Functional consequences of structural adaptation of the heart in hypertension.
Extent of myocardial shortening is inversely related to afterload. Maintenance of normal stroke volume (SV) in hypertension will therefore require elevation of cardiac performance. The question of whether left ventricular hypertrophy, which develops during chronic hypertension, enhances or depresses cardiac function has been examined experimentally. Cardiac function curves have been constructed and maximal cardiac output has been determined during rapid volume load in intact animals or in isolated perfused hearts from spontaneously hypertensive rats (SHR) and from normotensive rats. When preload, afterload, heart rate, and contractility are controlled, maximal performance is enhanced in the SHR heart, and its ability to increase contractility on elevations in afterload (homeometric autoregulation) is reset in proportion to the increase in arterial blood pressure. Although a reduced volume compliance of the SHR left ventricle has not been documented, its diastolic properties will still be influenced by the increased wall thickness. The reason is that a higher pressure is required to induce a given diastolic wall stress when wall thickness/radius ratio is increased according to Laplace's law. Since wall stress in turn determines the extent of myocardial shortening, maintenance of normal stroke volume in SHR calls for increased diastolic pressures or increased inotropic stimulation. The structural adaptation of the heart to hypertension will thus enhance its systolic performance, but will influence its diastolic properties so that secondary adjustments are required to enhance ventricular filling or the inotropic state of the heart, or both.
D000818:Animals; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology; D003971:Diastole; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D009200:Myocardial Contraction; D051381:Rats; D011918:Rats, Inbred SHR; D013599:Systole