LV dysfunction begins with some injury to, or stress on, the myocardium and is generally a progressive process. The principal manifestation of such progression is a change in the geometry and structure of the left ventricle such that the chamber dilates and/or hypertrophies and becomes more spherical—a process referred to as cardiac remodeling. Specific patterns of ventricular remodeling occur in response to the imposed augmentation in workload. With pressure overload, the increased wall tension during systole initiates parallel addition of new myofibrils, causing wall thickening and concentric hypertrophy. With volume overload the wall tension increases during diastole, initiating series addition of new sarcomeres, resulting in chamber enlargement and eccentric hypertrophy. Ventricular dilation allows the chamber to eject an adequate stroke volume with less muscle shortening, but wall stress is increased as described by the Laplace relationship:
Wall tension = P x R/2h where P = intracavity pressure, R = the radius of the chamber, and h = the thickness of the chamber wall.
Increasing wall tension requires higher oxygen demand for the same performance. Myocardial hypertrophy with increasing wall thickness allows the heart to overcome pressure overload with decreased wall tension.
Was this article helpful?