Rationale of echocardiographic assessment of left ventricular wall stress and midwall mechanics in hypertensive heart disease

Abstract

Active reduction of left ventricular chamber size during systole is the final effect of complex interaction mechanisms involving layers of differently oriented myocardial fibres, the shortening of which is less than the one measured as shortening of the left ventricular diameter at the level of the endocardium. This biological phenomenon is particularly evident in conditions such as arterial hypertension in which left ventricular geometry is altered. Due to the double effect of contraction on both the longitudinal (shortening) and transverse (thickening) axes of the myocardial fibres, the shortening of single myocardial fibres is amplified at the level of the endocardium and this amplification is a function of wall thickness. Increased wall thickness can enhance at the endocardial level the effect of myocardial fibres with reduced shortening, allowing preservation of ejection fraction despite depressed midwall shortening, through a 'contractile gradient' proceeding from epicardium to endocardium. This is detectable using tagged MRI or even quantitative echocardiography. This discrepancy between chamber and wall mechanics, seen in arterial hypertension and in other clinical conditions characterized by alteration of left ventricular geometry, is at the basis of the better prediction of cardiovascular risk in hypertensive patients by measures of left ventricular wall mechanics than by measures of left ventricular chamber function.