Determination of Left Ventricular Preload and Afterload by Quantitative Echocardiography in Man

Abstract

Left ventricular circumferential wall stress at end-diastole (preload) and at the end of isovolumic left ventricular contraction (afterload) was calculated in 48 subjects with chronic myocardial and valvular heart disease by using left ventricular internal dimensions and wall thickness measured by quantitative echocardiography, left ventricular end-diastolic pressure, and aortic end-diastolic pressure. These calculations were then compared with similar determinations made using quantitative angiocardiography. Left ventricular preload and afterload determined by quantitative echocardiography and quantitative angiocardiography correlated significantly (r = 0.978 and 0.864, respectively). Left ventricular preloads of 30 X 10 3 dynes/cm 2 in subjects with mitral stenosis and 39 X 10 3 dynes/cm 2 in subjects with coronary artery disease unassociated with left ventricular dysfunction or mitral regurgitation were close to or within the normal range (32 X 10 3 ± 4 X 10 3 dynes/cm 2 ). Left ventricular preload in subjects with compensated volume overload was comparable with the angiocardiographically calculated values of 63 x 10 3 , 57 X 10 3 , and 53 X 10 3 dynes/cm 2 in subjects with coronary artery disease plus mitral regurgitation, mitral regurgitation, and aortic regurgitation, respectively. Left ventricular preload was most elevated in subjects with coronary artery disease associated with segmental left ventricular dyskinesis or akinesis. No significant differences in left ventricular afterload were noted between subject groups, although those with hypertrophic cardiac disease had the lowest calculated values. Quantitative echocardiography is an accurate technique for measuring left ventricular circumferential wall stress (preload and afterload) when left ventricular end-diastolic pressure and aortic end-diastolic pressure can be obtained. KEY WORDScircumferential wall stress ultrasound left ventricular geometry left ventricular hypertrophy left ventricular wall thickness valvular heart disease coronary artery disease • The adaptive anatomic and functional alterations of the left ventricle produced by chronic myocardial or valvular heart disease c an be evaluated by measuring ventricular volume, intracavitary pressure, and mass. Quantitative angiocardiography (1) has facilitated description of the mechanical function of the ventricle in the normal state (2) and in a variety of abnormal conditions (3, 4). However, evaluation of ven-

Effect of glyceryl trinitrate on echocardiographic left ventricular dimensions during exercise in the upright position.

“…The Laplace relation, however, implies that wall stress would be reduced only in proportion to the decrease in left ventricular linear dimensions (such as the end-diastolic or end-systolic dimension) and not in proportion to the (much larger) associated decrease in left ventricular volume. Similar conclusions may be derived from calculations directly relating circumferential wall stress and left ventricular echocardiographic dimensions (Ratshin et al, 1974).…”

Wall stress and patterns of hypertrophy in the human left ventricle.

“…Recently, Ratshin, Rackley, and Russell have reported (34) on the use of a combined hemodynamic and ultrasonic technique, similar to that used in our study, for the measurement of LV wall stress. In their study close correlation was demonstrated between wall stresses calculated from biplane angiographic and ultrasonic techniques.…”

Echocardiographic determination of left ventricular stress-velocity relations.

“…The reliability of the echogram in estimating the internal LV minor axis, wall thickness, and circumferential wall stress has recently been demonstrated.9 10 All measurements were processed by the programmed calculator, and time plots of endocardial VCF, midwall VCF, and LV hoop stress were constructed ( fig. 1).…”