Immune thrombocytopenic purpura and myocardial infarction: a dilemma of management.

began 3 days before presentation. She had a history of diabetes mellitus, hypertension, hyperlipidemia, smoking, and family history of cardiovascular disease. She was managed for ITP that was diagnosed 6 years previously. Steroid therapy was stopped 4 months before her admission because of a normal platelet count. No history of bleeding was reported. On admission, 12-lead surface electrocardiogram revealed T wave inversion in inferior leads. Blood tests showed increased troponin levels (2.5 ng/ml, normal ≤ 0.2 ng/ml), while creatinine phosphokinase levels were normal. The diagnosis at admission was non-ST elevation acute myocardial infarction; she was clinically stable and had no recurrence of chest pain during her stay in both the emergency department and the coronary care unit. Physical examination was normal with no signs of heart failure or bleeding. Echocardiography revealed basal inferior and posterior wall motion abnormality, with estimated left ventricular ejection fraction of 45%. At presentation the platelet count was 26,000 μl, while the standard coagulation tests were normal. To prepare the patient for coronary angiography a hematologic consultation was requested and subsequently intravenous immunoglobulin and steroid treatment was started without antiplatelet or anticoagulant therapy. A few hours later she developed chest pain and transient ST-elevation in inferior leads of the ECG. Platelet count at the time of the event was 29,000 μl. Because of the spontaneous resolution of the ECG changes and chest pain after 20 minutes, conservative treatment including steroids was continued. Since the i mmune thrombocytopenic purpura is an autoimmune disease characterized by premature destruction of platelets by autoantibodies, causing thrombocytopenia and mucocutaneous bleeding [1]. The estimated incidence is 10 per 100,000 persons per year, with a female:male ratio of 3:1. The decision to treat ITP1 is based on platelet count and the extent of bleeding. Since severe bleeding is uncommon when the platelet count is above 30,000/μl, treatment is usually initiated when the count falls below this level [1]. Antiplatelet and anticoagulant therapy is a mainstay in the management of acute coronary syndrome, particularly in the presence of coronary intervention. Because of the bleeding risk in patients with ITP this therapy is generally contraindicated if the platelet count is below 30,000/μl [2]. Since there are no precise recommendations, this dilemma causes difficulty in managing concomitant acute coronary syndrome and ITP. Acute myocardial infarction is rare in patients with ITP. We describe a patient with ITP admitted for acute myocardial infarction and thrombocytopenia (26,000/μl).