Inotropy, calcium, and heart failure: a personal perspective.
The medical treatment of heart failure has improved significantly in the last decade, yet despite the reduction of morbidity and mortality, heart attacks and stroke cause 15 million deaths each year. Cardiovascular disease (CVD) constitutes 50% of all deaths worldwide. Indeed, heart disease represents a continuing global burden, despite all the advances. When considering the major objective of medical treatment of heart failure, the paradigm has shifted from increasing cardiac output of the failing heart by augmenting contractility to a decrease in afterload and inhibition of neurohumors affecting heart muscle. Nevertheless, a direct increase in contractility is still appropriate in some conditions of heart failure for a short-term beneficial effect. This article reviews certain aspects of cellular and molecular mechanisms to provide a framework for problem solving in this vital field.
Schwartz
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Institute of Molecular Pharmacology and Biophysics, University of Cincinnati College of Medicine, Ohio 45267-0828, USA.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D015220:Calcium Channels / Q000235:genetics / Q000378:metabolism; D000252:Calcium-Transporting ATPases / Q000235:genetics / Q000378:metabolism; D006333:Heart Failure / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*; D011379:Prognosis; D014158:Transcription, Genetic
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D000252:Calcium-Transporting ATPases; D002118:Calcium