Hyperthyroidism is associated with a marked effect on the cardiovascular system. Despite enhanced resting ventricular systolic performance, thyrotoxicosis has been implicated as a primary cause of cardiomegaly, congestive heart failure, and decreased exercise tolerance. To further assess potential alterations in ventricular function we have noninvasively studied diastolic performance in nine newly diagnosed and untreated hyperthyroid patients. Parameters including diastolic flow velocities, isovolumic relaxation time (IVRT), and the rate of diastolic flow deceleration were compared to those of an age- and sex-matched control population, and then repeat determinations were made after beta-adrenergic blockade and again when the patients were chemically and clinically euthyroid. Before treatment the IVRT was 33.0 ms, which was significantly (P less than 0.005) shorter than the control value (57.9 ms) and in combination with other measures of diastolic function indicated enhanced left ventricular relaxation. beta-Adrenergic blockade slowed the resting heart rate from 97 to 80 beats/min (P less than 0.005) and partially normalized the rate of diastolic deceleration, but had no effect on the IVRT (33.8 ms). When patients were euthyroid, the IVRT was 51.7 ms, and other measures of diastolic performance were the same as those in controls. The current data assessing resting diastolic function in hyperthyroidism are similar to those previously reported for systolic function. Our findings of enhanced cardiac diastolic performance do not support the hypothesis that thyrotoxicosis is associated with compromised left ventricular function and suggest the possibility that the cardiac symptoms that accompany hyperthyroidism may be due to noncardiac mechanisms.
Infections caused by species within the viridans streptococci have been associated with different clinical characteristics. We studied 36 patients with viridans streptococcal endocarditis. Complications were seen in 10 (32%) of 31 patients with native valve endocarditis and four (80%) of five with prosthetic valve endocarditis and included death in two, valve replacement in six, persistent infection in three, emboli in two, and congestive heart failure in nine. Two-dimensional echocardiograms demonstrated vegetations in 26 (72%) of 36, flail mitral valves in seven, disruption of aortic valve prosthesis in one, and perivalvular abscesses in three (two Streptococcus sanguis I and one Streptococcus intermedius I). All twelve patients with native valve endocarditis who suffered complications had vegetations detected by two-dimensional echocardiography, whereas seven patients with native valve endocarditis without vegetations, as detected by two-dimensional echocardiography, had no complications (P = .03). We found no significant correlation between streptococcal species and clinical outcome. To confirm our identifications, we sent 16 identical viridans streptococcal endocarditis isolates to five institutions; only three of 16 were identified as the same species by all five institutions. We conclude that viridans streptococcal endocarditis can be associated with a virulent clinical course and that there is marked variability in species designations of individual strains by different laboratories.
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