[Infective endocarditis complicating bilateral bacterial ophthalmitis: a case report].

A 53-year-old female suddenly went blind in her left eye on 3 June, 2000. She was admitted to the Department of Ophthalmology of our hospital under the diagnosis of endophthalmitis. Her left eye was enucleated, and Streptococcus agalactiae was found in the vitreous fluid. After left ophthalmectomy, inflammation recurred after cessation of antibiotic administration. Echocardiography demonstrated a vegetation of the posterior mitral valve. The diagnosis was infective endocarditis. She was transferred to the Department of Internal Medicine. Mitral regurgitation deteriorated during the course of medical therapy, but she was discharged on 13 September, 2000 because inflammation had improved remarkably and the vegetation had disappeared after administration of penicillin G, panipenem, cefotaxime and clindamycin. We suspected that embolism of the ophthalmic artery was the cause of the sudden blindness in her left eye. Infective endocarditis with bacterial endophthalmitis is very rare in Japan.

Influence of angiotensin II type 1-receptor antagonist CV11974 on infarct size and adjacent regional function after ischemia-reperfusion in dogs.

The presence of nonischemic regional dysfunction at the adjacent region of the ischemic myocardium was demonstrated in clinical studies. Recent studies demonstrated an angiotensin II type 1 (AT1)-receptor antagonist reduced myocardial ischemia-reperfusion injury. We investigated the role of the adjacent region after reperfusion by studying the effects of AT1-receptor antagonist on myocardial function and infarct size. We investigated 12 open-chest anesthetized dogs undergoing 90 min of left anterior descending coronary artery occlusion followed by 4 h of reperfusion. Six dogs injected with an AT1-receptor antagonist (CV11974) immediately after reperfusion were compared with 6 control dogs. Percent systolic shortening (%SS) was measured by two sets of the pair sonomicrometer crystals implanted to adjacent and remote nonischemic myocardium. After 4 h of reperfusion, infarct size was measured. There were no significant differences of the %SS at baseline between two regions. In both groups, %SS at adjacent region after reperfusion was significantly decreased as compared with remote region. There were no significant differences between the two groups. Infarct size, as a percentage of the area at risk, was smaller in the AT, group than in control group (25.49+/-7.53% vs 68.58+/-26.88% P<0.01). AT1-receptor antagonist reduces infarct size. This effect is not related to the change of regional myocardial function at adjacent region after reperfusion.