Left ventricular (LV) pseudoaneurysm is a clinicopathological entity that constitutes a rare mechanical complication of acute myocardial infarction (AMI).¹ It is formed when the cardiac rupture is contained by pericardium or scar tissue, without the presence of the myocardium as a tissue component.¹ It generally occurs in the inferior and posterior ventricular walls, given that ruptures of the anterior wall tend to lead to cardiac tamponade and sudden death, whereas the inferior-posterior face of the heart rests on the diaphragm, facilitating containment of the ventricular cavity by the pericardium.² Given its composition, there is a high risk of rupture, making surgical correction necessary.³

We report the case of a 67-year-old male patient, resident of the state of Bahia, Brazil, with hypertension for 10 years and diabetes for 5 years. He had been an ex-smoker for 32 years, with an estimated smoking history of 51 pack-years.

In 2019, he presented with AMI with ST-segment elevation in the anterior wall. However, he arrived at a unit with a hemodynamic service 8 days after diagnosis, without having received fibrinolytic therapy. Upon admission, he underwent coronary angiography, which showed 90% stenosis in diagonal branch and only parietal irregularities in the other coronary arteries. He underwent transluminal angioplasty and was discharged from the hospital. The patient was advised to undergo outpatient follow-up at the cardiology service, which he did not follow.

Five years later, the patient returned for a consultation requesting clearance for inguinal herniorrhaphy. He complained of dyspnea upon moderate exertion, such as walking uphill, but he stated that this symptom had been present since 2019, without progression. He denied association with chest pain or other anginal equivalents. The general surgeon reported that there was a mass in the LV on the chest tomography.

Upon physical examination, the patient had an active precordium, with an apparent, visible, and palpable apex beat in the fourth left intercostal space, between the left midclavicular line and the anterior axillary line, which was propulsive and measured 3 fingertips. The patient was using acetylsalicylic acid 100 mg/day, metoprolol succinate 50 mg every 12 hours, spironolactone 25 mg/day, atorvastatin 80 mg/day, enalapril 20 mg every 12 hours, and metformin XR 500 mg every 12 hours. The patient was admitted for diagnostic confirmation.

Radiography showed a mass adjacent to the LV (Figure 1), and electrocardiography indicated residual ST-segment elevation in the precordial leads (Figure 2).

Transthoracic echocardiography described akinesia of the middle and apical segments of the anteroseptal, anteroapical, apical LV walls and inferobasal and inferoseptal walls of the LV, in addition to the formation of a pseudoaneurysm in the inferolateral wall with important global systolic dysfunction and ejection fraction (EF) of 21%, by the Simpson method. We observed diastolic filling and tissue Doppler imaging compatible with type 3 diastolic dysfunction (restrictive pattern). The examination performed in 2019 revealed EF of 27% and segmental LV involvement with severe systolic dysfunction, with no mention of pseudoaneurysm formation.

Cardiac resonance imaging was performed, thus establishing diagnosis of LV pseudoaneurysm measuring 48 × 36 × 30 mm from the apical anterior segment, with neck size of 30 mm. Transmural late enhancement was greater than 50% throughout the apical and anteroseptal region (Figure 3).

The patient underwent a new coronary cineangiography according to the surgical intervention schedule, showing 75% stenosis in the bifurcation of the first marginal branch, 90% ostial stenosis of the second marginal branch, 75% to 90% stenosis middle third of the posterolateral branch, and 75% stenosis in the middle third of the right coronary artery (Figure 4).

The patient was referred for aneurysmectomy and revascularization of the marginal branch and the right coronary artery with saphenous vein graft. During surgery, the diagnosis of pseudoaneurysm was confirmed (Figure 5). During the postoperative period, he developed a stroke after an episode of atrial fibrillation with high ventricular response. Nonetheless, he was discharged approximately 7 days after the procedure without sequelae.

AMI is the most common cause of LV pseudoaneurysm (55%). Less frequently, pseudoaneurysms occur as a complication of cardiac surgery, chest trauma, as a consequence of endocarditis, and, rarely, after suppurative pericarditis or tumor infiltration.^1,4,5

Mechanical complications in the context of AMI are currently uncommon due to the effective implementation of early revascularization strategies. Although rare, cardiac rupture is one of the most feared events.³ In the case of pseudoaneurysm, approximately 30% to 45% have a chance of rupture; in this context, surgical intervention can substantially reduce this risk.^1,4,5

Some patients may present symptoms of heart failure due to LV dysfunction. However, approximately 10% are asymptomatic.⁴

Pseudoaneurysms can be detected on chest radiography as an area adjacent to the heart. On electrocardiography, there may be nonspecific repolarization changes.⁶

Echocardiography identifies changes in 90% of cases, but approximately 67% to 75% of cases are confused with aneurysm.^4,5,7 Left ventriculography, on the other hand, has been considered an important imaging modality, with a diagnostic accuracy of around 85%, given that it is possible to determine the neck of the pseudoaneurysm and the absence of surrounding coronary arteries.^3,7

In 2005, Konen et al. assessed 22 cardiac resonance images of patients with pseudoaneurysm or LV aneurysm. Delayed enhancement of pericardium was more common in patients with pseudoaneurysm, leading to a sensitivity of 100% and specificity of 83.3%. For these patients, the end-diastolic volume was greater than in those with true aneurysm. Therefore, this test plays an important role in differentiating both pathologies.⁸

Treatment for acute and symptomatic cases is limited to surgical correction, taking patients’ risks into consideration.¹

In 1998, Yeo et al. followed 52 patients with pseudoaneurysm for approximately 4 years. The majority were diagnosed incidentally; 42 patients underwent surgical correction, and mortality reached 7%. Ten patients were treated conservatively; they did not undergo the procedure due to high risk. After 2.3 years of study, 19 patients died, 6 of them in the conservative group. There were no reports of rupture.^9,10

Following this same model, in 2003, Moreno et al. followed 10 patients, all diagnosed with pseudoaneurysm and in conservative treatment, for 3.8 years, and none of them developed fatal rupture during this period. However, the incidence of stroke reached 33%, which suggests the possibility of chronic anticoagulation adjacent to treatment.¹⁰

According to Faustino et al., there is still no consensus on treatment for chronic cases, but surgical indication has become routine due to the risk of rupture and thrombotic embolization. In patients with pseudoaneurysms larger than 3 cm, procedure is indisputably necessary. In the case of patients with high surgical risk, the possibility of percutaneous procedure can be assessed. Since the condition may also be present in previously operated patients, the presence of adhesions makes intraoperative management difficult and increases mortality. Defects can be occluded with septal occluders, such as those used in congenital heart disease.^1,4,11

This case illustrates the importance of diagnosing the LV pseudoaneurysm, which led to impaired EF. It is a rare condition that can remain asymptomatic for years, but it presents a significant risk of complications. Regular surveillance and follow-up are essential, especially in patients with a history of AMI. Diagnosis and surgical intervention are essential due to the high risk of rupture, even in the absence of symptoms. Imaging modalities, such as magnetic resonance imaging, are crucial for assessment and treatment planning.