Left ventricular function and hyperthyroidism.

Abstract

Cardiac output, aortic pressure, and left ventricular pressure (using a catheter tip micro- manometer), angiographic end-diastolic volume and end-systolic volume were measured in seven thyrotoxic patients in sinus rhythm without heart failure. The following indices were calculated: dP/dt max, [(dP/dt)/TP] max, ejection fraction, mean velocity of fibre shortening, left ventricular mass, and the end-systolic pressure: end-systolic volume ratio (LVESP/LVESV). All measurements were made in the basal state and 20 minutes after 15 mg intravenous propranolol. After hyperthyroidism had been corrected with carbimazole, the same set of measurements was made in four now euthyroid patients in a basal state and while being atrially paced at the same heart rate as that found when they were hyperthyroid. The results were compared with those obtained in 11 normal patients of the same age studied in the basal state and during atrial pacing at the same heart rate as the thyrotoxic patients. After propranolol and when euthyroid, cardiac output, dP/dt max, [(dP/dt)/TP] max, ejection fraction, and mean velocity offibre shortening decreased, and left ventricular mass decreased with euthyroidism. Reduction of cardiac output was related to a decrease in heart rate and stroke volume. After propranolol, stroke volume decreased because there was a greater increase in LV end-systolic volume than in LV end-diastolic volume. In the euthyroid state stroke volume decreased because of a decrease in LV end-diastolic volume without a change in systolic volume. Comparison of thyrotoxic, euthyroid atrially paced, and normal atrially paced patients disclosed that the increase in cardiac output during hyperthyroidism was related to an increase in LV end-diastolic volume, ejection fraction, mean velocity of fibre shortening, and dP/dt max, and that LVESP/LVESV did not differ between thyrotoxic and normal atrially paced patients. These data suggest that the reduction in cardiac output is mediated by different mechanisms after intravenous propranolol and carbimazole treatment; and that the haemodynamics of hyperthyroidism are related to the interaction of peripheral factors (a decrease in systemic arterial resistance and an increase in blood volume) and cardiac factors (an increase in heart rate).