2001, Number 3
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Rev Hosp M Gea Glz 2001; 4 (3)
Physiopathological mechanisms in cardiac failure
Gutiérrez VI, Domínguez MA
Language: Spanish
References: 229
Page: 75-95
PDF size: 495.36 Kb.
ABSTRACT
Heart failure has been defined as the mechanical failure of the heart to maintain systemic perfusion commensurate with the requirements of metabolizing tissues.
Left-ventricular dysfunction generally leads to overt heart failure, and once overt heart failure occurs myocardial failure and remodeling are likely to be progressive.
When the heart is damaged by an insult, compensatory mechanisms are activated to stabilize myocardial performance. These mechanisms, through increase in heart rate, contractility, volume expansion, and hypertrophy, stabilize myocardial performance for a short time. However, continued chronic use of these compensatory mechanisms to support the failing heart has definite downside. Activation of neurohormonal, cytokine, and mechanical stretch signaling pathways alters gene expression, cardiac myocyte loss, and cell remodeling, which all contribute to the progression of the myocardial dysfunction and remodeling that is part of the natural history of heart failure. Evidence of an increased rate of apoptosis has been detected in failing heart at the time of transplantation in humans, as well as in hearts from animals with experimentally induced hypertrophy and cardiomyopathy.
This article will focus on each of the various pathophysiological abnormalities found in patients with severe heart failure with a review of current research on the pathogenesis of this increasingly common condition.
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