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.
Lakatta
E G
EG
Laboratory of Cardiovascular Science, National Institute on Aging, Baltimore.
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