In cardiology, ventricular remodeling (or cardiac remodeling) refers to changes in the size, shape, structure, and function of the heart. This can happen as a result of exercise (physiological remodeling) or after an injury to the heart muscle (pathological remodeling). The injury is typically due to acute myocardial infarction (usually transmural or ST-segment elevation infarction) but maybe from several causes that result in increased pressure or volume, causing pressure overload or volume overload (forms of strain) on the heart.
Chronic hypertension, congenital heart disease with intracardiac shunting, and valvular heart disease may also lead to remodeling. After the insult occurs, a series of histopathological and structural changes occur in the left ventricular myocardium that leads to a progressive decline in left ventricular performance. Ultimately, ventricular remodeling may result in diminished contractile (systolic) function and reduced stroke volume.
Physiological remodeling is reversible while pathological remodeling is mostly irreversible. Remodeling of the ventricles under left/right pressure demand makes mismatches inevitable — pathologic pressure mismatches between the pulmonary and systemic circulation guide compensatory remodeling of the left and right ventricles. The term "reverse remodeling" in cardiology implies an improvement in ventricular mechanics and function following a remote injury or pathological process.
Ventricular remodeling may include ventricular hypertrophy, ventricular dilation, cardiomegaly, and other changes. It is an aspect of cardiomyopathy, of which there are many types. Concentric hypertrophy is due to pressure overload, while eccentric hypertrophy is due to volume overload.
Remodeling of the heart is evaluated by performing an echocardiogram. The size and function of the atria and ventricles can be characterized using this test.
Many factors influence the time course and extent of the remodeling, including the severity of the injury, subsequent events (recurrent ischemia or infarction), neurohormonal activation, genetic factors and gene expression, and treatment. Medications may attenuate remodeling. Angiotensin-converting enzyme (ACE) inhibitors have been consistently shown to decrease remodeling 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 remodeling. Carvedilol, a 3rd generation beta blocker, may reverse the remodeling process by reducing left ventricular volumes and improving systolic function. Early correction of congenital heart defects, if appropriate, may prevent remodeling, as will treatment of chronic hypertension or valvular heart disease. Often, reverse remodeling, or improvement in left ventricular function, will also be seen.