Relation between left ventricular midwall function and coronary vasodilator capacity in arterial hypertension

In systemic hypertension, depressed left ventricular midwall shortening predicts an adverse outcome and is associated with increased left ventricular relative wall thickness, which has been proposed as an independent predictor of cardiovascular risk and reduced coronary reserve. This study was designed to investigate whether depressed midwall shortening is associated with more critical impairment of coronary function and with exercise-induced myocardial ischemia. Sixty untreated hypertensive patients without coronary artery stenosis and 20 normotensive volunteers underwent exercise ECG testing, standard and transesophageal echocardiography to assess the occurrence of exercise-induced myocardial ischemia, left ventricular mass, geometry, and midwall shortening, and coronary vasodilator capacity. Compared with hypertensive patients with normal midwall shortening, those with depressed function (n = 15) had higher minimum coronary resistance (1.19 +/- 0.27 versus 1.39 +/- 0.20 mm Hg/cm per second, P < 0.01) and prevalence of exercise-induced myocardial ischemia ( 36 versus 67%, P < 0.05). Within the hypertensive group, midwall shortening was inversely related to minimum coronary resistance (r = -0.42, P < 0.01). Compared with patients with an exercise ECG test negative for myocardial ischemia, those with a positive test result (n = 26) had higher minimum coronary resistance (1.13 +/- 0.21 versus 1.38 +/- 0.27 mm Hg/cm per second, P < 0.01) and lower midwall shortening (104 +/- 16 versus 93 +/- 14%, P < 0.01). We conclude that hypertensive patients with depressed midwall shortening have more severe impairment of coronary function and a higher prevalence of exercise-induced myocardial ischemia as compared with hypertensive patients with normal midwall shortening. These findings suggest that a decrease in myocardial performance may be related, at least in part, to chronic intermittent myocardial ischemia caused by a critical impairment of coronary vasodilator capacity.