Abnormal intracellular calcium handling in myocardium from patients with end-stage heart failure.
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.
D000293:Adolescent; D000328:Adult; D002118:Calcium / Q000378:metabolism*; D009202:Cardiomyopathies / Q000378:metabolism* / Q000503:physiopathology; D003971:Diastole / Q000187:drug effects; D005260:Female; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D007424:Intracellular Fluid / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*; D012433:Ryanodine / Q000494:pharmacology; D012508:Sarcolemma / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D013599:Systole / Q000187:drug effects; D013696:Temperature; D014700:Verapamil / Q000494:pharmacology
D012433:Ryanodine; D014700:Verapamil; D002118:Calcium