PMC9530630_01
Clinical data of the patient with LV pseudoaneurysm post-acute myocardial infarction. (A) ECG showed acute inferior-, posterior- and lateral wall myocardial infarction. (B) Coronary angiography showed LCX acute occlusion. Yellow arrows indicated the occluded point of the LCX. (C) The primary percutaneous coronary intervention of LCX. A yellow arrow marked the revascularization of the proximal segment of the LCX. (D) CT demonstrated hemopericardium which was marked by yellow arrows. (E) TTE showed an LV pseudoaneurysm formation and blood between the pseudoaneurysm and LV during the diastolic period. (F) TTE showed blood flow interruption during the systolic period. (G) CMR confirmed LV pseudoaneurysm formation in the lateral wall, which is marked by the yellow arrow. LV, left ventricle; ECG, electrocardiogram; LCX, left circumflex; TTE, transthoracic echocardiography; CMR, cardiac magnetic resonance imaging.
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F1
The electrocardiogram (ECG) of the patient showed ST segment elevation in leads II, III, aVF, V5-V6, and V7-V9, which suggested inferior-, posterior-, and lateral-wall AMI (Figure 1A). Primary percutaneous coronary intervention (PCI) of the occlusive proximal segment of the left circumflex (LCX) coronary artery (Figure 1B) was successfully performed (Figure 1C). Chest CT (CT) further confirmed that the pericardium effusion was bloody (Figure 1D). However, subsequent TTE reexamination revealed the presence of a 2.1*1.1 cm pseudoaneurysm with a width of 0.3 cm fissure in the lateral wall that connected the LV and the pseudoaneurysm (Figures 1E,F), while cardiac magnetic resonance (CMR) also demonstrated the LV pseudoaneurysm formation (Figure 1G). Interestingly, during diastole, the blood flowed between the LV and pseudoaneurysm (Figure 1E, Supplementary Video 1); while during systole, the fissure was closed due to myocardial contraction, and the blood flow was subsequently interrupted (Figure 1F). One year later, TTE reexamination revealed that the LV pseudoaneurysm was only about 0.3*0.5 cm, and the fissure was closed without blood flow between the ventricle and the pseudoaneurysm (Supplementary Figure 1, Supplementary Video 2).
Clinical diagnosis and treatment timeline of the patient. STEMI, ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention; DAPT, dual-antiplatelet therapy; SAPT, single antiplatelet therapy; ARNI, angiotensin receptor, and neprilysin inhibitor.
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One year later, TTE reexamination revealed that the LV pseudoaneurysm was only about 0.3*0.5 cm, and the fissure was closed without blood flow between the ventricle and the pseudoaneurysm (Supplementary Figure 1, Supplementary Video 2). The clinical diagnosis and treatment timeline of the patient was summarized in Figure 2.