An Atypical Left Ventricular Pseudoaneurysm Managed Conservatively

Abstract

Background

Left ventricle (LV) pseudoaneurysms pose a serious and life-threatening complication of myocardial infarction.

Case Summary

We present a case of a thrombosed LV pseudoaneurysm with clot extension into the LV cavity in an asymptomatic 62-year-old man presenting with nonsecific symptoms. Multimodal imaging was undertaken to confirm the diagnosis. Owing to the chronicity of the pseudoaneurysm, the patient was managed conservatively.

Discussion

This case illustrates an alternative management approach in a clinical scenario with a paucity of data and no clear guidelines.

Take-Home Messages

Multimodal imaging is critical to distinguish LV pseudoaneurysms from true aneurysms, particularly in atypical locations, as accurate diagnosis directly affects management decisions. Although surgical repair remains the standard treatment for LV pseudoaneurysms, select chronic cases may be candidates for conservative management. Long-term follow-up data is needed to validate this approach.

Graphical Abstract

History of Presentation

A 62-year-old man presented to his local hospital with nondermatomal right arm paresthesia, transient diaphoresis, and disorientation. He denied any prior history of chest pain, palpitations, or symptoms of heart failure. On examination, the patient was tachycardic without any signs of heart failure. Importantly, his neurologic examination was unremarkable. A 12-lead electrocardiogram demonstrated sinus rhythm with pathological Q waves and poor R-wave progression seen across the precordial leads (Figure 1). There was a dynamic rise in his troponin blood test, and the patient was transferred to a regional center for further comprehensive cardiac evaluation and management.

Take-Home Messages

• •Multimodal imaging is critical in distinguishing LV pseudoaneurysms from true aneurysms, particularly in atypical locations, as accurate diagnosis directly affects management decisions.
• •Although surgical repair remains the standard treatment for LV pseudoaneurysms, select chronic cases may be candidates for conservative management. Long-term follow-up data are needed to validate this approach.

Figure 1.

Admission Electrocardiogram

Electrocardiogram with Q waves and poor R-wave progression.

Past Medical History

The patient's past medical history was pertinent for hypertension and hypercholesterolemia with suboptimal medication compliance. Furthermore, he was an ex-smoker with a 50 pack/year history.

Differential Diagnosis

Initial differential diagnoses included a late-presenting anterior myocardial infarction, heart failure with reduced ejection fraction (HFrEF), and an atypical presentation of a transient ischemic attack with concomitant troponin leak.

Investigations

The patient's point-of-care troponin assay was initially negative on presentation (<0.04 μg/L) and increased to a positive level (0.85 μg/L) on repeat testing. His high-sensitivity troponin levels peaked at 1100 ng/L on day 2 of admission. His glycosylated hemoglobin was normal at 5.5%. A chest x-ray at the time of presentation showed cardiomegaly with enlargement and calcification of the left heart border, suggestive of a left ventricular aneurysm (Figure 2).

Figure 2.

Admission Chest X-Ray

Chest x-ray demonstrating increased cardiothoracic ratio at 0.53 with apparent bulging of the left heart border and suspected calcifications (green arrow).

Coronary angiogram demonstrated a chronic total occlusion of the left anterior descending (LAD) artery with ipsilateral collateralization as well as a chronic total occlusion of the right coronary artery (RCA) with epicardial collaterals from the proximal RCA and retrograde collaterals from the left system (Figure 3). There was minor disease in the codominant left circumflex artery (Figure 4). A left ventriculogram revealed severe segmental systolic dysfunction with a large cavity near the left ventricle (LV), suggestive of an aneurysm or pseudoaneurysm (Figure 5).

Figure 3.

Coronary Angiography of Left Anterior Descending Artery and Right Coronary Artery

Chronic total occlusion of the (Left) left anterior descending artery and (Right) right coronary artery with collateralization.

Figure 4.

Coronary Angiography

Codominant left circumflex artery with minor coronary artery disease.

Figure 5.

Left Ventriculogram

Left ventriculogram performed during coronary angiography demonstrating dilated left ventricle with a calcified mass at the apex. No contrast opacification was demonstrated outside the left ventricle.

Transthoracic echocardiogram (TTE) demonstrated akinesis of the LAD artery territory and confirmed a diagnosis of HFrEF, with an LV ejection fraction of 20%. Further, a cavity with a neck diameter of 3.23 cm was identified in continuity with the cardiac apex (Figure 6).

Figure 6.

Transthoracic Echocardiogram

Apical 2-chamber view demonstrating (Left) continuity of the left ventricle apex with pseudoaneurysm cavity (neck diameter: 3.23 cm) and (Right) large cavity in continuity with the left ventricle apex.

Cardiac computed tomography was performed to further characterize the LV cavity. This identified a 46 × 60 × 18 mm circumferentially calcified contained rupture in the midapical anterior wall with a 23 × 16.5 mm pedunculated thrombus extending into the LV cavity (Figure 7). Cardiac magnetic resonance imaging (CMR) demonstrated a transmural myocardial infarction of the LAD artery territory and confirmed a thrombus-filled cavity with clot extension into the LV (Figure 8). Based on all available imaging modalities, the consensus was that the cavity was a pseudoaneurysm in an atypical location.

Figure 7.

Cardiac Computed Tomography

(Left) Modified 4-chamber and (Right) modified 3-chamber views demonstrating thrombosed left ventricular pseudoaneurysm with circumferential calcification and thrombus extension into the left ventricular cavity.

Figure 8.

Cardiac Magnetic Resonance Imaging

Axial cardiac magnetic resonance imaging demonstrating thrombus extension into the left ventricular cavity.

Management

The patient was discussed at the multidisciplinary heart team meeting, where a decision was made to manage the pseudoaneurysm conservatively. Given the confirmed nonviability of the LAD artery territory on CMR and the patient's lack of symptoms, revascularization was deemed unlikely to improve prognosis. The mainstay of his management focused on the initiation and up-titration of guideline-directed medical therapy for HFrEF. Additionally, anticoagulation with warfarin was commenced to address the clot extension into the LV cavity, with an international normalized ratio target of 2 to 3.

Discussions

LV pseudoaneurysms are a rare but potentially life-threatening complication of myocardial infarction. They result from a contained rupture of the LV free wall, where the adherent pericardium or surrounding structures prevent complete cardiac rupture. This contrasts with true aneurysms, which involve a thinned out but structurally intact myocardial wall.¹ Accurate differentiation between the two is critical because of their divergent management strategies and prognostic implications. Anatomical location can provide an important clue in differentiating between them. True LV aneurysms most commonly form at the anterior or anterolateral wall and apex, as these regions are particularly prone to infarction-related remodeling.² In contrast, pseudoaneurysms more frequently arise in the basal or inferior walls, where myocardial rupture is more likely to be contained by pericardial adhesions or adjacent structures.³ However, exceptions exist, as in our case where a large pseudoaneurysm developed at the apex, reinforcing the need for multimodal imaging for accurate differentiation.

Multimodal imaging is essential in distinguishing LV pseudoaneurysms from true aneurysms. TTE is often the initial diagnostic modality, but it may be limited in defining the extent of the abnormality. A key echocardiographic criterion supporting the diagnosis of pseudoaneurysm is a neck-to-cavity ratio of <50%, which was present in our case.⁴ Computed tomography and CMR can further delineate structural characteristics, thrombus burden, and myocardial viability, aiding in both diagnosis and risk stratification. As in our case, the circumferential calcification confined to the border of the cavity suggested a ruptured thin-walled pseudoaneurysm as opposed to a true aneurysm, which usually has laminar thrombus and a heterogenous pattern of calcification mixed within it.

Surgical repair remains the cornerstone of management of LV pseudoaneurysms owing to their significant risk of rupture, which carries a mortality rate of 20% to 48% if left untreated.³ This is particularly pressing for large pseudoaneurysms (>3 cm). However, surgery itself carries substantial risk, with operative mortality reported as high as 23% in some series.⁵ Despite these general recommendations, there is emerging evidence suggesting that the risk of rupture with pseudoaneurysms may decrease over time.⁴ In select cases where pseudoaneurysms appear chronic, a conservative approach may be a reasonable alternative. In our case, the presence of a circumferentially calcified pseudoaneurysm suggested an element of chronicity and guided the decision for conservative management. Another critical consideration in this case was anticoagulation therapy. Pseudoaneurysms pose competing risks: thromboembolism due to stasis within the aneurysmal sac vs the potential for rupture. The decision to initiate anticoagulation was based on the presence of a large pedunculated thrombus extending into the LV cavity, indicating a significant risk of embolic events. However, there is limited evidence to guide anticoagulation decisions in pseudoaneurysm cases, as excessive anticoagulation could theoretically increase the risk of rupture. Given the chronic nature of the pseudoaneurysm and the stability of the thrombus on imaging, the risk-benefit assessment in this case favored anticoagulation with careful monitoring.

To our knowledge, this is one of the first reported cases of an incidentally discovered, thrombosed LV pseudoaneurysm that was managed conservatively with anticoagulation. Although the standard approach to pseudoaneurysms remains surgical repair, our case suggests that in select patients with chronic, calcified pseudoaneurysms and no viable myocardium, nonsurgical management may be considered. Given the lack of formal guidelines on conservative treatment, further studies are needed to better define patient selection criteria and long-term outcomes in medically managed LV pseudoaneurysms.

Follow-Up

A repeat TTE 3 months later confirmed marginal improvement in the LV ejection fraction despite optimal medical therapy, and the patient subsequently underwent primary prevention implantable cardioverter-defibrillator placement.

Conclusions

LV pseudoaneurysm is a rare but catastrophic complication of myocardial infarction. With the development and advancements in percutaneous coronary intervention services and techniques, clinicians may rarely encounter this phenomenon. This report highlights the unique presentation of an incidentally discovered pseudoaneurysm in a patient without cardiac symptoms. Although surgical repair is the primary treatment choice, multimodal imaging can play a vital role in characterizing the aneurysm and guiding personalized treatment strategies.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.