The anginal threshold was determined by atrial pacing in 23 patients with coronary artery disease. Twelve of the 23 subjects also performed supine exercise at progressive workloads until the onset of angina. Atrial pacing produced a fall in left ventricular stroke work index and left ventricular end-diastolic pressure (LVEDP); cardiac output increased, and, with the onset of angina, left ventricular dysfunction was sometimes evidenced, either by an increase in LVEDP or by an abnormal LVEDP in the postpacing period. In contrast, exercise consistently produced left ventricular dysfunction. The tension-time index at the onset of angina was similar whether the pain was induced by pacing or exercise.
The atrial rate that induced angina bore little relationship to either the clinical or anatomic severity (outlined by coronary arteriography) of coronary artery disease. The exercise workload that produced angina correlated inversely with the quantitated coronary disease. Although atrial pacing is a convenient tool for the study of ischemic ventricular dysfunction, exercise testing provides a more reliable index of functional and anatomic severity of coronary artery disease.
Oral administration of chlorothiazide depresses glomerular filtration, increases blood urea, maintains sodium output in the face of decreased filtered sodium load, and paradoxically for a diuretic, in these and in tests done shortly after intravenous administration, increases the efficiency of water reabsorption.
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