&NA;Intracellular Ca2+release and reuptake are essential for contraction and relaxation of normal heart muscle. Intracellular Ca2+transients were recorded with aequorin during isometric contraction of myocardium from patients with end‐stage heart failure. In contrast to controls, contractions and Ca2+transients of muscles from failing hearts were markedly prolonged, and the Ca2+transients exhibited 2 distinct components. Muscles from failing hearts showed a diminished capacity to restore low resting Ca2+levels during diastole. These experiments provide the first direct evidence from actively contracting human myocardium that intracellular Ca2+handling is abnormal and may cause systolic and diastolic dysfunction in heart failure. (Circulation Research1987;61:70‐76)