Ventricular dysfunction due to myocardial infarction is a result of a pathophysiological 'continuum', proceeding from a fully reversible alteration to the irreversible loss of myocardial tissue. Various studies have suggested that oxidative stress induced by acute ischemia may play a role for the progression of ventricular dysfunction to heart failure. Oxidative injury on the myocardium may be described as the result of two processes; a) a deficit of the endogenous anti-oxidant defence during ischemia, and b) a production of oxygen free radicals occurring during early reperfusion. Ventricular dysfunction may result from a direct action of oxygen free radicals on ion translocating proteins, particularly vulnerable to radical-induced oxidation at key sulfhydryl groups, and an indirect calcium-induced activation of proteases, leading to excitation-contraction uncoupling. A progressive increase in oxygen free radical injury and involvement of oxidative stress have been observed in the evolution of ventricular dysfunction, suggesting that oxidative stress may be an important determinant factor for prognosis. The specific role of oxidative stress in the progression of ischemia to failure is yet to be entirely defined; however, new therapeutic approaches may possibly influence the course of this progression by counteracting the oxidative injury.
|Number of pages||10|
|Journal||Heart Failure Reviews|
|Publication status||Published - 1999|
- Oxidative stress
- Ventricular dysfunction
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine