Hypertensive heart disease: Relationship of silent ischemia to coronary artery disease and left ventricular hypertrophy

ECG evidence of silent ischemia occurs commonly in patients with systemic hypertension, but its relationship to left ventricular hypertrophy (LVH), large-vessel coronary artery disease (CAD), and neurohumoral factors remains unclear. Accordingly we validated the results of the echocardiographic method used to measure left ventricular (LV) mass in the Soviet Union by comparison with necropsy measurements in 30 patients, and we examined the relationships in 46 men with essential hypertension among ST segment depression during ambulatory monitoring, exercise stress and transesophageal pacing (n = 38), and LV mass, catheterization evidence of CAD (n = 25), and neurohumoral factors (plasma catecholamines and platelet aggregability). Echocardiographic measurements of LV mass by both the Soviet and Penn methods were closely correlated with necropsy values ( r = 0.78 and 90, respectively; both p < 0.001). During ambulatory monitoring from 1 to 17 episodes of ≥ 1 mm ST depression occurred in 26 of 46 (65%) patients with hypertension; ischemia was also provoked by exercise or pacing stress in most but not all of these patients (65% and 80%, respectively). Neither ST depression nor the occurrence of additional episodes of symptomatic angina was related to the presence of coronary obstruction at catheterization; patients with and without ST depression did not differ in age, blood pressure, or LV mass. No systematic differences between patients with and without CAD or ST depression were noted in catecholamine levels or platelet aggregability, but the subset in whom ischemia developed at a lower heart rate (×) blood pressure product during pacing stress than during exercise stress had significantly lower norepinephrine levels at rest and during pacing stress (68 ± 34 versus 157 ± 47 ng/L, p < 0.02; and 86 ± 39 versus 254 ± 86 ng/L, p < 0.01). Thus asymptomatic ST depression occurs commonly during normal activity and induced stress in patients with systemic hypertension but is not consistently related to the presence of large-vessel CAD, LVH, or neurohumoral abnormalities.