966-39 Hypertension and Left Ventricular Hypertrophy Further Impair Utilization of the Reduced Coronary Reserve in Patients with Coronary Artery Stenosis

Abstract

Left ventricular hypertrophy (LVH) predisposes to an increased infarct size after coronary occlusion in dog. Aim of the study was to investigate the impact of the coexistence of LVH secondary to hypertension and coronary stenosis on the coronary vasodilator capacity in man. Coronary flow velocity in left anterior descending artery (LAD) was monitored by Transesophageal-Doppler at baseline and during low- and high-dose of iv. Dipyridamole (0.56 mg/Kg/4 min followed after 2 min by 0.28 mg/Kg/2 min) in 56 patients, divided as follows: 19 normal controls (N Group), 21 pts with hypertension, LVH and no CAD (LVH Group), and 16 pts with moderate LAD artery stenosis (≤ 75%) [10 without LVH (LAD Group) and 6 with LVH secondary to hypertension (LAD + LVH Group)]. All pts had Dipyridamole Echo test negative for left ventricular asynergy. Blood pressure and left ventricular mass were similar in N vs LAD pts, and in LVH vs LAD + LVH. Mean total coronary flow velocity was measured from Doppler recordings. Coronary reserve was computed as the ratio of high-dose Dipyridamole to Basal flow velocity. Minimum coronary resistance and the percent of coronary reserve recruited after low-dose Dipyridamole were also computed. Baseline coronary flow velocity was 29 ± 6 cm/sec in N, and significantly higher in LVH and CAD (39 ± 11 and 41 ± 11, respectively, p < 0.01). Coronary flow velocity after high-dose Dipyridamole was 92 ± 18 in N, and significantly lower only in LAD + LVH (68 ± 16, p < 0.05). Coronary reserve was 3.3 ± 0.7 in N, and significantly reduced in all pts subgroups (2.4 ± 0.4, 2.2 ± 0.6, 2.3 ± 0.4 in LVH, LAD, LAD + LVH; P < 0.01 vs N). Percent of coronary reserve recruited after low-dose Dipyridamole was 94 ± 8% in N, 91 ± 11% in LAD, and lower in LVH (79 ± 11%, P < 0.01 vs N) and in LAD + LVH (69 ± 10%, P < 0.05 vs LVH). Compared to N, minimum coronary resistance was significantly higher in LVH (p < 0.05) and LAD + LVH (p < 0.01) (0.94 ± 0.2 vs 1.20 ± 0.3 and 1.40 ± 0.4 mmHg/ml/min, respectively); it was also higher in LAD + LVH than in LAD alone (1.07 ± 0.2 mmHg/ml/min, p < 0.05). Coronary reserve is similarly reduced in pts with LVH secondary to hypertension, LAD stenosis alone, or LVH + LAD stenosis. Coexistence of hypertensive LVH with LAD stenosis is associated. compared to LAD stenosis alone, with significantly higher minimum coronary resistance and a hindered utilization of the reduced coronary reserve.