MECHANISMS OF CORONARY FLOW RESERVE IMPAIRMENT IN HUMAN HYPERTENSION - AN INTEGRATED APPROACH BY TRANSTHORACIC AND TRANSESOPHAGEAL ECHOCARDIOGRAPHY

The purpose of this study was to investigate the different mechanisms responsible for an impairment of coronary vasodilator capacity in hype rtensive subjects by an integrated echocardiographic approach, includi ng transesophageal Doppler echocardiography, which allows noninvasive monitoring of coronary flow velocity in the left anterior descending a rtery during pharmacological vasodilation. The study population consis ted of 17 healthy control subjects and 33 hypertensive subjects: 10 wi thout hypertrophy, 16 with mild to moderate hypertrophy, and 7 with se vere left ventricular hypertrophy. Mean systolic and diastolic flow ve locities were monitored basally (together with indexes of myocardial o xygen demand, such as heart rate, myocardial inotropism, and left Vent ricular wall stress) and during infusion of low-dose (0.56 mg/kg per 4 minutes) and high-dose (0.84 mg/kg per 9 minutes) dipyridamole. Coron ary reserve was assessed as the ratio of mean diastolic velocity after high-dose dipyridamole and basal diastolic velocity, and minimum coro nary resistance as the ratio of diastolic blood pressure and diastolic velocity after high-dose dipyridamole. Compared with the control grou p, in all hypertensive groups, coronary reserve was similarly decrease d (3.54+/-0.84 versus 2.59+/-0.42, 2.29+/-0.46, and 2.43+/-0.71; P<.01 ) and minimum resistance increased (0.56+/-0.15 versus 0.75+/-0.31, 0. 75+/-0.19, and 0.78+/-0.21 mm Hg . s(-1). cm(-1); P=NS). These results confirm that coronary reserve in hypertensive individuals is reduced even before the occurrence of left ventricular hypertrophy. The reduct ion in coronary reserve depends on both an increase in resting coronar y flow and an impairment in maximal vasodilator capacity. An increase in resting flow is dependent on higher heart rate and wall stress in h ypertensive subjects without ventricular hypertrophy and on increased myocardial mass in hypertensive subjects with hypertrophy. Hypertensiv e subjects with ventricular hypertrophy also demonstrated a significan tly blunted response to low-dose dipyridamole.