Heart failure is a pathophysiological condition in which the circulation of blood provided by the pumping activity of the heart fails to deliver oxygen at a rate commensurate with tissue metabolic requirements. Heart failure is most often caused by cardiac injury related to myocardial infarction, myocarditis, or cardiac toxins, or chronic pressure or volume overload of the heart related to hypertension or valvular heart disease. A complex array of neurohormonal and inflammatory responses to cardiac injury and/or overload induces a pathological process called ventricular remodeling, characterized by progressive myocyte hypertrophy and interstitial fibrosis, with associated abnormalities in myocellular metabolism and contractile function. The remodeling process serves to preserve stroke volume, so is not typically associated with clinical symptoms of heart failure in its early stages. The remodeling process is associated with progressive myocyte loss via apoptosis, and is strongly linked to clinical progression of disease. Symptomatic heart failure, manifest as congestion and reduced exercise capacity, occurs when the ventricular remodeling process has advanced to late stages, and is attributable to a combination of both cardiac and extra-cardiac factors that limit cardiac output reserve, regional blood flow, and peripheral oxygen utilization.
KeywordsMyocardial injury Myocardial infarction Preload Afterload Cardiac output Ventricular remodeling Neurohormonal activation Inflammation Apoptosis
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