Feldman T, Borow K M, Sarne D H, Neumann A, Lang R M
J Am Coll Cardiol. 1986 May;7(5):967-74. doi: 10.1016/s0735-1097(86)80213-3.
Hyperthyroidism has been reported to affect all of the major determinants of left ventricular performance in a manner that would augment ventricular shortening characteristics. The hypothesis tested in this study is that reduced afterload in conjunction with increased preload and heart rate, rather than augmented contractility, accounts for much of the increase in left ventricular performance noted previously in these patients. To investigate this hypothesis, 11 hyperthyroid patients were evaluated serially over 4 +/- 2 months. With therapy, serum total thyroxin (T4) decreased significantly (p less than 0.001). Ventricular hemodynamics were assessed by two-dimensional targeted M-mode echocardiograms and calibrated carotid pulse tracings. Ventricular preload was estimated by end-diastolic dimension, whereas afterload was measured as end-systolic wall stress. Overall left ventricular performance was quantitated by the extent and velocity of shortening, whereas myocardial work was assessed by ventricular systolic stress-length relations. With therapy, overall left ventricular performance declined (p less than 0.01). This change was associated with no change in end-diastolic dimension or end-systolic wall stress, and a 24% fall in heart rate (p less than 0.01). This latter finding has been shown previously to have no significant effect on left ventricular contractile state over the range of heart rates encountered in this study. In all cases, the end-systolic stress/rate-corrected shortening velocity relation fell with attainment of normal thyroid status, characteristic of a decline in contractility. There was a strong positive correlation between left ventricular contractility and serum thyroid hormone level (r = 0.83). In addition, ventricular minute work declined with therapy (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
