Background: The mechanisms of ventricular enlargement and dysfunction during postinfarct remodeling remain largely unknown. Although global left ventricular architectural changes after myocardial infarction are well documented, differences in function between adjacent and remote noninfarcted myocardium during left ventricular remodeling have not been investigated. These functional differences may relate to regional differences in wall stress during contraction and may contribute to chamber enlargement and global dysfunction after infarction.
Methods and results: Anteroapical infarcts were produced in seven sheep by ligation of the mid left anterior descending coronary artery and second diagonal branch at thoracotomy. Magnetic resonance short-axis and long-axis images tagged by spatial modulation of magnetization were obtained before and 1 week, 8 weeks, and 6 months after infarction. Left ventricular volumes, mass, ejection fraction, and lengths of infarcted and noninfarcted segments were measured. Circumferential and longitudinal shortening in the subendocardium and subepicardium, wall thickness, and histopathology were assessed in infarcted segments and regions adjacent to and remote from the infarct border. We found that a difference in circumferential and longitudinal segmental shortening between adjacent and remote noninfarcted myocardium present at 1 week persisted up to 6 months after myocardial infarction. However, partial improvement of function in adjacent regions occurred during infarct healing between 1 and 8 weeks after infarction. Left ventricular volume increased up to 6 months after infarction, out of proportion to the concomitant eccentric hypertrophy, whereas the ejection fraction fell. Left ventricular dilatation late in the remodeling process was secondary to lengthening of noninfarcted segments, which were free of significant fibrosis.
Conclusions: Left ventricular dilatation and eccentric hypertrophy during remodeling are associated with persistent differences in segmental function between adjacent and remote noninfarcted regions. These functional differences may reflect increased wall stress in adjacent noninfarcted regions and contribute to the global dilatation and dysfunction characteristic of left ventricular remodeling after infarction.