Resumen

ULATE-MONTERO, Guido  y  ULATE-CAMPOS, Adriana. Update in physiopathological mechanisms in heart failure. Acta méd. costarric [online]. 2008, vol.50, n.1, pp.5-12. ISSN 0001-6002.

Heart failure is one of the most frequent clinical syndromes in medical practice;it appears when the heart is unable to pump enough volume of blood to supply the tissue ’s requirements.This article reviews the most recent information regarding the mechanisms involved in the pathophysiology of heart failure,the main goal is to offer the knowledge necessary to understand and manage properly this condition.In heart failure,as a response to the low cardiac output,a series of neuroendocrine systemic mechanisms are activated,but they contribute to deteriorate the clinical status;this happens with the sympathetic and the renin-angiotensin-aldosterone systems,which end up producing endothelial damage,increase of oxidative radicals,apoptosis, cardiac fibrosis and generation of arrhythmias.Also there is an increase in the secretion of natriuretic peptides,which tend to regulate some of the exacerbated neuroendocrine responses, but with time their effect tend to diminish.At the cellular and molecular level a series of alterations occur in the regulation of intracellular Ca²⁺, as well as in some of the ionic currents that play a role in the generation of action potentials in cardiac myocytes.Cardiac remodeling precedes the clinical manifestations of heart failure and contributes to its deterioration.Chemical messengers like endothelin-1,norepinephrine and angiotensin II,activate the MAP kinases cascade and provoke cardiac hypertrophy favoring the development of ischemia and the appearance of arrhythmias.Pharmacological management of heart failure must aim the mechanisms affected,it must block the deleterious actions of the neuroendocrine systems,avoiding the loss of myocytes, the generation of fibrosis and the production of cardiac arrhythmias,in order to achieve this goal an appropriate management of intracellular levels of Ca²⁺ is required.

Palabras clave : Heart failure; cardiac remodeling; neurohumoral activation; excitation-contraction coupling; arrhythmias; apoptosis.

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