DIASTOLIC DYSFUNCTION IN CORONARY AND HYPERTENSIVE HEART-DISEASE

Diastolic dysfunction is an early sign in the temporal sequence of isc hemic events in coronary heart disease. The ischemic cascade, beginnin g with an oxygen demand supply imbalance and metabolic alterations, id entifies diastolic disorders of the left ventricle (LV) as an early ph enomenon, even before systolic dysfunction, ECG changes or chest pain occur. Although the physiology of diastolic function is complex, the f actors contributing to diastolic disturbances can be differentiated in to intrinsic and extrinsic LV abnormalities. Intrinsic mechanisms incl ude (i) impaired L-V relaxation, (ii) increased overall chamber stiffn ess, (iii) increased myocardial stiffness, and (iv) increased LV async hrony. All these factors are part of myocardial hypertrophy. The main determinant of active LV relaxation is the intracellular concentration of adenosine triphosphate (ATP). Cardiac hypertrophy, by increasing t otal coronary flow demand due to elevated left ventricular mass, slows the energy dependent process of relaxation resulting in a decreased c oncentration of calcium ATPase in the sarcoplasmic reticulum. Myocardi al hypertrophy additionally leads to an increase of myocardial mass re lative to the cavity volume. The degree of hypertrophy, which is the m ain determinant of chamber stiffness, shifts the diastolic pressure-vo lume relation such that the same volume is associated with a higher pr essure. The main, if not unique, determinant of myocardial diastolic t issue distensibility is the structure and concentration of the collage n. Consequently tissue stiffness is augmented in coronary disease with reparative interstitial fibrosis or scar following myocardial infarct ion and in myocardial hypertrophy in which the LV collagen concentrati on is elevated due to reactive fibrosis. An increase in regional async hrony of LV contraction and relaxation is a result of regional ischemi a as well as of LV hypertrophy and tissue fibrosis. So LV asynchrony, a common sign in coronary disease, is increased by additional LV hyper trophy and fibrosis. Factors extrinsic to the LV causing diastolic dis orders include (i) increased central blood volume, which will increase left ventricular pressure, without altering the LV pressure-volume re lation, and (ii) ventricular interaction mediated by pericardial restr aint, which may cause a parallel upward shift of the diastolic LV pres sure-volume relation. Improved understanding of LV relaxation and fill ing helps to treat LV diastolic disturbances. Yet, treating diastolic dysfunction in coronary and/or hypertensive heart disease, both intrin sic and extrinsic abnormalities should be considered.