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Musculoskeletal complaints have been reported to occur in as many as 44% of patients with infective endocarditis (IE). A 4-year retrospective review of 104 cases of IE in which new diagnostic criteria were used showed that 24 episodes (23%) began with musculoskeletal complaints. Sixteen of the 24 episodes (66%) involved osteoarticular infection (OAI) documented during the period of hospitalization. Thus, in 15% of the 104 cases of IE, OAI was documented. The 16 episodes occurred in 15 patients, all of whom were intravenous drug abusers (IVDAs). In contrast, OAI was documented in none of the 38 cases in the IE population that did not involve IVDAs. Only three episodes were associated with single rather than multiple bone or joint involvement. There were no deaths, and the patients' conditions seemed to respond well to appropriate therapy. OAIs appear to be uncommon in patients with IE who are not IVDAs. Musculoskeletal complaints in the IVDA population with IE, however, should prompt a careful search for OAI.

We hypothesized that ozone (O3) exposure acutely affects cardiovascular hemodynamics in humans and, in particular, in subjects with essential hypertension. We studied 10 nonmedicated hypertensive and six healthy male adults. Each subject, after catheterization of the right heart and a radial artery, was exposed in an environmentally controlled chamber to filtered air (FA) on one day and to 0.3 ppm O3 on the following day for 3 h with intermittent exercise. Relative to FA exposure, O3 exposure induced no statistically significant changes in cardiac index, ventricular performance, pulmonary artery pressure, pulmonary and systemic vascular resistances, ECG, serum cardiac enzymes, plasma catecholamines and atrial natriuretic factor, and SaO2. The overall results did not indicate major acute cardiovascular effects of O3 in either the hypertensive or the control subjects. However, mean preexposure to postexposure changes were significantly (p < 0.02) larger with O3 than with FA for rate-pressure product (1,353 beats/min/mm Hg) and for heart rate (8 beats/min); these responses were not significantly different between the hypertensive and the control subjects. Significant O3 effects were also observed for mean FEV1 (-6%), and AaPO2 (> 10 mm Hg increase), which were not significantly different between the two groups. These results suggest that O3 exposure can increase myocardial work and impair pulmonary gas exchange to a degree that might be clinically important in persons with significant preexisting cardiovascular impairment, with or without concomitant lung disease.

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