Ca(2+)-currents and intracellular [Ca2+]i-transients in single ventricular myocytes isolated from terminally failing human myocardium.

The purpose of the present study was to test the hypothesis that steps between the excitation of the cell membrane and contraction are altered in cardiac failure. Ca(2+)-currents and [Ca2+]i-transients were measured in single ventricular myocytes isolated from explanted hearts of patients with terminal heart failure undergoing transplantation, or from donors whose organs could not be used for technical reasons. Peak Ca(2+)-current densities were unchanged, as was the current-voltage relation. However, in myocytes isolated from severely failing hearts resting [Ca2+]i-levels were elevated, peak [Ca2+]i-transients were significantly smaller, and the diastolic decline of [Ca2+]i was markedly slowed. As the trigger for the release of Ca2+ from the sarcoplasmic reticulum is unchanged and the systolic [Ca2+]i-transient is reduced, severe heart failure can be described as partial electromechanical uncoupling.