Increased Regional Myocardial StiEfness of the Left Ventricle During Pacing-induced Angina in Man

The left ventricular diastolic pressure-volume.relationship shifts upward during angina, but why this happens is not known. To assess regional myocardial stiffness, we studied 12 patients who.had coronary artery disease using simultaneous left ventricular micromanometer pressure recording and Mmode echocardiography before and during angina induced. by pacing tachycardia. All patients had twoor three-vessel coronary artery disease that involved the posterior left ventricular wall circulation and had positive pacing stress tests, i.e., development ofangina and a postpacing rise in left ventricular end-diastolic pressure (15 3 to 31 6 mm Hg, p < 0.001). A marked upward shift in the relationship between the diastolic left ventricular pressure and the posterior wall thickness (h) occurred after pacing tachycardia, but the change in left ventricular posterior wall end-diastolic thickness was minimal (8.9 2.1 to 9.2 2.1 mm, NS). After pacing, the peak rate of left ventricular posterior wall thinning decreased (82 37 to 48 27 mm/sec, p < 0.005) and the time constant of relaxation derived from the best exponential fit to the isovolumic left ventricular pressure decay increased (49 5 to 58 7 msec,.p < 0.001). Diastolic active left ventricular pressure decay, extrapolated from the exponential fit, was subtracted from the measured left ventricular pressure (which is equal in magnitude but opposite in sign to the radial stress at the endocardium) to calculate residual left ventricular pressure (PR) and hence residual stress (6R = -PR). A radial stifiness modulus (ER) was determined by the slope of the PR VS log h plots before and after pacing. Over the same range of residual radial stress (aR), ER was always higher during pacing-induced angina, indicating increased residual myocardial stiffness. Increased myocardial stiffness in addition to a decreased rate of wall thinning and slow active pressure decay contribute to the upward shift in left ventricular pressure-wall thickness and pressure-volume relationships during pacing-induced angina.