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Archive for the ‘Stroke’ Category


Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Stroke is a leading cause of death worldwide and the most common cause of long-term disability amongst adults, more particularly in patients with diabetes mellitus and arterial hypertension. Increasing evidence suggests that disordered physiological variables following acute ischaemic stroke, especially hyperglycaemia, adversely affect outcomes.

 

Post-stroke hyperglycaemia is common (up to 50% of patients) and may be rather prolonged, regardless of diabetes status. A substantial body of evidence has demonstrated that hyperglycaemia has a deleterious effect upon clinical and morphological stroke outcomes. Therefore, hyperglycaemia represents an attractive physiological target for acute stroke therapies.

 

However, whether intensive glycaemic manipulation positively influences the fate of ischaemic tissue remains unknown. One major adverse event of management of hyperglycaemia with insulin (either glucose-potassium-insulin infusions or intensive insulin therapy) is the occurrence of hypoglycaemia, which can also induce cerebral damage.

 

Doctors all over the world have debated whether intensive glucose management, which requires the use of IV insulin to bring blood sugar levels down to 80-130 mg/dL, or standard glucose control using insulin shots, which aims to get glucose below 180 mg/dL, lead to better outcomes after stroke.

 

A period of hyperglycemia is common, with elevated blood glucose in the periinfarct period consistently linked with poor outcome in patients with and without diabetes. The mechanisms that underlie this deleterious effect of dysglycemia on ischemic neuronal tissue remain to be established, although in vitro research, functional imaging, and animal work have provided clues.

 

While prompt correction of hyperglycemia can be achieved, trials of acute insulin administration in stroke and other critical care populations have been equivocal. Diabetes mellitus and hyperglycemia per se are associated with poor cerebrovascular health, both in terms of stroke risk and outcome thereafter.

 

Interventions to control blood sugar are available but evidence of cerebrovascular efficacy are lacking. In diabetes, glycemic control should be part of a global approach to vascular risk while in acute stroke, theoretical data suggest intervention to lower markedly elevated blood glucose may be of benefit, especially if thrombolysis is administered.

 

Both hypoglycaemia and hyperglycaemia may lead to further brain injury and clinical deterioration; that is the reason these conditions should be avoided after stroke. Yet, when correcting hyperglycaemia, great care should be taken not to switch the patient into hypoglycaemia, and subsequently aggressive insulin administration treatment should be avoided.

 

Early identification and prompt management of hyperglycaemia, especially in acute ischaemic stroke, is recommended. Although the appropriate level of blood glucose during acute stroke is still debated, a reasonable approach is to keep the patient in a mildly hyperglycaemic state, rather than risking hypoglycaemia, using continuous glucose monitoring.

 

The primary results from the Stroke Hyperglycemia Insulin Network Effort (SHINE) study, a large, multisite clinical study showed that intensive glucose management did not improve functional outcomes at 90 days after stroke compared to standard glucose therapy. In addition, intense glucose therapy increased the risk of very low blood glucose (hypoglycemia) and required a higher level of care such as increased supervision from nursing staff, compared to standard treatment.

 

References:

 

https://www.nih.gov/news-events/news-releases/nih-study-provides-answer-long-held-debate-blood-sugar-control-after-stroke

 

https://www.ncbi.nlm.nih.gov/pubmed/27873213

 

https://www.ncbi.nlm.nih.gov/pubmed/19342845

 

https://www.ncbi.nlm.nih.gov/pubmed/20491782

 

https://www.ncbi.nlm.nih.gov/pubmed/21211743

 

https://www.ncbi.nlm.nih.gov/pubmed/18690907

 

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The Promise of Low-Dose Aspirin on Longevity in the Geriatric Population: No Effect on Outcomes in the US and Australia

Reporter: Aviva Lev-Ari, PhD, RN

UPDATED on 10/17/2018

https://www.nejm.org/doi/full/10.1056/NEJMoa1800722

Effect of Aspirin on Disability-free Survival in the Elderly

ORIGINAL ARTICLE

Effect of Aspirin on Disability-free Survival in the Healthy Elderly

J.J. McNeil and Others

    

McNeil et al. conducted the randomized, placebo-controlled Aspirin in Reducing Events in the Elderly (ASPREE) trial to investigate whether the daily use of aspirin, at a dose of 100 mg, in healthy, community-dwelling older adults would prolong a healthy life span, free from dementia and persistent physical disability. Trial participants were community-dwelling men and women from Australia and the United States who were 70 years of age or older (or ≥65 years of age among blacks and Hispanics in the United States).

Clinical Pearls

  Is there any evidence to support the use of aspirin for primary prevention of cardiovascular or other chronic disease in healthy older adults?

Several large, randomized trials have shown the efficacy of aspirin for the secondary prevention of cardiovascular disease among persons with a history of coronary heart disease or stroke. The evidence supporting a benefit of aspirin therapy in the primary prevention of cardiovascular or other chronic disease is less conclusive despite favorable trends suggesting that aspirin use reduces the incidence of cardiovascular events and possibly reduces the incidence of cancer and cancer-related mortality, particularly from colorectal cancer.

  Does the daily use of 100 mg of aspirin prolong a healthy lifespan in older adults without cardiovascular disease, dementia, or physical disability?

In the ASPREE trial, the daily use of 100 mg of enteric-coated aspirin did not differ significantly from placebo in influencing the rates of disability-free survival at a median of 4.7 years. The primary end point of death, dementia, or physical disability occurred in 921 participants in the aspirin group (21.5 events per 1000 person-years) and in 914 in the placebo group (21.2 events per 1000 person-years). The between-group difference was not significant (hazard ratio, 1.01; 95% confidence interval [CI], 0.92 to 1.11; P=0.79). Among participants who had a primary end-point event, death was the most common first event (in 911 participants [50% of the events] at a mean age of 77.5 years), dementia was the next most common (in 549 participants [30% of the events] at a mean age of 77.7 years), and persistent physical disability was the least common.

Morning Report Questions

Q. How does a daily aspirin dose of 100 mg influence rates of death from any cause and the risk of major hemorrhage in healthy older adults?

A. In the ASPREE trial, the secondary end point of death from any cause, denoting death as the first, second, or third event to occur in the primary end point, occurred in 558 participants in the aspirin group (12.7 events per 1000 person-years) and in 494 participants in the placebo group (11.1 events per 1000 person-years) (hazard ratio, 1.14; unadjusted 95% CI, 1.01 to 1.29). Because there was no adjustment for multiple comparisons of secondary end points, no inferences can be made regarding differences in mortality between the two groups. Major hemorrhage occurred in 3.8% of the participants in the aspirin group, as compared with 2.8% of those in the placebo group (hazard ratio, 1.38; 95% CI, 1.18 to 1.62; P<0.001). Fatal or nonfatal hemorrhagic stroke (including subarachnoid hemorrhage) occurred in 49 participants (0.5%) in the aspirin group and in 40 (0.4%) in the placebo group.

Q. How generalizable are the results of the ASPREE trial?

A. White participants comprised 91% of the overall trial cohort. Owing to the small number of blacks and Hispanics (including participants who were younger than 70 years of age) and other nonwhites, the applicability of the main findings of the ASPREE trial to these subgroups is unclear.

 

Daily Low-Dose Aspirin Found to Have No Effect on Healthy Life Span in Older People?

According to 3 articles published online The New England Journal of Medicine (16 September 2018), daily low-dose aspirin was found to have no effect on healthy life span in older people. This large NIH-funded study examined outcomes in United States and Australia

Results showed that in a large clinical trial to determine the risks and benefits of daily low-dose aspirin in healthy older adults without previous cardiovascular events,

Aspirin did not prolong healthy, independent living (life free of dementia or persistent physical disability).

Risk of dying from a range of causes, including cancer and heart disease, varied and will require further analysis and additional follow-up of study participants. These initial findings from the ASPirin in Reducing Events in the Elderly (ASPREE) trial, partially supported by the National Institutes of Health.

ASPREE is an international, randomized, double-blind, placebo-controlled trial that enrolled 19,114 older people (16,703 in Australia and 2,411 in the United States). The study began in 2010 and enrolled participants aged 70 and older; 65 was the minimum age of entry for African-American and Hispanic individuals in the United States because of their higher risk for dementia and cardiovascular disease. At study enrollment, ASPREE participants could not have dementia or a physical disability and had to be free of medical conditions requiring aspirin use. They were followed for an average of 4.7 years to determine outcomes.

In the total study population, treatment with 100 mg of low-dose aspirin per day did not affect survival free of dementia or disability. Among the people randomly assigned to take aspirin,

  • 90.3% remained alive at the end of the treatment without persistent physical disability or dementia, compared with 90.5% of those taking a placebo.
  • Rates of physical disability were similar, and rates of dementia were almost identical in both groups. However,
  • the group taking aspirin had an increased risk of death compared to the placebo group: 5.9% of participants taking aspirin and 5.2% taking placebo died during the study.

This effect of aspirin has not been noted in previous studies; and caution is needed in interpreting this finding. The higher death rate in the aspirin-treated group was due primarily to a higher rate of cancer deaths. A small increase in new cancer cases was reported in the group taking aspirin but the difference could have been due to chance. The authors also analyzed the ASPREE results to determine whether cardiovascular events took place. They found that

  • the rates for major cardiovascular events — including coronary heart disease, nonfatal heart attacks, and fatal and nonfatal ischemic stroke — were similar in the aspirin and the placebo groups. In the aspirin group, 448 people experienced cardiovascular events, compared with 474 people in the placebo group.

Significant bleeding — a known risk of regular aspirin use — was also measured. The authors noted that

  • aspirin was associated with a significantly increased risk of bleeding, primarily in the gastrointestinal tract and brain. Clinically significant bleeding — hemorrhagic stroke, bleeding in the brain, gastrointestinal hemorrhages or hemorrhages at other sites that required transfusion or hospitalization — occurred in 361 people (3.8%) on aspirin and in 265 (2.7%) taking the placebo.
  • As would be expected in an older adult population, cancer was a common cause of death, and 50% of the people who died in the trial had some type of cancer.
  • Heart disease and stroke accounted for 19% of the deaths and major bleeding for 5%.

The ASPREE team is continuing to analyze the results of this study and has implemented plans for monitoring participants. As these efforts continue, the authors emphasized that older adults should follow the advice from their own physicians about daily aspirin use. It is important to note that the new findings do not apply to people with a proven indication for aspirin such as stroke, heart attack or other cardiovascular disease. In addition, the study did not address aspirin’s effects in people younger than age 65. Also, since only 11% of participants had regularly taken low-dose aspirin prior to entering the study, the implications of ASPREE’s findings need further investigation to determine whether healthy older people who have been regularly using aspirin for disease prevention should continue or discontinue use.

SOURCE

From: OnTarget <ontarget@targethealth.com>

Date: September 23, 2018 at 10:47:06 PM EDT

To: avivalev-ari@alum.berkeley.edu

Subject: OnTarget Newsletter

 

Other 121 articles on ASPIRIN were published in this Open Access Online Scientific Journal, including the following:

https://pharmaceuticalintelligence.com/?s=Aspirin

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Two Classes of Antithrombotic Drugs: Anticoagulants and Antiplatelet drugs

Reporter: Aviva Lev-Ari, PhD, RN
These drugs are used to treat
  • strokes,
  • myocardial infarctions,
  • pulmonary embolisms,
  • disseminated intravascular coagulation (DIC) and
  • deep vein thrombosis (DVT)
— all potentially life-threatening conditions.
THERAPEUTIC STRATEGIES
• Degrade fibrinogen/fibrin (fibrinolytic agents)
GOAL: eliminate formed clots
• Inhibit clotting mechanism (anticoagulants)
GOAL: prevent progression of thrombosis
• Interfere either with platelet adhesion and/or aggregation (antiplatelet drugs)
GOAL: prevent initial clot formation
Antithrombotic therapy has had an enormous impact in several significant ways.
  • Heparin has made bypass surgery and dialysis possible by blocking clotting in external tubing.
  • Antithrombotic therapy has reduced the risk of blood clots in leg veins (also known as deep-vein thrombosis or DVT), a condition that can lead to death from pulmonary embolism (a clot that blocks an artery to the lungs) by more than 70 percent. And most importantly,
  • it has markedly reduced death from heart attacks, the risk of stroke in people with heart irregularities (atrial fibrillation), and the risk of major stroke in patients with mini-strokes.

Antithrombotic Therapy

This article was published in December 2008 as part of the special ASH anniversary brochure, 50 Years in Hematology: Research That Revolutionized Patient Care.

Normally, blood flows through our arteries and veins smoothly and efficiently, but if a clot, or thrombus, blocks the smooth flow of blood, the result – called thrombosis – can be serious and even cause death. Diseases arising from clots in blood vessels include heart attack and stroke, among others. These disorders collectively are the most common cause of death and disability in the developed world. We now have an array of drugs that can be used to prevent and treat thrombosis – and there are more on the way – but this was not always the case.

Classes of Antithrombotic Drugs

Image Source: http://www.hematology.org/About/History/50-Years/1523.aspx

The most important components of a thrombus are fibrin and platelets. Fibrin is a protein that forms a mesh that traps red blood cells, while platelets, a type of blood cell, form clumps that add to the mass of the thrombus. Both fibrin and platelets stabilize the thrombus and prevent it from falling apart. Fibrin is the more important component of clots that form in veins, and platelets are the more important component of clots that form in arteries where they can cause heart attacks and strokes by blocking the flow of blood in the heart and brain, respectively, although fibrin plays an important role in arterial thrombosis as well.

There are two classes of antithrombotic drugs: anticoagulants and antiplatelet drugs. Anticoagulants slow down clotting, thereby reducing fibrin formation and preventing clots from forming and growing. Antiplatelet agents prevent platelets from clumping and also prevent clots from forming and growing.

Anticoagulant Drugs

The anticoagulants heparin and dicumarol were discovered by chance, long before we understood how they worked. Heparin was first discovered in 1916 by a medical student at The Johns Hopkins University who was investigating a clotting product from extracts of dog liver and heart. In 1939, dicumarol (the precursor to warfarin) was extracted by a biochemist at the University of Wisconsin from moldy clover brought to him by a farmer whose prize bull had bled to death after eating the clover.

Both of these anticoagulants have been used effectively to prevent clots since 1940. These drugs produce a highly variable anticoagulant effect in patients, requiring their effect to be measured by special blood tests and their dose adjusted according to the results. Heparin acts immediately and is given intravenously (through the veins). Warfarin is swallowed in tablet form, but its anticoagulant effect is delayed for days. Therefore, until recently, patients requiring anticoagulants who were admitted to a hospital were started on a heparin infusion and were then discharged from the hospital after five to seven days on warfarin.

In the 1970s, three different groups of researchers in Stockholm, London, and Hamilton, Ontario, began work on low-molecular-weight heparin (LMWH). LMWH is produced by chemically splitting heparin into one-third of its original size. It has fewer side effects than heparin and produces a more predictable anticoagulant response. By the mid 1980s, LMWH preparations were being tested in clinical trials, and they have now replaced heparin for most indications. Because LMWH is injected subcutaneously (under the skin) in a fixed dose without the need for anticoagulant monitoring, patients can now be treated at home instead of at the hospital.

With the biotechnology revolution has come genetically engineered “designer” anticoagulant molecules that target specific clotting enzymes. Anti-clotting substances and their DNA were also extracted from an array of exotic creatures (ticks, leeches, snakes, and vampire bats) and converted into drugs by chemical synthesis or genetic engineering. Structural chemists next began to fabricate small molecules designed to fit into the active component of clotting enzymes, like a key into a lock.

The first successful synthetic anticoagulants were fondaparinux and bivalirudin. Bivalirudin, a synthetic molecule based on the structure of hirudin (the anti-clotting substance found in leeches), is an effective treatment for patients with heart attacks. Fondaparinux is a small molecule whose structure is based on the active component of the much larger LMWH and heparin molecules. It has advantages over LMWH and heparin and has recently been approved by the FDA. Newer designer drugs that target single clotting factors and that can be taken by mouth are undergoing clinical testing. If successful, we will have safer and more convenient replacements for warfarin, the only oral anticoagulant available for more than 60 years.

Antiplatelet Drugs

Blood platelets are inactive until damage to blood vessels or blood coagulation causes them to explode into sticky irregular cells that clump together and form a thrombus. The first antiplatelet drug was aspirin, which has been used to relieve pain for more than 100 years. In the mid-1960s, scientists showed that aspirin prevented platelets from clumping, and subsequent clinical trials showed that it reduces the risk of stroke and heart attack. In 1980, researchers showed that aspirin in very low doses (much lower than that required to relieve a headache) blocked the production of a chemical in platelets that is required for platelet clumping. During that time, better understanding of the process of platelet clumping allowed the development of designer antiplatelet drugs directed at specific targets. We now have more potent drugs, such as clopidogrel, dipyridamole, and abciximab. These drugs are used with aspirin and effectively prevent heart attack and stroke; they also prolong the lives of patients who have already had a heart attack.

SOURCE 
Anticoagulation Drugs:
  • heparin (FONDAPARINUX HEPARIN (Calciparine, Hepathrom, Lipo-Hepin, Liquaemin, Panheprin)
  • warfarin – 4-HYDROXYCOUMARIN (Coumadin) WARFARIN (Athrombin-K, Panwarfin)
  • rivaroxaban (Xarelto)
  • dabigatran (Pradaxa)
  • apixaban (Eliquis)
  • edoxaban (Savaysa)
  • enoxaparin (Lovenox)
  • fondaparinux (Arixtra)
  • ARGATROBAN BIVALIRUDIN (Angiomax)
  • DALTEPARIN (Fragmin)
  • DROTRECOGIN ALFA (ACTIVATED PROTEIN C) (Xigris)
  • HIRUDIN (Desirudin)
  • LEPIRUDIN (Refludan)
  • XIMELAGATRAN (Exanta)

ANTIDOTES

  • PHYTONADIONE (Vitamin K1)
  • PROTAMINE SULFATE AMINOCAPROIC ACID (EACA) (generic, Amicar) (in bleeding disorders)
Antiplatelet Drugs
  • ACETYL SALICYLIC ACID (aspirin) 
  • clopidogrel (Plavix)
  • dipyridamole (Persantine)
  • abciximab (Centocor)
  • EPTIFIBATIDE (Integrilin)
  • TICLOPIDINE (Ticlid)
  • TIROFIBAN (Aggrastat)

THROMBOLYTICS

  1. ANISTREPLASE (APSAC; Eminase)
  2. STREPTOKINASE (Streptase, Kabikinase)
  3. TISSUE PLASMINOGEN ACTIVATORS (tPAs):
  • ALTEPLASE (Activase),
  • RETEPLASE (Retavase),
  • TENECTEPLASE (TNKase)
  • UROKINASE (Abbokinase)

Fibrinolytic Drugs

Fibrinolytic therapy is used in selected patients with venous thromboembolism. For example, patients with massive or submassive PE can benefit from systemic or catheter-directed fibrinolytic therapy. The latter can also be used as an adjunct to anticoagulants for treatment of patients with extensive iliofemoral-vein thrombosis.

Arterial and venous thrombi are composed of platelets and fibrin, but the proportions differ.

  • Arterial thrombi are rich in platelets because of the high shear in the injured arteries. In contrast,
  • venous thrombi, which form under low shear conditions, contain relatively few platelets and are predominantly composed of fibrin and trapped red cells.
  • Because of the predominance of platelets, arterial thrombi appear white, whereas venous thrombi are red in color, reflecting the trapped red cells.

SOURCE

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A new mechanism of action to attack in the treatment of coronary artery disease (CAD), Novartis developed Ilaris (canakinumab), a human monoclonal antibody targeting the interleukin-1beta innate immunity pathway

Reporter: Aviva Lev-Ari, PhD, RN

 

Speaking at an ESC press briefing, Ridker said, “This is what personalized predictive medicine is all about.” Once a patient has experienced an MI, there is always residual risk of recurrence. Thus, he suggested that residual risk can be divided into

  • residual lipid-driven risk and
  • residual inflammatory-driven risk.

canakinumab might prove to be most useful if it were given to an identified high-responder group. Findings in the hs-CRP responders:

Patients whose hs-CRP declined to 1.8 mg/L or less had a much more robust response. In that subgroup, the number needed to treat to prevent a primary endpoint event was 50 at 2 years and 30 at 3.7 years.

He noted that after a single injection responders have a significant reduction in highly sensitive-CRP and it is those patients who would benefit from continuing on treatment.

“Maybe that first dose could be free,” Ridker added.

Co-investigator, Peter Libby, MD, of Massachusetts General Hospital, put it this way: 30 days after an MI, when a patient is on statin therapy and stable,

  • physicians could check LDL and then initiate more aggressive statin therapy if it is not well-controlled. Similarly,
  • physicians should check hs-CRP, and if it is elevated — 2.0 mg/L or higher — initiating anti-inflammatory therapy targeting interleukin-1 beta would be an option

Interestingly, the treatment had no effect on lipids, which suggests that the benefit was all attributable to the anti-inflammatory activity. 

In the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS), 150 mg of canakinumab every 3 months reduced high-sensitivity C-reactive protein (hs-CRP) levels by an average of 37% compared with placebo and achieved a 15% reduction in cardiovascular events — mostly MIs — compared with placebo, Paul Ridker, MD, reported here at the European Society of Cardiology 2017 congress.

The CANTOS findings were simultaneously published online by the New England Journal of Medicine.

After a median follow-up of 3.7 years, the event rate was 4.5 per 100 person-years in the placebo group versus 3.86 events per 100 person-years in the canakinumab 150 mg group. Two other arms — canakinumab 50 mg and 300 mg — also achieved reductions in events (4.11 and 3.90 per 100 person-years, respectively) but only the 150-mg dose achieved a statistically significant reduction.

There was no reduction in mortality. The trial recruited patients who had a history of MI and a hs-CRP level of 2.0 mg/L or higher.

  • There was no significant difference in all-cause mortality (HR for all canakinumab doses versus placebo, 0.94; 95% CI 0.83-1.06; P=0.31).

Benefits of Anti-inflammatory Canakinumab

although there was no cardiovascular mortality benefit, there was 30% reduction in need for bypass surgery, angioplasty, and heart failure — all of which means a significant improvement in quality of life. And treatment was also associated with a reduction in gout, rheumatoid arthritis, and osteoarthritis, he said.

Cancer Benefit

There was an apparent decrease in risk of cancer, a finding that was elucidated in a Lancet paper also published today. In the cancer analysis, also authored by Ridker, total cancer mortality was lower only in the 300-mg group, but “[i]ncident 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.”

Negative findings

  • Canakinumab was associated with a higher incidence of fatal infection than placebo — the rate was 0.18 in the 3,344 patient placebo group versus 0.32 among the 6,717 patients who received any dose of the drug, which worked out to 23 deaths versus 78 deaths (P=0.02).
  • VIEW VIDEO

Study Author Paul M. Ridker. Interviewed by Peggy Peck, Editor-in-Chief of MedPage Today

https://www.medpagetoday.com/meetingcoverage/esc/67529

  • VIEW VIDEO

Clinical Impact or No Clinical Impact

Anthony DeMaria, MD discusses the major trials from ESC and what impact, if any, they will have on clinical practice.
Benefit vs Price
On June 28 heart failure specialist Milton Packer, MD, wrote this in his MedPage Today blog: “My prediction: [canakinumab] may cost $64,000 for a 15-20% reduction in the risk of a major cardiovascular event, without decreasing cardiovascular death by itself.
Amgen’s Repatha (evolocumab) is a PCSK9 inhibitor that aggressively lowers lipids and is approved for patients who fail statin therapy, including patients with heterozygous or homozygous familial hypercholesterolemia. But while the lipid reductions with the PCSK9 therapy are impressive, and the FOURIER trial found a 15% reduction in events with treatment, neither evolocumab nor alirocumab (Praluent), a PCSK9 inhibitor from Sanofi/Regeneron have achieved wide uptake as payers balk at the high price tags for the drugs.
Other anti-inflammatory agents:
Ridker said. For example, “we have a [National Heart, Lung, and Blood Institute] trial of methotrexate (RA agent) that is on-going. If that proves to be effective, it would be only pennies per treatment.” At the press conference, Ridker said the methotrexate trial has “randomized about 4,000 patients, and we will need to get to 7,000 so it will be a few years before we have results.”

SOURCE

https://www.medpagetoday.com/meetingcoverage/esc/67529

176 articles on monoclonal antibody

https://pharmaceuticalintelligence.com/?s=monoclonal+antibody

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Expanded Stroke Thrombectomy Guidelines: FDA expands treatment window for use (Up to 24 Hours Post-Stroke) of clot retrieval devices (Stryker’s Trevo Stent) in certain stroke patients

Reporter: Aviva Lev-Ari, PhD, RN

 

The stent retriever from Stryker was cleared for thrombectomy-eligible patients as initial therapy to reduce paralysis and other stroke disability only as an addition to tissue plasminogen activator (tPA). Previously, the device was approved only for use within 6 hours of ischemic stroke onset.

 

FDA Clears Trevo Stent Retriever for Up to 24 Hours Post-Stroke

FDA move follows expanded stroke thrombectomy guidelines

by Nicole Lou, Reporter, MedPage Today/CRTonline.org

“Time is critical following the onset of stroke symptoms. Expanding the treatment window from 6 to 24 hours will significantly increase the number of stroke patients who may benefit from treatment,” said Carlos Peña, PhD, director of the division of neurological and physical medicine devices at the FDA’s Center for Devices and Radiological Health, in a statement. “Healthcare providers and their patients now have better tools for treating stroke and potentially preventing long-term disability.”

The American Heart Association and American Stroke Association recently revised their guidelines to recommend stent retriever use up to 24 hours after symptom onset. This was announced at the International Stroke Conference in January, where the DEFUSE 3 trial added to the evidence from DAWN in demonstrating benefits to relatively late endovascular thrombectomy.

In particular, DAWN data were used to support the FDA’s latest decision. Trial investigators had reported more functional independence when patients were randomized to Trevo thrombectomy over medical management alone.

SOURCE

https://www.medpagetoday.com/cardiology/strokes/71183

 

FDA expands treatment window for use of clot retrieval devices in certain stroke patients

For Immediate Release

February 15, 2018

Summary

FDA expands treatment window for use of clot retrieval devices in certain stroke patients

Release

The U.S. Food and Drug Administration today cleared the use of the Trevo clot retrieval device to treat certain stroke patients up to 24 hours after symptom onset, expanding the device’s indication to a broader group of patients. This device is cleared for use as an initial therapy for strokes due to blood clots (also known as an acute ischemic stroke) to reduce paralysis, speech difficulties and other stroke disabilities and only as an addition to treatment with a medication that dissolves blood blots called tissue plasminogen activator (t-PA). The device was previously cleared for use in patients six hours after symptom onset.

“Time is critical following the onset of stroke symptoms. Expanding the treatment window from 6 to 24 hours will significantly increase the number of stroke patients who may benefit from treatment,” said Carlos Peña, Ph.D., director of the division of neurological and physical medicine devices at the FDA’s Center for Devices and Radiological Health. “Health care providers and their patients now have better tools for treating stroke and potentially preventing long-term disability.”

A stroke is a serious medical condition that requires emergency care and can cause lasting brain damage, long-term disability or even death. According to the Centers for Disease Control and Prevention, stroke is the fifth leading cause of death in the U.S. and is a major cause of serious disability for adults. About 795,000 people in the U.S. have a stroke each year. Ischemic strokes represent about 87 percent of all strokes.

The Trevo device was first cleared by the FDA in 2012 to remove a blood clot and restore blood flow in stroke patients who could not receive t-PA or for those patients who did not respond to t-PA therapy. In 2016, the FDA allowed expanded marketing of the device for certain patients in addition to treatment with t-PA if used within six hours of the onset of symptoms. Today’s expanded indication increases the amount of time that the device can be used once the symptoms are present.

Trevo is a clot removal device that is inserted through a catheter up into the blood vessel to the site of the blood clot. When the shaped section at the end of the device is fully expanded (up to three to six millimeters in diameter), it grips the clot, allowing the physician to retrieve the clot by pulling it back through the blood vessel along with the device for removal through a catheter or sheath.

The FDA evaluated data from a clinical trial comparing 107 patients treated with the Trevo device and medical management to 99 patients who had only medical management. About 48 percent of patients treated with the Trevo device were functionally independent (ranging from no symptoms to slight disability) three months after their stroke compared to 13 percent of patients who were not treated with the Trevo device.

Risks associated with using the Trevo device include a failure to retrieve the blood clot, embolization (blockage) to new territories in the brain, arterial dissections and vascular perforations, and access site complications at the femoral (thigh) artery entry point.

Trevo was reviewed through the premarket notification (510(k)) pathway. A 510(k) is a premarket submission made by device manufacturers to the FDA to demonstrate that the new device is substantially equivalent to a legally marketed predicate device. The FDA granted premarket clearance of the Trevo device to Concentric Medical Inc.

The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation’s food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.

SOURCE

https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm596983.htm

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