The findings, by researchers at the Ohio State University Dorothy M. Davis Heart and Lung Research Institute, show that specialized proteins called ryanodine receptors (RyRs) malfunction in the failing heart. The RyRs form channels that become leaky, leading to calcium imbalances that prevent the heart from contracting effectively and relaxing adequately. The condition worsens until the heart can no longer work as a pump.
The root causes of heart failure are not known.
"We found some drastic changes in the way muscle cells in the failing heart handle calcium," says principal investigator Sandor Gyorke, professor of physiology and cell biology at the OSU Davis Heart and Lung Research Institute. "Discovery of this mechanism suggests at least one potential target for treating the causes of this disease in a rational manner."
Currently, the only way to correct heart failure is by heart transplantation.
About 4.9 million Americans are currently living with heart failure, and an estimated 265,000 of them die of it yearly. Those with the condition are at six to nine times greater risk of experiencing sudden cardiac death than someone in the general population. From 1992 to 2002, deaths from heart failure rose 35 percent and the incidence is expected to keep rising.
Calcium plays a fundamental role in muscle contraction, particularly in heart muscle. A heart contraction begins when the heart's pacemaker sends an electrical signal to heart-muscle cells. The electrical signal triggers the release of calcium from a large storage site within each muscle cell. The released calcium activates the muscle cell's contractile machinery, which causes the cell, and the heart as a whole, to contract.