A growing left ventricular aneurysm after myocardial infarction: pathological confirmation of subepicardial aneurysm
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IMAGE–CARDIOLOGY
A growing left ventricular aneurysm after myocardial infarction: pathological confirmation of subepicardial aneurysm Hitomi Horinouchi1 · Tomoo Nagai1 · Mai Ishihara2 · Seiji Tamiya1 · Yuji Ikari1 Received: 5 August 2020 / Accepted: 22 September 2020 © The Japan Society of Ultrasonics in Medicine 2020
A 67-year-old woman with a history of hypertension, diabetes mellitus, surgical treatment of colon and cervical cancers, and recent cerebral infarction, who complained of epigastralgia lasting 3 days, was admitted due to inferior myocardial infarction. She received successful percutaneous coronary interventions for her occluded right coronary artery with thrombus followed by intracoronary administration of tissue plasminogen activator (TPA). The door to balloon time was 140 min, and her final angiogram indicated TIMI 3 reflow. Although her hemodynamic condition was stabilized without arrhythmic events during the hospitalization except for one sustained ventricular tachycardia event, which was successfully treated by cardioversion, she started to suffer aspiration pneumonia. Serial routine follow-up echocardiograms found a growing left ventricular aneurysm in her infarcted myocardium (Fig. 1a). She refused any further surgical intervention, and passed away after 2 months’ hospitalization due to refractory respiratory infection. An autopsy was performed, and a large left ventricular aneurysm (70 × 50 mm) with aneurysmal neck (Fig. 1b) was observed macroscopically. Microscopically, the aneurysmal wall did not involve the parietal pericardium with hematoxylin–eosin stain (Fig. 1c, upper). A mural thrombus was also detected (TH). An immunological stain with desmin (Fig. 1c, lower) further revealed a thin layer of myocardium (arrow heads). These findings were consistent with a diagnosis of left ventricular subepicardial aneurysm (SEA). SEA of the left ventricle is a rare complication of myocardial infarction, with an incidence of 0.3–1% at autopsy
[1, 2], A typical morphologic feature is an abrupt interruption of the left ventricular myocardium by the mouth with an aneurysmal neck. Microscopically, the aneurysmal wall is composed of epicardium with or without a thin myocardial layer [3]. Several risk factors for SEA include strenuous physical activity, hypertension, large infarct size, presence of inflammatory reactions, high intraventricular pressure, use of thrombolytic therapy, and a longer time to reperfusion after infarction [3]. As SEA is prone to rupture from its formation, serial echocardiographic studies are necessary to detect unruptured SEA [4], and early surgical treatment is advocated [5]. In our case, the time to reperfusion after the infarction might has been prolonged as the patient had complained of epigastralgia for 3 days before admission, although the precise onset time was uncertain. Furthermore, the use of TPA and multiple comorbidities may have caused serious damage to the infarcted myocardium and contributed to SEA formation. As the patient refused any aggressive intervention an
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