Rupture of the ventricular myocardium is an often lethal complication after myocardial infarction. Due to the dramatic hemodynamics and the short time frame between ventricular rupture and surgical closure of the defect, additional therapeutic strategies are needed. Here we report the successful therapy of ventricular rupture by percutaneous intrapericardial instillation of fibrin glue in a 72-year-old male patient with postinfarct angina secondary to anterior myocardial infarction. 1. Case Report Rupture of the ventricular myocardium after myocardial infarction is a dramatic and often lethal complication. Due to the dramatic hemodynamic dysfunction, immediate therapies are imperative. As surgical repair of the defect is often not available, percutaneous intrapericardial instillation of fibrin glue can be an alternative. A 72-year-old male patient with postinfarct angina secondary to anterior myocardial infarction was transferred to our center from a community hospital after administration of systemic thrombolytic therapy using streptokinase. Coronary angiography showed single vessel disease with high grade stenosis of the LAD. Stent implantation was successfully performed with uncomplicated postinterventional course. On day three, the patient developed another episode of angina. Recatheterization excluded acute restenosis or stent thrombosis. On the same day, the patient developed rapid onset cardiogenic shock with need for resuscitation, intubation, high dose catecholamine treatment, and an intra-aortic balloon pump. Echocardiography showed an acute pericardial tamponade suggesting a ventricular rupture (Figure 1(a)). Pericardiocentesis was performed, and large amounts of blood could be aspirated and were directly retransfused. Hemodynamics stabilised only under constant aspiration. As ultima ratio, we instillated a total of 30？mL of a two-component fibrin glue normally used for bleeding ulcers in gastroenterology. This resulted in a sustained hemodynamic stabilization. The patient could be weaned off the balloon pump and catecholamines in the following three days. Echocardiography showed a stable minor pericardial effusion of 100？mL without any signs of hemodynamic relevance (Figure 1(b)). Unfortunately, on day nine, the patient gradually developed signs of progressive cardiogenic shock again with the need of cathecolamine treatment and finally died from pump failure on day 13. Serial echocardiographic evaluations were negative for relevant pericardial effusion. Autopsy revealed a fibrin glue induced focal peri-epicardial adhesion and extensive
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