Spontaneous Intramural Hematoma of the Left Ventricle
A 66-year-old man was admitted to our emergency department for treatment of acute thromboses of multiple abdominal vessels (abdominal aorta, splenic artery and vein, inferior mesenteric artery, and portal vein). Chest computed tomography (CT) performed 2 days before admission showed no abnormality in the left ventricular myocardium (Figure 1). Laboratory findings suggested a hematologic disorder, and therapeutic anticoagulation with heparin was initiated. A bone marrow biopsy was conducted that revealed chronic myelomonocytic leukemia as the underlying disease. Three days after admission, the patient reported severe chest pain. Blood testing revealed elevated levels of high-sensitivity troponin T (155 ng/L [normal <14 ng/L]), normal levels of creatine kinase (30 U/L [normal<190 U/L]), activated partial thromboplastin time of 78 seconds (therapeutic activated partial thromboplastin time range, 45–75 seconds), and a slightly increased international normalized ratio of 1.3 (normal <1.2). ECG showed sinus tachycardia but no changes indicating myocardial ischemia. Triple rule-out CT was performed and excluded relevant coronary artery disease (Figure 2), pulmonary embolism, and abnormalities of the aorta. Instead, hemopericardium and a focal, expansive, lens-shaped hypodense lesion in the inferolateral wall of the left ventricle (LV) was found (Figure 3), which was not seen on the foregoing chest CT (see Figure 1). Subsequent transthoracic echocardiography confirmed pericardial tamponade, and an emergency pericardiocentesis was conducted. This was unsuccessful, and therefore surgical subxiphoidal pericardial drainage was performed. Follow-up transthoracic echocardiography 6 days after the intervention showed a small residual pericardial hematoma that was hemodynamically relevant. In addition, a new pseudoaneurysm in the inferolateral wall of the LV at the site of the previous hypodense mass was detected (Figure 4 and Movie I in the online-only Data Supplement) and confirmed by cardiac CT (Movie II in the online-only Data Supplement). Because of the small size of the pseudoaneurysm and the associated risk of operative treatment, conservative management was decided. Seven days later, follow-up CT showed a growing pseudoaneurysm (Figure 5), and the patient was scheduled for urgent operation. The pseudoaneurysm was resected (Figure 6) and the defect in the LV wall was closed by using a bovine pericardial patch. Transthoracic echocardiography performed 5 days after surgery showed regular postoperative results (Movie III in the online-only Data Supplement) with a normal LV ejection fraction of 67%. Cardiac CT, which was also performed 5 days after surgery, similarly showed normal postoperative findings with no residual pseudoaneurysm. The patient recovered well and was transferred to a rehabilitation hospital 7 days after surgery.
Pseudoaneurysm formation is a well-known complication after myocardial infarction, cardiac intervention, or cardiac surgery.1 In our patient, preexisting myocardial damage attributable to cardiac intervention or cardiac surgery could be excluded. Myocardial infarction as a possible reason for pseudoaneurysm formation was highly unlikely for the following reasons. First, cardiac CT showed patent coronary arteries without relevant stenoses (see Figure 1). Second, ECG showed no changes that were typical for myocardial infarction. Third, the isolated elevation of high-sensitivity troponin in the absence of elevated creatine kinase levels can be explained by pericardial tamponade. Fourth, a tissue sample of the myocardium adjacent to the pseudoaneurysm was analyzed histopathologically and revealed no signs of infarction. Finally, the expanding, lens-shaped mass in the inferolateral wall of the LV does not resemble the common appearance of myocardial infarction in CT.
Thus, we believe that this case is the first to demonstrate spontaneous hemorrhage into the wall of the LV leading to pseudoaneurysm formation, most probably because of anticoagulation at the upper limit, and with a concomitant hematologic disorder.
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.115.019396/-/DC1.
- © 2016 American Heart Association, Inc.