OUTCOME AFTER THROMBOLYTIC THERAPY OF 9 CASES OF MYOPERICARDITIS MISDIAGNOSED AS MYOCARDIAL-INFARCTION

Anecdotal reports have suggested that cardiovascular complications may occur if thrombolytic therapy is performed in cases of pericarditis m isdiagnosed as acute myocardial infarction. From 1980 to 1993, 47 case s of myopericarditis mimicking myocardial infarction have been admitte d to our institution. The misdiagnosis was made because of clinical on set characterized by a typical chest pain and/or localized ST segment elevation. Since 1987, nine (9/9 males, age 40 +/- 14 years) out of th e 47 patients (19%) have been treated with a thrombolytic agent (strep tokinase 4/9, rf-PA 5/9) followed by intravenous heparin. This treatme nt was started during the pre-hospital phase (2/9) and while in hospit al (7/9). No pericardial rub was present; ST segment elevation was mai nly localized in inferior and lateral leads, no Q wave developed; medi an creatine kinase rise was 268 units (range 38 to 1280), and only one patient had a small pericardial effusion. The mean level of fibrinoge n after thrombolysis was 1.72 g. l(-1) (range 0.1O to 4.50). In all ca ses, typical ECG changes were present suggesting pericarditis with a s ubsequent return to a normal EGG. No severe cardiac or pericardial com plication or arrhythmia occurred only one patient developed a non-comp ressive and resolvable pericardial effusion. Cardiac catheterizations (coronary and left ventricular angiographies) were normal when perform ed (5/9). Long-term follow-up (mean 46+/-29 months) was favourable wit hout any coronary events. In conclusion, thrombolytic therapy,vas unco mplicated in our patients with myopericarditis simulating evolving myo cardial infarction.