Epicardial Coronary Artery Size in Hypertensive and Physiologic Left Ventricular Hypertrophy

Background In the hypertensive heart, epicardial arteries are not enlarged, despite increased total coronary flow related to augmented cardiac workload, wall stress, and left ventricular (LV) mass. The aims of this study were to assess the impact of different hemodynamic factors and LV mass on baseline left main coronary artery (LMA) size in hypertensive LV hypertrophy (LVH) and physiologic LVH, used as a pressure-independent model of hypertrophy. Methods In 104 subjects without coronary disease (26 normotensive subjects without LVH, 15 athletes with physiologic LVH, and 63 untreated hypertensive subjects [28 without and 35 with LVH]), LMA size and coronary flow reserve (CFR) were measured by transesophageal echocardiography, and LV mass, volumes, stroke work, and wall stress were measured by transthoracic echocardiography. Results The LMA area in normotensive control subjects, athletes, and hypertensive subjects without and with LVH was 13.2 ± 4.2, 17.5 ± 2.9, 10.1 ± 3.2 and 13.1 ± 3.9 mm2. In normotensive control subjects, LMA size increased with body surface area, rate–pressure product, stroke work, and LV mass or wall thickness (r = 0.39, 0.39, 0.47 and 0.67 or 0.62, P< .05-0.01). In athletes with physiologic LVH, LMA area increased with CFR (0.65, P< .01). In the whole hypertensive population, LMA lumen increased with LV mass (r = 0.40, P< .01), and decreased with office systolic blood pressure (r = −0.48, P< .01). Conclusions In the hypertensive LVH, baseline LMA area is not increased and is inversely related to office systolic blood pressure. In the physiologic LVH, increase in baseline LMA size seems to reflect effect of high-flow stimuli. Background In the hypertensive heart, epicardial arteries are not enlarged, despite increased total coronary flow related to augmented cardiac workload, wall stress, and left ventricular (LV) mass. The aims of this study were to assess the impact of different hemodynamic factors and LV mass on baseline left main coronary artery (LMA) size in hypertensive LV hypertrophy (LVH) and physiologic LVH, used as a pressure-independent model of hypertrophy. Methods In 104 subjects without coronary disease (26 normotensive subjects without LVH, 15 athletes with physiologic LVH, and 63 untreated hypertensive subjects [28 without and 35 with LVH]), LMA size and coronary flow reserve (CFR) were measured by transesophageal echocardiography, and LV mass, volumes, stroke work, and wall stress were measured by transthoracic echocardiography. Results The LMA area in normotensive control subjects, athletes, and hypertensive subjects without and with LVH was 13.2 ± 4.2, 17.5 ± 2.9, 10.1 ± 3.2 and 13.1 ± 3.9 mm2. In normotensive control subjects, LMA size increased with body surface area, rate–pressure product, stroke work, and LV mass or wall thickness (r = 0.39, 0.39, 0.47 and 0.67 or 0.62, P< .05-0.01). In athletes with physiologic LVH, LMA area increased with CFR (0.65, P< .01). In the whole hypertensive population, LMA lumen increased with LV mass (r = 0.40, P< .01), and decreased with office systolic blood pressure (r = −0.48, P< .01). Conclusions In the hypertensive LVH, baseline LMA area is not increased and is inversely related to office systolic blood pressure. In the physiologic LVH, increase in baseline LMA size seems to reflect effect of high-flow stimuli.