American Heart Association 2016 meeting highlights
Woodruff Health Sciences Center | Nov. 15, 2016
Emory University School of Medicine researchers have been presenting dozens of research abstracts — oral presentations and posters — at the 2016 American Heart Association Scientific Sessions meeting in New Orleans this week. Here are just a few.
Highlighted clinical research topics: Telomeres + circulating progenitor cells, food deserts, and troponin as a risk marker for atrial fibrillation.
Highlighted basic research topics: Mesenchymal stem cells as a treatment for heart attack in animal models, a gradual release drug for atrial fibrillation, and how microparticles from stored blood affect blood vessels.
Aging, in general, depletes our bodies’ regenerative capacities. Arshed Quyyumi, MD, and colleagues at Emory Clinical Cardiovascular Research Institute have shown how circulating progenitor cells or CPCs, which regenerate blood vessels and correlate with outcomes in cardiovascular disease, are a finite resource and depleted with unhealthy aging.
Working with Quyyumi, research fellow Muhammad Hammadah, MD, is presenting data on how leukocyte telomere length interacts with the levels of CPCs, in a study of mental stress ischemia in 566 patients with stable coronary artery disease. Telomeres, the ends of chromosomes, tend to shorten with aging and cellular stress. Their length has been a widely studied biomarker.
Emory researchers have previously shown that people living in “food deserts” in the Atlanta area are more likely to have a higher burden of cardiovascular risk factors and higher markers of cardiovascular risk. Research fellow Heval Mohamed Kelli, MD, followed up on this work with a larger group of patients from the Emory Cardiovascular Biobank. Food deserts are defined by the USDA by two components: low-income and low access to healthy food. Here, Kelli showed that neighborhood income is the stronger statistical driver of adverse cardiovascular outcomes.
The biomarker troponin is routinely used to assess acute damage to the cardiac muscle. In addition, at low levels, it predicted the development of atrial fibrillation in a group of patients with suspected coronary artery disease (Emory Cardiovascular Biobank). Higher levels (more than the median of 4.7 pg/mL) doubled the risk of incident AF over five years. Also notable: the biomarkers FDP, suPAR, CRP, and HSP70 were not associated with atrial fibrillation after adjustment for traditional cardiovascular risk factors. Presented by William Schultz, MD, working with Quyyumi and colleagues. For background, please see related work on troponin + mental stress ischemia by Hammadah.
Cell therapy, using the patient’s own cells to reduce damage to the heart after a heart attack, has been a hot topic. Mesenchymal stem cells are derived from the bone marrow and can’t replace heart muscle. But they do exert anti-inflammatory and anti-oxidative effects, Eric Shin, MD, Rebecca Levit, MD, and colleagues showed in a rat model of heart attack. The researchers encapsulated the cells in a way previously described by Levit.
The drug amiodarone is often prescribed for control of heart arrhythmias such as atrial fibrillation, but can have toxic effects upon the lungs, eyes, thyroid and liver. Rebecca Levit, MD, Andres Garcia, PhD (from Georgia Tech) and colleagues have developed a method to deliver amiodarone directly to the heart in an extended release gel to reduce off-target toxicity. The method, including a minimally invasive delivery device, was tested in rats and pigs.
The effects of transfusions of old stored blood on surgery or intensive care patients have been debated and tested in clinical trials. Red blood cells are known to generate “microparticles” during storage. Adam Mitchell, MD, Charles Searles, MD, and colleagues investigated the effects of these microparticles on human endothelial cells.