The researchers suggested that their findings could lead to new treatments to reduce people's risk for this condition, in which the heart suddenly stops beating due to electrical instability.
The findings were to be presented Sunday at the American Chemical Society's annual meeting in Indianapolis.
"Sudden cardiac death due to this electrical instability causes an estimated 325,000 deaths annually in the United States alone," Dr. Mukesh Jain, of Case Western Reserve University in Cleveland, said in a chemical society news release. "That includes the three out of four heart disease deaths in people aged 35 to 44."
"In all too many cases, there is no second chance. The first event is the last event," Jain said. "Our research points the way toward possible ways of easing that toll -- new drugs that could reduce that risk, for example."
Sudden cardiac death most often strikes in the morning, between 6 a.m. and 10 a.m., followed by a smaller peak in the late afternoon. Scientists have long believed that there's a link between sudden cardiac death, the leading cause of heart attacks, and people's circadian rhythm, the 24-hour body clock in the brain that regulates sleep cycles.
The researchers said they discovered a protein, known as KLF15, that plays a role in the regulation of the heart's electrical activity. Levels of this protein change throughout the day like clockwork to allow substances to enter and leave cells in the heart in order to maintain a normal heartbeat.
Initially, the researchers discovered that patients with heart failure have lower levels of this protein. Using lab mice, the researchers then found that mice with low levels of KLF15 have the same heart problems as people with sudden cardiac death.
"It turns out that people with low KLF15 levels are the ones that are most susceptible to these sudden-death episodes that occur in the early morning hours," Jain said. "We think that if we could in some way boost KLF15 levels in patients with heart problems, maybe we can reduce the occurrence of these arrhythmias and [sudden cardiac death]."
The researchers said they're examining drugs that increase levels of KLF15 in the body. They noted, however, that this protein also affects other body processes.
"If we can find out how these compounds are boosting KLF15 levels, then maybe we can make much more targeted and specific therapies for the heart that would prevent [sudden cardiac death], but leave the other KLF15-related processes alone," Jain said. He added that other researchers are trying to develop genetic tests to identify people with a mutation in the KLF15 gene that could put them at risk for sudden cardiac death.
The American Heart Association provides more information on cardiac arrest.
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