Calcium Metabolism in the Normal and Failing Heart

Abstract
An abnormality in calcium flux is more likely to account for the depressed contractility of failing myocardium than any other biochemical defect; studies at the molecular level are gradually delineating the specific nature of the abnormality. It has become clear that mitochondrial uptake of calcium is increased in the failing myocardial cell, with profound effects on the amount available to initiate contraction.

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