CHOLESTEROL CRYSTAL EMBOLIZATION AS A COM PLICATION OF FIBRINOLYTIC TREATMENT OF ACUTE MYOCARDIAL-INFARCTION

A 63-year-old male patient admitted with acute inferior myocardial inf arction was treated with tissue plasminogen activator (rt-PA) and hepa rin. 4 hours after the initiation of the rt-PA infusion he showed pain ful cutaneous alterations on the lower trunk, mistaken as drug-induced rash and later correctly identified as livedo reticularis. Simultaneo usly, renal function deteriorated. Assuming hypersensitivity vasculiti s, we instituted immunosuppressive treatment which proved to be ineffe ctive. Skin biopsy including the deeper layers showed multiple cholest erol emboli. Anticoagulants were stopped and we noticed no further cho lesterol embolism or further decline of renal function. 10 previous pu blications have mentioned a causal relationship between systemic fibri nolytic treatment and the cholesterol crystal embolism syndrome. In 7 cases, however, angiographic procedures were used or the interval betw een fibrinolysis and the occurrence of cholesterol crystal embolism wa s too long to exclude spontaneous or heparin-induced cholesterol cryst al embolism. The short interval in our own case points clearly to the systemic fibrinolytic therapy as the culprit. We would like to draw at tention to the possibility that in individuals with advanced atheroscl erotic lesions of the aorta or major arteries, systemic fibrinolytic t reatment of myocardial infarction may give rise to the cholesterol cry stal embolism syndrome.