Extremely high blood pressure that leads to strokes, heart attacks and acute kidney damage, classified as hypertensive emergency, is five times higher in inner-city African-American patients than the national average, according to a recent study co-lead by a Rutgers researcher.
The study, which is the largest one of its kind to compare the development of hypertensive emergency in a United States inner city, appears in the journal Blood Pressure.
One in three adults have high blood pressure known as hypertension, with the highest rates among African-Americans. In addition to being very common, high blood pressure in African-Americans develops earlier in life but has lower control rates compared to other racial-ethnic groups. Higher than average blood pressure results in the development of serious health complications that come with it. The study sought to determine the prevalence and risk factors of high blood pressure escalating to severe cases among African-Americans.
The cholesterol-lowering drugs called statins have demonstrated substantial benefits in reducing the risk of heart attacks and strokes caused by blood clots (ischemic strokes) in at-risk patients. Since statins are associated with a low risk of side effects, the benefits of taking them outweigh the risks, according to a scientific statement from the American Heart Association that reviewed multiple studies evaluating the safety and potential side effects of these drugs. It is published in the Association’s journal Circulation: Arteriosclerosis, Thrombosis and Vascular Biology.
According to the statement, one in four Americans over the age of 40 takes a statin drug, but up to 10 percent of people in the United States stop taking them because they experience symptoms that they may assume are due to the drug, but may not be.
“In most cases, you should not stop taking your statin medication if you think you are having side effects from the drug — instead, talk to your healthcare provider about your concerns. Stopping a statin can significantly increase the risk of a heart attack or stroke caused by a blocked artery,” said Mark Creager, M.D., former president of the American Heart Association and director of the Heart and Vascular Center at Dartmouth-Hitchcock Medical Center in Lebanon, New Hampshire.
A study led by Massachusetts General Hospital (MGH) investigators may lead to a significant expansion in the number of stroke patients who can safely be treated with intravenous tPA (tissue plasminogen activator), the “clot busting” drug that has greatly reduced stroke-related disability and deaths in eligible patients. The report, published online in Annals of Neurology, describes the results of a trial using MR-based imaging technologies to identify patients likely to be within 4.5 hours of stroke onset, even though their initial symptoms had not been witnessed.
“In up to 25 percent of stroke patients, the start of their symptoms is unwitnessed, preventing them from receiving tPA,” says Lee Schwamm, MD, executive vice chair of the MGH Department of Neurology and director of the MGH Comprehensive Stroke Center, co-lead and corresponding author of the paper. “For many of these patients, the first time anything is noticed is when they get up from sleeping. Our study showed — for the first time — that tPA could be given safely to patients with stroke of unwitnessed onset if their imaging suggested the stroke was very early in its progression and they met other treatment criteria. These results pave the way for a large randomized trial of tPA in patients with unwitnessed strokes.”
While immune cells called neutrophils are known to act as infantry in the body’s war on germs, a National Institutes of Health-funded study suggests they can act as medics as well. By studying rodents, researchers showed that instead of attacking germs, some neutrophils may help heal the brain after an intracerebral hemorrhage, a form of stroke caused by ruptured blood vessels. The study suggests that two neutrophil-related proteins may play critical roles in protecting the brain from stroke-induced damage and could be used as treatments for intracerebral hemorrhage.
“Intracerebral hemorrhage is a damaging and often fatal form of stroke for which there are no effective medicines,” said Jaroslaw Aronowski, M.D., Ph.D., professor, department of neurology, at the University of Texas Health Science Center at Houston, and senior author of the study published in Nature Communications. “Our results are a hopeful first step towards developing a treatment for this devastating form of stroke.”
The overall rate of stroke in the United States has been declining in recent years and while that has been good news, a new study suggests it may be primarily good news for men. The research, published in the August 9, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology, found that while the stroke rate for men declined during the study period, for women it remained the same.
“For years, women have had a lower overall rate of stroke compared with men, but now men appear to be approaching similar rates. While any decrease in rates of stroke is of course a good thing, it leaves one to wonder why women’s rates are not going down to the same extent,” said study author Tracy E. Madsen, MD, ScM, of the Alpert Medical School of Brown University in Providence, R.I. “At the end of our study, stroke rates for men and women were nearly the same.”
Recent figures from the Centers for Disease Control and Prevention (CDC) show that stroke has decreased to the fifth leading cause of death for men yet it remains the fourth leading cause of death for women.
Many patients with an irregular heartbeat, known as atrial fibrillation, are not receiving recommended blood thinning medication they need to prevent strokes, according to a study published today in the Journal of the American College of Cardiology.
People who have atrial fibrillation are at a very high risk for stroke. However, if they take blood thinners known as oral anticoagulants (OACs), it can reduce their risk by two-thirds. Recent clinical trials have also shown that a new type of blood thinner known as a direct oral anticoagulant (DOAC) can be just as — or even more — effective in preventing stroke in these patients.
“When DOACs were first introduced in 2010, there was an increase in use of oral anticoagulation,” said Lucas N. Marzec, MD, the study’s lead author and a clinical cardiac electrophysiologist at the University of Colorado and researcher with the Colorado Cardiovascular Outcomes Research Consortium in Aurora, Colorado. “However, there are still wide disparities in how they are prescribed. For example, we found that patients at the highest risk of stroke were the least likely to be treated with a DOAC.”
Determining the cause of an ischemic stroke — one caused by an interruption of blood supply — is critical to preventing a second stroke and is a primary focus in the evaluation of stroke patients. But despite that importance, physicians have long lacked a robust and objective means of doing so. Now a team of investigators at the Athinoula A. Martinos Center for Biomedical Imaging at the Massachusetts General Hospital (MGH) and the MGH Stroke Service have developed a software package that provides evidence-based, automated support for diagnosing the cause of stroke. Their study validating the package — called Causative Classification of Stroke (CCS) — was published online in JAMA Neurology.
“This was a much-needed study because, although stroke classifications systems are often used in research and clinical practice, these systems are not always able to produce subtypes with discrete pathophysiological, diagnostic and prognostic characteristics,” says Hakan Ay, MD, a vascular neurologist, Martinos Center investigator and senior author of the JAMA Neurology paper. “We found that the CCS-based classifications provided better correlations between clinical and imaging stroke features and were better able to discriminate among stroke outcomes than were two conventional, non-automated classification methods.”
Tiny particles in air pollution have been associated with cardiovascular disease, which can lead to premature death. But how particles inhaled into the lungs can affect blood vessels and the heart has remained a mystery. Now, scientists have found evidence in human and animal studies that inhaled nanoparticles can travel from the lungs into the bloodstream, potentially explaining the link between air pollution and cardiovascular disease. Their results appear in the journal ACS Nano.
The World Health Organization estimates that in 2012, about 72 percent of premature deaths related to outdoor air pollution were due to ischemic heart disease and strokes. Pulmonary disease, respiratory infections and lung cancer were linked to the other 28 percent. Many scientists have suspected that fine particles travel from the lungs into the bloodstream, but evidence supporting this assumption in humans has been challenging to collect. So Mark Miller and colleagues at the University of Edinburgh in the United Kingdom and the National Institute for Public Health and the Environment in the Netherlands used a selection of specialized techniques to track the fate of inhaled gold nanoparticles.
Researchers at The University of Manchester have discovered that a potential new drug reduces the number of brain cells destroyed by stroke and then helps to repair the damage.
A reduction in blood flow to the brain caused by stroke is a major cause of death and disability, and there are few effective treatments.
A team of scientists at The University of Manchester has now found that a potential new stroke drug not only works in rodents by limiting the death of existing brain cells but also by promoting the birth of new neurons (so-called neurogenesis).
Despite their different triggers, the same molecular chain of events appears to be responsible for brain cell death from strokes, injuries and even such neurodegenerative diseases as Alzheimer’s. Now, researchers at Johns Hopkins say they have pinpointed the protein at the end of that chain of events, one that delivers the fatal strike by carving up a cell’s DNA. The find, they say, potentially opens up a new avenue for the development of drugs to prevent, stop or weaken the process.
A report on the research appears in the Oct. 7 issue of the journal Science.
The new experiments, conducted in laboratory-grown cells, build on earlier work by research partners Ted Dawson, M.D., Ph.D., now director of the Institute for Cell Engineering at the Johns Hopkins University School of Medicine, and Valina Dawson, Ph.D., professor of neurology. Their research groups found that despite their very different causes and symptoms, injury, stroke, Alzheimer’s disease, Parkinson’s disease and the rare, fatal genetic disorder Huntington’s disease have a shared mechanism of a distinct form of “programmed” brain cell death they named parthanatos after the personification of death in Greek mythology and PARP, an enzyme involved in the process.