Approximately 4.9 million Americans are presently living with heart failure, and an estimated 265,000 patients die from the condition annually.

Researchers at the Ohio State University Dorothy M. Davis Heart and Lung Research Institute, led by Sandor Gyorke, have identified a molecular defect that allows calcium to leak out of heart-muscle cells, resulting in a chemical imbalance that diminishes the heart's ability to contract and relax adequately.

Calcium plays an essential role in heart-muscle contraction. It is stored in the cells until the heart's natural pacemaker sends an electrical signal for its release. The amount of calcium stored determines the strength of the heartbeat and how much blood the heart ejects when it contracts.

Calcium Channels Malfunction

When the electrical signal has been received, calcium is released into the cell via thousands of channels. The calcium then activates a contraction in each cell and in the heart as a whole.

The channels close tightly after each release of calcium, and molecular pumps suck the calcium back into storage to prepare for the next contraction.

Heart failure occurs when the channels do not close tightly after a contraction, researchers suggest. Strong contractions are not possible when too little calcium is in storage, and the heart muscle cannot relax when too much calcium remains released in the cell.

The condition causes the heart to grow progressively weaker over time.

Potential Non-Surgical Solution

Approximately 4.9 million Americans are presently living with heart failure, and an estimated 265,000 patients die from the condition annually. They are at six to nine times greater risk of experiencing sudden cardiac death than someone in the general population. Deaths from heart failure rose 35 percent between 1992 and 2002, and the incidence is expected to keep rising.

Heart transplant surgery is currently the only effective method of correcting heart failure, but Gyorke hopes this new information will lead to less radical forms of treatment.

"We found some drastic changes in the way muscle cells in the failing heart handle calcium," he notes. "Discovery of this mechanism suggests at least one potential target for treating the causes of this disease in a rational manner."