Intramyocardial Spontaneous Hematoma Mimicking an Acute Myocardial Infarction
An 80-year-old man affected by rheumatoid arthritis and chronic myeloid leukemia who was a smoker and hypertensive was admitted to the coronary care unit for first ST-elevation myocardial infarction. The diagnosis was suspected on the basis of the presence of chest pain associated with ST-segment elevation in leads III and aVF and a cardiac troponin T level of 0.30 ng/dL. At coronary angiography, performed 2 hours after pain onset, a 50% stenosis of the proximal right coronary artery with a translucent filling defect that suggested a parietal thrombus at the cardiac crux was found (see online-only Data Supplement Movie I); the left coronary artery had diffuse atherosclerosis in the absence of significant stenosis. Therefore, no interventional procedure was performed and the patient was treated with aspirin and clopidogrel. The echocardiogram performed soon after coronary catheterization showed an expansive lesion in the basal segment of the inferior wall characterized by echodensity intermediate between blood and tissue (Figure 1A). Myocardial contrast echocardiography documented that the expansive lesion was characterized by a reduced and irregular microvascular network compatible with both hemangioma1 and intramyocardial hematoma2 (Figures 1B and 2⇓A; online-only Data Supplement Movies II and III). Magnetic Resonance Imaging further clarified the diagnosis. In fact, T2-weighted fat-suppressed images documented the presence of a hyperintense expansive lesion compatible with both hemangioma and intramyocardial hematoma (Figure 2B), but first-pass perfusion imaging showed marked signal loss in the lesion (Figure 3A), with no enhancement within the first minute (Figure 3B; online-only Data Supplement Movies IV and V). At late enhancement, a mild subendocardial perfusion defect remained only in the midventricular inferior wall. This pattern is typical of intramyocardial hemorrhage, whereas the contrast enhancement pattern of hemangioma is characterized by slow peripheral contrast uptake.3
When the diagnosis of intramyocardial hematoma was established, antiplatelet and heparin treatment was discontinued, but the next day, an echocardiogram documented a large intraventricular mural thrombus that dissolved rapidly within 2 days of heparin treatment. The patient was then screened for possible thrombotic and hemorrhagic disorders, and in fact, antiphospholipid antibodies were found to be elevated in his blood (cardiolipid antibody IgM 16 U/mL). These antibodies can be associated with both rheumatoid arthritis and chronic myeloid leukemia and are responsible for thrombosis and hemorrhagic disorders.4 Thus, in this patient, antiphospholipid syndrome was a likely cause of both intramyocardial hemorrhage presenting as ST-segment elevation acute myocardial infarction and intraventricular mural thrombosis.
The patient has been discharged with aspirin and oral anticoagulant treatment (online-only Data Supplement Movies VI and VII). A control echocardiogram performed 6 months after the acute events documented that the expansive lesion remained confined to the basal segment of the inferior wall, in the absence of parietal thrombi. The patient is currently doing well.
The online-only Data Supplement, consisting of Movies I through VII, is available with this article at http://circ.ahajournals.org/cgi/content/full/116/15/e371/DC1.
Vargas-Barron J, Romero-Cardenas A, Roldan FJ, Molina-Carrion M, Avila-Casado C, Villavicencio R, Martinez-Sanchez C, Lupi-Herrera E, Zabalgoitia M. Long term follow-up of intramyocardial dissecting hematomas complicating acute myocardial infarction. J Am Soc Echocardiogr. 2005; 18: 1422.
Moniotte S, Geva T, Perez-Atayde A, Fulton DR, Pigula FA, Powell AJ. Cardiac hemangioma. Circulation. 2005; 112: e103–e104.