A scar cannot generate force, so the infarcted segment becomes akinetic or dyskinetic — it either does not move or bulges outward during systole. The remaining viable myocardium must therefore produce the same stroke volume from less muscle. It compensates in two ways: acutely through the Frank–Starling mechanism, where increased end-diastolic volume stretches the surviving myocytes and increases their force of contraction, and chronically through neurohormonal activation — sympathetic drive and the renin–angiotensin–aldosterone system — which raises contractility and preserves blood pressure.
These compensations are effective in the short term but become maladaptive. Increased wall stress in the border zone and the surviving ventricle stimulates hypertrophy and interstitial fibrosis. The ventricle dilates, and because the infarcted region is thin and non-contractile, the dilation is asymmetric: the scar thins further and the chamber becomes more spherical. This is adverse remodeling. The Laplace relationship, \(\sigma = \frac{P \cdot r}{2h}\), explains why it is self-reinforcing: as the chamber radius \(r\) increases and the wall thickness \(h\) decreases, wall stress \(\sigma\) rises for the same pressure \(P\), which drives further dilation and further thinning.
The functional endpoint is a ventricle that is larger, more spherical, and less efficient. Ejection fraction falls, filling pressures rise, and the patient develops heart failure. The extent of remodeling depends on infarct size, infarct location, and whether reperfusion was achieved early enough to salvage myocardium at the border zone.