Post-Infarction Left Ventricular Aneurysms: Etiology, Pathogenesis, Diagnosis, and Treatment

A post-infarction left ventricular (LV) aneurysm is a localized bulging of the LV wall, occurring after a myocardial infarction (MI) in the area of transmural necrosis and scarring. This condition is a serious complication affecting the contractile function of the heart and the patient’s survival prognosis.

Two fundamentally different types of damage are identified.

True LV aneurysm

• The wall in this case is formed by all layers of the myocardium (scarred, thinned, but continuous myocardium).
• The aneurysm cavity communicates with the LV cavity via a wide neck.
• It has a low risk of rupture but leads to systolic dysfunction, arrhythmias, and thrombosis.

False aneurysm (pseudoaneurysm) of the LV

• Occurs when the free wall of the LV ruptures. In such a case, the aneurysm wall is formed by pericardium/fibrous tissue, not myocardium.
• Typically, it has a narrow neck and a sac-like cavity.
• It has an extremely high risk of rupture and cardiac tamponade, thus it is considered a life-threatening condition usually requiring surgical intervention.

Epidemiology

Thanks to early reperfusion, the incidence of LV aneurysm development has significantly decreased and is estimated at about 5–8% among patients with previous transmural MI.

False LV aneurysm occurs much less frequently — in about 0.2–0.5% of patients post-MI, often localized in the inferior and lateral walls. Despite its rarity, pseudoaneurysm is associated with high mortality due to the risk of sudden rupture (according to various retrospective studies, mortality without surgery can reach 80% in the first years of observation).

Epidemiology

Development of true LV aneurysm

1. Acute transmural myocardial infarction: necrosis of the entire myocardial layer, most often in the anterior descending artery territory.
2. Early remodeling phase: the necrotized wall becomes thinned, loses contractility, and develops akinesia or dyskinesia. Under the influence of intraluminal pressure, the section gradually bulges.
3. Fibrosis and scar formation: necrotic tissue is replaced by fibrous scar, which preserves wall integrity but poorly resists stretching.
4. Chronic remodeling and aneurysm: lead to stable, fixed bulging with a thinned, scarred wall and altered LV geometry, resulting in progressive systolic dysfunction, mitral regurgitation, and intracavitary thrombus formation.

Development of LV pseudoaneurysm

1. Rupture of the free LV wall: often occurs in the course of acute or subacute transmural MI. Sometimes rupture may appear as sluggish “leakage” of blood.
2. Pericardial restraint of rupture: blood from the LV cavity moves into the pericardial space but does not cause immediate tamponade due to local pericardial adhesions or clot formation.
3. Formation of pseudoaneurysm cavity: a cavity forms, typically communicating with the LV through a narrow opening. The wall is represented by the pericardium, fibrin, blood clots, and granulation tissue, without a full myocardial layer.
4. Progression and risk of rupture: the cavity can expand, increasing pressure and the risk of recurrent, potentially fatal rupture and tamponade. Additional possible complications include thromboembolisms, severe congestive heart failure, and arrhythmias. Upon final wall rupture, blood from the LV cavity bursts into the pericardium, causing acute tamponade and rapidly leading to death without immediate surgical intervention.

Classification

By wall structure

• True aneurysm: the wall consists of a thinned, scar-altered myocardium (includes all layers of the wall).
• False (pseudoaneurysm): occurs when the LV free wall ruptures, limited by the pericardium, blood clot, or scar tissue, with a lack of intact myocardial wall.

By time post-myocardial infarction

• Acute: up to 2 weeks post-MI.
• Subacute: weeks 2–6.
• Chronic: more than 6–8 weeks post-MI.

By form of aneurysmal protrusion

• Diffuse: broad base, with a gradual transition from the normal wall to the aneurysm zone.
• Saccular: localized, more sharply demarcated bulging. Such a form more often raises suspicion towards pseudoaneurysm, especially with a markedly narrow neck.

Clinical manifestations

Symptoms may range from no complaints to critical conditions.

True LV aneurysm:

• Dyspnea and signs of chronic heart failure (CHF): a result of decreased contractility and LV systolic dysfunction.
• Angina: occurs with persistent myocardial ischemia.
• Arrhythmias: ventricular extrasystoles, stable or unstable ventricular tachycardia due to scar substrate.
• Embolic complications: strokes, peripheral artery emboli in the presence of an intracardiac clot.
• Asymptomatic course: in some patients, the aneurysm is detected asymptomatically during echocardiography or MRI.

False LV aneurysm:

• Hidden symptoms: may present with mild symptoms or nonspecific complaints (dyspnea, weakness, atypical chest pain).
• Often manifests with signs of heart failure, severe dyspnea.
• Ventricular arrhythmias and thromboembolism may occur.
• Fatal rupture: the main threat is sudden rupture leading to hemopericardium and cardiac tamponade, which may result in sudden collapse and death.

Diagnosis

Laboratory methods

There are no specific laboratory markers for LV aneurysm, but the following are used in practice:

• Cardiospecific troponins, CK-MB: elevated in the acute phase of MI, helping to date the event.
• BNP/NT-proBNP: reflects the severity of CHF and pressure/volume overload, often elevated in significant aneurysms.
• Complete blood count, creatinine, electrolytes, coagulation profile, and other parameters are necessary for the assessment of comorbid conditions, surgical preparation, and anticoagulant therapy monitoring.

Instrumental methods

1. Echocardiography (transthoracic and transesophageal): a key method for primary diagnosis and differentiation of true and false aneurysms.

• True aneurysm: localized thinning and bulging of the LV wall; broad opening between the LV cavity and aneurysm; dyskinesia/akinesia in the aneurysm zone; possible presence of mural thrombotic masses.
• False aneurysm: narrow neck with a sudden transition from the LV cavity into the aneurysmal cavity; wall appears thin and heterogeneous, without a typical myocardial layer; pericardial effusion is often detected; a Doppler study reveals turbulent flow through the narrow opening.

2. Coronary angiography: it is conducted to assess the coronary bed, plan surgical intervention, and clarify ischemic etiology. Recommended before surgical correction of both true and false aneurysms.

3. Computed tomography (CT) and magnetic resonance imaging (MRI) of the heart.

• Cardiac MRI: to evaluate the structure and function of the left ventricle, the thickness and composition of the wall, the volume and shape of the aneurysm, and the presence of blood clots. Allows for clear differentiation between a true aneurysm (scarred myocardium) and a pseudoaneurysm (wall without myocardium, limited by the pericardium).
• Heart CT: an alternative to MRI; visualizes calcifications, pericardial changes, and the anatomy of the pseudoaneurysm neck.

Find more scientifically accurate content on our social media

Subscribe and don’t miss out the latest resources

Treatment for left ventricular aneurysm

Medication therapy

Aimed at treating the consequences of myocardial infarction and chronic heart failure, preventing thromboembolism and arrhythmias, and optimizing condition before/instead of surgery. The main groups of drugs are:

• Antiplatelet therapy: aspirin and P2Y12 inhibitors are considered a standard therapy after myocardial infarction and stenting, in the absence of a high risk of bleeding.
• Anticoagulants: vitamin K antagonists or non-vitamin K antagonist oral anticoagulants (NOACs) in the presence of intraventricular thrombus, at high risk of embolism, or large aneurysms with significant blood stasis, provided there is no high risk of bleeding.
• Angiotensin-converting enzyme inhibitors (ACEIs)/angiotensin receptor blocker (ARBs)/angiotensin receptor-neprilysin inhibitors (ARNIs): reduce remodeling and improve prognosis in systolic dysfunction of LV.
• Beta-blockers: reduce the risk of arrhythmias, decrease myocardial workload, and improve survival.
• Mineralocorticoid receptor antagonists and SGLT2 inhibitors: in CHF with reduced ejection fraction, they represent a standard of modern therapy.
• Diuretics: for control of symptoms of congestive CHF.
• Antiarrhythmics therapy, implantable cardioverter-defibrillator (ICD): implantation of a cardioverter-defibrillator may be discussed for life-threatening ventricular arrhythmias.

Surgical therapy

True left ventricular aneurysm (indications):

1. Symptomatic CHF with severe systolic dysfunction of LV associated with aneurysmal deformation.
2. Refractory angina in the presence of significant coronary disease.
3. Life-threatening ventricular arrhythmias associated with the scarred area of the aneurysm.
4. Recurrent systemic embolism in the context of intraventricular clot, not controlled medically.

Main types of surgeries:

• Resection of the aneurysm sac with reconstruction of the left ventricular cavity using a patch;
• Linear aneurysmoplasty and other modifications;
• Often combined with coronary artery bypass grafting (CABG) and/or mitral valve plasty (in cases of ischemic mitral regurgitation).

False pseudoaneurysm of LV (indications):

Due to the high likelihood of rupture, LV pseudoaneurysm is usually considered an absolute indication for surgical treatment, especially when identified in the first few months after MI and when the cavity size is >3 cm.

Main approaches:

• Open surgical correction: suturing or closure of the pseudoaneurysm neck with a patch (pericardial or synthetic); reconstruction of the free wall of LV; simultaneous CABG if necessary.
• Percutaneous closure: discussed in patients with high surgical risk and a well-defined pseudoaneurysm neck.
• Conservative tactics (only medication and observation) are possible only in individual patients with chronic, stable, small pseudoaneurysms and high surgical risk, but they are associated with a significant risk of sudden death.