Calcium does not contribute to heart failure

In animal models, the group headed by Karl Toischer from University of Göttingen, showed that pharmacological decrease of calcium leak from the sarcoplasmatic reticulum into heart muscle cells can correct arrhythmia but did not improve pumping malfunction. Mice that had their arrhythmias corrected by Rycal S36, a modulator of cardiac ryanodine receptor (RyR2)-mediated calcium leak, survived longer than other mice with similar models of heart disease, suggesting that targeting calcium leak in this way could have some therapeutic value.

Heart failure is a leading cause of death and disability worldwide, and about 5.7 million adults in the US are affected by heart failure each year. Plugging the leak in mice with heart disease did not prevent the defective cardiac remodeling associated with heart failure, but did correct arrhythmia. The researchers also found that increasing calcium leak in mouse and human cells did not exacerbate heart failure, confirming that leaky cells contribute more to arrhythmia than heart muscle remodeling.