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Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction

Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction
Literature review current through: Jan 2024.
This topic last updated: Jul 28, 2023.

INTRODUCTION — Left ventricular (LV) aneurysms and pseudoaneurysms are two complications of myocardial infarction (MI) that can lead to death or significant morbidity. This topic reviews the diagnosis and management of patients with aneurysms or pseudoaneurysms caused by MI.

Aneurysms are also found in diseases such as hypertrophic cardiomyopathy and Chagas disease. Their diagnosis and management are discussed separately. (See "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis" and "Hypertrophic cardiomyopathy: Morphologic variants and the pathophysiology of left ventricular outflow tract obstruction", section on 'Midcavity obstructive HCM'.)

LEFT VENTRICULAR ANEURYSM

Pathophysiology — LV aneurysms are caused by severe ischemic injury to the myocardium. In the early phase of LV aneurysm formation, the histologic findings in the ventricular wall include muscle necrosis and an intense inflammatory reaction. The injured myocardium is gradually replaced with scar tissue formation. The "border zone" of the aneurysm (ie, between the aneurysm and the normal myocardium) is characterized by patchy fibrosis and abnormal alignment of the muscle fibers [1-3].

In more mature aneurysms, the wall of the aneurysm typically consists of a white fibrous scar and is thin. The scar is composed of hyalinized fibrous tissue (image 1) [1-3]. The endocardial surface is smooth and nontrabeculated (image 2) [1]. The aneurysm is filled with organized clot in over 50 percent of cases (image 3 and image 4). The mural thrombus may calcify over time and the aneurysmal wall may itself become calcified (image 5 and image 6). Dense adhesions between the aneurysm and the overlying pericardium are common [1,2].

These structural changes result in abnormal hemodynamics, metabolic stress, and adverse remodeling that causes or exacerbates preexisting myocardial injury [4-6]:

Hemodynamic abnormalities – In patients with an LV aneurysm, the aneurysmal segment of the LV bulges during systole, which effectively results in loss of forward stroke volume.

Metabolic stress – In patients with an LV aneurysm, the enlarged ventricle causes an increase in wall tension via La Place's Law and an increase in oxygen demand [7]. In the presence of obstructive coronary artery disease, increased metabolic stress may exacerbate angina. (See "Approach to the patient with suspected angina pectoris".)

The end result of metabolic stress and prolonged ischemia is a globally dilated and dysfunctional LV.

Epidemiology — LV aneurysms are rare and typically occur as a complication of acute MI. Other causes of LV aneurysm include prior cardiac surgery, Chagas disease, and hypertrophic cardiomyopathy.

In patients with MI who are treated with modern reperfusion techniques (eg, percutaneous coronary intervention), the incidence of LV aneurysm has not been well studied. However, its incidence with modern reperfusion therapy is likely lower than its incidence during the era of widespread thrombolytic use, which was 7 to 19 percent of patients with a Q-wave MI [8,9].

The risk factors for LV aneurysm after MI include anterior wall infarction, delayed or incomplete reperfusion, and the absence of extensive collateralization. Approximately 70 to 85 percent of LV aneurysms are located in the anterior or apical walls and are associated with total occlusion of the left anterior descending (LAD) coronary artery and the absence of collateralization (image 7 and image 8) [1-3,10]. Only 10 to 15 percent of LV aneurysms involve the inferior-basal walls (image 9 and image 10). Lateral LV aneurysms are exceedingly rare, in part due to the dual blood supply from either the LAD or the right coronary artery (figure 1) [1-3,10].

Clinical manifestations — In patients with acute MI, the presence of an LV aneurysm is typically identified with imaging performed for diagnosis and management of acute MI. Among patients who present remotely from the index acute MI, the aneurysm may be detected during the evaluation of worsening signs or symptoms, which include:

Angina – In patients with an LV aneurysm, increased oxygen consumption caused by elevated filling pressure and wall tension may promote angina.

Heart failure – In patients with an MI significant enough to cause an LV aneurysm, LV systolic dysfunction is typically present. In our experience, most patients with an LV aneurysm have heart failure (HF) symptoms.

Ventricular arrhythmias Ventricular arrhythmias are common in patients with an LV aneurysm. In addition to the common mechanisms of ventricular arrhythmias in patients with LV systolic dysfunction, patients with an LV aneurysm are prone to scar-related reentrant arrhythmias, which occur at the border zone between the aneurysmal and normal portions of the LV wall [11-13]. (See "Enhanced cardiac automaticity" and "Reentry and the development of cardiac arrhythmias".)

Systemic embolization – Patients with an LV aneurysm rarely present with stroke or systemic embolization [14,15]. However, a mural thrombus is present at autopsy or during surgery in more than 50 percent of patients with LV aneurysm [2,11,16].

Sudden death – Patients with an LV aneurysm may present with sudden death as the result of a ventricular arrhythmia or aneurysm rupture [17]. (See 'Prognosis and risk of rupture' below.)

Evaluation for LV aneurysm — The evaluation for LV aneurysm includes the following:

History and physical examination – A history of MI is the most common history among patients with an LV aneurysm. Cardiac surgery, Chagas disease, and hypertrophic cardiomyopathy are less common diseases that cause LV aneurysm.

The physical examination may reveal one or more of the following findings:

Cardiac enlargement with a diffuse apical impulse that is displaced to the left of the midclavicular line. (See "Examination of the precordial pulsation".)

An area of dyskinesis can occasionally be appreciated with palpation of the apex or left lateral chest wall, in the area of the anterior wall of the LV.

A third or fourth heart sound is often heard, indicating blood flow into a dilated and stiffened LV chamber. (See "Auscultation of heart sounds".)

A systolic murmur of mitral regurgitation may be appreciated due to the distortion of LV geometry that results in the absence of leaflet apposition, tethering of the chordae, papillary muscle dysfunction, and/or annular dilation. (See "Auscultation of cardiac murmurs in adults".)

ECG – The electrocardiogram may record evidence of a large anterior MI or persistent ST-segment elevation, but these findings are not specific for LV aneurysm and could represent a large scar without aneurysm formation (waveform 1).

Chest radiograph – The presence of an LV aneurysm may be identified on chest radiography (image 10 and image 7 and image 8 and image 11), but other imaging techniques are more likely to establish the presence or absence of an LV aneurysm.

Initial imaging (echocardiography) – In patients suspected of having an LV aneurysm, echocardiography is typically the first step in evaluation (movie 1 and movie 2) [18,19]. In most patients, echocardiography is sufficient to establish the diagnosis. In patients with nondiagnostic echocardiographic images or who require further characterization of the ventricular wall (eg, to differentiate between aneurysm and pseudoaneurysm), additional imaging may be required.

The echocardiographic appearance of an LV aneurysm includes a large area of myocardium that is akinetic or dyskinetic during systole and abnormal ventricular wall deformation during diastole. LV aneurysms arise from a broad base or "neck" (movie 1 and movie 2), which differentiates them from the smaller neck of an LV pseudoaneurysm. (See 'Diagnosis' below.)

Additional imaging – In patients in whom echocardiography cannot definitively establish the diagnosis of LV aneurysm, we typically obtain cardiovascular magnetic resonance (CMR) imaging, which is considered the gold standard for diagnosis of LV aneurysm. If CMR imaging cannot be obtained (eg, in the presence of retained or implanted metallic bodies), other options for the diagnosis of LV aneurysm include coronary computed tomographic angiography (CCTA), radionuclide ventriculography, and contrast ventriculography. Examples of LV aneurysm imaging findings include:

CMR (image 12)

CCTA (figure 1 and image 2 and image 3 and image 4 and image 5 and image 6 and image 9 and image 13 and image 14)

Radionuclide ventriculography (image 15)

Contrast ventriculography (image 14 and image 16)

Assessment for LV thrombus – In patients diagnosed with an LV aneurysm, a dedicated study for assessment of LV thrombus should be performed. The approach to diagnosis of LV thrombus is discussed separately. (See "Left ventricular thrombus after acute myocardial infarction", section on 'Diagnosis'.)

Diagnosis — For the purpose of this topic review, an LV aneurysm is a well-delineated area of myocardium that is thin, scarred, and has no functional myocardium (ie, akinetic, dyskinetic).

The pathologic findings of LV aneurysm are discussed elsewhere in this topic. (See 'Pathophysiology' above.)

The differential diagnosis includes LV pseudoaneurysm and LV diverticulum. In contrast with an LV pseudoaneurysm, a true LV aneurysm arises from a broad base or "neck" and the myocardium, though fibrotic and scarred, is not interrupted. The characteristics of LV pseudoaneurysms are discussed elsewhere in this topic (see 'Diagnosis' below). An LV diverticulum is a rare finding that occurs either as a congenital anomaly or in patients with hypertrophic cardiomyopathy [20,21].

Management

Therapy for reduced systolic function — All patients with an LV aneurysm and LV systolic dysfunction should receive therapy appropriate for ischemic cardiomyopathy (eg, revascularization, medical therapy, cardiac resynchronization therapy) [22]. The general approach to the management of LV systolic dysfunction is described elsewhere. (See "Overview of the management of heart failure with reduced ejection fraction in adults" and "Treatment of ischemic cardiomyopathy".)

Anticoagulation — We evaluate for the presence of thrombus in all patients with evidence of an LV aneurysm. Our approach to anticoagulation is discussed separately. (See "Left ventricular thrombus after acute myocardial infarction", section on 'Prevention of embolic events'.)

Role of aneurysmectomy — The scenarios in which aneurysmectomy may be considered include:

Patients with an LV aneurysm who require cardiac surgery – In patients with an LV aneurysm who will undergo cardiac surgery (eg, coronary artery bypass graft surgery [CABG]), LV aneurysmectomy may be included as part of the planned surgery. The decision to perform aneurysmectomy at the time of cardiac surgery is typically determined by the surgeon who must decide whether aneurysmectomy is required to successfully perform the planned surgery (eg, mitral valve surgery) or is likely to be of benefit regardless of the planned surgery.

North American guidelines give a weak recommendation for performance of aneurysmectomy at the time of CABG in patients with the features noted above, while European guidelines do not mention aneurysmectomy [23,24].

There are no reliable data to guide patient selection or the exact approach to surgery (eg, Dor myoplasty, linear repair) [25]. Some patients enrolled in the STICH trial likely had an LV aneurysm and aneurysmectomy, but the anatomy and surgery performed in STICH were not well described, which limits the direct application of this trial's results to patients with an LV aneurysm [26]. Further details on this study are described elsewhere in this topic. (See 'Surgery for left ventricular enlargement' below.)

Patients with an LV aneurysm without another indication for cardiac surgery In patients with HF who receive maximal medical therapy and have no indication for cardiac surgery but who have a large aneurysm, large LV thrombus, or arrhythmias due to an aneurysm, isolated LV aneurysmectomy is an option for therapy if no other options (eg, radiofrequency ablation, heart transplantation) are feasible or appropriate.

Isolated aneurysmectomy is not mentioned in professional guidelines, and its efficacy is unclear.

Approach to severe heart failure — In patients with an LV aneurysm who have severe HF symptoms (eg, New York Heart Association class IV HF symptoms) refractory to optimal medical and device-based treatments, we continue optimal therapy and evaluate the patient for the appropriateness of advanced HF therapies such as heart transplantation and durable mechanical circulatory support. In rare scenarios, aneurysmectomy may be an option for therapy. (See 'Role of aneurysmectomy' above.)

Approach to ventricular arrhythmias — In patients with an LV aneurysm who have refractory ventricular arrhythmias despite optimal medical management, VT ablation is an option that may reduce the frequency of ventricular arrhythmias. In most patients with an LV aneurysm who are under consideration for VT ablation, an assessment for advanced HF therapies is warranted. (See "Electrical storm and incessant ventricular tachycardia", section on 'Subsequent management'.)

Longitudinal monitoring — In patients diagnosed with LV aneurysm, we typically monitor for changes in LV function, changes in aneurysm dimensions, and related complications with echocardiography. Following acute MI and aneurysm formation, we may obtain imaging every 6 to 12 months to monitor for adverse remodeling and thrombus formation. After approximately one year, the frequency of echocardiographic monitoring is individualized to the patient.

Prognosis and risk of rupture — The natural history of patients with LV aneurysm who survive the initial MI is not well described. However, the presence of an LV aneurysm likely confers a worse prognosis than for similar patients who do not have an LV aneurysm. Based on our experience, morbidity and mortality in patients with an LV aneurysm is related to its size, whether the aneurysmal segment is dyskinetic or akinetic, the extent of coronary disease (single versus multivessel), and the overall function of the LV.

The risk factors for LV aneurysm rupture are unclear. The risk of aneurysm rupture may increase with the size of the aneurysm and decrease as the aneurysm becomes older and more fibrotic. In our experience, rupture is rare. There are no data that allow for accurate estimation of the risk of this fatal complication.

LEFT VENTRICULAR PSEUDOANEURYSM

Epidemiology and clinical presentation — LV pseudoaneurysm is a rare complication of MI, cardiac surgery, and trauma [27]. Risk factors for LV pseudoaneurysm are similar to those of ventricular free wall rupture (see "Acute myocardial infarction: Mechanical complications", section on 'Risk factors'). Right ventricular pseudoaneurysms are typically associated with prior cardiac surgery in patients with congenital heart disease [28].

The most frequent symptoms associated with LV pseudoaneurysm are chest pain and dyspnea [27,28]. Rarely, a pseudoaneurysm may present as persistent pericarditis. Sudden cardiac death was the presenting manifestation in approximately 3 percent. Between 12 and 25 percent of patients who have a ventricular pseudoaneurysm may be asymptomatic. Additional features of the presentation include:

Murmur – Murmurs are present in about two-thirds of patients [27]. The murmur is often present in both systole and diastole, but if isolated to systole, it may be indistinguishable from the murmur of mitral regurgitation.

ECG changes – ECG changes occur in more than 95 percent of patients and include ST-segment elevation in 20 percent and nonspecific changes in the remainder.

Chest radiography – In patients with a pseudoaneurysm, chest radiography may show cardiomegaly with or without calcification.

Evaluation — Similar to LV aneurysm, LV pseudoaneurysm should be suspected in patients who present with signs or symptoms of acute MI or HF. In patients with prior cardiac surgery or trauma, a high index of suspicion is required to pursue specific testing for an LV pseudoaneurysm.

Acute presentation with STEMI – In patients who present with acute MI (typically ST-elevation MI [STEMI]), the evaluation for acute MI typically includes a detailed history, physical examination, ECG, and chest radiography. If these or other studies (eg, point-of-care ultrasonography [POCUS]) suggest the presence of an LV pseudoaneurysm (eg, mass on chest radiography, circumferential pericardial effusion) in a patient who will undergo percutaneous coronary intervention (PCI), contrast ventriculography should be performed during the PCI procedure. In similar patients in whom contrast ventriculography cannot be performed, transthoracic or transesophageal echocardiography should be performed as soon as possible.

If the diagnosis is unclear after contrast ventriculography or echocardiography, CMR imaging or CCTA should be performed when clinically feasible.

Presentation without STEMI – In patients who present nonurgently, echocardiography, CMR imaging, or CCTA are all reasonable options for initial imaging.

Findings on imaging studies commonly obtained to assess for LV aneurysm include:

Echocardiography – On echocardiography, LV pseudoaneurysms have a narrow neck that is typically less than 40 percent of the maximal aneurysm diameter and causes an abrupt interruption in the ventricular myocardium. In contrast, true aneurysms are nearly as wide at the neck as they are at the apex (movie 1 and movie 2 and image 17) and there is no interruption of the ventricular myocardium (though it may be fibrotic or scarred).

Computed tomography or magnetic resonance imaging – The findings on CCTA and CMR imaging are similar to those on echocardiography, but CCTA and CMR can often identify the location of the aneurysm with greater detail (image 18) [29,30]. In addition, CCTA and CMR allow for more accurate measurement of the characteristics of the pseudoaneurysm (eg, ratio between the maximal internal width of the orifice to the maximal parallel internal diameter) and may provide other information relevant to management (eg, coronary anatomy with CCTA, characterization of the pseudoaneurysm tissue with CMR).

Contrast ventriculography – Contrast ventriculography demonstrates a narrow orifice leading to a saccular collection of blood that is contiguous with the LV cavity and that does not contain evidence of coronary artery circulation (image 19) [31]. Ventriculography leads to a definitive diagnosis in over 85 percent of patients [27].

Diagnosis — An LV pseudoaneurysm, also referred to as a false aneurysm or contained rupture, forms when the myocardium ruptures and the rupture is contained by adherent pericardium or scar tissue [32]. LV pseudoaneurysm is clinically diagnosed by identifying an outpouching of the LV that arises from a breach in the myocardial wall and is contained only by pericardium (ie, not myocardium).

The differential diagnosis includes true LV aneurysm and LV diverticulum. Unlike a true LV aneurysm, an LV pseudoaneurysm contains no endocardium or myocardium.

Treatment and prognosis — The treatment of patients with an LV pseudoaneurysm typically involves acute hemodynamic stabilization and urgent surgical repair:

Acute management – Patients who present with acute MI and pseudoaneurysm should be treated with all therapies appropriate for STEMI. (See "Overview of the acute management of ST-elevation myocardial infarction".)

For patients who present with cardiogenic shock, therapy may also include inotropic support and temporary mechanical circulatory support as appropriate. The approach to treatment of cardiogenic shock in acute MI is discussed separately. (See "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction".)

Surgical repair – In patients with LV pseudoaneurysm, medical therapy alone is associated with a high risk of mortality that may exceed 50 percent [27]. Thus, in patients who can safely undergo surgery, surgical repair is required. The goal of surgery is to prevent rupture and improve myocardial function. In patients who cannot undergo surgical repair, other options for treatment may include durable mechanical circulatory support device placement and urgent heart transplantation. Catheter-based occlusion has been reported, but the efficacy of this procedure is unclear [33].

Surgery is typically performed urgently. Surgery consists of resection of the pseudoaneurysm and repair of the LV wall defect with reapproximation of the myocardium with or without use of a patch [34]. The mortality after pseudoaneurysm repair is described in older studies in which the perioperative mortality was less than 10 percent and greater in patients who required additional surgery (eg, mitral valve replacement) [35,36].

SURGERY FOR LEFT VENTRICULAR ENLARGEMENT — In patients who have ventricular enlargement without an aneurysm, we suggest not performing LV restoration surgery. The benefit of this surgery is unclear and other surgical options for end-stage HF (eg, LV assist device placement, transplantation) may be available.

The rationale for surgical LV restoration is to reduce LV volume to improve mechanical function of the LV. Surgical LV restoration was evaluated in the STICH trial, which included 1000 patients with ischemic cardiomyopathy and an anterior akinetic or dyskinetic region of myocardium amenable to ventricular reconstruction [26]. Among patients randomly assigned to either LV reconstruction with coronary artery bypass graft surgery (CABG) or CABG alone, the risk of death or HF hospitalization was similar (58 versus 59 percent; hazard ratio 0.99, 95% CI 0.84-1.17).

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Non-ST-elevation acute coronary syndromes (non-ST-elevation myocardial infarction)" and "Society guideline links: ST-elevation myocardial infarction (STEMI)".)

SUMMARY AND RECOMMENDATIONS

Left ventricular aneurysm

Epidemiology – Left ventricular (LV) aneurysms are rare and typically occur as a complication of acute myocardial infarction (MI). Other causes of LV aneurysm include prior cardiac surgery, Chagas disease, and hypertrophic cardiomyopathy.

The risk factors for LV aneurysm after MI include anterior wall infarction, delayed or incomplete reperfusion, and the absence of extensive collateralization. (See 'Epidemiology' above.)

Clinical manifestations –In patients with acute MI, the presence of an LV aneurysm is typically identified with imaging performed for diagnosis and management of acute MI. Other syndromes that may indicate the presence of an LV aneurysm include angina, heart failure (HF), ventricular arrhythmias, systemic embolization, and sudden death.

Evaluation for LV aneurysm In patients suspected of having an LV aneurysm, echocardiography is typically the first step in evaluation (movie 1 and movie 2) [18,19]. In most patients, echocardiography is sufficient to establish the diagnosis. In patients with nondiagnostic echocardiographic images or who require further characterization of the ventricular wall (eg, to differentiate between aneurysm and pseudoaneurysm), additional imaging with cardiac computed tomographic angiography (CCTA), cardiovascular magnetic resonance (CMR) imaging (image 12), nuclear imaging (image 15), or contrast ventriculography (image 16) may be required.

In patients diagnosed with an LV aneurysm, a dedicated study for assessment of LV thrombus should be performed. The approach to diagnosis of LV thrombus is discussed separately. (See "Left ventricular thrombus after acute myocardial infarction", section on 'Diagnosis'.)

Management

-Therapy for reduced systolic function – All patients with an LV aneurysm and LV systolic dysfunction should receive therapy appropriate for ischemic cardiomyopathy (eg, revascularization, medical therapy, device therapy) [22]. The general approach to the management of LV systolic dysfunction is described elsewhere. (See "Overview of the management of heart failure with reduced ejection fraction in adults" and "Treatment of ischemic cardiomyopathy".)

-Anticoagulation – We evaluate for the presence of thrombus in all patients with evidence of an LV aneurysm. Our approach to anticoagulation is discussed separately. (See "Left ventricular thrombus after acute myocardial infarction", section on 'Prevention of embolic events'.)

-Aneurysmectomy in addition to other cardiac surgery – In patients with an LV aneurysm who will undergo cardiac surgery (eg, coronary artery bypass graft surgery [CABG]), LV aneurysmectomy may be included as part of the planned surgery. The decision to perform aneurysmectomy at the time of cardiac surgery is typically determined by the surgeon who must decide whether aneurysmectomy is required to successfully perform the planned surgery (eg, mitral valve surgery) or is likely to be of benefit regardless of the planned surgery. (See 'Role of aneurysmectomy' above.)

-Isolated aneurysmectomy – In patients with HF who receive maximal medical therapy but who have a large aneurysm, large LV thrombus, or arrhythmias due to an aneurysm, isolated LV aneurysmectomy is an option for therapy if no other options (eg, radiofrequency ablation, heart transplantation) are feasible or appropriate.

-Approach to severe heart failure – In patients with an LV aneurysm who have severe HF symptoms (eg, New York Heart Association class IV HF symptoms) refractory to optimal medical and device-based treatments, we continue optimal therapy and evaluate the patient for the appropriateness of advanced HF therapies such as heart transplantation and durable mechanical circulatory support. (See 'Approach to severe heart failure' above.)

-Approach to ventricular arrhythmias – In patients with an LV aneurysm who have refractory ventricular arrhythmias despite optimal medical management, ventricular tachycardia (VT) ablation is an option that may reduce the frequency of ventricular arrhythmias. (See "Electrical storm and incessant ventricular tachycardia", section on 'Subsequent management'.)

-Longitudinal monitoring – In patients diagnosed with LV aneurysm, we typically monitor for changes in LV function, changes in aneurysm dimensions, and related complications with routine echocardiography at least every three months. (See 'Longitudinal monitoring' above.)

Left ventricular pseudoaneurysm

Epidemiology and clinical presentation – LV pseudoaneurysm is a rare complication of MI, cardiac surgery, and trauma. The first indication of an LV pseudoaneurysm may be sudden death, which results from rupture of the pseudoaneurysm. Right ventricular pseudoaneurysms are typically associated with prior cardiac surgery in patients with congenital heart disease. (See 'Epidemiology and clinical presentation' above.)

Evaluation – Similar to LV aneurysm, LV pseudoaneurysm should be suspected in patients who present with signs or symptoms of acute MI or HF. In patients with prior cardiac surgery or trauma, a high index of suspicion is required to pursue specific testing for an LV pseudoaneurysm.

The initial approach to diagnosis is contrast ventriculography (image 19) for patients with ST-elevation MI (STEMI) who will undergo percutaneous coronary intervention (PCI) and echocardiography (image 17) for other patients. (See 'Evaluation' above.)

Diagnosis – An LV pseudoaneurysm, also referred to as a false aneurysm or contained rupture, forms when the myocardium ruptures and the rupture is contained by adherent pericardium or scar tissue [32]. LV pseudoaneurysm is clinically diagnosed by identifying an outpouching of the LV that arises from a breach in the myocardial wall and is contained only by pericardium (ie, not myocardium). (See 'Diagnosis' above.)

The differential diagnosis includes true LV aneurysm and LV diverticulum. Unlike a true LV aneurysm, an LV pseudoaneurysm contains no endocardium or myocardium.

Treatment and prognosis — The treatment of patients with an LV pseudoaneurysm typically involves acute hemodynamic stabilization and definitive repair:

-Acute management – Patients who present with acute MI and pseudoaneurysm should be treated with all therapies appropriate for STEMI. (See "Overview of the acute management of ST-elevation myocardial infarction".)

For patients who present with cardiogenic shock, therapy may also include inotropic support and temporary mechanical circulatory support as appropriate. (See "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction".)

-Surgical repair – In patients with LV pseudoaneurysm, medical therapy alone is associated with a high risk of mortality that may exceed 50 percent. Thus, in patients who can safely undergo surgery, surgical repair is required. In patients who cannot undergo surgical repair, other options for treatment may include durable mechanical circulatory support device placement and urgent heart transplantation. (See 'Treatment and prognosis' above.)

Surgery for left ventricular enlargement – In patients who have ventricular enlargement without an aneurysm, we suggest not performing LV restoration surgery (Grade 2B).

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Oz M Shapira, MD, who contributed to earlier versions of this topic review.

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References

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