A 63-year-old man was admitted because of current chest pain with perspiration for 6 hours. Electrocardiography showed complete right bundle-branch block and ST-segment elevation on leads II, III, aVF, and V2 through V6 (Figure 1); we therefore suspected an anterior and inferior wall acute myocardial infarction. Coronary angiography revealed total occlusion of the proximal left anterior descending artery (Figure 2 and Movie I in the online-only Data Supplement); the left circumflex and right coronary arteries showed no abnormalities. The left anterior descending artery was recanalized by percutaneous catheter intervention. The patient complained of chest pain the next afternoon after percutaneous catheter intervention, and the ECG was not changed. A transthoracic echocardiogram was performed, which demonstrated that the apical segments of the left ventricular walls were akinetic with normal thickness in the 4-chamber view (Movie II in the online-only Data Supplement), but the apex myocardium was dyskinetic with a perforation (2 mm in diameter) connected to a small apical aneurysm (10×5 mm) covered by intact epicardium that communicated with the left ventricular cavity as demonstrated by color Doppler (Figure 3A and 3B and Movie III in the online-only Data Supplement) from the apical 2-chamber view. This was consistent with a subepicardial aneurysm (SEA). On the follow-up echocardiography performed 8 days after infarction, there was a small thrombus at the apex, and the false aneurysm could not be seen (Figure 3C and Movie IV in the online-only Data Supplement).
Electrocardiography showed complete right bundle-branch block and ST-segment elevation on leads II, III, aVF, and V2 through V6.
Coronary angiography revealed total occlusion (arrow) of the proximal left anterior descending artery.
Apical 2-chamber view showed an apical myocardial perforation (2 mm in diameter) connected to a small apical aneurysm (10×5 mm) covered by intact epicardium (A), which communicated with the left ventricular cavity as demonstrated by color Doppler (B). Follow-up echocardiography performed 8 days after infarction showed a small thrombus at the apex, and the false aneurysm could not be seen (C).
To confirm the diagnosis, cardiac magnetic resonance imaging (MRI) was performed. Axial (Figure 4A) and short-axis (Figure 4B) first-pass perfusion steady-state free-precession MRIs demonstrated an area of microvascular obstruction in the apical wall (solid arrows) with an small aneurysm (open arrow) compatible with a left ventricular rupture. The magnified view (Figure 4C) of the steady-state free-precession MRI confirmed an apical thrombus (arrow) at the area of the ruptured orifice (open arrow) covered by intact epicardium. The 2-chamber-view (Figure 4D) delayed-enhancement inversion-recovery MRI (steady-state free-precession–gradient recalled echocardiography) after intravenous gadolinium injection showed apical acute myocardial infarction with a persistent area of microvascular obstruction (arrowheads), small apical thrombus, and a small aneurysm with clot covered by epicardium (arrow).
A, Cine (steady-state free-precession) cardiac magnetic resonance imaging of the 2-chamber view in the diastolic phase clearly showing a diverticulum-like cavity (arrowhead) with thrombus (white arrow) inside. B, In cine imaging of the 2-chamber view in the systolic phase, the diverticulum-like cavity disappeared, which indicated the formation of an aneurysm. The intact epicardium could be seen in this phase (white solid arrow), which was consistent with a subepicardial aneurysm. The thrombus (black arrow) still could be seen in the left ventricular apex. C, Late gadolinium enhancement (LGE) imaging of the short axis. The scar (arrowheads) was demonstrated by enhanced myocardium, whereas significant microvascular obstruction was detected as the hypoenhancement (white arrow) within the necrotic area. D, LGE imaging of the 2-chamber view. Enhanced myocardium was detached in the apex, and thromboses (open arrow) can be seen in the left ventricle and inside the diverticulum.
To prevent epicardial rupture or sudden death, an aneurysmectomy was performed 28 days after infarction. During surgery, a small ruptured orifice filled with thrombus in the left ventricular apex was evident. A ventricular aneurysm resection and coronary artery bypass saphenous vein to left anterior descending artery side anastomosis operation were performed.
Pathological examination showed that the endocardial layer and muscle layer structure ruptured, but the epicardial layer was intact with fibrous tissue and a small number of myocardial cells (Figure 5). The patient was discharged from hospital 10 days after surgery in good condition.
Gross pathological examination showed that the epicardial layer of the apical surface was intact (1*), but the endocardial layer and muscle layer structure ruptured (2, arrow), covered by thrombus (3 and 4). Histological examination showed that the epicardial layer was integrity (arrow) with fibrous tissue and a small number of myocardial cells (5).
Discussion
There are several potentially life-threatening complications: arrhythmias, cardiogenic shock, and ventricular wall rupture with the formation of aneurysm. In left ventricular complete free wall ruptures account for almost 4% of patient deaths after acute myocardial infarction (33% occur within the first 24 hours, 85% within the first week),1 complete septal ruptures (accounting for 1%–5% of all infarct-related deaths),2 and the formation of false aneurysms. Although true aneurysms typically do not require emergency treatment, false aneurysms, or pseudoaneurysms, are the result of a complete rupture of the ventricular wall with containment of the resulting hematoma by adherent pericardium and thus have a high mortality rate. SEA is rare; of 1814 hearts examined after postmortem arteriography from autopsy subjects at the Johns Hopkins Hospital, 704 had 1140 infarcts, and only 3 SEAs were found (0.2% of infarcts).3 Because SEAs are precursors to pseudoaneurysms with a high propensity to rupture, immediate treatment is often lifesaving. Although conservative management has been reported to be successful in asymptomatic chronic SEAs,4 surgical treatment is still considered the standard of care, especially for symptomatic acute SEAs, as in our case. The options include aneurysmectomy (resection) or aneurysmorrhaphy (patch repair). In addition to an elevated risk of death, patients with SEAs are initially difficult to diagnose owing to a lack of specific symptoms. Although the transthoracic echocardiography demonstrated the abnormality, sometimes the features are not distinct enough to differentiate aneurysm subtypes, and MRI or computed tomography may be helpful for accurate diagnosis. Because SEAs have a high risk of rupture, if patients have a history of acute myocardial infarction or signs of coronary artery disease, the cardiac surgery therapy should be performed as soon as the diagnosis confirmed.
In a patient with continued chest pain after acute myocardial infarction, subendocardial left ventricular aneurysm/impending rupture should be considered as an uncommon life-threatening differential diagnosis. In our case, the SEA was found by transthoracic echocardiography and was confirmed on a dedicated cardiac MRI. Emergency surgery guided by these imaging findings most likely saved the patient’s life.
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