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Archive for the ‘Cardio-Oncology’ Category

Reporter: Aviva Lev-Ari, PhD, RN

March 26, 2018, by NCI Staff

Some people who have been treated for breast cancer or lymphoma have a higher risk of developing congestive heart failure than people who haven’t had cancer, results from a new study show.

The study researchers retrospectively compared heart failure rates in people who were diagnosed with breast cancer or lymphoma with those in people who did not have cancer. Although the risk of developing heart failure was relatively low overall, people who had been treated for cancer had more than twice the risk of developing heart failure than those who had never had cancer, they found, and the risk was evident as early as one year after their cancer diagnosis. The increased risk persisted for at least 20 years.

“As more cancer patients live longer, they are living long enough to manifest the long-term cardiac effects of cancer treatment,” said Lori Minasian, M.D., of NCI’s Division of Cancer Prevention, who was not involved in the study. “Increasingly, cardiologists and cardiovascular investigators have seen the need to evaluate the short- and long-term cardiac effects of cancer treatment.”

The bottom line, said study investigator Carolyn Larsen, M.D., of the Mayo Clinic, is that people who have been treated for breast cancer or lymphoma and their physicians should be aware of these risks, and patients should be assessed annually for signs of heart failure.

Dr. Larsen presented the study findingsExit Disclaimer at the American College of Cardiology (ACC) Annual Scientific Session on March 10.

Some Cancer Treatments Can Damage the Heart

Congestive heart failure (also referred to as heart failure) is a condition in which weakened or damaged heart muscles are unable to effectively pump blood to the rest of the body. Heart disease, diabetes, and high blood pressure are all risk factors for heart failure, as are some cancer treatments such as chemotherapy, chest radiation, immunotherapy, and some targeted therapies.

To assess the long-term risk of heart failure in people with cancer, Mayo Clinic researchers analyzed data from the Rochester Epidemiology Project. They focused on participants who were diagnosed with breast cancer or lymphoma from 1985 to 2010 and compared them with matched controls—people without cancer who were the same age and sex, and who had similar risk factors for heart disease.

Some people with breast cancer or lymphoma are “treated with therapies that can be toxic to the heart, particularly anthracyclines,” explained Dr. Larsen. Among the patients with cancer included in the analysis, nearly all had been treated with chemotherapy and 84% had received an anthracycline.

Within 5 years of their cancer diagnosis, the risk of heart failure was three times higher in people treated for breast cancer or lymphoma than in people without cancer, the researchers found. Within 20 years, 10% of the cancer survivors had developed heart failure, compared with 6% of control subjects.

The risk of heart failure was even higher for certain people with cancer. For example, people who were diagnosed with cancer at age 80 or older had three times the risk of heart failure as those who were diagnosed at a younger age. And heart failure risk was twice as high for survivors who had diabetes compared with those without diabetes.

In addition, they found that the risk of heart failure was two times higher for patients who were treated with doxorubicin (an anthracycline-based chemotherapy drug) compared with patients who received other cancer treatments.

What the Results Mean for People with Cancer

The study findings “add more information about the long-term risk after chemotherapy to the existing knowledge base and provide that data in an epidemiology study rather than a clinical trial—so the findings may be more applicable to a general population of breast cancer and lymphoma patients,” Dr. Larsen said.

Many clinical trials exclude patients with heart disease from participating, Dr. Minasian explained. Consequently, data from clinical trials may not reveal the extent to which heart failure risks are increased in those with pre-existing risk factors.

Nevertheless, Dr. Larsen stressed that “not every breast cancer or lymphoma patient is going to develop heart failure.”

Overall, 7% of those in the study treated for cancer developed heart failure, compared with approximately 3% of those in the control group. “It’s the minority” of people who develop heart failure, she said.

The researchers’ main goal, she added, “is to raise awareness of the risk of heart failure and to encourage a heart-healthy lifestyle in cancer survivors.” A heart-healthy lifestyle includes healthy eating, managing weight and stress, maintaining physical activity, and quitting smoking.

In addition, breast cancer and lymphoma survivors should be assessed for signs or symptoms of heart failure and for additional risk factors such as high blood pressure, diabetes, and smoking, Dr. Larsen said. Treating or controlling those risk factors may mitigate heart failure risk

Patients should also “be mindful that the risk of heart failure doesn’t end when they finish their cancer treatment,” Dr. Minasian added.

Ongoing Cardiotoxicity Research

Researchers are actively investigating approaches to lessen or prevent heart damage from cancer treatments. One trial—sponsored by NCI and the National Heart, Lung, and Blood Institute—is testing the cholesterol-lowering medication atorvastatin for reducing heart damage in women with breast cancer who are receiving anthracycline treatment.

Along the same lines, two studies presented at the ACC conference found that cardiac drugs may protect women with breast cancer from cardiotoxicity of cancer treatment.

In one study, the drugs lisinopril and carvedilol both prevented cardiotoxicity in women with breast cancerExit Disclaimer who were receiving the targeted therapy trastuzumab and who had been previously treated with anthracycline chemotherapy. In the other study, carvedilol reduced some measures of heart damageExit Disclaimer in women with breast cancer who were receiving anthracycline chemotherapy.

Organizations such as the ACC are also helping to better educate cardiologists and oncologists about heart failure risk factors in people with cancer “so we’re better able to take care of these patients,” Dr. Minasian said.

Earlier this year, for example, the American Heart Association published its first-ever statement on breast cancer and heart disease.

In it, the organization stressed the importance of managing cardiac risk factors in older women who have been treated for breast cancer, “because [cardiovascular disease], if not recognized and treated, can pose a greater health risk than the cancer itself.”

SOURCE

https://www.cancer.gov/news-events/cancer-currents-blog/2018/increased-heart-failure-risk

Other related articles published in this Open Access Online Scientific Journal include the following

Chapter 19: Relations between Cancer and Cardiovascular Diseases

19.1 Cancer, Respiration and the Peril of the Heart in Cancer Patients

19.2 Reuben Shaw, Ph.D., a geneticist and researcher at the Salk
Institute: Metabolism Influences Cancer

19.3 Heart Tumors: Etiology and Classification

19.4 Amyloidosis with Cardiomyopathy

19.5 Stabilizers that prevent Transthyretin-mediated Cardiomyocyte Amyloidotic Toxicity

19.6 Cancer Symptom Science: On the Mechanisms underlying the Expression of Cancer-related Symptoms

19.7  Therapies

19.7.1  Cardio-Oncology and Onco-Cardiology Programs: Treatments for Cancer Patients with a History of Cardiovascular Disease

19.7.2 Radiation and Chemotherapy Therapy: The Pharmacological Risk for Developing Cardiovascular Disease

19.8  3rd Annual Canadian Cardiac Oncology Network Conference, June 20 –21, 2013, Ottawa Convention Centre

SOURCE

Series C: e-Books on Cancer & Oncology

Series C Content Consultant: Larry H. Bernstein, MD, FCAP

 

VOLUME TWO 

Cancer Therapies:

Metabolic, Genomics, Interventional, Immunotherapy and Nanotechnology in Therapy Delivery (Series C Book 2). On Amazon.com since 5/18/2017

http://www.amazon.com/dp/B071VQ6YYK

71VQ6YYK

Authors, Curators and Editors

Larry H Bernstein, MD, FCAP

larry.bernstein@gmail.com

and

Stephen J Williams, PhD

sjwilliamspa@comcast.net

Guest Authors and CuratorsTilda Barliya, PhDtildabarliya@gmail.comDemet Sag, PhD, demet.sag@gmail.comDror Nir, PhDdror.nir@radbee.comZiv Raviv, PhDzraviv06@gmail.comDanut Dragoi, PhDDanut.daa@gmail.comEvelina Cohn, PhDecohn2011@yahoo.comAviva Lev-Ari, PhD, RN, avivalev-ari@alum.berkeley.edu

Leaders in Pharmaceutical Business Intelligence

LINKs to other e-Books on Cancer on Amazon.com by Our Team

Cancer Biology and Genomics for Disease Diagnosis

(Series C Book 1) – on Amazon.com since 8/11/2015

http://www.amazon.com/dp/B013RVYR2K

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COVID concern in Cardiology: Asymptomatic patients who have been previously infected demonstrating evidence on MRI of scarring or myocarditis

Reporters: Justin D. Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN

 

The Voice of Dr. Justin D. Pearlman, MD, PhD, FACC

Indeed, many viruses can cause inflammation and weakening of the heart.

So far there is no established action to take for prevention, and management is based on clinical manifestations of heart failure: shortness of breath, particularly if worse laying flat or worse with exertion, leg swelling (edema), blood tests showing elevated brain natriuretic peptide (BNP or proBNP, a marker of heart muscle strain), and a basic metabolic panel that may show “pre-renal azotemia” (elevation of BUN and Creatinine, typically in a ratio >20:1) and/or hyponatremia (sodium concentration below 135 mEq/dL). If any of the above are suspected, it is reasonable to get transthoracic echocardiography for systolic and diastolic function. If either systolic or diastolic function by ultrasound show significant impairment not improved by usual therapy (diuretic, ACEI/ARB/ARNI, blocker, aldosterone inhibitor e.g. spironolactone) then an MRI scar map may be considered (MRI scar maps show retention of gadolinium contrast agent by injured heart muscle, first demonstrated by Dr. Justin Pearlman during angiogenesis research MRI studies).

There is no controversy in the above, the controversy is a rush to expanded referral for cardiac MRI without clear clinical evidence of heart impairment, at a stage when there is no established therapy for possible detection of myocarditis (cardiac inflammation). General unproven measures for inflammation may include taking ginger and tumeric supplements if well tolerated by the stomach, drinking 2 cups/day of Rooibos Tea if well tolerated by the liver.

Canakinumab was recommended by one research group to treat inflammation and risk to the heart if the blood test hsCRP is elevated (in addition to potential weakening of muscle, inflammation activates complement, makes atherosclerosis lesions unstable, and thus may elevate risk of heart attack, stroke, renal failure or limb loss from blocked blood delivery). The canakinumab studies were published in NEJM and LANCET with claims of significant improvement in outcomes, but that was not approved by FDA or confirmed by other groups, even though it has biologic plausibility. https://www.thelancet.com/journals/lancet/article/PIIS0140-67361732247-X/fulltext

 

Some Heart Societies Agree on Cautions for COVID-Myocarditis Screening

— Official response has been modest, though

Such evidence of myocardial injury and inflammation on CMR turned up in a German study among people who recovered from largely mild or moderate cases of COVID-19 compared with healthy controls and risk factor-matched controls.

Then an Ohio State University study showed CMR findings suggestive of myocarditis in 15% of collegiate athletes after asymptomatic or mild SARS-CoV-2 infection.

But an open letter from some 50 medical professionals across disciplines emphasized that “prevalence, clinical significance and long-term implications” of such findings aren’t known. The letter called on the 18 professional societies to which it was sent on Tuesday to release clear guidance against CMR screening in the general population to look for post-COVID heart damage in the absence of symptoms.

The Society for Cardiac Magnetic Resonance quickly responded with a brief statement from its chief executive officer, Chiara Bucciarelli-Ducci, MD, PhD, agreeing that routine CMR in asymptomatic patients after COVID-19 “is currently not justified… and it should not be encouraged.”

She referred clinicians to the multisociety guidelines on clinical indications of CMR when deciding whether to scan COVID-19 patients. “While CMR is an excellent imaging tool for diagnosing myocarditis in patients with suspected disease, we do not recommend its use in patients without symptoms,” she added.

The American Heart Association didn’t put out any written statement but offered spokesperson Manesh Patel, MD, chair of its Diagnostic and Interventional Cath Committee.

“The American Heart Association’s position on this is that in general we agree that routine cardiac MRI should not be conducted unless in the course of a study” for COVID-19 patients, he said. “There’s a lot of evolving information around people with COVID, and certainly asymptomatic status, whether it’s recent or prior, it’s not clearly known what the MRI findings will mean or what the long-term implications are without both a control group and an understanding around population.”

The ACC opted against taking a stand. It provided MedPage Today with the following statement from ACC President Athena Poppas, MD:

“We appreciate the authors’ concerns about the potential mischaracterization of the long-term impact of myocarditis after a COVID-19 diagnosis and the need for well-designed clinical trials and careful, long term follow-up. The pandemic is requiring everyone make real-time decisions on how to best care for heart disease patients who may be impacted by COVID-19. The ACC is committed to helping synthesize and provide the most up-to-date, high quality information possible to the cardiovascular care team. We will continue to review and assess the scientific data surrounding cardiac health and COVID-19 and issue guidance to help our care team.”

While the open letter noted that some post-COVID patients have been asking for CMR, Walsh noted that primary care would likely see the brunt of any such influx. She personally has not had any patients ask to be screened.

SOURCE

https://www.medpagetoday.com/infectiousdisease/covid19/88704?xid=nl_covidupdate_2020-09-21

Effect of interleukin-1β inhibition with canakinumab on incident lung cancer in patients with atherosclerosis: exploratory results from a randomised, double-blind, placebo-controlled trial

Summary

Background

Inflammation in the tumour microenvironment mediated by interleukin 1β is hypothesised to have a major role in cancer invasiveness, progression, and metastases. We did an additional analysis in the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS), a randomised trial of the role of interleukin-1β inhibition in atherosclerosis, with the aim of establishing whether inhibition of a major product of the Nod-like receptor protein 3 (NLRP3) inflammasome with canakinumab might alter cancer incidence.

Methods

We did a randomised, double-blind, placebo-controlled trial of canakinumab in 10 061 patients with atherosclerosis who had had a myocardial infarction, were free of previously diagnosed cancer, and had concentrations of high-sensitivity C-reactive protein (hsCRP) of 2 mg/L or greater. To assess dose–response effects, patients were randomly assigned by computer-generated codes to three canakinumab doses (50 mg, 150 mg, and 300 mg, subcutaneously every 3 months) or placebo. Participants were followed up for incident cancer diagnoses, which were adjudicated by an oncology endpoint committee masked to drug or dose allocation. Analysis was by intention to treat. The trial is registered with ClinicalTrials.govNCT01327846. The trial is closed (the last patient visit was in June, 2017).

Findings

Baseline concentrations of hsCRP (median 6·0 mg/L vs 4·2 mg/L; p<0·0001) and interleukin 6 (3·2 vs 2·6 ng/L; p<0·0001) were significantly higher among participants subsequently diagnosed with lung cancer than among those not diagnosed with cancer. During median follow-up of 3·7 years, compared with placebo, canakinumab was associated with dose-dependent reductions in concentrations of hsCRP of 26–41% and of interleukin 6 of 25–43% (p<0·0001 for all comparisons). Total cancer mortality (n=196) was significantly lower in the pooled canakinumab group than in the placebo group (p=0·0007 for trend across groups), but was significantly lower than placebo only in the 300 mg group individually (hazard ratio [HR] 0·49 [95% CI 0·31–0·75]; p=0·0009). Incident lung cancer (n=129) was significantly less frequent in the 150 mg (HR 0·61 [95% CI 0·39–0·97]; p=0·034) and 300 mg groups (HR 0·33 [95% CI 0·18–0·59]; p<0·0001; p<0·0001 for trend across groups). Lung cancer mortality was significantly less common in the canakinumab 300 mg group than in the placebo group (HR 0·23 [95% CI 0·10–0·54]; p=0·0002) and in the pooled canakinumab population than in the placebo group (p=0·0002 for trend across groups). Fatal infections or sepsis were significantly more common in the canakinumab groups than in the placebo group. All-cause mortality did not differ significantly between the canakinumab and placebo groups (HR 0·94 [95% CI 0·83–1·06]; p=0·31).

Interpretation

Our hypothesis-generating data suggest the possibility that anti-inflammatory therapy with canakinumab targeting the interleukin-1β innate immunity pathway could significantly reduce incident lung cancer and lung cancer mortality. Replication of these data in formal settings of cancer screening and treatment is required.

Funding

Novartis Pharmaceuticals.

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Imaging (ECHO) marker that would identify early cardiotoxic effects: The impact of high-dose immunosuppression for ICI myocarditis Cardiac Echo Tracks Checkpoint Inhibitor Damage – Predicting cardiac injury before EF falls

Reporter: Aviva Lev-Ari, PhD, RN

The present study is the first to use Global longitudinal strain (GLS) specifically to identify immune checkpoint inhibitors (ICI) myocarditis, Abraham and Aras noted.

The study compared 101 ICI myocarditis cases from a multicenter international registry (30 with serial GLS) against a random sample of 92 ICI users at Neilan’s institution who did not present with myocarditis (14 with serial GLS) during a study period from 2013 through 2019.

Despite not propensity-matching these patients, the investigators ended up with two groups with similar age (around 65), sex (>60% men), and cancer type (most commonly melanoma and lung cancer).

Before ICI therapy, GLS was similar between groups (20.3% among cases and 20.6% among controls, P=0.60).

Patients who had myocarditis still had a normal ejection fraction in 60% of cases.

One major limitation of the study was that serial echocardiograms had not been routinely performed on people with myocarditis. “[T]hus, it was not possible to determine if the GLS decrease occurred prior to the development of myocarditis,” Neilan and colleagues acknowledged.

Furthermore, 97% of ICI myocarditis cases presented with elevated troponin levels, so it’s “unclear if GLS assessment has incremental value to such readily available biomarkers,” the editorialists pointed out.

“Additional work is needed to test if the GLS decrease occurs prior to the development of clinical myocarditis, can provide an early method of detection, and whether tailoring immunosuppressive therapy based on the measurement of GLS at presentation with myocarditis may be of value,” the authors said.

 

SOURCES

 

  • Cardiac Echo Tracks Checkpoint Inhibitor Damage

https://www.medpagetoday.com/cardiology/chf/84682?xid=nl_mpt_DHE_2020-02-04&eun=g99985d0r&utm_source=Sailthru&utm_medium=email&utm_campaign=Daily%20Headlines%20Top%20Cat%20HeC%20%202020-02-04&utm_term=NL_Daily_DHE_dual-gmail-definition

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Human Heart can be damaged by the presence of cancer elsewhere in the body. This finding surprised physicians and researchers.

Reporter: Aviva Lev-Ari, PhD, RN

 

See more at:

http://www.bidmc.org/Centers-and-Departments/Departments/Cardiovascular-Institute/CVI-Newsletter/Archives/Feb16/HeartCancer.aspx#sthash.hlqDqew7.dpuf

 

SOURCE

http://www.bidmc.org/Centers-and-Departments/Departments/Cardiovascular-Institute/CVI-Newsletter/Archives/Feb16/HeartCancer.aspx

 

Heart 2015;101:1874-1880 doi:10.1136/heartjnl-2015-307848
  • Heart failure and cardiomyopathies
  • Original article

Cardiovascular biomarkers in patients with cancer and their association with all-cause mortality

Author Affiliations

  1. 1Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna,Vienna, Austria

  2. 2Division of Oncology and Hematology, Department of Internal Medicine I, Medical University of Vienna, Austria

  3. 3Division of Cardio-Thoracic-Vascular Anesthesia and Intensive Care Medicine, Department of Anesthesia, Medical University of Vienna, Vienna, Austria

  4. 4Complexity Research, Vienna, Austria

  5. 5Department of Gynecology, Medical University of Vienna, Vienna, Austria

  6. 6Department of Otorhinolaryngology, Head and Neck Surgery, Medical University of Vienna, Austria

Abstract

Objective Patients with cancer may display elevated levels of B-type natriuretic peptide (BNP) and high-sensitive troponin T (hsTnT) without clinical manifestation of cardiac disease. This study aimed to evaluate circulating cardiovascular hormones and hsTnT and their association with mortality in cancer.

Methods We prospectively enrolled 555 consecutive patients with a primary diagnosis of cancer and without prior cardiotoxic anticancer therapy. N-terminal pro BNP (NT-proBNP), mid-regional pro-atrial natriuretic peptide (MR-proANP), mid-regional pro-adrenomedullin (MR-proADM), C-terminal pro-endothelin-1 (CT-proET-1), copeptin, hsTnT, proinflammatory markers interleukin 6 (IL-6) and C reactive protein (CRP), and cytokines serum amyloid A (SAA), haptoglobin and fibronectin were measured. All-cause mortality was defined as primary endpoint.

Results During a median follow-up of 25 (IQR 16–31) months, 186 (34%) patients died. All cardiovascular hormones and hsTnT levels rose with tumour stage progression. All markers were significant predictors of mortality with HRs per IQR of 1.54 (95% CI 1.24 to 1.90, p<0.001) for NT-proBNP, 1.40 (95% CI 1.10 to 1.79, p<0.01) for MR-proANP, 1.31 (95% CI 1.19 to 1.44, p<0.001) for MR-proADM, 1.21 (95% CI 1.14 to 1.30, p<0.001) for CT-proET-1, 1.22 (95% CI 1.04 to 1.42, p=0.014) for copeptin and 1.21 (95% CI 1.13 to 1.32, p<0.001) for hsTnT, independent of age, gender, tumour entity and stage, and presence of cardiac comorbidities. NT-proBNP, MR-proANP, MR-proADM and hsTnT displayed a significant correlation with IL-6 and CRP.

Conclusions Circulating levels of cardiovascular peptides like NT-proBNP, MR-proANP, MR-proADM, CT-pro-ET-1 and hsTnT were elevated in an unselected population of patients with cancer prior to induction of any cardiotoxic anticancer therapy. The aforementioned markers and copeptin were strongly related to all-cause mortality, suggesting the presence of subclinical functional and morphological myocardial damage directly linked to disease progression.

SOURCE

http://heart.bmj.com/content/101/23/1874

Can Cancer Itself Damage the Heart?

Both treated and untreated cancer patients had impaired heart function

Seville, Spain – 3 December 2015: Research presented today at EuroEcho-Imaging 2015 raises the possibility that cancer itself may damage heart muscle irrespective of exposure to cancer drug therapies.1 Researchers from the UK’s first dedicated cardio-oncology clinic found that both treated and untreated cancer patients had impaired heart function.

The annual meeting of the European Association of Cardiovascular Imaging (EACVI), a registered branch of the European Society of Cardiology (ESC), is held 2 to 5 December 2015 in Seville, Spain.

“It is well known that chemotherapy is potentially toxic to the heart, making cancer patients more prone to cardiovascular complications such as heart failure, hypertension or myocardial ischaemia,” said Dr Rajdeep S. Khattar, last author of the abstract and consultant cardiologist at the Royal Brompton Hospital in London, UK. “Our study raises the possibility that tumour growth itself may also damage the heart which could have important implications for monitoring.”

The definition of cardiotoxicity is based on a reduced ejection fraction (less than 55%) and symptoms of heart failure. Ejection fraction is a coarse measure of left ventricular function and is assessed by echocardiography. It refers to the percentage of blood pumped into the circulation when the heart contracts. For example, if there is 100 ml of blood in the left ventricle and 65 ml is pumped out, the ejection fraction is 65%.

The current study applied a more subtle measure of left ventricular function using echocardiography called strain. It indicates how well the myocardial fibres contract. Previous studies have shown that cancer patients who have had chemotherapy can have a normal ejection fraction but reduced strain and that this may predict subsequent cardiotoxicity.

Dr Khattar said: “Our study carried this finding a step further to see if untreated cancer patients with a normal ejection fraction also had reduced strain measurements.”

The study compared myocardial strain in three groups with a normal ejection fraction (55% or more): 43 patients with cancer who were currently being treated or had received treatment in the past, 36 patients with as yet untreated cancer, and 20 healthy individuals matched to the cancer groups for age and gender.

The researchers found that both groups of cancer patients had similarly reduced strain measurements, indicating impaired heart function, compared to the healthy individuals.

“All of the cancer patients had a preserved ejection fraction so by this coarse measure their hearts were functioning normally,” said Dr Khattar. “But the strain measurements showed that they did have myocardial dysfunction.”

He continued: “What was really new was the finding of reduced strain, and therefore myocardial dysfunction, in the group of patients with cancer who had not yet received treatment. This raises the possibility that the tumour itself may have a direct and deleterious effect on the function of the heart.”

Patients with reduced strain before they start their cancer drug therapies may be predisposed to developing heart failure during the course of their treatment. “These patients might need closer monitoring,” said Dr Khattar. “This would be a real change because at the moment, cancer patients don’t, as a matter of routine, have a cardiovascular risk assessment by a cardiologist.”

This is only the second study in humans which suggests that cancer might have a direct effect on the heart. A study published in September found elevated cardiovascular biomarkers in patients with as yet untreated cancer.2,3 “It could be that the tumour produces these inflammatory markers which then leads to the reduction in myocardial function that we found,” said Dr Khattar.

Dr Khattar will continue to follow the patients in the current study to find out if their rates of heart failure and death are predicted by the strain measurements. He said: “If it transpires that the patients with reduced strain prior to cancer treatment are more prone to heart failure and death then it would be important to implement closer monitoring of patients with cancer than is conducted currently.”

SOURCE

http://emjreviews.com/press/can-cancer-itself-damage-the-heart/

 

Early Signs of Heart Damage

The first study was published in September 2015 in the journal Heart. It investigated the presence of cardiovascular biomarkers in cancer patients. Biomarkers are biologically active substances whose presence in the bloodstream indicate the presence or severity of disease. The study’s authors performed blood tests on 555 patients who had been diagnosed with cancer, but not yet treated for it. The tests measured several hormones and proteins closely associated with heart function.

The researchers discovered that the cardiovascular biomarker levels rose as patients’ tumors advanced and that they were significant predictors of death. This was true regardless of the patient’s age, gender, tumor type and whether cardiac disease was apparent at the time of cancer diagnosis.

The second study was the subject of a December 2015 presentation by British doctors at a European conference on echocardiography — a diagnostic technology that uses high-frequency sound waves to produce images of the heart. The researchers used a new-ish echocardiographic test called “strain” to evaluate the heart muscle’s ability to contract while pumping blood.

Strain was measured in three groups of people: 43 with cancer who had already been treated, 36 with cancer who had not yet been treated, and 20 healthy people with similar demographic characteristics. Both groups of cancer patients showed signs of heart dysfunction, while the healthy patients did not.

A More Sensitive Metric

Both the findings and the strain technique used to generate them are significant breakthroughs, according to Chang.

“For the past 50 years, we’ve been relying on ejection fraction to know what’s going on in the heart,” says Chang. “It is a crude measure compared to strain.”

Ejection fraction, also measured with echocardiography, is the traditional metric for gauging heart strength. It’s the percentage of blood that’s ejected or pumped out from the left ventricle of the heart during each heartbeat. Normal ejection fraction is 55 to 75 percent.

Ejection fraction has been a reliable indicator of cardiotoxicity caused principally by radiation to the chest and chemotherapy with anthracyclines, a class of drugs used for breast cancer, leukemia and lymphoma, Chang says. It does not, however, indicate the more subtle signs of dysfunction that are now suspected as being caused by the mere presence of tumor cells.

In other words, heart muscle damage can and does occur even before it can be detected on the basis of ejection fraction measurements, whereas analysis of strain can pick up cardiac dysfunction at the very earliest stage, when the damage is most easily treated.

http://www.bidmc.org/Centers-and-Departments/Departments/Cardiovascular-Institute/CVI-Newsletter/Archives/Feb16/HeartCancer.aspx#sthash.hlqDqew7.dpuf

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