Key result
Chronic post-MI LV dysfunction leads to progressive dilatation and symptomatic HF at 1.5-3 years.
This review highlights the pathophysiological mechanisms of post-myocardial infarction remodeling, emphasizing that infarct size, location, and early hemodynamics drive progressive left ventricular dilatation and symptomatic heart failure.
May support extended post-MI surveillance for LV dysfunction; hypothesis-generating for therapies targeting the 1.5-3 year window.
A major consequence of chronic cardiac dysfunction is chronic overload of contractile myocardium. Various aetiologies, in reaction to this, may induce compensatory mechanisms consisting of excentric (dilatation) and concentric hypertrophy. Chronic left ventricular dysfunction is caused most frequently by myocardial infarction. Left ventricular dilatation and hypertrophy occurs in patients with extensive infarction. Dilatation may at first be compensatory, restoring stroke volume within 4 weeks of the infarct. However, as dilatation progresses, left ventricular ejection fraction and stroke volume deteriorate during exercise and at rest, and finally pulmonary capillary wedge pressure increases and patients become symptomatic 1.5-3 years after the infarct. Major determinants of progressive left ventricular dilatation and deterioration of haemodynamics are a depressed left ventricular ejection fraction, angiographically determined infarct size, stroke volume early (4 days) after myocardial infarction, infarct location (anterior/inferior) and the grade (TIMI) of perfusion of the infarct-associated coronary artery. Chronic loading and unloading may accelerate or decelerate this process. Efficiency and energy reserve (phosphocreatine) of the dilated ventricles is reduced. Further intrinsic changes in surviving myocardium include morphological and functional disturbance of coronary microcirculation.
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Ertl et al. (1993) conducted a review in Chronic cardiac dysfunction and heart failure. Chronic left ventricular dysfunction post-myocardial infarction leads to progressive dilatation, deterioration of hemodynamics, and symptomatic heart failure 1.5-3 years after the infarct.
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