, Tedrow UB, Nof E, Inada K, Koplan BA, Michaud GF, John RM, Epstein LM, Stevenson WG. Acute failure of catheter ablation for ventricular tachycardia due to structural heart disease: causes and significance. J Am Heart Assoc. 2013; 2(3):e000072.
    View in: PubMed
  3. Ng J, Barbhaiya C, Chopra N, Reichlin T, Nof E, Tadros T, Stevenson WG, John RM. Automatic external defibrillators-friend or foe? Am J Emerg Med. 2013 Aug; 31(8):1292.e1-2.
    View in: PubMed
  4. Steven D, Sultan A, Reddy V, Luker J, Altenburg M, Hoffmann B, Rostock T, Servatius H, Stevenson WG, Willems S, Michaud GF. Benefit of pulmonary vein isolation guided by loss of pace capture on the ablation line: results from a prospective 2-center randomized trial. J Am Coll Cardiol. 2013 Jul 2; 62(1):44-50.
    View in: PubMed
  5. Kojodjojo P, Tokuda M, Bohnen M, Michaud GF, Koplan BA, Epstein LM, Albert CM, John RM, Stevenson WG, Tedrow UB. Electrocardiographic left ventricular scar burden predicts clinical outcomes following infarct-related ventricular tachycardia ablation. Heart Rhythm. 2013 Aug; 10(8):1119-24.
    View in: PubMed
  6. Nof E, Stevenson WG, Epstein LM, Tedrow UB, Koplan BA. Catheter Ablation of Atrial Arrhythmias After Cardiac Transplantation: Findings at EP Study Utility of 3-D Mapping and Outcomes. J Cardiovasc Electrophysiol. 2013 May; 24(5):498-502.
    View in: PubMed
  7. Michaud GF, Stevenson WG. Feeling a little loopy? J Cardiovasc Electrophysiol. 2013 May; 24(5):553-5.
    View in: PubMed
  8. Epstein AE, Dimarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Tracy CM, Epstein AE, Darbar D, Dimarco JP, Dunbar SB, Estes NA, Ferguson TB, Hammill SC, Karasik PE, Link MS, Marine JE, Schoenfeld MH, Shanker AJ, Silka MJ, Stevenson LW, Stevenson WG, Varosy PD, Anderson JL, Jacobs AK, Halperin JL, Albert NM, Creager MA, Demets D, Ettinger SM, Guyton RA, Hochman JS, Kushner FG, Ohman EM, Stevenson W, Yancy CW. 2012 ACCF/AHA/HRS Focused Update Incorporated Into the ACCF/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation. 2013 Jan 22; 127(3):e283-352.
    View in: PubMed
  9. Tracy CM, Epstein AE, Darbar D, Dimarco JP, Dunbar SB, Mark Estes NA, Ferguson TB, Hammill SC, Karasik PE, Link MS, Marine JE, Schoenfeld MH, Shanker AJ, Silka MJ, Stevenson LW, Stevenson WG, Varosy PD, Epstein AE, Dimarco JP, Ellenbogen KA, Mark Estes NA, Freedman RA, Gettes LS, Marc Gillinov A, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Kristin Newby L, Page RL, Schoenfeld MH, Silka MJ, Warner Stevenson L, Sweeney MO, Anderson JL, Jacobs AK, Halperin JL, Albert NM, Creager MA, Demets D, Ettinger SM, Guyton RA, Hochman JS, Kushner FG, Ohman EM, Stevenson W, Yancy CW. 2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Thorac Cardiovasc Surg. 2012 Dec; 144(6):e127-45.
    View in: PubMed
  10. John RM, Tedrow UB, Koplan BA, Albert CM, Epstein LM, Sweeney MO, Miller AL, Michaud GF, Stevenson WG. Ventricular arrhythmias and sudden cardiac death. Lancet. 2012 Oct 27; 380(9852):1520-9.
    View in: PubMed
  11. Tracy CM, Epstein AE, Darbar D, DiMarco JP, Dunbar SB, Estes NA, Ferguson TB, Hammill SC, Karasik PE, Link MS, Marine JE, Schoenfeld MH, Shanker AJ, Silka MJ, Stevenson LW, Stevenson WG, Varosy PD, Ellenbogen KA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hayes DL, Page RL, Stevenson LW, Sweeney MO. 2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2012 Oct 2; 126(14):1784-800.
    View in: PubMed
  12. Tracy CM, Epstein AE, Darbar D, Dimarco JP, Dunbar SB, Estes NA, Ferguson TB, Hammill SC, Karasik PE, Link MS, Marine JE, Schoenfeld MH, Shanker AJ, Silka MJ, Stevenson LW, Stevenson WG, Varosy PD. 2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Heart Rhythm. 2012 Oct; 9(10):1737-53.
    View in: PubMed
  13. Tokuda M, Tedrow UB, Kojodjojo P, Inada K, Koplan BA, Michaud GF, John RM, Epstein LM, Stevenson WG. Catheter ablation of ventricular tachycardia in nonischemic heart disease. Circ Arrhythm Electrophysiol. 2012 Oct 1; 5(5):992-1000.
    View in: PubMed
  14. John RM, Stevenson WG. Ventricular arrhythmias in patients with implanted cardioverter defibrillators. Trends Cardiovasc Med. 2012 Oct; 22(7):169-73.
    View in: PubMed
  15. Waldo AL, Wilber DJ, Marchlinski FE, Stevenson WG, Aker B, Boo LM, Jackman WM. Safety of the open-irrigated ablation catheter for radiofrequency ablation: safety analysis from six clinical studies. Pacing Clin Electrophysiol. 2012 Sep; 35(9):1081-9.
    View in: PubMed
  16. Tedrow UB, Sobieszczyk P, Stevenson WG. Transvenous ethanol ablation of ventricular tachycardia. Heart Rhythm. 2012 Oct; 9(10):1640-1.
    View in: PubMed
  17. Stevenson WG, Tedrow UB. Ablation for ventricular tachycardia during stable sinus rhythm. Circulation. 2012 May 8; 125(18):2175-7.
    View in: PubMed
  18. Wissner E, Stevenson WG, Kuck KH. Catheter ablation of ventricular tachycardia in ischaemic and non-ischaemic cardiomyopathy: where are we today? A clinical review. Eur Heart J. 2012 Jun; 33(12):1440-50.
    View in: PubMed
  19. Vollmann D, Stevenson WG, Lüthje L, Sohns C, John RM, Zabel M, Michaud GF. Misleading long post-pacing interval after entrainment of typical atrial flutter from the cavotricuspid isthmus. J Am Coll Cardiol. 2012 Feb 28; 59(9):819-24.
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  20. Stevenson WG, Hernandez AF, Carson PE, Fang JC, Katz SD, Spertus JA, Sweitzer NK, Tang WH, Albert NM, Butler J, Westlake Canary CA, Collins SP, Colvin-Adams M, Ezekowitz JA, Givertz MM, Hershberger RE, Rogers JG, Teerlink JR, Walsh MN, Stough WG, Starling RC. Indications for cardiac resynchronization therapy: 2011 update from the Heart Failure Society of America Guideline Committee. J Card Fail. 2012 Feb; 18(2):94-106.
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  21. Inada K, Tokuda M, Roberts-Thomson KC, Steven D, Seiler J, Tedrow UB, Stevenson WG. Relation of high-pass filtered unipolar electrograms to bipolar electrograms during ventricular mapping. Pacing Clin Electrophysiol. 2012 Feb; 35(2):157-63.
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  22. Albert CM, Chen PS, Anderson ME, Cain ME, Fishman GI, Narayan SM, Olgin JE, Spooner PM, Stevenson WG, Van Wagoner DR, Packer DL. Full report from the first annual Heart Rhythm Society Research Forum: a vision for our research future, “dream, discover, develop, deliver”. Heart Rhythm. 2011 Dec; 8(12):e1-12.
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  23. Stevenson WG, John RM. Ventricular arrhythmias in patients with implanted defibrillators. Circulation. 2011 Oct 18; 124(16):e411-4.
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  24. Tokuda M, Sobieszczyk P, Eisenhauer AC, Kojodjojo P, Inada K, Koplan BA, Michaud GF, John RM, Epstein LM, Sacher F, Stevenson WG, Tedrow UB. Transcoronary ethanol ablation for recurrent ventricular tachycardia after failed catheter ablation: an update. Circ Arrhythm Electrophysiol. 2011 Dec; 4(6):889-96.
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  25. John RM, Stevenson WG. Catheter-based ablation for ventricular arrhythmias. Curr Cardiol Rep. 2011 Oct; 13(5):399-406.
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  26. Martinek M, Stevenson WG, Inada K, Tokuda M, Tedrow UB. QRS characteristics fail to reliably identify ventricular tachycardias that require epicardial ablation in ischemic heart disease. J Cardiovasc Electrophysiol. 2012 Feb; 23(2):188-93.
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  27. Asimaki A, Tandri H, Duffy ER, Winterfield JR, Mackey-Bojack S, Picken MM, Cooper LT, Wilber DJ, Marcus FI, Basso C, Thiene G, Tsatsopoulou A, Protonotarios N, Stevenson WG, McKenna WJ, Gautam S, Remick DG, Calkins H, Saffitz JE. Altered desmosomal proteins in granulomatous myocarditis and potential pathogenic links to arrhythmogenic right ventricular cardiomyopathy. Circ Arrhythm Electrophysiol. 2011 Oct; 4(5):743-52.
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  28. Wijnmaalen AP, Roberts-Thomson KC, Steven D, Klautz RJ, Willems S, Schalij MJ, Stevenson WG, Zeppenfeld K. Catheter ablation of ventricular tachycardia after left ventricular reconstructive surgery for ischemic cardiomyopathy. Heart Rhythm. 2012 Jan; 9(1):10-7.
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  29. Stevenson WG, Couper GS. A surgical option for ventricular tachycardia caused by nonischemic cardiomyopathy. Circ Arrhythm Electrophysiol. 2011 Aug; 4(4):429-31.
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  30. Tokuda M, Kojodjojo P, Epstein LM, Koplan BA, Michaud GF, Tedrow UB, Stevenson WG, John RM. Outcomes of cardiac perforation complicating catheter ablation of ventricular arrhythmias. Circ Arrhythm Electrophysiol. 2011 Oct; 4(5):660-6.
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  31. Kosmidou I, Inada K, Seiler J, Koplan B, Stevenson WG, Tedrow UB. Role of repeat procedures for catheter ablation of postinfarction ventricular tachycardia. Heart Rhythm. 2011 Oct; 8(10):1516-22.
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  32. Bohnen M, Stevenson WG, Tedrow UB, Michaud GF, John RM, Epstein LM, Albert CM, Koplan BA. Incidence and predictors of major complications from contemporary catheter ablation to treat cardiac arrhythmias. Heart Rhythm. 2011 Nov; 8(11):1661-6.
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  33. Wijnmaalen AP, Stevenson WG, Schalij MJ, Field ME, Stephenson K, Tedrow UB, Koplan BA, Putter H, Epstein LM, Zeppenfeld K. ECG identification of scar-related ventricular tachycardia with a left bundle-branch block configuration. Circ Arrhythm Electrophysiol. 2011 Aug; 4(4):486-93.
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  34. Steven D, Roberts-Thomson KC, Inada K, Seiler J, Koplan BA, Tedrow UB, Sweeney MO, Epstein LE, Stevenson WG. Long-term follow-up in patients with presumptive Brugada syndrome treated with implanted defibrillators. J Cardiovasc Electrophysiol. 2011 Oct; 22(10):1115-9.
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  35. Bohnen M, Shea JB, Michaud GF, John R, Stevenson WG, Epstein LM, Tedrow UB, Albert C, Koplan BA. Quality of life with atrial fibrillation: do the spouses suffer as much as the patients? Pacing Clin Electrophysiol. 2011 Jul; 34(7):804-9.
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  36. Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, Halperin JL, Kay GN, Le Huezey JY, Lowe JE, Olsson SB, Prystowsky EN, Tamargo JL, Wann LS, Smith SC, Priori SG, Estes NA, Ezekowitz MD, Jackman WM, January CT, Lowe JE, Page RL, Slotwiner DJ, Stevenson WG, Tracy CM, Jacobs AK, Anderson JL, Albert N, Buller CE, Creager MA, Ettinger SM, Guyton RA, Halperin JL, Hochman JS, Kushner FG, Ohman EM, Stevenson WG, Tarkington LG, Yancy CW. 2011 ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2011 Mar 15; 123(10):e269-367.
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  37. Wann LS, Curtis AB, Ellenbogen KA, Estes NA, Ezekowitz MD, Jackman WM, January CT, Lowe JE, Page RL, Slotwiner DJ, Stevenson WG, Tracy CM, Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, Halperin JL, Kay GN, Le Heuzey JY, Lowe JE, Olsson SB, Prystowsky EN, Tamargo JL, Wann LS, Jacobs AK, Anderson JL, Albert N, Creager MA, Ettinger SM, Guyton RA, Halperin JL, Hochman JS, Kushner FG, Ohman EM, Stevenson WG, Yancy CW. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update on Dabigatran): a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2011 Mar 15; 123(10):1144-50.
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  38. Wann LS, Curtis AB, Ellenbogen KA, Estes NA, Ezekowitz MD, Jackman WM, January CT, Lowe JE, Page RL, Slotwiner DJ, Stevenson WG, Tracy CM. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update on dabigatran): a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. J Am Coll Cardiol. 2011 Mar 15; 57(11):1330-7.
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  39. Wann LS, Curtis AB, Ellenbogen KA, Estes NA, Ezekowitz MD, Jackman WM, January CT, Lowe JE, Page RL, Slotwiner DJ, Stevenson WG, Tracy CM, Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, Halperin JL, Kay GN, Le Heuzey JY, Lowe JE, Olsson SB, Prystowsky EN, Tamargo JL, Wann LS, Jacobs AK, Anderson JL, Albert N, Creager MA, Ettinger SM, Guyton RA, Halperin JL, Hochman JS, Kushner FG, Ohman EM, Stevenson WG, Yancy CW. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update on dabigatran). A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Heart Rhythm. 2011 Mar; 8(3):e1-8.
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  40. Dukkipati SR, d’Avila A, Soejima K, Bala R, Inada K, Singh S, Stevenson WG, Marchlinski FE, Reddy VY. Long-term outcomes of combined epicardial and endocardial ablation of monomorphic ventricular tachycardia related to hypertrophic cardiomyopathy. Circ Arrhythm Electrophysiol. 2011 Apr; 4(2):185-94.
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  41. Tedrow UB, Stevenson WG. Recording and interpreting unipolar electrograms to guide catheter ablation. Heart Rhythm. 2011 May; 8(5):791-6.
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  42. Wann LS, Curtis AB, January CT, Ellenbogen KA, Lowe JE, Estes NA, Page RL, Ezekowitz MD, Slotwiner DJ, Jackman WM, Stevenson WG, Tracy CM, Fuster V, Rydén LE, Cannom DS, Le Heuzey JY, Crijns HJ, Lowe JE, Curtis AB, Olsson SB, Ellenbogen KA, Prystowsky EN, Halperin JL, Tamargo JL, Kay GN, Wann LS, Jacobs AK, Anderson JL, Albert N, Hochman JS, Buller CE, Kushner FG, Creager MA, Ohman EM, Ettinger SM, Stevenson WG, Guyton RA, Tarkington LG, Halperin JL, Yancy CW. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (Updating the 2006 Guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2011 Jan 11; 57(2):223-42.
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  43. Wann LS, Curtis AB, January CT, Ellenbogen KA, Lowe JE, Estes NA, Page RL, Ezekowitz MD, Slotwiner DJ, Jackman WM, Stevenson WG, Tracy CM, Fuster V, Rydén LE, Cannom DS, Le Heuzey JY, Crijns HJ, Lowe JE, Curtis AB, Olsson S, Ellenbogen KA, Prystowsky EN, Halperin JL, Tamargo JL, Kay GN, Wann LS, Jacobs AK, Anderson JL, Albert N, Hochman JS, Buller CE, Kushner FG, Creager MA, Ohman EM, Ettinger SM, Stevenson WG, Guyton RA, Tarkington LG, Halperin JL, Yancy CW. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (Updating the 2006 Guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Heart Rhythm. 2011 Jan; 8(1):157-76.
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  44. Wann LS, Curtis AB, January CT, Ellenbogen KA, Lowe JE, Estes NA, Page RL, Ezekowitz MD, Slotwiner DJ, Jackman WM, Stevenson WG, Tracy CM, Fuster V, Rydén LE, Cannom DS, Le Heuzey JY, Crijns HJ, Lowe JE, Curtis AB, Olsson S, Ellenbogen KA, Prystowsky EN, Halperin JL, Tamargo JL, Kay GN, Wann L, Jacobs AK, Anderson JL, Albert N, Hochman JS, Buller CE, Kushner FG, Creager MA, Ohman EM, Ettinger SM, Stevenson WG, Guyton RA, Tarkington LG, Halperin JL, Yancy CW. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (updating the 2006 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011 Jan 4; 123(1):104-23.
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  45. Stevenson WG, Asirvatham SJ. Teaching rounds in cardiac electrophysiology. Circ Arrhythm Electrophysiol. 2010 Dec; 3(6):563.
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  46. Rosman JZ, John RM, Stevenson WG, Epstein LM, Tedrow UB, Koplan BA, Albert CM, Michaud GF. Resetting criteria during ventricular overdrive pacing successfully differentiate orthodromic reentrant tachycardia from atrioventricular nodal reentrant tachycardia despite interobserver disagreement concerning QRS fusion. Heart Rhythm. 2011 Jan; 8(1):2-7.
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  47. Gautam S, John RM, Stevenson WG, Jain R, Epstein LM, Tedrow U, Koplan BA, McClennen S, Michaud GF. Effect of therapeutic INR on activated clotting times, heparin dosage, and bleeding risk during ablation of atrial fibrillation. J Cardiovasc Electrophysiol. 2011 Mar; 22(3):248-54.
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  48. Inada K, Seiler J, Roberts-Thomson KC, Steven D, Rosman J, John RM, Sobieszczyk P, Stevenson WG, Tedrow UB. Substrate characterization and catheter ablation for monomorphic ventricular tachycardia in patients with apical hypertrophic cardiomyopathy. J Cardiovasc Electrophysiol. 2011 Jan; 22(1):41-8.
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  49. Sacher F, Roberts-Thomson K, Maury P, Tedrow U, Nault I, Steven D, Hocini M, Koplan B, Leroux L, Derval N, Seiler J, Wright MJ, Epstein L, Haissaguerre M, Jais P, Stevenson WG. Epicardial ventricular tachycardia ablation a multicenter safety study. J Am Coll Cardiol. 2010 May 25; 55(21):2366-72.
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  50. Britton KA, Stevenson WG, Levy BD, Katz JT, Loscalzo J. Clinical problem-solving. The beat goes on. N Engl J Med. 2010 May 6; 362(18):1721-6.
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  51. Ross JJ, Britton KA, Desai AS, Stevenson WG. Interactive medical case. The beat goes on. N Engl J Med. 2010 Apr 15; 362(15):e53.
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  52. Tedrow UB, Stevenson WG. Arrhythmias: Catheter ablation for prevention of ventricular tachycardia. Nat Rev Cardiol. 2010 Apr; 7(4):181-2.
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  53. Sacher F, Wright M, Tedrow UB, O’Neill MD, Jais P, Hocini M, Macdonald R, Davies DW, Kanagaratnam P, Derval N, Epstein L, Peters NS, Stevenson WG, Haissaguerre M. Wolff-Parkinson-White ablation after a prior failure: a 7-year multicentre experience. Europace. 2010 Jun; 12(6):835-41.
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  54. Inada K, Roberts-Thomson KC, Seiler J, Steven D, Tedrow UB, Koplan BA, Stevenson WG. Mortality and safety of catheter ablation for antiarrhythmic drug-refractory ventricular tachycardia in elderly patients with coronary artery disease. Heart Rhythm. 2010 Jun; 7(6):740-4.
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  55. Steven D, Seiler J, Roberts-Thomson KC, Inada K, Stevenson WG. Mapping of atrial tachycardias after catheter ablation for atrial fibrillation: use of bi-atrial activation patterns to facilitate recognition of origin. Heart Rhythm. 2010 May; 7(5):664-72.
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  56. Stevenson WG, Tedrow U. Preventing ventricular tachycardia with catheter ablation. Lancet. 2010 Jan 2; 375(9708):4-6.
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  57. Al-Khatib SM, Calkins H, Eloff BC, Packer DL, Ellenbogen KA, Hammill SC, Natale A, Page RL, Prystowsky E, Jackman WM, Stevenson WG, Waldo AL, Wilber D, Kowey P, Yaross MS, Mark DB, Reiffel J, Finkle JK, Marinac-Dabic D, Pinnow E, Sager P, Sedrakyan A, Canos D, Gross T, Berliner E, Krucoff MW. Planning the Safety of Atrial Fibrillation Ablation Registry Initiative (SAFARI) as a Collaborative Pan-Stakeholder Critical Path Registry Model: a Cardiac Safety Research Consortium “Incubator” Think Tank. Am Heart J. 2010 Jan; 159(1):17-24.
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  58. Seiler J, Stevenson WG. Atrial fibrillation in congestive heart failure. Cardiol Rev. 2010 Jan-Feb; 18(1):38-50.
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  59. Steven D, Roberts-Thomson KC, Seiler J, Inada K, Tedrow UB, Mitchell RN, Sobieszczyk PS, Eisenhauer AC, Couper GS, Stevenson WG. Ventricular tachycardia arising from the aortomitral continuity in structural heart disease: characteristics and therapeutic considerations for an anatomically challenging area of origin. Circ Arrhythm Electrophysiol. 2009 Dec; 2(6):660-6.
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  60. Roberts-Thomson KC, Seiler J, Steven D, Inada K, Michaud GF, John RM, Koplan BA, Epstein LM, Stevenson WG, Tedrow UB. Percutaneous access of the epicardial space for mapping ventricular and supraventricular arrhythmias in patients with and without prior cardiac surgery. J Cardiovasc Electrophysiol. 2010 Apr; 21(4):406-11.
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  61. Steven D, Reddy VY, Inada K, Roberts-Thomson KC, Seiler J, Stevenson WG, Michaud GF. Loss of pace capture on the ablation line: a new marker for complete radiofrequency lesions to achieve pulmonary vein isolation. Heart Rhythm. 2010 Mar; 7(3):323-30.
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  62. Roberts-Thomson KC, Steven D, Seiler J, Inada K, Koplan BA, Tedrow UB, Epstein LM, Stevenson WG. Coronary artery injury due to catheter ablation in adults: presentations and outcomes. Circulation. 2009 Oct 13; 120(15):1465-73.
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  63. See VY, Roberts-Thomson KC, Stevenson WG, Camp PC, Koplan BA. Atrial arrhythmias after lung transplantation: epidemiology, mechanisms at electrophysiology study, and outcomes. Circ Arrhythm Electrophysiol. 2009 Oct; 2(5):504-10.
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  64. Stevenson WG, Saltzman JR. Gastroesophageal reflux and atrial-esophageal fistula. Heart Rhythm. 2009 Oct; 6(10):1463-4.
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  65. Aliot EM, Stevenson WG, Almendral-Garrote JM, Bogun F, Calkins CH, Delacretaz E, Della Bella P, Hindricks G, Jaïs P, Josephson ME, Kautzner J, Kay GN, Kuck KH, Lerman BB, Marchlinski F, Reddy V, Schalij MJ, Schilling R, Soejima K, Wilber D. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). Heart Rhythm. 2009 Jun; 6(6):886-933.
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  66. Aliot EM, Stevenson WG, Almendral-Garrote JM, Bogun F, Calkins CH, Delacretaz E, Bella PD, Hindricks G, Jaïs P, Josephson ME, Kautzner J, Kay GN, Kuck KH, Lerman BB, Marchlinski F, Reddy V, Schalij MJ, Schilling R, Soejima K, Wilber D. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). Europace. 2009 Jun; 11(6):771-817.
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  67. Raymond JM, Sacher F, Winslow R, Tedrow U, Stevenson WG. Catheter ablation for scar-related ventricular tachycardias. Curr Probl Cardiol. 2009 May; 34(5):225-70.
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  68. Lee JC, Steven D, Roberts-Thomson KC, Raymond JM, Stevenson WG, Tedrow UB. Atrial tachycardias adjacent to the phrenic nerve: recognition, potential problems, and solutions. Heart Rhythm. 2009 Aug; 6(8):1186-91.
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  69. Steven D, Roberts-Thomson KC, Seiler J, Michaud GF, John RM, Stevenson WG. Fibrillation in the superior vena cava mimicking atrial tachycardia. Circ Arrhythm Electrophysiol. 2009 Apr; 2(2):e4-7.
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  70. Roberts-Thomson KC, Seiler J, Steven D, Inada K, John R, Michaud G, Stevenson WG. Short AV response to atrial extrastimuli during narrow complex tachycardia: what is the mechanism? J Cardiovasc Electrophysiol. 2009 Aug; 20(8):946-8.
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  71. Koplan BA, Stevenson WG. Ventricular tachycardia and sudden cardiac death. Mayo Clin Proc. 2009 Mar; 84(3):289-97.
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  72. Khairy P, Stevenson WG. Catheter ablation in tetralogy of Fallot. Heart Rhythm. 2009 Jul; 6(7):1069-74.
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  73. Stevenson WG, Tedrow UB, Koplan BA. Management of ventricular tachycardia complicating cardiac surgery. Heart Rhythm. 2009 Aug; 6(8 Suppl):S66-9.
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  74. Lee JC, Epstein LM, Huffer LL, Stevenson WG, Koplan BA, Tedrow UB. ICD lead proarrhythmia cured by lead extraction. Heart Rhythm. 2009 May; 6(5):613-8.
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  75. Tedrow U, Stevenson WG. Strategies for epicardial mapping and ablation of ventricular tachycardia. J Cardiovasc Electrophysiol. 2009 Jun; 20(6):710-3.
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  76. Stevenson WG. Ventricular scars and ventricular tachycardia. Trans Am Clin Climatol Assoc. 2009; 120:403-12.
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  77. Stevenson WG, Wilber DJ, Natale A, Jackman WM, Marchlinski FE, Talbert T, Gonzalez MD, Worley SJ, Daoud EG, Hwang C, Schuger C, Bump TE, Jazayeri M, Tomassoni GF, Kopelman HA, Soejima K, Nakagawa H. Irrigated radiofrequency catheter ablation guided by electroanatomic mapping for recurrent ventricular tachycardia after myocardial infarction: the multicenter thermocool ventricular tachycardia ablation trial. Circulation. 2008 Dec 16; 118(25):2773-82.
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  78. Seiler J, Lee JC, Roberts-Thomson KC, Stevenson WG. Intracardiac echocardiography guided catheter ablation of incessant ventricular tachycardia from the posterior papillary muscle causing tachycardia–mediated cardiomyopathy. Heart Rhythm. 2009 Mar; 6(3):389-92.
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  79. Eckart RE, Field ME, Hruczkowski TW, Forman DE, Dorbala S, Di Carli MF, Albert CE, Maisel WH, Epstein LM, Stevenson WG. Association of electrocardiographic morphology of exercise-induced ventricular arrhythmia with mortality. Ann Intern Med. 2008 Oct 7; 149(7):451-60, W82.
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  80. Goldberger JJ, Cain ME, Hohnloser SH, Kadish AH, Knight BP, Lauer MS, Maron BJ, Page RL, Passman RS, Siscovick D, Stevenson WG, Zipes DP. American Heart Association/american College of Cardiology Foundation/heart Rhythm Society scientific statement on noninvasive risk stratification techniques for identifying patients at risk for sudden cardiac death: a scientific statement from the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention. Heart Rhythm. 2008 Oct; 5(10):e1-21.
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  81. Goldberger JJ, Cain ME, Hohnloser SH, Kadish AH, Knight BP, Lauer MS, Maron BJ, Page RL, Passman RS, Siscovick D, Siscovick D, Stevenson WG, Zipes DP. American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society scientific statement on noninvasive risk stratification techniques for identifying patients at risk for sudden cardiac death: a scientific statement from the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention. Circulation. 2008 Sep 30; 118(14):1497-1518.
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  82. Goldberger JJ, Cain ME, Hohnloser SH, Kadish AH, Knight BP, Lauer MS, Maron BJ, Page RL, Passman RS, Siscovick D, Stevenson WG, Zipes DP. American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society Scientific Statement on Noninvasive Risk Stratification Techniques for Identifying Patients at Risk for Sudden Cardiac Death. A scientific statement from the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention. J Am Coll Cardiol. 2008 Sep 30; 52(14):1179-99.
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  83. Seiler J, Roberts-Thomson KC, Raymond JM, Vest J, Delacretaz E, Stevenson WG. Steam pops during irrigated radiofrequency ablation: feasibility of impedance monitoring for prevention. Heart Rhythm. 2008 Oct; 5(10):1411-6.
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  84. Roy D, Talajic M, Nattel S, Wyse DG, Dorian P, Lee KL, Bourassa MG, Arnold JM, Buxton AE, Camm AJ, Connolly SJ, Dubuc M, Ducharme A, Guerra PG, Hohnloser SH, Lambert J, Le Heuzey JY, O’Hara G, Pedersen OD, Rouleau JL, Singh BN, Stevenson LW, Stevenson WG, Thibault B, Waldo AL. Rhythm control versus rate control for atrial fibrillation and heart failure. N Engl J Med. 2008 Jun 19; 358(25):2667-77.
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  85. Sacher F, Tedrow UB, Field ME, Raymond JM, Koplan BA, Epstein LM, Stevenson WG. Ventricular tachycardia ablation: evolution of patients and procedures over 8 years. Circ Arrhythm Electrophysiol. 2008 Aug; 1(3):153-61.
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  86. Vest JA, Seiler J, Stevenson WG. Clinical use of cooled radiofrequency ablation. J Cardiovasc Electrophysiol. 2008 Jul; 19(7):769-73.
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  87. Stevenson WG, Berul CI. Arrhythmia and Electrophysiology: the eagle can land. Circ Arrhythm Electrophysiol. 2008 Apr; 1(1):1.
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  88. Roberts-Thomson KC, Seiler J, Raymond JM, Stevenson WG. Exercise induced tachycardia with atrioventricular dissociation: what is the mechanism? Heart Rhythm. 2009 Mar; 6(3):426-8.
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  89. Zeppenfeld K, Stevenson WG. Ablation of ventricular tachycardia in patients with structural heart disease. Pacing Clin Electrophysiol. 2008 Mar; 31(3):358-74.
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  90. Cooper JM, Sapp JL, Robinson D, Epstein LM, Stevenson WG. A rewarming maneuver demonstrates the contribution of blood flow to electrode cooling during internally irrigated RF ablation. J Cardiovasc Electrophysiol. 2008 Apr; 19(4):409-14.
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  91. Zeppenfeld K, Schalij MJ, Bartelings MM, Tedrow UB, Koplan BA, Soejima K, Stevenson WG. Catheter ablation of ventricular tachycardia after repair of congenital heart disease: electroanatomic identification of the critical right ventricular isthmus. Circulation. 2007 Nov 13; 116(20):2241-52.
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  92. Eckart RE, Hruczkowski TW, Tedrow UB, Koplan BA, Epstein LM, Stevenson WG. Sustained ventricular tachycardia associated with corrective valve surgery. Circulation. 2007 Oct 30; 116(18):2005-11.
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  93. Sacher F, Sobieszczyk P, Tedrow U, Eisenhauer AC, Field ME, Selwyn A, Raymond JM, Koplan B, Epstein LM, Stevenson WG. Transcoronary ethanol ventricular tachycardia ablation in the modern electrophysiology era. Heart Rhythm. 2008 Jan; 5(1):62-8.
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  94. Sacher F, Vest J, Raymond JM, Stevenson WG. Incessant donor-to-recipient atrial tachycardia after bilateral lung transplantation. Heart Rhythm. 2008 Jan; 5(1):149-51.
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  95. Sacher F, Vest J, Raymond JM, Stevenson WG. Atrial pacing inducing narrow QRS tachycardia followed by wide complex tachycardia. J Cardiovasc Electrophysiol. 2007 Nov; 18(11):1213-5.
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  96. Stevenson WG, Soejima K. Catheter ablation for ventricular tachycardia. Circulation. 2007 May 29; 115(21):2750-60.
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  97. Koplan BA, Stevenson WG. Sudden arrhythmic death syndrome. Heart. 2007 May; 93(5):547-8.
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  98. Parkash R, Stevenson WG. Atrial fibrillation and clinical events in chronic heart failure. J Am Coll Cardiol. 2007 Jan 23; 49(3):376; author reply 376-7.
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  99. Sacher F, Jais P, Stephenson K, O’Neill MD, Hocini M, Clementy J, Stevenson WG, Haissaguerre M. Phrenic nerve injury after catheter ablation of atrial fibrillation. Indian Pacing Electrophysiol J. 2007; 7(1):1-6.
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  100. Tedrow UB, Stevenson WG, Wood MA, Shepard RK, Hall K, Pellegrini CP, Ellenbogen KA. Activation sequence modification during cardiac resynchronization by manipulation of left ventricular epicardial pacing stimulus strength. Pacing Clin Electrophysiol. 2007 Jan; 30(1):65-9.
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  101. Dzau VJ, Antman EM, Black HR, Hayes DL, Manson JE, Plutzky J, Popma JJ, Stevenson W. The cardiovascular disease continuum validated: clinical evidence of improved patient outcomes: part I: Pathophysiology and clinical trial evidence (risk factors through stable coronary artery disease). Circulation. 2006 Dec 19; 114(25):2850-70.
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  102. Dzau VJ, Antman EM, Black HR, Hayes DL, Manson JE, Plutzky J, Popma JJ, Stevenson W. The cardiovascular disease continuum validated: clinical evidence of improved patient outcomes: part II: Clinical trial evidence (acute coronary syndromes through renal disease) and future directions. Circulation. 2006 Dec 19; 114(25):2871-91.
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  103. Stevenson WG, Tedrow U. Management of atrial fibrillation in patients with heart failure. Heart Rhythm. 2007 Mar; 4(3 Suppl):S28-30.
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  104. Tedrow U, Stevenson WG. Substrate mapping and the aging atrium. Heart Rhythm. 2007 Feb; 4(2):145-6.
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  105. Eckart RE, Hruczkowski TW, Stevenson WG, Epstein LM. Myopotentials leading to ventricular fibrillation detection after advisory defibrillator generator replacement. Pacing Clin Electrophysiol. 2006 Nov; 29(11):1273-6.
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  106. Perloff JK, Middlekauf HR, Child JS, Stevenson WG, Miner PD, Goldberg GD. Usefulness of post-ventriculotomy signal averaged electrocardiograms in congenital heart disease. Am J Cardiol. 2006 Dec 15; 98(12):1646-51.
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  107. Koplan BA, Epstein LM, Albert CM, Stevenson WG. Survival in octogenarians receiving implantable defibrillators. Am Heart J. 2006 Oct; 152(4):714-9.
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  108. Veenhuyzen GD, Hruczkowski T, Dhir SK, Stevenson WG. Another way to prove the presence and participation of an accessory pathway in supraventricular tachycardia? J Cardiovasc Electrophysiol. 2006 Oct; 17(10):1147-9.
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  109. Yan AT, Shayne AJ, Brown KA, Gupta SN, Chan CW, Luu TM, Di Carli MF, Reynolds HG, Stevenson WG, Kwong RY. Characterization of the peri-infarct zone by contrast-enhanced cardiac magnetic resonance imaging is a powerful predictor of post-myocardial infarction mortality. Circulation. 2006 Jul 4; 114(1):32-9.
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  110. Sapp JL, Cooper JM, Zei P, Stevenson WG. Large radiofrequency ablation lesions can be created with a retractable infusion-needle catheter. J Cardiovasc Electrophysiol. 2006 Jun; 17(6):657-61.
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  111. Field ME, Miyazaki H, Epstein LM, Stevenson WG. Narrow complex tachycardia after slow pathway ablation: continue ablating? J Cardiovasc Electrophysiol. 2006 May; 17(5):557-9.
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  112. Tedrow UB, Kramer DB, Stevenson LW, Stevenson WG, Baughman KL, Epstein LM, Lewis EF. Relation of right ventricular peak systolic pressure to major adverse events in patients undergoing cardiac resynchronization therapy. Am J Cardiol. 2006 Jun 15; 97(12):1737-40.
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  113. Ames A, Stevenson WG. Cardiology patient page. Catheter ablation of atrial fibrillation. Circulation. 2006 Apr 4; 113(13):e666-8.
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  114. Koplan BA, Soejima K, Baughman K, Epstein LM, Stevenson WG. Refractory ventricular tachycardia secondary to cardiac sarcoid: electrophysiologic characteristics, mapping, and ablation. Heart Rhythm. 2006 Aug; 3(8):924-9.
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  115. Zei PC, Stevenson WG. Epicardial catheter mapping and ablation of ventricular tachycardia. Heart Rhythm. 2006 Mar; 3(3):360-3.
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  116. Miyazaki H, Stevenson WG, Stephenson K, Soejima K, Epstein LM. Entrainment mapping for rapid distinction of left and right atrial tachycardias. Heart Rhythm. 2006 May; 3(5):516-23.
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  117. Parkash R, Stevenson WG, Epstein LM, Maisel WH. Predicting early mortality after implantable defibrillator implantation: a clinical risk score for optimal patient selection. Am Heart J. 2006 Feb; 151(2):397-403.
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  118. Stevenson WG, Epstein LM. Endpoints for ablation of atrial fibrillation. Heart Rhythm. 2006 Feb; 3(2):146-7.
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  119. Stevenson LW, Stevenson WG. Cost-effectiveness of ICDs. N Engl J Med. 2006 Jan 12; 354(2):205-7; author reply 205-7.
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  120. Nazarian S, Maisel WH, Miles JS, Tsang S, Stevenson LW, Stevenson WG. Impact of implantable cardioverter defibrillators on survival and recurrent hospitalization in advanced heart failure. Am Heart J. 2005 Nov; 150(5):955-60.
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  121. Intini A, Goldstein RN, Jia P, Ramanathan C, Ryu K, Giannattasio B, Gilkeson R, Stambler BS, Brugada P, Stevenson WG, Rudy Y, Waldo AL. Electrocardiographic imaging (ECGI), a novel diagnostic modality used for mapping of focal left ventricular tachycardia in a young athlete. Heart Rhythm. 2005 Nov; 2(11):1250-2.
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  122. Parkash R, Maisel WH, Toca FM, Stevenson WG. Atrial fibrillation in heart failure: high mortality risk even if ventricular function is preserved. Am Heart J. 2005 Oct; 150(4):701-6.
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  123. Reynolds DW, Chen PS, Deal BJ, Donahue JK, Ellenbogen KA, Epstein AE, Friedman PA, Hammill SC, Hohnloser SH, Kanter RJ, Lindsay BD, Natale A, Saffitz J, Stevenson WG. Highlights of Heart Rhythm 2005, the Annual Scientific Sessions of the Heart Rhythm Society, May 4-7, 2005, New Orleans, Louisiana. Heart Rhythm. 2005 Sep; 2(9):1025-33.
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  124. Stevenson WG, Soejima K. Recording techniques for clinical electrophysiology. J Cardiovasc Electrophysiol. 2005 Sep; 16(9):1017-22.
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  125. Tedrow U, Stevenson WG, Benzaquen LR. Apical left ventricular aneurysm presenting with malignant ventricular tachycardia responsive to aneurysmectomy. Heart. 2005 May; 91(5):623.
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  126. Brunckhorst CB, Delacretaz E, Soejima K, Maisel WH, Friedman PL, Stevenson WG. Impact of changing activation sequence on bipolar electrogram amplitude for voltage mapping of left ventricular infarcts causing ventricular tachycardia. J Interv Card Electrophysiol. 2005 Mar; 12(2):137-41.
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  127. Stevenson WG. Catheter ablation of monomorphic ventricular tachycardia. Curr Opin Cardiol. 2005 Jan; 20(1):42-7.
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  128. Stevenson WG. To freeze or burn the epicardium? Heart Rhythm. 2005 Jan; 2(1):91-2.
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  129. Stevenson WG, Chaitman BR, Ellenbogen KA, Epstein AE, Gross WL, Hayes DL, Strickberger SA, Sweeney MO. Clinical assessment and management of patients with implanted cardioverter-defibrillators presenting to nonelectrophysiologists. Circulation. 2004 Dec 21; 110(25):3866-9.
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  130. Tedrow U, Maisel WH, Epstein LM, Soejima K, Stevenson WG. Feasibility of adjusting paced left ventricular activation by manipulating stimulus strength. J Am Coll Cardiol. 2004 Dec 7; 44(11):2249-52.
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  131. Stevenson WG, Stevenson LW. Atrial fibrillation and heart failure–five more years. N Engl J Med. 2004 Dec 2; 351(23):2437-40.
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  132. Brunckhorst CB, Delacretaz E, Soejima K, Jackman WM, Nakagawa H, Kuck KH, Ben-Haim SA, Seifert B, Stevenson WG. Ventricular mapping during atrial and right ventricular pacing: relation of electrogram parameters to ventricular tachycardia reentry circuits after myocardial infarction. J Interv Card Electrophysiol. 2004 Dec; 11(3):183-91.
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  133. Curtis AB, Abraham WT, Chen PS, Ellenbogen KA, Epstein AE, Friedman PA, Hohnloser SH, Kanter RJ, Stevenson WG. Highlights of Heart Rhythm 2004, the Annual Scientific Sessions of the Heart Rhythm Society: May 19 to 22, 2004, in San Francisco, California. J Am Coll Cardiol. 2004 Oct 19; 44(8):1550-6.
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  134. Stevenson WG, Cooper J, Sapp J. Optimizing RF output for cooled RF ablation. J Cardiovasc Electrophysiol. 2004 Oct; 15(10 Suppl):S24-7.
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  135. Soejima K, Stevenson WG. Athens, athletes, and arrhythmias: the cardiologist’s dilemma. J Am Coll Cardiol. 2004 Sep 1; 44(5):1059-61.
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  136. Cooper JM, Sapp JL, Tedrow U, Pellegrini CP, Robinson D, Epstein LM, Stevenson WG. Ablation with an internally irrigated radiofrequency catheter: learning how to avoid steam pops. Heart Rhythm. 2004 Sep; 1(3):329-33.
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  137. Soejima K, Couper G, Cooper JM, Sapp JL, Epstein LM, Stevenson WG. Subxiphoid surgical approach for epicardial catheter-based mapping and ablation in patients with prior cardiac surgery or difficult pericardial access. Circulation. 2004 Sep 7; 110(10):1197-201.
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  138. Brunckhorst CB, Delacretaz E, Soejima K, Maisel WH, Friedman PL, Stevenson WG. Identification of the ventricular tachycardia isthmus after infarction by pace mapping. Circulation. 2004 Aug 10; 110(6):652-9.
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  139. Friedman PL, Dubuc M, Green MS, Jackman WM, Keane DT, Marinchak RA, Nazari J, Packer DL, Skanes A, Steinberg JS, Stevenson WG, Tchou PJ, Wilber DJ, Worley SJ. Catheter cryoablation of supraventricular tachycardia: results of the multicenter prospective “frosty” trial. Heart Rhythm. 2004 Jul; 1(2):129-38.
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  140. Sapp JL, Soejima K, Cooper JM, Epstein LM, Stevenson WG. Ablation lesion size correlates with pacing threshold: a physiological basis for use of pacing to assess ablation lesions. Pacing Clin Electrophysiol. 2004 Jul; 27(7):933-7.
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  141. Soejima K, Stevenson WG, Sapp JL, Selwyn AP, Couper G, Epstein LM. Endocardial and epicardial radiofrequency ablation of ventricular tachycardia associated with dilated cardiomyopathy: the importance of low-voltage scars. J Am Coll Cardiol. 2004 May 19; 43(10):1834-42.
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  142. Tedrow U, Sweeney MO, Stevenson WG. Physiology of cardiac resynchronization. Curr Cardiol Rep. 2004 May; 6(3):189-93.
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  143. Sapp JL, Cooper JM, Soejima K, Sorrell T, Lopera G, Satti SD, Koplan BA, Epstein LM, Edelman E, Rogers C, Stevenson WG. Deep myocardial ablation lesions can be created with a retractable needle-tipped catheter. Pacing Clin Electrophysiol. 2004 May; 27(5):594-9.
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  144. Stevenson WG, Sweeney MO. Single site left ventricular pacing for cardiac resynchronization. Circulation. 2004 Apr 13; 109(14):1694-6.
    View in: PubMed
  145. Koplan BA, Parkash R, Couper G, Stevenson WG. Combined epicardial-endocardial approach to ablation of inappropriate sinus tachycardia. J Cardiovasc Electrophysiol. 2004 Feb; 15(2):237-40.
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  146. Lopera G, Stevenson WG, Soejima K, Maisel WH, Koplan B, Sapp JL, Satti SD, Epstein LM. Identification and ablation of three types of ventricular tachycardia involving the his-purkinje system in patients with heart disease. J Cardiovasc Electrophysiol. 2004 Jan; 15(1):52-8.
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  147. Blomström-Lundqvist C, Scheinman MM, Aliot EM, Alpert JS, Calkins H, Camm AJ, Campbell WB, Haines DE, Kuck KH, Lerman BB, Miller DD, Shaeffer CW, Stevenson WG, Tomaselli GF, Antman EM, Smith SC, Alpert JS, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Hiratzka LF, Hunt SA, Jacobs AK, Russell RO, Priori SG, Blanc JJ, Budaj A, Burgos EF, Cowie M, Deckers JW, Garcia MA, Klein WW, Lekakis J, Lindahl B, Mazzotta G, Morais JC, Oto A, Smiseth O, Trappe HJ. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias–executive summary. a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society. J Am Coll Cardiol. 2003 Oct 15; 42(8):1493-531.
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  148. Blomström-Lundqvist C, Scheinman MM, Aliot EM, Alpert JS, Calkins H, Camm AJ, Campbell WB, Haines DE, Kuck KH, Lerman BB, Miller DD, Shaeffer CW, Stevenson WG, Tomaselli GF, Antman EM, Smith SC, Alpert JS, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Hiratzka LF, Hunt SA, Jacobs AK, Russell RO, Priori SG, Blanc JJ, Budaj A, Burgos EF, Cowie M, Deckers JW, Garcia MA, Klein WW, Lekakis J, Lindahl B, Mazzotta G, Morais JC, Oto A, Smiseth O, Trappe HJ. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias–executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation. 2003 Oct 14; 108(15):1871-909.
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  149. Delacretaz E, Soejima K, Brunckhorst CB, Maisel WH, Friedman PL, Stevenson WG. Assessment of radiofrequency ablation effect from unipolar pacing threshold. Pacing Clin Electrophysiol. 2003 Oct; 26(10):1993-6.
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  150. Soejima K, Stevenson WG. Catheter ablation of ventricular tachycardia in patients with ischemic heart disease. Curr Cardiol Rep. 2003 Sep; 5(5):364-8.
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  151. Tung S, Soejima K, Maisel WH, Suzuki M, Epstein L, Stevenson WG. Recognition of far-field electrograms during entrainment mapping of ventricular tachycardia. J Am Coll Cardiol. 2003 Jul 2; 42(1):110-5.
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  152. Stevenson WG, Soejima K. Inside or out? Another option for incessant ventricular tachycardia. J Am Coll Cardiol. 2003 Jun 4; 41(11):2044-5.
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  153. Brunckhorst CB, Stevenson WG, Soejima K, Maisel WH, Delacretaz E, Friedman PL, Ben-Haim SA. Relationship of slow conduction detected by pace-mapping to ventricular tachycardia re-entry circuit sites after infarction. J Am Coll Cardiol. 2003 Mar 5; 41(5):802-9.
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  154. Koplan BA, Stevenson WG, Epstein LM, Aranki SF, Maisel WH. Development and validation of a simple risk score to predict the need for permanent pacing after cardiac valve surgery. J Am Coll Cardiol. 2003 Mar 5; 41(5):795-801.
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  155. Ellison KE, Stevenson WG, Sweeney MO, Epstein LM, Maisel WH. Management of arrhythmias in heart failure. Congest Heart Fail. 2003 Mar-Apr; 9(2):91-9.
    View in: PubMed
  156. Stevenson WG, Epstein LM. Predicting sudden death risk for heart failure patients in the implantable cardioverter-defibrillator age. Circulation. 2003 Feb 4; 107(4):514-6.
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  157. Maisel WH, Stevenson WG, Epstein LM. Changing trends in pacemaker and implantable cardioverter defibrillator generator advisories. Pacing Clin Electrophysiol. 2002 Dec; 25(12):1670-8.
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  158. Khan HH, Maisel WH, Ho C, Suzuki M, Soejima K, Solomon S, Stevenson WG. Effect of radiofrequency catheter ablation of ventricular tachycardia on left ventricular function in patients with prior myocardial infarction. J Interv Card Electrophysiol. 2002 Dec; 7(3):243-7.
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  159. Fenelon G, Stambler BS, Huvelle E, Brugada P, Stevenson WG. Left ventricular dysfunction is associated with prolonged average ventricular fibrillation cycle length in patients with implantable cardioverter defibrillators. J Interv Card Electrophysiol. 2002 Dec; 7(3):249-54.
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  160. Soejima K, Stevenson WG, Maisel WH, Sapp JL, Epstein LM. Electrically unexcitable scar mapping based on pacing threshold for identification of the reentry circuit isthmus: feasibility for guiding ventricular tachycardia ablation. Circulation. 2002 Sep 24; 106(13):1678-83.
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  161. Maisel WH, Stevenson WG. Syncope–getting to the heart of the matter. N Engl J Med. 2002 Sep 19; 347(12):931-3.
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  162. Maisel WH, Stevenson WG, Epstein LM. Reduced atrial blood flow in patients with coronary artery disease. Coron Artery Dis. 2002 Aug; 13(5):283-90.
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  163. Soejima K, Stevenson WG. Ventricular tachycardia associated with myocardial infarct scar: a spectrum of therapies for a single patient. Circulation. 2002 Jul 9; 106(2):176-9.
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  164. Brunckhorst CB, Stevenson WG, Jackman WM, Kuck KH, Soejima K, Nakagawa H, Cappato R, Ben-Haim SA. Ventricular mapping during atrial and ventricular pacing. Relationship of multipotential electrograms to ventricular tachycardia reentry circuits after myocardial infarction. Eur Heart J. 2002 Jul; 23(14):1131-8.
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  165. Friedman RA, Walsh EP, Silka MJ, Calkins H, Stevenson WG, Rhodes LA, Deal BJ, Wolff GS, Demaso DR, Hanisch D, Van Hare GF. NASPE Expert Consensus Conference: Radiofrequency catheter ablation in children with and without congenital heart disease. Report of the writing committee. North American Society of Pacing and Electrophysiology. Pacing Clin Electrophysiol. 2002 Jun; 25(6):1000-17.
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  166. Stevenson WG, Ellison KE, Sweeney MO, Epstein LM, Maisel WH. Management of arrhythmias in heart failure. Cardiol Rev. 2002 Jan-Feb; 10(1):8-14.
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  167. Maisel WH, Rawn JD, Stevenson WG. Atrial fibrillation after cardiac surgery. Ann Intern Med. 2001 Dec 18; 135(12):1061-73.
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  168. Sapp J, Soejima K, Couper GS, Stevenson WG. Electrophysiology and anatomic characterization of an epicardial accessory pathway. J Cardiovasc Electrophysiol. 2001 Dec; 12(12):1411-4.
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  169. Sweeney MO, Ellison KE, Stevenson WG. Implantable cardioverter defibrillators in heart failure. Cardiol Clin. 2001 Nov; 19(4):653-67.
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  170. Maisel WH, Stevenson WG, Tung S, Blier LE, Brunckhorst CB. Less is more: 4:2:1 block. Circulation. 2001 Sep 4; 104(10):E50.
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  171. Delacrétaz E, Stevenson WG. Catheter ablation of ventricular tachycardia in patients with coronary heart disease. Part II: Clinical aspects, limitations, and recent developments. Pacing Clin Electrophysiol. 2001 Sep; 24(9 Pt 1):1403-11.
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  172. Maisel WH, Sweeney MO, Stevenson WG, Ellison KE, Epstein LM. Recalls and safety alerts involving pacemakers and implantable cardioverter-defibrillator generators. JAMA. 2001 Aug 15; 286(7):793-9.
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  173. Soejima K, Suzuki M, Maisel WH, Brunckhorst CB, Delacretaz E, Blier L, Tung S, Khan H, Stevenson WG. Catheter ablation in patients with multiple and unstable ventricular tachycardias after myocardial infarction: short ablation lines guided by reentry circuit isthmuses and sinus rhythm mapping. Circulation. 2001 Aug 7; 104(6):664-9.
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  174. Delacretaz E, Stevenson WG. Catheter ablation of ventricular tachycardia in patients with coronary heart disease: part I: Mapping. Pacing Clin Electrophysiol. 2001 Aug; 24(8 Pt 1):1261-77.
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  175. Delacretaz E, Ganz LI, Soejima K, Friedman PL, Walsh EP, Triedman JK, Sloss LJ, Landzberg MJ, Stevenson WG. Multi atrial maco-re-entry circuits in adults with repaired congenital heart disease: entrainment mapping combined with three-dimensional electroanatomic mapping. J Am Coll Cardiol. 2001 May; 37(6):1665-76.
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  176. Soejima K, Delacretaz E, Suzuki M, Brunckhorst CB, Maisel WH, Friedman PL, Stevenson WG. Saline-cooled versus standard radiofrequency catheter ablation for infarct-related ventricular tachycardias. Circulation. 2001 Apr 10; 103(14):1858-62.
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  177. Soejima K, Stevenson WG, Maisel WH, Delacretaz E, Brunckhorst CB, Ellison KE, Friedman PL. The N + 1 difference: a new measure for entrainment mapping. J Am Coll Cardiol. 2001 Apr; 37(5):1386-94.
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  178. Delacretaz E, Soejima K, Gottipaty VK, Brunckhorst CB, Friedman PL, Stevenson WG. Single catheter determination of local electrogram prematurity using simultaneous unipolar and bipolar recordings to replace the surface ECG as a timing reference. Pacing Clin Electrophysiol. 2001 Apr; 24(4 Pt 1):441-9.
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  179. Stevenson WG, Maisel WH. Electrocardiography artifact: what you do not know, you do not recognize. Am J Med. 2001 Apr 1; 110(5):402-3.
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  180. Stevenson WG, Soejima K. Knowing where to look. J Cardiovasc Electrophysiol. 2001 Mar; 12(3):367-8.
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  181. Stevenson WG, Stevenson LW. Prevention of sudden death in heart failure. J Cardiovasc Electrophysiol. 2001 Jan; 12(1):112-4.
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  182. Stevenson WG, Delacretaz E. Radiofrequency catheter ablation of ventricular tachycardia. Heart. 2000 Nov; 84(5):553-9.
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  183. Stevenson WG, Delacretaz E. Strategies for catheter ablation of scar-related ventricular tachycardia. Curr Cardiol Rep. 2000 Nov; 2(6):537-44.
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  184. Soejima K, Stevenson WG, Delacretaz E, Brunckhorst CB, Maisel WH, Friedman PL. Identification of left atrial origin of ectopic tachycardia during right atrial mapping: analysis of double potentials at the posteromedial right atrium. J Cardiovasc Electrophysiol. 2000 Sep; 11(9):975-80.
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  185. Weinfeld MS, Drazner MH, Stevenson WG, Stevenson LW. Early outcome of initiating amiodarone for atrial fibrillation in advanced heart failure. J Heart Lung Transplant. 2000 Jul; 19(7):638-43.
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  186. Maisel WH, Stevenson WG. Sudden death and the electrophysiological effects of angiotensin-converting enzyme inhibitors. J Card Fail. 2000 Jun; 6(2):80-2.
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  187. Ellison KE, Stevenson WG, Sweeney MO, Lefroy DC, Delacretaz E, Friedman PL. Catheter ablation for hemodynamically unstable monomorphic ventricular tachycardia. J Cardiovasc Electrophysiol. 2000 Jan; 11(1):41-4.
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  188. Delacretaz E, Stevenson WG, Ellison KE, Maisel WH, Friedman PL. Mapping and radiofrequency catheter ablation of the three types of sustained monomorphic ventricular tachycardia in nonischemic heart disease. J Cardiovasc Electrophysiol. 2000 Jan; 11(1):11-7.
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  189. Delacretaz E, Soejima K, Stevenson WG, Friedman PL. Short ventriculoatrial intervals during orthodromic atrioventricular reciprocating tachycardia: what is the mechanism? J Cardiovasc Electrophysiol. 2000 Jan; 11(1):121-4.
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  190. Soejima K, Delacretaz E, Stevenson WG, Friedman PL. DDD-pacing-induced cardiomyopathy following AV node ablation for persistent atrial tachycardia. J Interv Card Electrophysiol. 1999 Dec; 3(4):321-3.
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  191. Stevenson WG, Stevenson LW. Atrial fibrillation in heart failure. N Engl J Med. 1999 Sep 16; 341(12):910-1.
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  192. Kocovic DZ, Harada T, Friedman PL, Stevenson WG. Characteristics of electrograms recorded at reentry circuit sites and bystanders during ventricular tachycardia after myocardial infarction. J Am Coll Cardiol. 1999 Aug; 34(2):381-8.
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  193. Delacretaz E, Stevenson WG, Winters GL, Mitchell RN, Stewart S, Lynch K, Friedman PL. Ablation of ventricular tachycardia with a saline-cooled radiofrequency catheter: anatomic and histologic characteristics of the lesions in humans. J Cardiovasc Electrophysiol. 1999 Jun; 10(6):860-5.
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  194. Delacretaz E, Stevenson WG, Winters GL, Friedman PL. Radiofrequency ablation of atrial flutter. Circulation. 1999 Apr 13; 99(14):E1-2.
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  195. Friedman PL, Stevenson WG. Proarrhythmia. Am J Cardiol. 1998 Oct 16; 82(8A):50N-58N.
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  196. Ellison KE, Friedman PL, Ganz LI, Stevenson WG. Entrainment mapping and radiofrequency catheter ablation of ventricular tachycardia in right ventricular dysplasia. J Am Coll Cardiol. 1998 Sep; 32(3):724-8.
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  197. Lefroy DC, Fang JC, Stevenson LW, Hartley LH, Friedman PL, Stevenson WG. Recipient-to-donor atrioatrial conduction after orthotopic heart transplantation: surface electrocardiographic features and estimated prevalence. Am J Cardiol. 1998 Aug 15; 82(4):444-50.
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  198. Stevenson WG, Friedman PL, Kocovic D, Sager PT, Saxon LA, Pavri B. Radiofrequency catheter ablation of ventricular tachycardia after myocardial infarction. Circulation. 1998 Jul 28; 98(4):308-14.
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  199. Stevenson WG, Delacretaz E, Friedman PL, Ellison KE. Identification and ablation of macroreentrant ventricular tachycardia with the CARTO electroanatomical mapping system. Pacing Clin Electrophysiol. 1998 Jul; 21(7):1448-56.
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  200. Lefroy DC, Ellison KE, Friedman PL, Stevenson WG. Arrhythmia of the month: shortening of ventriculoatrial conduction time during radiofrequency catheter ablation of a concealed accessory pathway. J Cardiovasc Electrophysiol. 1998 Apr; 9(4):445-7.
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  201. Ganz LI, Couper GS, Friedman PL, Stevenson WG, Ellison K. Use of telemetered permanent pacemaker intracardiac electrograms to diagnose ventricular tachycardia. Am J Cardiol. 1997 Dec 1; 80(11):1511-3.
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  202. stevenson WG, Friedman PL, Ganz LI. Radiofrequency catheter ablation of ventricular tachycardia late after myocardial infarction. J Cardiovasc Electrophysiol. 1997 Nov; 8(11):1309-19.
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  203. Stevenson WG, Ellison KE, Lefroy DC, Friedman PL. Ablation therapy for cardiac arrhythmias. Am J Cardiol. 1997 Oct 23; 80(8A):56G-66G.
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  204. Ellison KE, Stevenson WG, Couper GS, Friedman PL. Ablation of ventricular tachycardia due to a postinfarct ventricular septal defect: identification and transection of a broad reentry loop. J Cardiovasc Electrophysiol. 1997 Oct; 8(10):1163-6.
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  205. Harada T, Stevenson WG, Kocovic DZ, Friedman PL. Catheter ablation of ventricular tachycardia after myocardial infarction: relation of endocardial sinus rhythm late potentials to the reentry circuit. J Am Coll Cardiol. 1997 Oct; 30(4):1015-23.
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  206. Stevenson WG, Sweeney MO. Arrhythmias and sudden death in heart failure. Jpn Circ J. 1997 Sep; 61(9):727-40.
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  207. Maisel WH, Kuntz KM, Reimold SC, Lee TH, Antman EM, Friedman PL, Stevenson WG. Risk of initiating antiarrhythmic drug therapy for atrial fibrillation in patients admitted to a university hospital. Ann Intern Med. 1997 Aug 15; 127(4):281-4.
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  208. Stevenson WG, Sweeney MO. Pharmacologic and nonpharmacologic treatment of ventricular arrhythmias in heart failure. Curr Opin Cardiol. 1997 May; 12(3):242-50.
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  209. Stevenson WG, Friedman PL, Sager PT, Saxon LA, Kocovic D, Harada T, Wiener I, Khan H. Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping. J Am Coll Cardiol. 1997 May; 29(6):1180-9.
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  210. Hadjis TA, Stevenson WG, Harada T, Friedman PL, Sager P, Saxon LA. Preferential locations for critical reentry circuit sites causing ventricular tachycardia after inferior wall myocardial infarction. J Cardiovasc Electrophysiol. 1997 Apr; 8(4):363-70.
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Food Insecurity in Africa and GMOs

Reporter and Curator: Larry H. Bernstein, MD, FCAP 

Article ID #103: Food Insecurity in Africa and GMOs. Published on 1/13/2014

WordCloud Image Produced by Adam Tubman

 

This Report is a presentation from several articles since mid-2013 on the food shortage in Sub-Saharan Africa, where crop yields are among the lowest in the worlds.  In this series we have presented modiable  and epigenetic causes of CVD, among other topics, including diabetes, obesity, and exercise.  We have mentioned that while magnesium, fiber, a sufficient source of n-3 polyunsaturated fatty acids (from seafood or seaweed, or from flaxseed), and a functional methyl transporter as well as a source of methionine ( which requires a meat source, as B9 folate is plant sourced and does not fix the problem).  In this discussion we have both a voluntary and an involuntary course of living that leads to CVD and brain dysfunction, depending on where one lives, a “perfect storm”.

Part 1.  Tensions over Food Insecurity in Africa   Oct 8, 2013

Sharon Schmickle

Sub-Saharan Africa’s agricultural yields are among the lowest in the world, and nearly one-third of its people are malnourished. That much, tragically, is well established. Less clear are the reasons Africa’s farm output remains depressed despite hands-on work and billions of dollars invested by individuals, organizations and governments. News reports often explore specific aspects of the problem such as drought. This series takes the novel approach of looking at intertwined tensions underlying the many problems. Through stories told across the continent, Sharon Schmickle focus on several key themes:

  • Africa is caught in an ideological struggle over the nature and scope of agriculture with European—and, sometimes, American—organizations pitted against agribusiness and many agricultural scientists.
  • Institutions have failed African farmers. Public and private agencies often work at cross purposes, neglecting to follow through on crop-saving opportunities. Investments in research and agricultural extension have been inadequate.

Scientists have made impressive gains against the scourges that threaten crops. But they risk losing their breakthroughs against malnutrition, crop-destroying pests and drought if they overlook local tastes and customs.

The series, which also incorporates the work of local journalists, begins with an overview of Tanzania where government officials are divided in the global ideological standoff. Despite a government initiative called Kilimo Kwanza (Farmers First), many farmers lack access to the improved seeds and tissue cultures that could help them thwart yield-stealing diseases and pests. And many farmers are so locked into practices of the past that change comes hard if at all.

This narrative is not twisted to an anti-GMO slant, and could be viewed as a need for GMO harvests without the independence to develop them, and the struggle against a powerful industrial source that takes from an impoverished people.

Sharon Schmickle has been a journalist for MinnPost.com since 2007, and before that she worked for the Minneapolis Star Tribune where she reported from the paper’s Washington bureau…

http://pulitzercenter.org/sites/default/files/styles/responsive_cropped/public/09-16-13/1382/lunch_line_at_engaruka_primary_school_0.jpg

Roiling tensions underlie efforts to improve food security in Africa, often pulling at cross purposes on farmers, consumers and their countries.

Tanzania: Mixed Feelings on Genetically Modified Crops
Tanzania faces the question of whether food from GM crops will sell at markets like this one in Dar es Salaam. Image by Sharon Schmickle. Tanzania, 2013.

Part 2.  Nathanael Johnson lets the anti-GMO movement off the hook

By MICHAEL EISEN | Published: JAN 10, 2014

For the last six months, Nathanael Johnson has been writing about GMOs for the lefty environmental magazine Grist. The goal of his ultimately 26 part series was to try and bring some journalistic sanity to a topic that has gotten nasty in recent years. As Grist editor Scott Rosenberg is quoted on Dan Charles’ blog:
GMOs “were a unique problem for us,” says Rosenberg. On the one hand, most of Grist’s readers and supporters despise GMOs, seeing them as a tool of corporate agribusiness and chemical-dependent farming.

On the other hand, says Rosenberg, he’d been struck by the passion of people who defended this technology, especially scientists. It convinced him that the issue deserved a fresh look.

I’ve enjoyed reading the series. Johnson has investigated a wide range of issues related to GMOs with a generally empirical eye – trying to find data to help answer questions, while avoiding the polemicism that dominates discussions of the topic. Although I don’t think everything he has written is right, the series is a very useful starting point for people trying to wrap the heads around what can be a complex topic. He has clearly tried to delve deeply into every topic, and to not let dogma or propaganda from either side affect his conclusions.

Unfortunately, if the series has had an effect on what I presume is its target audience – the anti-GMO readers of Grist – it hasn’t shown up in online debates about GMOs. When I and others have pointed to Johnson’s series in response to outrageous statements from anti-GMO campaigners, he is dismissed as either a naive fool or just another Monsanto tool.

So I was surprised to read his concluding piece in the series, “What I learned from six months of GMO research: None of it matters“.

The most astonishing thing about the vicious public brawl over GMOs is that the stakes are so low.

His basic point is that a lot of hot air and political energy is spent trying to decide between two alternative futures that aren’t all that different.

In the GMO-free future, farming still looks pretty much the same. Without insect-resistant crops, farmers spray more broad-spectrum insecticides, which do some collateral damage to surrounding food webs. Without herbicide-resistant crops, farmers spray less glyphosate, which slows the spread of glyphosate-resistant weeds and perhaps leads to healthier soil biota. Farmers also till their fields more often, which kills soil biota, and releases a lot more greenhouse gases.

The banning of GMOs hasn’t led to a transformation of agriculture because GM seed was never a linchpin supporting the conventional food system: Farmers could always do fine without it. Eaters no longer worry about the small potential threat of GMO health hazards, but they are subject to new risks: GMOs were neither the first, nor have they been the last, agricultural innovation, and each of these technologies comes with its own potential hazards. Plant scientists will have increased their use of mutagenesis and epigenetic manipulation, perhaps. We no longer have biotech patents, but we still have traditional seed-breeding patents. Life goes on.

In the other alternate future, where the pro-GMO side wins, we see less insecticide, more herbicide, and less tillage. In this world, with regulations lifted, a surge of small business and garage-biotechnologists got to work on creative solutions for the problems of agriculture.

Genetic engineering is just one tool in the tinkerer’s belt. Newer tools are already available, and scientists continue to make breakthroughs with traditional breeding. So in this future, a few more genetically engineered plants and animals get their chance to compete. Some make the world a little better, while others cause unexpected problems. But the science has moved beyond basic genetic engineering, and most of the risks and benefits of progress are coming from other technologies. Life goes on.

In many ways he’s right. GMOs on the market today – and most of the ones planned – are about making agriculture more efficient and profitable for farmers and seed providers. This is not a trivial thing, but would global agriculture collapse without these GMOs? Of course not.

We rarely see transformative technologies coming. And remember that we are still in the very early days of genetic engineering of crops and animals. I suspect that you could go back and look at the early days of almost any new technology and convincingly downplay its transformative potential.

Most new technologies ultimately fail to deliver. But the proper stance to take is to say that we just don’t know. What we do know is that there are many pressing and complex problems facing the future of agriculture. And, given that there is no compelling reason not to allow GM techniques to proceed, why take this tool out of the hands of scientists?

People care about GMOs because they symbolize corporate control of the food system, or unsustainable agriculture, or the basic unhealthiness of our modern diet. On the other side, people care about GMOs because they symbolize the victory of human ingenuity over hunger and suffering, or the triumph of market forces, or the wonder of science.

What is most disturbing about the GMO debate – and why it matters – is that the anti-GMO movement at almost every turn rejects empiricism as a means of understanding the world and making decisions about it. GMO opponents have largely rejected Johnson and his series.

They do not appear to believe that the kind of questions that Johnson asks – “Does insect resistant corn reduce the amount of insecticide used on farms?” – can even be asked. They already know the answer, and are completely unmoved by evidence.

The world faces so many challenges now, and we can only solve them if we believe that the world can be understood by studying it, that we can think up and generate possible solutions to the challenges we face, and that we can make rational decisions about which ones to use or not to use.

– See more at: http://www.michaeleisen.org/blog/?p=1530#sthash.GVFidZev.dpuf

Part 3.  Africa: Context is Crucial to Seeing Challenge of Hunger

October 17, 2013 / Des Moines Register
http://pulitzercenter.org/sites/default/files/styles/slideshow/public/10-16-13/farmerprocessingmilkintobutter640.jpg

Women farmers are processing more of their milk. Image by Sharon Schmickle. Tanzania, 2013.

To understand food security in sub-Saharan Africa, context is crucial. Some 500 million small farms feed 80 percent of the people who live in regions that are perilously close to hunger.
Published Oct 17, 2013  SHARON SCHMICKLE

Iowans who take in this year’s World Food Prize Borlaug Dialogue in Des Moines can gain a wealth of expert perspectives on the important challenge of nourishing a growing world population during the next century.
Learning the full measure of the challenge, though, calls for reaching beyond the lectures and panel discussions — reaching into the local reasons it has been so difficult to achieve global food security.
Context is crucial in a world where some 500 million small farms feed 80 percent of the people who live in regions that are perilously close to hunger.
To visit farms in those regions is to learn why it has been so difficult to stand up to the moral challenge the late Norman Borlaug delivered time and again, insisting that access to adequate food is a basic human right.
It is to meet female farmers like Sharifa Said Nambanga, who struggles to feed five children with the rice she can grow on a small plot in Zanzibar. Women do a hefty share of the farm work around the world. Often, though, they are shut off from the extension services that should deliver improved seeds, fertilizer and the know-how to use agriculture’s modern methods. Feeling abandoned, they limp along as best they can on their own.
It is to meet pastoralists like Parmelo Ndiimu. He is a Maasai elder who watches helplessly while the trees he needs to feed his goats are cut to make charcoal for cooking in urban kitchens. “If we won’t be able to feed our goats, we will not be able to feed our children,” Ndiimu said. “And we will be gone.”
It is to meet Tanzanian farmers who work their small plots throughout a full growing season only to see weevils destroy half their bean harvest. They know firsthand the tension between farmers and the ever evolving pests that attack crops in the field and after harvest.
It is to see corn planted from family seed wither in the field, stalks barren and green leaves giving way to limp yellow strips. Theoretically, the simple remedy should be improved seeds. But nothing is simple in the process of getting those improved seeds to small-scale farmers, especially when the improvement involved genetic modification of the plants.
In his later years, Borlaug addressed context in sub-Saharan Africa, recognizing that along with improved seed, farmers also needed to knock down barriers in their marketing, storage and processing systems. He challenged African leaders to invest more in agriculture.
Within that framework, it is clear that millions of small-scale farmers — especially those in Africa — operate amid tensions that limit their opportunities to extract more food from the technology that has filled porridge bowls and bread baskets elsewhere.

Part 4. Betting on the Impact of Synthetic Biology In Healthcare – By Jenny Rooke

Jenny Rooke drives innovation in the life sciences field through investing and business building around brilliant scientists and engineers with novel technologies. Prior, Jenny held multiple executive roles at U.S. Genomics.

I am an ardent believer in the potential of synthetic biology – its technologies, methods, and talented practitioners – to transform human life on just about every dimension: What we eat, how we make things, the character of our environment and how we move through it, how we are born, and, eventually, how long we live.

My more circumspect investor side is forced to admit that the evidence base of practical (not to mention profitable) applications of synthetic biology remains, shall we say, a work in progress. The first wave of synthetic biology companies that focused on energy/biofuels has been largely disappointing commercially, despite some notable technical successes, due in part to challenges related to scale-up, feedstock economics, and distribution.

It seems reasonable to search for proof cases of synthetic biology’s utility in human health; after all, the vast majority of biotechnology’s impact to date (practically and financially) has been in healthcare, including the creation of entirely novel categories of therapeutics and molecular diagnostics.

To be fair, it’s early yet to expect too many synthetic biology success stories in medicine. Synthetic biology as a field is just over a decade old and if it takes on average a decade for a new drug to move from the lab to the market, well, the math is obvious. In addition, there remain a great deal of technical, clinical, and safety risk inherent to applying synthetic biology technologies to human health problems (consider the painful lessons from the analogous field of gene therapy). This helps explain the reluctance of incumbent healthcare companies and traditional healthcare investors to make big bets on synthetic biology until the technology’s practical utility is more proven.

In 2011 and 2012, the Bill & Melinda Gates Foundation put out a call for grant applications to “Apply Synthetic Biology to Global Health Challenges” under its Global Health division, which aims to harness advances in science and technology to save lives in developing countries. The foundation’s Grand Challenges Explorations, or GCE, program is an ideal mechanism for fostering applications of synthetic biology.

Synthetic biology will play a critical role in enabling novel, affordable healthcare solutions for developing countries. Image source: GrandChallenges.org

For more information on the Grand Challenges in Global Health program, including a brief description of each project and a discussion of observed themes, see the review article “Synthetic biology as a source of global health innovation” (Syst Synth Biol (2013) 7:67–72).