ALTERED DIASTOLIC [CA2-FAILURE(](I) HANDLING IN HUMAN VENTRICULAR MYOCYTES FROM PATIENTS WITH TERMINAL HEART)

To investigate whether the slow diastolic decay of [Ca2+](i) in myocar dium of patients with heart failure is a result of alterations of the Ca2+ adenosine triphosphatase of the sarcoplasmic reticulum or the sar colemma, [Ca2+](i) transients were recorded in voltage-clamped ventric ular cells isolated from hearts of patients with terminal heart failur e or from undiseased donor hearts. To isolate the [Ca2+](i)-reuptake f unction of the sarcoplasmic reticulum, myocytes were dialyzed via the patch pipette with Na+-free solution and incubated in Ca2+-free and Na +-free solution to inhibit Na+/Ca2+ exchange. After superfusion with C a2+-containing, Na+-free medium, the sarcoplasmic reticulum was loaded with Ca2+ through repetitive voltage-clamp pulses to +10 mV. Under th ese conditions, [Ca2+](i) decay was significantly slower in myocytes f rom patients with heart failure (538 +/- 66 msec) than in controls (30 5 +/- 16 msec; p < 0.05). After the addition of 10 mmol/L of caffeine, [Ca2+](i) levels did not show appreciable decay between two voltage-c lamp pulses in diseased and undiseased myocytes. We conclude that dias tolic decay of [Ca2+](i) in ventricular myocytes from patients with te rminal heart failure is partially the result of a decreased rate of Ca 2+ reuptake by the sarcoplasmic reticulum. Sarcolemmal Ca2+ adenosine triphosphatase does not contribute significantly to cytoplasmic [Ca2+] (i) removal during an individual heartbeat.