ree wall rupture in the setting of acute myocardial infarction is known to have mortality of more than 90% only with medical therapy. 1 A new therapeutic option, percutaneous intrapericardial fibrin-glue therapy, was recently introduced for the oozing type of cardiac rupture, with success in some cases, 2-4 although the longterm effects of this treatment have not been reported; in particular, whether adhesions from the fibrin-glue could potentially impair left ventricular diastolic function. Case ReportA 82-year-old woman was admitted to the emergency room because of vomiting and syncope. She had a history of hypertension and cerebral infarction. On arrival, her pulse rate was 88 beats/min and blood pressure was 94/52 mmHg. The jugular vein was markedly dilated with distant heart sounds, but no rales. Peripheral oxygen saturation was 94% while she was receiving 30% oxygen. Electrocardiogram showed a normal sinus rhythm, ST segment elevation in leads V5, V6, I and aVL, small q wave in V6 and aVL, and tall R wave in V1 and V2. Two-dimensional Circulation Journal Vol.66, July 2002 echocardiography showed an echo-free space that was suggestive of 200-300 ml of pericardial effusion. The left ventricular cavity was relatively small with an akinetic area in the posterolateral wall. Within 1 h of admission, her hemodynamic state deteriorated, with a progressive decline in blood pressure and an increase in venous pressure. Pericardiocentesis confirmed bloody pericardial effusion and resulted in a dramatic restoration of arterial blood pressure. These findings strongly suggested cardiac tamponade caused by free wall rupture in the clinical setting of acute posterolateral myocardial infarction.Because of the patient's advanced age and her stable hemodynamic state, percutaneous intrapericardial fibringlue fixation therapy using fibrin-glue (Beriplast ® ) was selected as the treatment to repair the ruptured myocardium. Because the patient had dementia, written informed consent was obtained from her family before the procedure. The agent was composed of 6 ml of solution A (800 mg human fibrinogen, 750 units coagulation factor VIII, and 10,000 KIE aprotinin solution) and 6 ml of solution B (2,500 units thrombin and 10 ml calcium chloride). Solutions A and B were infused separately into the intrapericardial space through the drainage catheter. On the second hospital day, the bloody pericardial drainage gradually declined to 50 ml/day and blood pressure was maintained. Metoprolol was started to reduce left ventricular contractility, and captopril and nitrate were given for cardiac unloading. On the 14th hospital day, echocardiography showed no pericardial effusion and a relatively higher atrial component and normal deceleration time of the E wave (244 ms) on transmitral Doppler flow (Fig 1). Coronary angiography could not be

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