Many factors influence the time course and extent of<unk> , including the severity of the injury, secondary events (recurrent ischemia or infarction), neurohormonal activation, genetic factors and gene expression, and treatment. Medications may attenuate<unk> . Angiotensin-converting enzyme (ACE) inhibitors have been consistently shown to decrease<unk>  in animal models or transmural infarction and chronic pressure overload. Clinical trials have shown that ACE inhibitor therapy after myocardial infarction leads to improved myocardial performance, improved ejection fraction, and decreased mortality compared to patients treated with placebo. Likewise, inhibition of aldosterone, either directly or indirectly, leads to improvement in<unk> . Carvedilol, a 3rd generation beta blocker, may actually reverse the<unk>  process by reducing left<unk>  volumes and improving systolic function. Early correction of congenital heart defects, if appropriate, may prevent<unk> , as will treatment of chronic hypertension or valvular heart disease. Often, reverse<unk> , or improvement in left<unk>  function, will also be seen.
Ventricular remodeling
Myocardial scarring
Cardiac fibrosis
Pacemaker crosstalk
Myocardial stunning
Cardiomyocyte proliferation
Coronary vasospasm
Ventricular hypertrophy