Hemodynamic overload and the regulation of myofibrillar protein degradation.

T he growth and hypertrophy of left ventricular myocardium in response to pressure or volume overload or segmental loss of functional myocardium was once considered a purely beneficial, structural adaptation to reduce or normalize systolic and/or diastolic wall stress.' This concept has been challenged, however, by a growing body of evidence indicating that most forms of left ventricular hypertrophy (LVH) are associated with increased morbidity and mortality caused by progressive left ventricular contractile dysfunction, irreversible muscle injury, and the ultimate development of congestive heart failure. Thus, a rational approach to the patient with structural heart disease associated with LVH requires a clear understanding of the underlying metabolic processes responsible for the growth of cardiac muscle in response to hemodynamic overload and the resultant changes in muscle structure that may be responsible for this progressive functional