Clinical viral infections and temporal bone histologic studies of patients with AIDS

The brain, eye, and inner ear are each protected from blood-borne infectious agents by a barrier that has some anatomic and functional differences. In patients with AIDS, opportunistic infections of the central nervous system and eye are frequent. Little is known about the incidence of middle and inner ear infections in patients with AIDS, but deafness and severe vertigo are uncommon. We studied 14 homosexual men with AIDS, aged 28 to 55 years, for 1 to 2 years until death. No patient had deafness, but one had vertigo. Adenovirus type 6 and cytomegalovirus were isolated from the middle ear cavity in four patients. Temporal bone histology demonstrated acute otitis media in four, chronic otitis media in two, and serous otitis media in three. Adenovirus type 6 and cytomegalovirus, either alone or with herpes simplex virus type 1, were isolated from inner fluids of three patients. Histologic inner ear findings were abnormal in only one patient. Viruses were isolated or histologically identified in the brains of four patients and in the eyes of five patients. In our patients viral infections were nearly as common in the inner ears as in the brain and eye, suggesting that protection from the blood-labyrinth barrier was similar to that from the other barriers. Because the inner ear viral infections were asymptomatic and there was an absence of pathologic damage and inflammation, we suggest that some viral inner ear infections in patients with AIDS are nonpathogenic and elicit no inflammation or that the viral infections occur terminally and elicit no inflammation because of immunosuppression from the AIDS. (OTOLARYNGOL HEAD NECK SURG 1995; 113:695-701.)     

Outcome after thrombolytic therapy of nine cases of myopericarditis misdiagnosed as myocardial infarction

Anecdotal reports have suggested that cardiovascular complicationsmay occur if thrombolytic therapy is performed in cases of pericarditismisdiagnosed as acute myocardial infarction. From 1980 to 1993,47 cases of myopericarditis mimicking myocardial infarctionhave been admitted to our institution. The misdiagnosis wasmade because of clinical onset characterized by a typical chestpain, and/or localized ST segment elevation. Since 1987, nine(919 males, age 40±14 years) out of the 47 patients (19%)have been treated with a thrombolytic agent (streptokinase 419,rt-PA 519) followed by intravenous heparin. This treatment wasstarted during the pre-hospital pliase (2/9) and while in hospital(7/9). No pericardial rub was present; ST segment elevationwas mainly localized in inferior and lateral leads; no Q wavedeveloped; median creatine kinase rise was 268 units (range38 to 1280), and only one patient had a small pericardial effusion.The mean level of fibrinogen after thrombolysis was 1.72 g.l^–1 (range 0.10 to 4.50). In all cases, typical ECG cliangeswere present suggesting pericarditis with a subsequent returnto a normal ECG. No severe cardiac or pericardial complicationor arrhytlxmia occurred; only one patient developed a non-compressiveand resolvable pericardial effusion. Cardiac catheterizations(coronary and left ventricular angiographies) were normal whenperformed (5/9). Long-term follow-up (mean 46±29 months)was favourable without any coronary events. In conclusion, thrombolytictherapy was uncomplicated in our patients with myopericarditissimulating evolving myocardial infarction.     

Delayed Response to Radiofrequency Ablation of Accessory Connections

This article summarizes delayed interruption in anomalous conduction through accessory connections following radiofrequency ablation attempts in three patients. The time course of the delayed interruption in accessory connection conduction suggests that such an effect is unlikely to occur after the first week following unsuccessful radiofrequency ablation.