Pathophysiology of the hypertrophied heart in man
Krayenbuehl, H. P. ; Hess, O. ; Hirzel, H.
In: European Heart Journal, 1982, vol. 3, p. 125-131
Ajouter à la liste personnelle- Summary
- Increase in sympathetic drive, the Frank-Starling effect and myocardial hypertrophy represent the three compensatory mechanisms in chronic mechanical overloading of the heart. Chronic pressure overload is associated with concentric and chronic volume overload with eccentric hypertrophy. The changes in ventricular geometry have an important influence on the ejection dynamics of the heart; the magnitude of fiber shortening is the predominant mechanism for systolic reduction of cavity size in eccentric hypertrophy whereas in concentric hypertrophy the contribution of systolic wall thickening to ejection becomes very important. The main abnormality of diastolic function in patients with left ventricular (LV) hypertrophy is the increase of chamber stiffness indicated by the steepened slope of the diastolic pressure-volume relationship. In contrast LV diastolic myocardial stiffness as evaluated from the stress-strain relationship remains relatively unaltered in hypertrophy unless there is massive admixture of fibrosis in the LV wall (congestive cardiomyopathy). Finally LV relaxation (rate of pressure decay) is often impaired in hypertrophied states although the relationship of abnormalities of relaxation to alterations of systolic function remains to be established. There has been considerable debate whether in secondary LV hypertrophy from chronic pressure or volume overload myocardial contractility is normal or depressed. We have recently shown that in patients with myocardial hypertrophy from aortic stenosis ejection phase indexes of contractility are correlated inversely to peak systolic wall stress and that this relationship is modulated according to the actual inotropic state. The patients on the downward shifted curve (depressed contractile state) had a significantly increased LV angiographic mass. Thus advanced LV hypertrophy in chronic pressure overload appears to be associated with compromised contractile state. The structural and metabolic abnormalities which may be ultimately responsible for the depression of contractility of the hypertrophied human myocardium encompass the following findings: reduced intracellular volume fraction of myofibrils; massive increase of the average fiber diameter and increased variability of the thickness of the individual fibers and reduced activity of the myofibrillar ATPase