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Ventricular aneurysm
Ventricular aneurysm
Ventricular aneurysm
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Aneurysm of heart
Heart left ventricular aneurysm short axis view

Ventricular aneurysms are one of the many complications that may occur after a heart attack. The word aneurysm refers to a bulge or 'pocketing' of the wall or lining of a vessel commonly occurring in the blood vessels at the base of the septum, or within the aorta. In the heart, they usually arise from a patch of weakened tissue in a ventricular wall, which swells into a bubble filled with blood.[1] This, in turn, may block the passageways leading out of the heart, leading to severely constricted blood flow to the body. Ventricular aneurysms can be fatal. They are usually non-rupturing because they are lined by scar tissue.

A left ventricular aneurysm can be associated with ST elevation.[2]

Signs and symptoms

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Ventricular aneurysms usually grow at a very slow pace, but can still pose problems. Usually, this type of aneurysm grows in the left ventricle. This bubble has the potential to block blood flow to the rest of the body, and thus limit the patient's stamina. In other cases, a similarly developed pseudoaneurysm ("false aneurysm") may burst, sometimes resulting in the death of the patient. Also, blood clots may form on the inside of ventricular aneurysms, and form embolisms. If such a clot escapes from the aneurysm, it will be moved in the circulation throughout the body. If it gets stuck inside a blood vessel, it may cause ischemia in a limb, a painful condition that can lead to reduced movement and tissue death in the limb.[1] Alternatively, if a clot blocks a vessel going to the brain, it can cause a stroke. In certain cases, ventricular aneurysms cause ventricular failure or arrhythmia. At this stage, treatment is necessary.[citation needed]

Causes

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Ventricular aneurysms are usually complications resulting from a heart attack. When the heart muscle (cardiac muscle) partially dies during a heart attack, a layer of muscle may survive, and, being severely weakened, start to become an aneurysm. Blood may flow into the surrounding dead muscle and inflate the weakened flap of muscle into a bubble. It may also be congenital.[citation needed]

Diagnosis

[edit]
Left ventricular aneurysm
An ECG of a person with a left ventricular aneurysm. Note the ST elevation in the anterior leads.

When a person visits the hospital or doctor with other symptoms, especially with a history of heart problems, they will normally be required to undergo an electrocardiogram, which monitors electrical activity within the heart and shows abnormalities when a cardiac aneurysm is present. It can also appear as a bulge on a chest x-ray, and a more accurate diagnosis will then be made using an echocardiogram, which uses ultrasound to 'photograph' the heart and how it functions while it beats.[citation needed]

  • Left ventricular aneurysm as seen on ultrasound[3]
  • Left ventricular aneurysm as seen on ultrasound[3]

Differential diagnosis

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It should also not be confused with a pseudoaneurysm,[4][5] coronary artery aneurysm or a myocardial rupture (which involves a hole in the wall, not just a bulge.)

Cardiac Diverticulum

[edit]

Cardiac diverticulum or ventricular diverticulum is defined as a congenital malformation of the fibrous or muscular part of the heart which is only visible during chest x-rays or during an echocardiogram reading.[6] This should not be confused with ventricular diverticulum, as the latter is a sub type derived from the latter in congenital cases. it is usually asymptomatic and is only detected using imaging. Fibrous diverticulum is characterised by a calcification if present at the tip ( apex) or a thrombi that may detaches to form an emboli. Muscular diverticulum is characterised by appendix forming at the ether of the ventricles.[7] it is a rare anomaly and can be diagnosed prenatal. Diagnosis is usually done by a chest X-ray and silhouette is viewed around the heart. Echocardiogram reading present a similar picture to ventricular aneurysms on the ST segment. Management is dependent on the situation presented and the severity of the case. Usually, surgical resection is advised but in prenatal cases, due to combination with other cardiac abnormalities, especially in latter trimesters, but pericardiocentesis is useful technique to reduce pleural effusion or/ and secondary disorders.[vague]

Treatment

[edit]

Some people live with this type of aneurysm for many years without any specific treatment. Treatment is limited to surgery (ventricular reduction) for this defect of the heart. However, surgery is not required in most cases but, limiting the patient's physical activity levels to lower the risk of making the aneurysm bigger is advised. Also, ACE Inhibitors seem to prevent Left Ventricular remodeling and aneurysm formation.[citation needed]

Blood thinning agents may be given to help reduce the likelihood of blood thickening and clots forming, along with the use of drugs to correct the irregular rhythm of the heart (seen on the electrocardiogram)[citation needed]

See also

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References

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Further reading

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Ventricular aneurysm

View on Grokipedia
from Grokipedia
A ventricular aneurysm is a localized outpouching or bulge in the wall of one of the heart's lower chambers (ventricles), most commonly the left ventricle, caused by thinning and weakening of the myocardial tissue, which fails to contract properly during . This condition arises predominantly as a complication of acute (heart attack), where scar tissue replaces damaged heart muscle, leading to paradoxical expansion of the affected area. It affects the heart's pumping efficiency and can lead to serious complications if untreated. Ventricular aneurysms are classified as true aneurysms, involving all layers of the ventricular wall, or pseudoaneurysms (false aneurysms), which are contained by rather than myocardium and carry a higher of rupture. The most frequent is ischemic, accounting for 85-90% of cases, particularly after anterior wall infarctions due to occlusion, though rare non-ischemic causes include congenital defects, trauma, , or . Incidence has declined significantly with advances in , from 7-19% in the thrombolytic era to less than 5% currently, with U.S. data indicating about 0.2% among acute admissions. Many ventricular aneurysms are asymptomatic and discovered incidentally on follow-up , but symptomatic cases—often involving larger aneurysms—manifest with symptoms such as dyspnea, fatigue, and ; from ; or arrhythmias like . Complications include thromboembolic events from thrombi, reduced cardiac output leading to congestive , and, in pseudoaneurysms, a high risk of rupture with mortality rates up to 50% if untreated. relies on multimodality , with as the initial modality to detect wall motion abnormalities and distinguish aneurysm types based on neck-to-sac ratios, supplemented by cardiac MRI for precise assessment of size and . Management begins with guideline-directed medical therapy, including beta-blockers, ACE inhibitors, and anticoagulation for prevention to stabilize small or aneurysms, achieving up to 90% five-year survival. For symptomatic or high-risk cases (e.g., New York Heart Association class III-IV, intractable s, or large aneurysms >25% of left ventricular volume), surgical intervention such as aneurysmectomy with ventricular reconstruction or coronary artery bypass grafting is indicated, though randomized trials like STICH show no overall survival benefit when added to medical therapy alone. varies widely, with five-year mortality ranging from 10% for small aneurysms to over 50% for complicated cases, improved by early and device therapy like implantable cardioverter-defibrillators for control.

Overview

Definition

A ventricular aneurysm is defined as a localized outpouching or bulge in the wall of a heart ventricle resulting from weakening of the myocardium, most commonly affecting the left ventricle but occasionally involving the right ventricle. This condition represents a structural abnormality where the ventricular wall fails to contract effectively, leading to dyskinetic motion during the . Ventricular aneurysms are often associated with prior , though other etiologies may contribute. Ventricular aneurysms are classified into two main types: true aneurysms and false (or pseudo) aneurysms. A true aneurysm involves the full thickness of the ventricular wall, including all three layers (, myocardium, and epicardium), resulting in a broad-based bulge with persistent thinning and . In contrast, a false aneurysm arises from a contained rupture of the ventricular wall, where the outpouching is bounded externally by , , or adhesions rather than intact myocardial layers, creating a narrow-necked sac with a higher of rupture. This distinction is critical for management, as false aneurysms require more urgent intervention due to their precarious containment. Anatomically, ventricular aneurysms can be categorized by their location, predominantly in the left ventricle, with subtypes including apical (most common, often involving the apex), anterior (extending from the front wall), septal (affecting the ), and inferior (along the diaphragmatic surface). Right ventricular aneurysms, while far less frequent, may occur in similar locations but are typically smaller and associated with different hemodynamic implications. The condition was first recognized at in 1757 by John Hunter, marking an early description of ventricular wall bulging as a pathological entity. Modern understanding advanced significantly in the mid-20th century, with the first angiographic confirmation reported in 1951, enabling noninvasive visualization and precise diagnosis.

Epidemiology

Ventricular aneurysms most commonly develop as a complication of acute (AMI), with true left ventricular aneurysms occurring in approximately 30% to 35% of cases involving transmural infarcts, though rates vary widely based on infarct location and treatment timing. In the pre-reperfusion era, incidence rates reached 10% to 30% among post-AMI patients, but timely interventions such as primary (PCI) have reduced this to under 5% in ST-elevation myocardial infarction (STEMI) cases by the 2020s, reflecting improved myocardial salvage and limited infarct expansion. For instance, analysis of over 11 million U.S. AMI admissions from 1999 to 2016 identified left ventricular aneurysms in only 0.2% of cases, underscoring the overall rarity in contemporary cohorts. Demographic patterns show ventricular aneurysms are more prevalent in males over 60 years, aligning with the higher baseline risk of AMI in this group, though affected cohorts often include a notable proportion of females with comorbidities. Higher persists in regions with delayed AMI treatment, where access to is limited, compared to urban centers with rapid intervention capabilities. Congenital forms remain rare, with a prevalence of 0.02% to 0.76% in and angiographic studies, with apical variants detected in about 0.3% to 0.4% of cases, typically identified incidentally in younger patients without prior . Key risk factors include large transmural infarcts, particularly those involving the anterior wall due to occlusion, and delayed exceeding 6 hours post-AMI onset, which exacerbates wall thinning and remodeling. Comorbidities such as and further elevate risk by promoting extensive coronary disease and impaired healing, while failure to restore infarct patency independently contributes to formation in up to 22% of anterior AMI cases. Global trends indicate a sustained decline in developed countries, driven by widespread PCI adoption; U.S. National Inpatient Sample data from major registries demonstrate stable low incidence rates below 5% in recent decades, with 2024 studies confirming this pattern amid advancing reperfusion strategies. In contrast, emerging data from diverse cohorts suggest persistent higher rates in areas with suboptimal AMI care, highlighting disparities in therapeutic access.

Pathophysiology

Etiology

The primary etiology of ventricular aneurysms is ischemic secondary to acute , which accounts for 85-90% of cases. This complication arises from transmural myocardial caused by prolonged coronary occlusion, typically involving the . Secondary causes include congenital anomalies, such as isolated left ventricular diverticula or aneurysms, with a reported prevalence of about 0.4% in adults. Traumatic injuries, particularly blunt chest trauma, can also lead to ventricular aneurysms through direct myocardial damage. Infectious etiologies encompass , which frequently results in apical aneurysms due to chronic , and less commonly . Idiopathic forms may manifest as apical aneurysms associated with . Rare etiologies include granulomatous diseases such as , which can cause granulomatous infiltration leading to aneurysmal dilation, or iatrogenic factors such as post-cardiac surgery complications. Right ventricular aneurysms are often linked to arrhythmogenic right ventricular dysplasia, characterized by fibrofatty replacement of myocardium. Multifactorial aspects include genetic predispositions, such as mutations in genes underlying arrhythmogenic right ventricular dysplasia or , which contribute to aneurysm formation alongside environmental triggers.

Formation Mechanisms

Ventricular aneurysms typically form following a transmural , where ischemic of the full-thickness myocardium initiates a cascade of remodeling events. The sequence begins with myocyte death and subsequent thinning of the infarcted wall, as necrotic tissue is resorbed without adequate compensatory in the affected segment. This is followed by progressive , where is replaced by dense formation, resulting in a non-contractile, thinned ventricular wall that bulges outward. Key processes driving this formation include impaired collagen synthesis, which weakens the structural integrity of the myocardium, and activation of matrix metalloproteinases (MMPs), such as MMP-9, that degrade the components like and . This degradation exacerbates wall thinning and promotes dyskinetic motion, leading to paradoxical systolic expansion where the aneurysmal segment herniates during ventricular contraction instead of contributing to ejection. Hemodynamic factors further accelerate dilation, as increased wall stress—governed by , where stress is proportional to pressure times radius divided by twice the wall thickness—amplifies tension in the thinned, akinetic region, fostering progressive enlargement of the aneurysm. The development occurs in distinct stages: in the acute phase (1-2 weeks post-myocardial infarction), inflammation and early thinning predominate due to myocyte necrosis and inflammatory cell infiltration; the subacute phase (2-8 weeks) involves ongoing fibrosis and scar maturation; and the chronic phase (>8 weeks) features a stabilized aneurysm with persistent risk of thrombus formation within the dyskinetic pouch. Recent studies from 2024 and 2025 have underscored the role of persistent inflammation, particularly via interleukin-6 (IL-6) pathways, in delaying healing and promoting adverse remodeling in the reperfusion era, where incomplete resolution of inflammatory signals contributes to excessive matrix degradation and aneurysm progression.

Clinical Manifestations

Signs and Symptoms

Many patients with ventricular aneurysms, particularly left ventricular (LV) aneurysms, are asymptomatic and are detected incidentally during follow-up imaging after (MI). Symptomatic presentations often include dyspnea on exertion due to reduced , persistent fatigue, and resembling post-MI . Cardiac-specific signs may encompass persistent ST-segment elevation on electrocardiogram (ECG), an S3 gallop on , and displacement of the apical impulse on . Systemic symptoms can involve arising from ventricular arrhythmias or syncope; in rare right ventricular aneurysm cases, signs of such as jugular venous distension may occur. Symptoms typically emerge 2-4 weeks post-MI during and tend to worsen with larger aneurysms, such as those exceeding a substantial portion of the LV wall. These aneurysms are also associated with complications like .

Complications

Ventricular aneurysms are associated with several cardiovascular complications, primarily due to altered ventricular geometry and myocardial scarring. Ventricular arrhythmias, including ventricular tachycardia (VT) and ventricular fibrillation (VF), occur in nearly one-third of patients, originating at the junction between normal myocardium and the aneurysmal segment, and carry a significant risk of sudden cardiac death. Congestive heart failure is common in ventricular aneurysm cases due to reduced left ventricular ejection fraction and adverse remodeling, contributing to the 20% to 35% incidence observed in post-AMI patients, with mortality risk increasing when ejection fraction falls below 20% to 30%. Additionally, mitral regurgitation may arise from papillary muscle dysfunction due to ischemia or displacement in the aneurysmal region. Thromboembolic events represent another major , stemming from thrombus formation within akinetic aneurysmal segments. These thrombi can lead to systemic , with a notable of ; anticoagulation is typically recommended for at least three months post-event to mitigate this . Peripheral arterial embolism is also possible but less common. Rare but serious complications include rupture, which is rare but more common in early, immature aneurysms and is often fatal, as well as or free wall perforation. Pseudoaneurysms, distinguished by their contained rupture through the myocardial wall, exhibit a higher rupture of 30% to 50% if untreated, leading to elevated mortality. Prognostically, untreated ventricular aneurysms are linked to approximately 50% five-year overall, with variations from 30% to 80% depending on the study and aneurysm size, primarily driven by and arrhythmias; surgical intervention improves five-year survival to 68% to 79%. A 2024 review in the Journal of the highlights that while modern management, including timely , has reduced rupture incidence, the burden of ventricular arrhythmias persists, necessitating ongoing monitoring and targeted therapies.

Diagnosis

Diagnostic Methods

Transthoracic echocardiography (TTE) serves as the first-line imaging modality for detecting left ventricular aneurysms, providing real-time assessment of wall motion abnormalities, aneurysm size, and the presence of intracavitary thrombi. It exhibits high diagnostic performance, with exceeding 90% for identifying aneurysms compared to invasive ventriculography. Contrast-enhanced TTE can enhance visualization in patients with suboptimal acoustic windows, aiding in the differentiation of true aneurysms from pseudoaneurysms. Cardiac magnetic resonance imaging (CMR) is considered the gold standard for detailed tissue characterization in ventricular aneurysms, particularly for evaluating myocardial through late enhancement and assessing mural with high accuracy. It offers superior quantification of left ventricular volumes and function when is inconclusive, making it invaluable for planning interventions. Computed tomography (CT) complements these by providing excellent delineation of pseudoaneurysms, coronary , and aneurysm morphology, especially in cases requiring preoperative evaluation. Electrocardiography (ECG) often reveals persistent ST-segment elevation beyond two weeks post-myocardial in anterior ventricular s, alongside pathological Q waves, though this pattern has variable sensitivity around 38-50% but high specificity for aneurysm detection. ECG monitoring, such as Holter, is recommended for screening ventricular arrhythmias associated with aneurysms, given their propensity to cause life-threatening rhythms. Invasive coronary combined with left ventriculography remains the reference standard for confirming aneurysm location, assessing myocardial viability, and evaluating coronary patency prior to surgical consideration. This approach allows precise measurement of aneurysm size as a of the left ventricular and identifies residual ischemia. Laboratory evaluations include B-type natriuretic peptide (BNP) levels, which are typically elevated in patients with ventricular aneurysms complicated by , correlating with systolic dysfunction severity. levels may be assessed in acute presentations to confirm recent as the underlying , though they normalize in chronic aneurysm cases.

Differential Diagnosis

The differential diagnosis of ventricular aneurysm encompasses a range of cardiac and non-cardiac conditions that may present with similar clinical symptoms such as , , or arrhythmias, or mimic the condition radiologically through apparent outpouchings or wall motion abnormalities on imaging. Accurate distinction is crucial to guide appropriate management, as misdiagnosis can lead to unnecessary interventions or delayed treatment for life-threatening entities. Cardiac mimics include post-myocardial (MI) , which manifests as non-aneurysmal regional wall bulging due to akinesia or without a discrete aneurysmal sac, often resolving with ; cardiac tumors such as hydatid cysts or metastatic lesions, which appear as fixed masses with heterogeneous echogenicity and lack dyskinetic motion; and the apical variant of (HCM), characterized by myocardial hypertrophy and crypts leading to localized thinning and ballooning rather than true aneurysmal dilation. Vascular conditions like may simulate ventricular aneurysm through acute chest pain and hemodynamic instability, potentially causing secondary left ventricular dysfunction via coronary ostial involvement, while can produce a pseudo-mass effect on imaging, compressing the ventricle and mimicking aneurysmal expansion with associated physiology. Non-cardiac mimics encompass , which can appear as a posterior mediastinal outpouching on chest or , compressing cardiac structures and causing exertional dyspnea; mediastinal cysts, presenting as avascular, fluid-filled lesions adjacent to the ventricle that lack contractility; and , featuring transient apical ballooning with stress-induced catecholamine surge, reversible on follow-up imaging. Key discriminators include echocardiographic assessment of wall motion—true aneurysms exhibit paradoxical , whereas tumors remain fixed and diverticula show synchronous contraction—and anatomical features such as neck width, where pseudoaneurysms have a narrow (ratio 0.25–0.5) compared to the broad base of true aneurysms or diverticula. Cardiac diverticula, congenital outpouchings containing all myocardial layers with narrow necks, contract synchronously unlike the dyskinetic aneurysms. Advanced imaging modalities like cardiac MRI or CT can further differentiate these by evaluating tissue composition, flow dynamics, and reversibility.

Management

Medical Treatment

Medical treatment of ventricular aneurysm primarily focuses on managing associated complications such as , arrhythmias, and through and device-based interventions, while optimizing factors. Beta-blockers, such as metoprolol, are utilized to control arrhythmias and prevent adverse in patients with post-myocardial left ventricular aneurysms. These agents reduce and myocardial oxygen demand, contributing to improved survival as part of guideline-directed medical therapy (GDMT). (ACE) inhibitors, angiotensin receptor blockers (ARBs), or angiotensin receptor-neprilysin inhibitors (ARNIs, such as ) are administered for reduction to mitigate left ventricular dysfunction and remodeling. Anticoagulation is essential for preventing formation within the , particularly in the presence of , which occurs in over 50% of cases. is traditionally used with a target international normalized ratio (INR) of 2 to 3 for at least the first 3 months post-infarction, or longer in cases of large aneurysms, friable thrombi, or impaired left ventricular function; however, direct oral anticoagulants (DOACs, such as ) are reasonable alternatives with evidence of noninferior efficacy and lower bleeding risk. For heart failure symptoms associated with left ventricular dysfunction, diuretics provide relief from congestion, while aldosterone antagonists like address fluid retention and improve outcomes as part of GDMT. Sodium-glucose cotransporter-2 (SGLT2) inhibitors, such as dapagliflozin or empagliflozin, are recommended per 2022 American College of Cardiology/ (ACC/AHA) guidelines for patients with reduced (≤40%) to reduce hospitalization for and cardiovascular mortality, independent of status. Modern GDMT, including these agents, achieves up to 90% five-year survival in small or asymptomatic cases. Device therapy includes implantable cardioverter-defibrillators (ICDs) for primary prevention of sudden cardiac death in patients with less than 35%, as per ACC/ guidelines. (CRT) is indicated for those with QRS duration greater than 150 ms, , and ≤35% on guideline-directed medical therapy, to improve synchrony and reduce mortality by up to 36%. Lifestyle modifications, including , heart-healthy diet, and supervised exercise through , are integral to prevent recurrence and enhance . Ongoing monitoring with serial is advised to assess aneurysm stability and ventricular function.

Surgical Interventions

Surgical interventions for ventricular aneurysms are indicated in patients with symptomatic refractory to medical therapy, particularly those in New York Heart Association (NYHA) class III or IV, or when the aneurysm involves a large dyskinetic segment exceeding 35% of the left ventricular wall or an end-systolic volume index (LVESVI) of at least 60 mL/m². Additional indications include large intraneurysmal thrombi at risk of or persistent ventricular arrhythmias unresponsive to pharmacological treatment or (ICD) therapy. Preoperative assessment typically relies on modalities such as or cardiac magnetic resonance to confirm aneurysm size, viability, and geometry, as detailed in diagnostic protocols. The primary surgical procedures aim to exclude the aneurysmal segment and restore left ventricular geometry. Aneurysmectomy with patch repair involves resecting the non-viable aneurysmal wall and reconstructing the ventricle using a Dacron or autologous pericardial patch to close the defect. The endoventricular circular patch plasty, commonly known as the Dor procedure, encircles the aneurysm's border with a patch to exclude the akinetic or dyskinetic area while preserving the endocardial layer, thereby improving ventricular function and reducing wall stress. These techniques are performed via under , with careful attention to myocardial protection. Concomitant interventions are frequently required due to underlying ischemic . Coronary artery bypass grafting (CABG) is performed in the majority of cases to achieve complete , particularly when left ventricular (LVEF) is ≤35%, as it enhances long-term outcomes by addressing residual ischemia. or replacement may be undertaken if moderate to severe is present, contributing to heart failure symptoms. Postoperative outcomes demonstrate significant improvements in cardiac function, though risks remain. Perioperative mortality ranges from 5% to 15%, influenced by factors such as age, comorbidities, and aneurysm complexity. Successful repair typically increases LVEF by 10% to 20% and reduces LVESVI by approximately 37%, alleviating symptoms and decreasing rehospitalization rates. Long-term survival is favorable, with 5-year rates of 70% to 80% and 10-year survival approaching 60% to 80% in selected cohorts, as reported in recent analyses. Minimally invasive options are emerging for suitable candidates to reduce recovery time and complications. Hybrid approaches, such as ventricular restoration using devices like the Revivent TC System, deploy anchors via to partition the aneurysm without open , achieving 1-year survival rates up to 90% in trials. Robotic-assisted repairs and combined (PCI) with surgical reconstruction offer alternatives for high-risk patients. Ventricular assist devices (VADs) serve as a bridge to definitive or transplant in cases of severe associated with aneurysms, stabilizing prior to intervention.

References

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