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Cardiac remodeling: Basic aspects

Jay N Cohn, MD
Section Editor
Wilson S Colucci, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC


Heart failure (HF) is associated with significant morbidity and mortality attributable largely to cardiac structural changes with associated cardiac dysfunction. (See "Prognosis of heart failure".)

Cardiac dysfunction is defined as an alteration in the relationship between preload (often defined by left ventricular filling pressure) and stroke volume. This relationship is depicted by Frank-Starling curves, which identify a shift downward and to the right as cardiac dysfunction (figure 1).

Remodeling is defined as alteration in the structure (dimensions, mass, shape) of the heart (called cardiac or ventricular remodeling) in response to hemodynamic load and/or cardiac injury in association with neurohormonal activation. Remodeling may be described as physiologic or pathologic [1]; alternatively, remodeling may be classified as adaptive or maladaptive [2].

The remodeling process frequently includes increases in myocardial mass. The heart can respond to environmental stimuli by growth (increased myocardial mass) or shrinkage (atrophy) with a dynamic range of at least 100 percent [3]. Myocardial hypertrophy is most properly defined as increased cardiomyocyte size which may occur with or without an increase in overall myocardial mass; however, the term "hypertrophy" has also been used to denote increased myocardial mass and/or wall thickness.

Physiologic remodeling is a compensatory change in the dimensions and function of the heart in response to physiologic stimuli such as exercise and pregnancy. This type of remodeling is seen in athletes and has been called "athlete's heart." (See "Definition and classification of the cardiomyopathies", section on 'Athlete's heart'.)

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Literature review current through: Dec 2017. | This topic last updated: Aug 23, 2017.
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