Cardiovascular Medicine

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Cardiovascular Medicine

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News Article | May 3, 2017
Site: www.eurekalert.org

According to a new Finnish study, cardiorespiratory fitness is inversely related to risk of fatty liver. The research was conducted at the University of Turku, Finland, and shows that, despite the person's weight, achieving moderate cardiorespiratory fitness can protect from fatty liver. In the national Cardiovascular Risk in Young Finns Study, researchers measured the cardiorespiratory fitness of 463 Finns with a cycle ergometer exercise test and determined fatty liver with an ultrasound. The participants were 30-47 years of age. -The study revealed that cardiorespiratory fitness is inversely related to the risk of fatty liver - despite physical activity, smoking, alcohol use, serum lipids, insulin, glucose, and C-reactive protein. Importantly, the same results could be seen in participants who were obese, says Researcher Kristiina Pälve from Research Centre of Applied and Preventive Cardiovascular Medicine of the University of Turku. The research results are significant for public health: despite the person's weight, achieving a moderate level of cardiorespiratory fitness can protect from fatty liver. Fatty liver is a significant and expanding public health concern. It is related to several metabolic disturbances, increased risk of cardiovascular disease and type 2 diabetes. The research article was published in April in the Medicine & Science in Sports & Exercise journal. Pälve KS, Pahkala K, Suomela E, Aatola H, Hulkkonen J, Juonala M, Lehtimäki T, Rönnemaa T, Viikari JS, Kähönen M, Hutri-Kähönen N, Telama R, Tammelin T, Raitakari OT.: Cardiorespiratory Fitness and Risk of Fatty Liver. The Young Finns Study. Medicine & Science in Sports & Exercise. 2017 Apr 11. doi: 10.1111/MSS.0000000000001288. https:/ MD Kristiina Pälve, Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku tel. +358 2 333 7220, krsoma@utu.fi


News Article | April 18, 2017
Site: news.yahoo.com

(Reuters Health) - More than nine million people may miss out on cholesterol-lowering drugs that prevent heart attacks and strokes if doctors choose one set of medical guidelines over another, according to a new study. That's because the government-backed U.S. Preventive Services Task Force (USPSTF) set a higher threshold for use of the drugs, known as statins, than the American College of Cardiology and the American Heart Association (ACC/AHA). "I would say we’re still searching for the perfect guidelines," said lead author Michael Pencina, of Duke University in Durham, North Carolina. The 2013 ACC/AHA guidelines recommend statins for people ages 40 to 75 with at least a 7.5 percent risk of having a heart attack or stroke in the next 10 years. (The ACC/AHA cardiovascular risk estimator tool is available online here: http://bit.ly/2pPwoXh.) The ACC/AHA also recommends statins for people with cardiovascular disease, for diabetics between ages 40 and 75 and for adults with high levels of “bad” low-density lipoprotein cholesterol. The 2016 USPSTF recommendation endorses statins for people ages 40 to 75 with at least a 10 percent or greater risk of a heart attack or stroke over the next decade and at least one cardiovascular risk factor like diabetes or high blood pressure. Pencina told Reuters Health fewer people would be using statins under the more conservative USPSTF guidelines. "What we wanted to do is quantify the impact and look at what it means in terms of numbers." The researchers applied the recommendations to nationally representative data collected from 3,416 people without a history of cardiovascular disease between 2009 and 2014. Overall, 21.5 percent were already on statins to prevent heart attacks and strokes. An additional 24.3 percent would be on statins if all doctors followed the ACC/AHA guidelines, compared to an additional 15.8 percent if all doctors followed the USPSTF recommendation. The difference between the two guidelines represents about 9.3 million people in the United States, the researchers write in JAMA. Under the USPSTF guidelines, some diabetics would be excluded from statin use. More than half of those excluded would be middle-aged adults with a more than 30 percent average risk of a cardiovascular event over the next 30 years. "About one in three people are going to experience a cardiovascular event over the next 30 years," said Pencina. In a statement to Reuters Health, the USPSTF said its recommendations are based on the best available evidence about a preventive service's benefits and harms. "Because the USPSTF makes recommendations that are closely tied to the available evidence, we focused on recommending statins for the people who the evidence showed were most likely to benefit, though ultimately this decision should be made through a conversation between each patient and their doctor," the statement continued. In its review of evidence, the USPSTF focused on 19 trials involving a total of 71,344 people who had no history of cardiovascular disease. Overall, people were 14 percent less likely to die during the study period if they were taking statins than if they were taking a dummy pill or nothing at all. The risk of serious side effects from statins was also low. The USPSTF is always more conservative in its recommendations than professional organizations - not just for cholesterol, said Dr. Steve Nissen, chairman of the Robert and Suzanne Tomsich Department of Cardiovascular Medicine at the Cleveland Clinic. "Whether you treat or not treat is frankly something that should be a discussion between patient and physician," he told Reuters Health. "That’s how I do it." Nissen, who was not involved in the new study, said some entity should step in to clear up the confusion between the USPSTF, ACC/AHA and several other statin guidelines. "I’m not terribly happy to have multiple guidelines floating around out there," he said. Pencina said it's important for patients to be informed about their risk of cardiovascular disease and understand the risks and benefits of statins. "Both sets of guidelines - to their credit - recommend an informed decision between the patient and the clinician," he said. "Those are crucial."


A Finnish study coordinated by the Research Centre of Applied and Preventive Cardiovascular Medicine at the University of Turku shows that exposure to cardiovascular risk factors, such as high blood pressure, elevated serum LDL-cholesterol and smoking in childhood and adolescence, is associated with poorer learning ability and memory in middle age. With the aging population, cognitive deficits, such as difficulties in learning and memory, are becoming more common. Cardiovascular risk factors contribute to the occurrence of these deficits. Results from a longitudinal Finnish study show that the effects of cardiovascular risk factors on the brain begin already long before the occurrence of visible changes in cognitive performance. - Previous studies have focused on adulthood and old age, whereas this study brings novel information on the associations between cardiovascular risk factors and cognitive performance throughout the whole lifespan, says Senior Researcher Suvi Rovio from the Research Centre of Applied and Preventive Cardiovascular Medicine at the University of Turku. The results of this study can be exploited by turning the focus of prevention of the cardiovascular risk factors actively to children and adolescence in order to promote brain health in adulthood. High blood pressure, elevated serum cholesterol levels and smoking can be regulated through healthy lifestyle choices. The cognitive performance of over 2,000 participants was measured at the age of 34-49 years. The results showed that high blood pressure and serum LDL-cholesterol level measured in childhood and adolescence as well as smoking in adolescence were associated with poorer cognitive performance in midlife. This association remained regardless of the presence of such risk factors in adulthood. The difference in cognitive performance between those participants whose risk factor levels often exceeded the guideline values for cardiovascular risk factors and those always remaining within the guideline values was equivalent to the difference caused by six years of aging. This study is part of the ongoing national Cardiovascular Risk in Young Finns Study coordinated by the Research Centre of Applied and Preventive Cardiovascular Medicine at the University of Turku. Initially, 3,596 participants have been followed up repeatedly for 31 years for their cardiovascular risk factors from childhood to adulthood. The results were published in the Journal of the American College of Cardiology in May 2017. Cardiovascular Risk Factors From Childhood and Midlife Cognitive Performance The Young Finns Study Suvi P. Rovio et al. Journal of the American College of Cardiology Volume 69, Issue 18, May 2017 DOI: 10.1016/j.jacc.2017.02.060


PHILADELPHIA--A new strategy - an injectable antibody - for lowering blood lipids and thereby potentially preventing coronary artery disease and other conditions caused by the build-up of fats, cholesterol, and other substances on the artery walls, is supported by findings from two new studies from researchers in the Perelman School of Medicine at the University of Pennsylvania. The new approach targets a protein called ANGPTL3, a regulator of enzymes that clear triglycerides and other fat molecules from the blood. Research in recent years has hinted that inherited mutations in the ANGPTL3 gene that disable its function can decrease triglyceride, LDL cholesterol and HDL cholesterol levels. As reported in a paper published today online in the New England Journal of Medicine, researchers from Penn Medicine, Regeneron Pharmaceuticals, and a group of international collaborators studied ANGPTL3 in both humans and mice. They found that blocking ANGPTL3 activity with an investigative injectable antibody, known as evinacumab, reduced triglycerides by up to 76 percent and lowered LDL cholesterol 23 percent in human study participants, and largely reversed signs of atherosclerosis in a mouse models. Researchers also included a human genetics study of approximately 188,000 people, which found that carriers of mutations that disable ANGPTL3 had nearly 40 percent fewer incidents of coronary artery disease as compared to those with fully functioning ANGPTL3. "In the clinic, I treat many patients with very high triglycerides, but our current medications aren't lowering triglycerides enough in many cases. I'm delighted at the prospect of a new treatment that's a lot more potent, all the more because it lowers LDL at the same time," said study co-author Richard L. Dunbar, MD, assistant professor of Cardiovascular Medicine and member of Penn's Division of Translational Medicine and Human Genetics. "It's very reassuring to see that people with this genetic defect actually seem to be protected from heart disease. I think that really bodes well for a therapeutic that's targeting the ANGPTL3 pathway." In a separate study, published in the March issue of the Journal of the American College of Cardiology (JACC) researchers from Penn Medicine, Harvard Medical School, Washington University in St. Louis, and nine other institutions, who also studied humans and mice, reported on a similar set of findings. Among these was the discovery from another large population sample that carriers of ANGPTL3-inactivating mutations had a 34 percent lower rate of coronary artery disease compared to non-carriers. "We used different lines of evidence to show that ANGPTL3 deficiency is associated with a reduced risk of coronary artery disease," said study co-author Kiran Musunuru, MD, PhD, MPH, an associate professor of Cardiovascular Medicine at Penn. "But ultimately we were able to identify that fact that carriers of this genetic mutation did in fact experience a benefit - with little other health risk." The trial of research on ANGPTL3 as a potential target for atherosclerosis prevention began over a decade ago when scientists reported on two cases of familial hypolipidemia, a rare inherited condition involving abnormally low blood levels of cholesterol and triglycerides. Most cases of familial hypolipidemia are linked to other gene mutations that cause liver and digestive problems, but in members of this American family with the condition, Musunuru found mutations in the gene for ANGPTL3, and no associated health problems. In the NEJM study from Dunbar and colleagues, the antibody had similar effects in an initial clinical trial in 83 people, lowering the blood levels of triglycerides measured after fasting by about 75 percent at the highest dose, and lowering LDL cholesterol by about 30 percent. Statins and other drugs are already widely used to lower LDL cholesterol, but there are fewer options for lowering triglycerides. "For treating high triglyceride levels there's really nothing out there that's quite this potent, so that's where I expect this new approach to have its greatest therapeutic benefit," Dunbar said. Hypertriglyceridemia, a condition in which fasting triglyceride levels are greater than 150 mg/dL, is estimated to affect at least tens of millions of American adults. It is associated with coronary artery disease and other forms of atherosclerosis, and can lead to potentially fatal inflammation of the pancreas. In principle, the strategy of targeting ANGPTL3 could have an even broader use in treating atherosclerosis in the general population. The researchers found that in a mouse model of atherosclerosis, treatment with evinacumab reduced the area of atherosclerotic lesions by 39 percent. The population study findings, including those from the JACC study, suggest that even the partial inactivation of ANGPTL3--carriers typically have one mutant copy of the gene and one working copy--may be powerfully protective against coronary artery disease, which has long been one of the leading causes of death in developed countries. In the JACC study, for example, carriers of inactivating ANGPTL3 mutations had only a 17 percent reduction in triglycerides on average. But that modest reduction was associated with a 34 percent reduction in coronary artery disease risk. Moreover, Musunuru and his colleagues found that the people in their sample with the lowest blood levels of ANGPTL3 had a 35 percent lower rate of heart attacks compared to those with the highest ANGPTL3 levels. Dunbar noted that the population study findings probably have lain to rest a lingering concern about targeting ANGPTL3, namely its effect in lowering not just LDL and triglycerides but also the so-called "good cholesterol," known as HDL cholesterol. "If lowering HDL were a major concern, then I don't think we would have seen the evidence of overall benefit that we did in this study," he said. The two studies together suggest that single copies of inactivating ANGPTL3 mutations are found in roughly one of every 250 people of European descent, whereas people with mutations in both copies of the gene--as in the family studied by Musunuru and colleagues--are much rarer. According to Dunbar, the next logical step would be to take evinacumab into larger clinical trials to study its safety, effectiveness, and optimal dosing. "The effect of even a single dose lasts for several months, and it's plausible that with multiple doses we would see an even deeper and more sustained effect," he said. Additional Penn authors on the NEJM study include Scott Damrauer, MD, Aeron Small, and Daniel J. Rader MD, and the Journal of the American College of Cardiology study include Xiao Wang, PhD, Daniel J. Rader, MD, and Danish Saleheen, MBBS, PhD. Funding sources for the studies detailed in this press release included grants from the National Heart, Lung, and Blood Institute (NHLBI) (R01HL131961), (K08HL114642), (R01HL118744), (R01HL127564) and (R21HL120781) and Regeneron Pharmaceuticals. Editor's Note: Dunbar has received grant support from and consulted for Regeneron Pharmaceuticals, Inc. Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $6.7 billion enterprise. The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 20 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $392 million awarded in the 2016 fiscal year. The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center -- which are recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report -- Chester County Hospital; Lancaster General Health; Penn Wissahickon Hospice; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine. Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2016, Penn Medicine provided $393 million to benefit our community.


News Article | May 28, 2017
Site: www.sciencedaily.com

A new strategy -- an injectable antibody -- for lowering blood lipids and thereby potentially preventing coronary artery disease and other conditions caused by the build-up of fats, cholesterol, and other substances on the artery walls, is supported by findings from two new studies from researchers in the Perelman School of Medicine at the University of Pennsylvania. The new approach targets a protein called ANGPTL3, a regulator of enzymes that clear triglycerides and other fat molecules from the blood. Research in recent years has hinted that inherited mutations in the ANGPTL3 gene that disable its function can decrease triglyceride, LDL cholesterol and HDL cholesterol levels. As reported in a paper published online in the New England Journal of Medicine, researchers from Penn Medicine, Regeneron Pharmaceuticals, and a group of international collaborators studied ANGPTL3 in both humans and mice. They found that blocking ANGPTL3 activity with an investigative injectable antibody, known as evinacumab, reduced triglycerides by up to 76 percent and lowered LDL cholesterol 23 percent in human study participants, and largely reversed signs of atherosclerosis in a mouse models. Researchers also included a human genetics study of approximately 188,000 people, which found that carriers of mutations that disable ANGPTL3 had nearly 40 percent fewer incidents of coronary artery disease as compared to those with fully functioning ANGPTL3. "In the clinic, I treat many patients with very high triglycerides, but our current medications aren't lowering triglycerides enough in many cases. I'm delighted at the prospect of a new treatment that's a lot more potent, all the more because it lowers LDL at the same time," said study co-author Richard L. Dunbar, MD, assistant professor of Cardiovascular Medicine and member of Penn's Division of Translational Medicine and Human Genetics. "It's very reassuring to see that people with this genetic defect actually seem to be protected from heart disease. I think that really bodes well for a therapeutic that's targeting the ANGPTL3 pathway." In a separate study, published in the March issue of the Journal of the American College of Cardiology (JACC) researchers from Penn Medicine, Harvard Medical School, Washington University in St. Louis, and nine other institutions, who also studied humans and mice, reported on a similar set of findings. Among these was the discovery from another large population sample that carriers of ANGPTL3-inactivating mutations had a 34 percent lower rate of coronary artery disease compared to non-carriers. "We used different lines of evidence to show that ANGPTL3 deficiency is associated with a reduced risk of coronary artery disease," said study co-author Kiran Musunuru, MD, PhD, MPH, an associate professor of Cardiovascular Medicine at Penn. "But ultimately we were able to identify that fact that carriers of this genetic mutation did in fact experience a benefit -- with little other health risk." The trial of research on ANGPTL3 as a potential target for atherosclerosis prevention began over a decade ago when scientists reported on two cases of familial hypolipidemia, a rare inherited condition involving abnormally low blood levels of cholesterol and triglycerides. Most cases of familial hypolipidemia are linked to other gene mutations that cause liver and digestive problems, but in members of this American family with the condition, Musunuru found mutations in the gene for ANGPTL3, and no associated health problems. In the NEJM study from Dunbar and colleagues, the antibody had similar effects in an initial clinical trial in 83 people, lowering the blood levels of triglycerides measured after fasting by about 75 percent at the highest dose, and lowering LDL cholesterol by about 30 percent. Statins and other drugs are already widely used to lower LDL cholesterol, but there are fewer options for lowering triglycerides. "For treating high triglyceride levels there's really nothing out there that's quite this potent, so that's where I expect this new approach to have its greatest therapeutic benefit," Dunbar said. Hypertriglyceridemia, a condition in which fasting triglyceride levels are greater than 150 mg/dL, is estimated to affect at least tens of millions of American adults. It is associated with coronary artery disease and other forms of atherosclerosis, and can lead to potentially fatal inflammation of the pancreas. In principle, the strategy of targeting ANGPTL3 could have an even broader use in treating atherosclerosis in the general population. The researchers found that in a mouse model of atherosclerosis, treatment with evinacumab reduced the area of atherosclerotic lesions by 39 percent. The population study findings, including those from the JACC study, suggest that even the partial inactivation of ANGPTL3 -- carriers typically have one mutant copy of the gene and one working copy -- may be powerfully protective against coronary artery disease, which has long been one of the leading causes of death in developed countries. In the JACC study, for example, carriers of inactivating ANGPTL3 mutations had only a 17 percent reduction in triglycerides on average. But that modest reduction was associated with a 34 percent reduction in coronary artery disease risk. Moreover, Musunuru and his colleagues found that the people in their sample with the lowest blood levels of ANGPTL3 had a 35 percent lower rate of heart attacks compared to those with the highest ANGPTL3 levels. Dunbar noted that the population study findings probably have lain to rest a lingering concern about targeting ANGPTL3, namely its effect in lowering not just LDL and triglycerides but also the so-called "good cholesterol," known as HDL cholesterol. "If lowering HDL were a major concern, then I don't think we would have seen the evidence of overall benefit that we did in this study," he said. The two studies together suggest that single copies of inactivating ANGPTL3 mutations are found in roughly one of every 250 people of European descent, whereas people with mutations in both copies of the gene -- as in the family studied by Musunuru and colleagues -- are much rarer. According to Dunbar, the next logical step would be to take evinacumab into larger clinical trials to study its safety, effectiveness, and optimal dosing. "The effect of even a single dose lasts for several months, and it's plausible that with multiple doses we would see an even deeper and more sustained effect," he said.


SAN CARLOS, Calif.--(BUSINESS WIRE)--BioCardia®, Inc. (OTC:BCDA) today announced publication of a study in the International Heart Journal.1 According to the study, delivery of stem cell therapy to the heart using the Helix™ transendocardial delivery system results in superior cell delivery than either percutaneous intra-coronary infusion or direct injection in an open chest procedure. Use of the Helix system resulted in 18 times higher retention of injected cells in the myocardium than intra-coronary artery infusion, and three times higher than direct injection to the heart using a straight needle. Yoshiake Mitsutake, MD from Stanford University’s Division of Cardiovascular Medicine was the lead author of the article. The authors commented, “Our study indicated that the efficacy of cell delivery using a transendocardial helical infusion delivery system was more efficient than either transepicardial injection or intra-coronary infusion. The Helix transendocardial delivery system has the potential to improve local cell delivery and retention in cardiovascular cell-based therapy, thus potentially improving clinical outcomes.” Recognizing that there have been variable results for stem cell therapies for cardiovascular disease to date, the authors, who included researchers from BioCardia and Stanford University, intended to study the impact of optimizing the delivery method on cell retention, as a potential strategy to improve patient outcomes. In this pre-clinical study, 12 swine subjects underwent collection of bone marrow cells and delivery of processed stem cells via one of the three delivery methods. PET-CT images were acquired one hour after cell injections to determine cell retention. The Helix system is used in the company’s investigational CardiAMP® therapy, which is designed to deliver a high dose of a patient’s own bone marrow cells directly to the point of cardiac dysfunction, potentially stimulating the body’s natural healing mechanism after a heart attack. The therapy, including the Helix system, is currently being studied in the U.S. in the CardiAMP Heart Failure Trial, a phase III, multi-center, randomized, double-blinded, sham-controlled study which is enrolling up to 260 patients at up to 40 centers nationwide. For information about eligibility or enrollment in the CardiAMP Trial, please visit www.clinicaltrials.gov or ask your cardiologist. The Helix system is actively being used, or has been used, in nine other clinical trials, including EXCELLENT (EXpanded CELL ENdocardiac Transplantation), RECARDIO (Phase I Trial of Endocavitary Injection of Bone Marrow Derived CD133+ Cells in Ischemic Refractory Cardiomyopathy), and TRIDENT (TRansendocardial Stem Cell Injection Delivery Effects on Neomyogenesis Study). The company recently entered into new agreements, or amended existing agreements, with AstraZeneca and the University of Washington with respect to evaluating the Helix system for their therapeutic programs. “The Helix system is an integral part of our investigational CardiAMP therapy, and we are pleased to see these promising results relative to how it may improve tissue retention of cell therapy,” said BioCardia Chief Executive Officer Peter Altman. “We look forward to continued enrollment in our CardiAMP Phase III trial to understand how the investigational therapy may help U.S. heart failure patients in need.” BioCardia, Inc., headquartered in San Carlos, CA, is developing regenerative biologic therapies to treat cardiovascular disease. CardiAMP® and CardiALLO® cell therapies are the company’s biotherapeutic product candidates in clinical development. For more information, visit www.BioCardia.com. This press release contains forward-looking statements as that term is defined under the Private Securities Litigation Reform Act of 1995. Such forward-looking statements include, among other things, the potential efficacy and outcomes from use of our products and therapies and references to the enrollment of our Phase III trial. Actual results could differ from those projected in any forward-looking statements due to numerous factors. Such factors include, among others, the inherent uncertainties associated with developing new products or technologies, unexpected expenditures, the ability to raise the additional funding needed to continue to pursue BioCardia’s business and product development plans, competition in the industry in which BioCardia operates and overall market conditions, and whether the combined funds will support BioCardia’s operations and enable BioCardia to advance its pivotal Phase 3 CardiAMP cell therapy program. These forward-looking statements are made as of the date of this press release, and BioCardia assumes no obligation to update the forward-looking statements.


News Article | May 24, 2017
Site: www.eurekalert.org

In a Correspondence in The New England Journal of Medicine, researchers led by Susan Cheng, MD, MPH, of Brigham and Women's Hospital, explore the impact of efforts to reduce risk factors for stroke in black patients. Cheng and colleagues write, "There has been a disparity between blacks and whites in the rates at which the contributions of risk factors for stroke have diminished. Given the potential for interventions to modify the risk of stroke, targeted efforts to address particular risk factors may reduce the overall burden of stroke among blacks." Cheng is available to speak with media about this publication. Physician and researcher, Division of Cardiovascular Medicine, Brigham and Women's Hospital Senior author of this NEJM Correspondence WHERE The New England Journal of Medicine WHAT Researchers examined trends in the contributions of major risk factors for stroke -- hypertension, obesity, diabetes, hypercholesterolemia, and smoking -- in 15,350 adults, 26 percent of whom were black. Over an average of 24 years, 1,243 participants experienced a stroke. Researchers determined the population attributable risk, an estimate of the proportion of disease in the study population that can be attributed to an exposure. They found that the contributions of major risk factors for stroke - such as hypertension, smoking and diabetes - are decreasing, likely reflecting increasing awareness and treatment. The contributions of all risk factors combined decreased from 73 percent in 1990 to 41 percent in 2010 across the entire participant sample However, when analyzing according to race, researchers found that the contribution of all risk factors combined was associated with a greater decline in the risk of stroke among whites (66 percent in 1990 to 34 percent in 2010) than among blacks (84 percent in 1990 to 63 percent in 2010). The difference was primarily driven by the disparity in the reduction of hypertension. Researchers note that for most risk factors that contribute to the incidence of stroke, declining trends among men were similar to those among women. WHY Cheng, a physician and researcher in the Division of Cardiovascular Medicine at BWH is the author of over 100 peer-reviewed publications. Most recently, she was senior author on a separate paper, published in the British Medical Journal, about the prognosis and heritability of high blood pressure that begins early in life. Her research focuses on how aging promotes the development of cardiovascular risk and disease.


News Article | May 14, 2017
Site: www.futurity.org

The prevalence of women with heart disease delivering babies increased by 24 percent from 2003-2012, report researchers. This jump, reported in the American Journal of Cardiology, may prompt greater awareness of heart disease in women of childbearing age and heighten individual screening of heart disease in pregnant patients. Heart disease is the most common cause of death among pregnant women in the United States and other developed countries. There remain significant gaps in understanding of the prevalence, trends, and outcomes of heart disease in pregnancy in the US population. Investigation of trends and outcomes in heart disease and pregnancy has been limited. In this study, researchers used the Healthcare Cost and Utilization Project’s National Inpatient Sample to better determine the trends and relationship between women with heart disease and delivering babies. To do this, they studied existing heart conditions and outcomes using a large sample of women with heart disease (81,295) and without heart disease (39,894,032). “We learned that in addition to the high and growing prevalence of women with heart disease delivering babies, the reasons are mainly related to increases in women delivering babies with diseases such as cardiomyopathy, adult congenital heart disease, and pulmonary hypertension,” says lead author Kathleen Stergiopoulos, professor of medicine in Stony Brook University’s Division of Cardiovascular Medicine, and a specialist in heart disease in women at the Stony Brook Heart Institute. The study also shows that major adverse cardiac events in pregnant women with heart disease increased by nearly 19 percent, and there is a significant and gradual increase in these events for women who have delivered babies and have heart disease. The most common events for women with heart disease were heart failure and arrhythmia. According to Stergiopoulos, while a maternal death is a rare event, the findings should affect clinical practices when caring for women with heart disease who are pregnant. She emphasizes that future strategies to mitigate risk in these women include individualized preconception counseling and heart disease risk stratification, meticulous pregnancy follow-up, and a coordinated approach to labor and delivery for those with heart disease that includes specialists from cardiology, maternal fetal medicine, obstetrical anesthesiology, and neonatology. Support for the research came from the American Heart Association and an American Medical Association Foundation Seed Grant.


Multicenter study shows AF ablation is safe and just as effective in patients with CHD compared to those with normal hearts PHILADELPHIA--Congenital heart disease (CHD) includes a range of defects that occur in the heart which patients are born with, such as a hole in the heart's wall, a leaky valve or even an inversion in the heart's orientation. CHD was once a severe condition often resulting in early death, but now, more and more CHD patients are living long and healthy lives. Therefore, as this population grows, so does the number of patients who are treated for other complications of their disease, such as early onset atrial fibrillation (AF), a quivering or irregular heartbeat that can lead to blood clots, stroke, heart failure and other complications. AF is often treated with a catheter ablation, a minimally invasive procedure in which the areas of the heart causing the irregularity are cauterized, but until now, there was limited data to support the safety and efficacy of treating CHD patients with an AF ablation. In a new study presented today at the Heart Rhythm Society's 38th Annual Scientific Session in Chicago, researchers from the Perelman School of Medicine at the University of Pennsylvania have found that CHD patients--even with complex defects--can safely undergo ablation for AF, with similar success rates as patients with normal hearts. "Treatment for atrial fibrillation is critical, whether the patient has a normal heart or whether they have complex congenital heart disease," said the study's presenter Jackson J. Liang, DO, a third-year cardiovascular disease fellow in the Perelman School of Medicine at the University of Pennsylvania. "In fact, atrial fibrillation can be especially detrimental in patients with complex congenital heart disease since they may be more reliant on the "atrial kick" provided during sinus rhythm. Unfortunately for some CHD patients, AF ablation may be more challenging due to the presence of complex anatomy, and the optimal ablation strategy for these patients remains to be defined." In this multicenter study, researchers performed a retrospective analysis of 69 CHD patients who underwent AF ablation, by collecting data from Penn, University of Colorado, University of California San Francisco, and Texas Cardiac Arrhythmia Institute at St. David's Medical Center. Researchers looked at those who underwent AF ablation for paroxysmal (intermittent) or persistent AF between 2008 and 2016. They identified the type of CHD, and tracked the ablation strategy - pulmonary vein isolation (PVI), PVI with additional ablation, or non-PV ablation only. "Some physicians may not be aware that catheter ablation can be performed to treat atrial fibrillation in patients with congenital heart disease, and instead they may prescribe anti-arrhythmic medications," said David Frankel, MD, an assistant professor of Cardiovascular Medicine at Penn. "We hope this study will increase awareness of catheter ablation as a viable treatment option for atrial fibrillation in these patients." Of the 69 patients, 34 had paroxysmal AF and 25 had complex CHD. The team defined complete success as freedom from recurrent AF for one year off antiarrhythmic medications, and partial success as freedom from AF recurrences for one year on previously ineffective anti-arrhythmic medications. At one year, researchers concluded that 53 percent of the patients had complete success with an additional 13 percent experiencing partial success. 92 percent of patients underwent a PVI approach, while seven percent had a non-PVI ablation alone. "We also found that 12 patients needed a repeat ablation within the first year, but most notably, there were no major procedural complications identified and only five minor complications, which is on par with rates in non-CHD patients," said Liang. "While PVI should remain the cornerstone of ablation, an individualized approach utilizing pre-procedural imaging to help to define the anatomy is necessary to improve outcomes in patients with CHD." Researchers conclude that AF ablation in this complex population was safe and effective, with similar outcomes to those seen in non-CHD patients, despite anatomical differences. However, they noted that more research is needed to further define the challenges and optimal ablation strategies in CHD patients. Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $6.7 billion enterprise. The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 20 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $392 million awarded in the 2016 fiscal year. The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center -- which are recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report -- Chester County Hospital; Lancaster General Health; Penn Wissahickon Hospice; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine. Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2016, Penn Medicine provided $393 million to benefit our community.


News Article | May 10, 2017
Site: www.eurekalert.org

PHILADELPHIA - Bacteria in the gut microbiome drive the formation of cerebral cavernous malformations (CCMs), clusters of dilated, thin-walled blood vessels in the brain that can cause stroke and seizures, according to new research published this week in Nature by researchers from the Perelman School of Medicine at the University of Pennsylvania. Led by Mark Kahn, MD, a professor of Cardiovascular Medicine, the team's research suggests that altering the microbiome in CCM patients may be an effective therapy for this cerebrovascular disease. CCM disease, which occurs in about one in 100 to 200 people, can present in two forms. One is sporadic, accounting for 80 percent of cases, and is most frequent in older individuals. The remaining 20 percent are familial, inherited cases. In 2016, the Kahn lab discovered the molecular mechanism in endothelial cells that underlies the formation of CCMs. In the current Nature study, the team discovered that this molecular pathway is activated by TLR4, a receptor for the bacterial molecule lipopolysaccharide (LPS). Activation of TLR4 on brain endothelial cells by LPS vastly accelerated CCM formation. Conversely, if TLR4 was removed from endothelial cells genetically, or if the mice were treated with drugs that block TLR4 function, CCM formation is prevented. Since TLR4 primarily responds to LPS from Gram-negative bacteria, Alan Tang, an MD-PhD student in the Kahn lab, proposed that bacteria from the animal's gut microbiome may drive CCM formation. To test this theory, he examined CCM formation in mice that were housed under germ-free conditions (in collaboration with the Children's Hospital of Philadelphia through the PennCHOP Microbiome Program Core Facility) or treated with antibiotics to reduce the number of bacteria living in the gut. In both cases, CCM formation was dramatically reduced, demonstrating a key role for bacteria in the pathology of CCM disease. The team next sought evidence that bacterial LPS-TLR4 signaling might also support CCM formation in human patients. They worked with researchers at the University of New Mexico (UNM) and the University of California, San Francisco (UCSF) who have studied several hundred patients who carry an identical mutation in one CCM gene but display a widely variable disease course. "Some of these patients experience severe stroke by the age of two and others have no symptoms over their lifetime," Kahn said. "What makes the disease outcome so variable?" Working with the team from UNM and UCSF, they discovered that genetic variations that raise the amount of TLR4 that is produced are associated with higher numbers of CCM lesions, suggesting that the key role for LPS-TLR4 signaling identified in mice is also present in humans. These studies identify an unexpected, direct link between the microbiome and a common cerebrovascular disease. "This suggests that treatments designed to block TLR4 signaling or alter the microbiome may be used to treat this disease," Kahn said. These studies were in part supported by the National Institutes of Health (R01HL094326, P01NS092521) and a PennCHOP Microbiome Program Pilot & Feasibility Award Grant. Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $6.7 billion enterprise. The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 20 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $392 million awarded in the 2016 fiscal year. The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center -- which are recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report -- Chester County Hospital; Lancaster General Health; Penn Wissahickon Hospice; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine. Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2016, Penn Medicine provided $393 million to benefit our community.

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