Heart failure affects more then 5 million Americans and usually develops when the heart is unable to pump enough blood to the body. As the heart tries to compensate by pumping faster, it usually grows larger and becomes less effective.
A heart attack, high blood pressure, abnormal heart valves and diabetes predispose someone to heart failure. But symptoms are often missed until the person begins to feel fatigued and has trouble breathing. By then, it is often too late, said Liggett.
One in five chronic heart failure patients is dead within a year of diagnosis. More than half of those diagnosed die within five years, and only one in four survives for 10 years.
When someone experiences heart failure, adrenalin binds to the heart cell's beta-adrenergic receptors and stimulates the heart to work harder.
Beta blockers are among the most commonly prescribed medications for heart failure. In many patients, they relieve the heart by blocking the response from the receptors. The two most commonly prescribed beta blockers are carvedilol and metoprolol, commonly sold under the trade names Coreg and Toprol, respectively.
"It's really protecting the heart from chronic overstimulation," Kass said.
But the effectiveness of beta blockers varies from one patient to the next. It can take as long as a year to determine if they're working, and side effects include dizziness, fatigue, fluid retention and erectile dysfunction, Liggett said.
"You could say that up to 50 percent of the patients on beta blockers have less than an optimal response," he said.
The study does not resolve why beta blockers work better in some people than others. But the results may lead to screening tests that narrow down which patients are right for beta blockers.
"We'll be able to say, `Here's a group we could screen for,' and if you believe in it strongly enough, you could say you don't need to go on them," Kass said.
There are probably several other genetic variations that work this way, Liggett said, and he continues to search for them.
In their study, Liggett and a team of researchers compiled genetic profiles of 2,000 black and white volunteers in Cincinnati, Kansas City and Atlanta. Some volunteers had heart failure, while others were healthy.
The profiles showed a variation in GRK5, a gene known to curb receptor activity in heart failure patients. Most people had genes that produced a protein called glutamine in cells throughout their bodies, including heart cells. Some had another protein called leucine.
