By AMERICAN HEART ASSOCIATION NEWS
Editor’s note: This is one in a series of Cardiovascular Genome-Phenome Study Discovery grants awarded by the American Heart Association to speed personalized treatments and prevention for heart disease.
Heart failure means the heart can’t keep up with its workload — providing your body with the oxygen and nutrients it needs — by pumping enough blood.
“While initially understood to occur when the heart was severely weakened by heart attacks, viruses or genetic mutations, heart failure can occur without any apparent weakness of the heart muscle,” said Nancy K. Sweitzer, M.D., director of the UA Sarver Heart Center, professor of medicine and chief of the Division of Cardiology in the University of Arizona College of Medicine–Tucson.
In heart failure with preserved ejection fraction, or HFpEF, the heart can’t fill normally with blood because the muscle is stiff or thickened. HFpEF, which affects about half of the nearly 6 million U.S. adults with heart failure, remains an enigma to many researchers, including Sweitzer, who plans to compare blood proteins to study why some people with HFpEF do poorly and others do well.
“We will measure blood protein levels in patients with HFpEF who die or are hospitalized compared to healthier patients,” said Sweitzer, one of 10 researchers each recently awarded $160,000 by the American Heart Association, with funding from AstraZeneca, to study new ways to individualize the treatment and prevention of heart disease.
HFpEF hits older people, especially women, more frequently. And because of the aging population, the prevalence of the condition is increasing. It frustrates doctors because it’s hard to diagnose, and there is no test to implicate the disease when people experience symptoms such as shortness of breath. And while there are treatments for heart failure’s risk factors, there is no cure for the condition.
Sweitzer said her team will use a technique that tests a large library of proteins to see what turns up. The hope is that it will provide new clues about why HFpEF happens and why some people become very sick — leading to new treatment possibilities.
Identifying proteins in this work will provide clues to biologic pathways important in HFpEF. Scientists can then study those clues to improve understanding of HFpEF and develop treatments better targeted at the actual disease mechanisms, she said.
“It has been suggested that HFpEF is actually more than one disease,” she said. “We will also look for protein signatures in subpopulations of HFpEF patients to see if we need to treat different things in different people.”
The need to take a deeper dive is critical, Sweitzer said.
“HFpEF is one of the few heart diseases affecting increasing numbers of people each year. It accounts for a disparate amount of Medicare spending,” said Sweitzer. “Use of discovery proteomics holds promise to unlock clues about why this disease happens, and when it does, why some people land in the hospital with severe, even life-threatening illness, while others are only mildly short of breath.”
Heart failure, one of the most common reasons people 65 and older go into the hospital, is being studied from different angles. Another researcher, Sanjiv Shah, M.D., director of the heart failure with preserved ejection fraction program at Northwestern University, is examining why some people with high blood pressure, a major risk factor for heart disease, develop heart failure while others don’t.