Defect in the molecular level in the cells of the heart may be responsible for causing heart failures.
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.
Researchers had found some drastic changes in the way muscle cells in the failing heart handle calcium. 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. 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.
This calcium storage site is known as the sarcoplasmic reticulum (SR), and it resembles a convoluted, flattened sack within the cell. The delicate, membrane-bound walls of the SR are penetrated with thousands of RyR channels. These serve as gatekeepers that allow calcium to flood into the cell to initiate contraction.
The amount of calcium stored in the SR determines the strength of the heartbeat and how much blood the heart ejects when it contracts. At the end of a contraction, the channels close tightly. Molecular pumps, also located in the walls of the SR, then suck the released calcium back into the SR to prepare for the next contraction.