Excitation-contraction coupling in heart failure.
A central feature of the excitation-contraction cycle-myocardial Ca2+ handling--is altered in humans with cardiomyopathy. Many adaptive changes in excitation-contraction mechanisms observed in aged or hypertensive animals also supervene in the failing human heart. Heart failure may thus emerge when such changes lead to systolic or diastolic insufficiency.
Laboratory of Cardiovascular Science, National Institute on Aging, Baltimore.
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Lakatta
D000222:Adaptation, Physiological; D000255:Adenosine Triphosphate / Q000378:metabolism; D000375:Aging / Q000502:physiology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D004573:Electrolytes / Q000378:metabolism; D006329:Heart Conduction System / Q000503:physiopathology*; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D008564:Membrane Potentials / Q000502:physiology; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000378:metabolism / Q000494:pharmacology
D004573:Electrolytes; D018377:Neurotransmitter Agents; D000255:Adenosine Triphosphate; D002118:Calcium