Left ventricular aneurysm

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Left ventricular (LV) aneurysm forms when intraventricular tension stretches the injured heart muscle during each cardiac cycle. It is a complication of myocardial infarction (MI) and it is categorized into true and false aneurysms, based on the nature of it’s wall. It is usually asymptomatic but may present as chest pain and dyspnea, and it should be suspected in patients with sustained ST elevation after MI. The diagnosis is based on echocardiographic findings.

The British vascular surgeons, John and William Hunter, first described the aneurysm in 1880. In 1967, Gorlin and colleagues reported that aneurysms can be strongly suspected in up to 75% of patients with myocardial infarction.^[1]

Based on the nature of the wall and its components, left ventricular aneurysms are classified as true or false aneurysms.^[2]

A true left ventricular aneurysm has an aneurysmal sac which contains the endocardium, epicardium, and thinned fibrous tissue (scar) which is a remnant of the left ventricular muscle.

Unlike a true aneurysm which contains some myocardial elements in its wall, the walls of a false aneurysm are composed of organized hematoma and pericardium and lack any element of the original myocardial wall.

Aneurysms form when intraventricular tension stretches the noncontracting, infarcted heart muscle, producing the expansion of the thin layer of necrotic muscle and fibrous tissue, which bulge with each cardiac contraction. The wall of a mature aneurysm is a white fibrous scar which becomes more densely fibrotic with the passage of time. The outward bulge with each cardiac contraction compromises the left ventricular stroke volume. On histopathological analysis, hyalinized fibrous tissue is the predominant finding. It usually takes 1 month for fibrous tissue to form.^[1][3]

Myocardial infarction is the most common cause of left ventricular (LV) aneurysm formation. Less common causes include HCM, trauma, idiopathic and congenital abnormalities.^[4][5][2][6]

True LV aneurysm must be differentiated from false aneurysms.^{[7] [8]}

It was estimated that LV aneurysm develops in 30%-35% of patients with Q wave MI, but this has decreased significantly due to improvements in the management of patients with acute MI.^[9] Currently it is estimated that true left ventricular aneurysms develop in less than 5% of all patients with STEMI.^[10] According to this report, the use of thrombolytic agents has decreased the incidence of LV aneurysm from 18.8% to 7.2%.^[10]

The most potent risk factor for the development of LV aneurysm is ST elevation MI. Other risk factors include:^{[10][2][11][12]}

• Hypertrophic cardiomyopathy (HCM)
• Dilated cardiomyopathy (DCM)
• Advanced age
• Hypertension
• Use of corticosteroids

The clue to the diagnosis of LV aneurysm following MI is a persistent ST elevation without chest pain, and there is no recommendation to screen patients for LV aneurysm.

If left untreated, it may lead to heart failure and persistent anginal pain. For false aneurysms, rupture and hemodynamic compromise are the usual outcomes if left untreated. Improvements in STEMI management, control of hypertension and avoidance of corticosteroids in STEMI have led to a better prognosis and decreased mortality.^[12]

Mural thrombosis, heart failure, persistent angina, and arrhythmia, are the major complications.

The symptoms of left ventricular aneurysm depends on the size of the aneurysm. Small and medium sized aneurysms are usually asymptomatic but large sized aneurysms may present as persistent chest pain and dyspnea despite the proper treatment of the underlying cardiac condition.

Physical findings on cardiac examination in patients with LV aneurysm include diffuse and displaced apical impulse, S3 and/or S4 heart sounds and mitral regurgitation murmur.

A persistent ST elevation is suggestive of LV aneurysm.^[12]

A bulge of the silhouette of the left ventricle on chest x-ray is the characteristic finding for LV aneurysm. ^[12]

Chest CT scan with or without contrast may reveal the size and the location of LV aneurysm, it can also show the presence of calcifications in it.

Cardiac MRI is helpful for the diagnosis of LV aneurysm and it may be emerging as the preferred noninvasive technique for the preoperative assessment of LV shape, thinning, and resectability.^[13]

• Echocardiography is the modality of choice for the diagnosis of LV aneurysm. ^[14][15]
• It can measure the size and location of the aneurysm, and it is helpful for distinguishing true from false aneurysms based on the mouth size.
• Echocardiography is useful to diagnose dyskinesia or akinesia during systole.
• Echocardiography is helpful to diagnose mural thrombosis in aneurysm sac.
• Color flow echocardiography is helpful to establish the diagnosis based on in and out flow in the aneurysm.

Medical therapy is indicated for small and medium-sized LV aneurysms. Medical therapy is targeted at decreasing the cardiac work load (afterload reduction), anti ischemic therapy for chest pain and anti coagulation if mural thrombosis exist.^[16]

• Afterload reduction:

ACE inhibitors are the drug of choice for decreasing the afterload.

• Anti ischemic therapy:

Many medications are used for treating underlying ischemic event and decreasing ischemic burden. The medications include:^[16]

Nitrates | Beta Blockers | Calcium Channel Blockers | Potassium Channel Openers | Newer Anti-anginal Agents

• Surgical aneurysmectomy is recommended for large symptomatic aneurysms that cause angina pectoris or heart failure. Appropriate CABG is indicated at the time of aneurysmectomy.^[17]
• Another indication for surgical intervention is in patients who can not tolerate long term anticoagulation therapy.^[18]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Aneurysm was first described by John Hunter in 1880.

• British vascular surgeons, John and William Hunter, first described an aneurysm in 1880.
• In 1967, Gorlin and colleagues reported that a strong suspicion of aneurysm could be obtained in 75% of patients with myocardial infarction.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

The main classification method is based on the components of the wall of the aneurysm, and it classifies LV aneurysms into true and false (pseudo) aneurysms.

Based on the nature of the wall of the aneurysm and its components, left ventricular aneurysms are classified as true or false aneurysms.^[1]

A true left ventricular aneurysm has an aneurysmal sac which contains the endocardium, epicardium, and thinned fibrous tissue (scar) that is a remnant of the left ventricular muscle.

Unlike a true aneurysm, which contains some myocardial elements in its wall, the walls of a false aneurysm are composed of organized hematoma and pericardium and lack any element of the original myocardial wall.

Left ventricular aneurysm may also be classified by location as anterolateral (apical) or posterior.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Aneurysms form when the intraventricular tension stretches the non contracting, infarcted heart muscle, resulting in an expansion of the thin layer of necrotic muscle and fibrous tissue, which bulges with each cardiac contraction. The wall of a mature aneurysm is a white fibrous scar. It becomes more densely fibrotic as the time passes, and bulges outward with each cardiac contraction, resulting in a reduction of the left ventricular stroke volume. On microscopy, hyalinized fibrous tissue is the predominant finding. It usually takes 1 month for fibrous tissue to form.

• Hyalinized fibrous tissue is the predominant finding.
  • However, a small number of viable muscle cells are also usually present.^[1]
• It usually takes 1 month for fibrous tissue to form.
  • Collagen tissue is formed during the first 10 days.
  • When an aneurysm is present within 1 week of a first myocardial infarction, the wall is composed largely of necrotic muscle and it is therefore not a true aneurysm by definition.^[2]

• The wall of a mature aneurysm is a white fibrous scar.
  • The aneurysmal portion of the LV wall is thin. A mural thrombosis (which can be calcified), may be seen attached to the endocardial surface.^[3]
  • The endocardium beneath retains its trabeculations; the area of scarring is not clearly demarcated from the rest of the wall.
• The wall of the aneurysm becomes more densely fibrotic as the time passes, it bulges outward with each cardiac contraction and compromises the left ventricular stroke volume.

The gross pathologic features of LV aneurysm are shown below.^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Myocardial infarction is the most common cause of left ventricular (LV) aneurysm formation. Less common causes include HCM, trauma, idiopathic and congenital abnormalities.

The most common cause of LV aneurysm is myocardial infarction. It accounts for approximately 90% of apical aneurysms.^[1] Other less common causes include:^{[2][3][4][5][6][7]}

• Hypertrophic cardiomyopathy (HCM)
• Dilated cardiomyopathy (DCM)
• Trauma
• Idiopathic
• Congenital
• Iatrogenic
• Sarcoidosis
• Chagas disease
• Endocarditis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

True left ventricular (LV) aneurysm must be differentiated from pseudo aneurysm and LV diverticulum.

True LV aneurysm must be differentiated from false aneurysms.^{[1] [2]}

Left ventricular diverticulum is another differential diagnosis of LV aneurysm.^[3][4]

• It is defined as an outpouching structure that contains endocardium, myocardium, and pericardium.
• It displays normal contraction and is considered to be congenital.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

It is estimated that 5% of all patients with STEMI will develop LV aneurysm.

It was estimated that LV aneurysm develops in 30%-35% of patients with Q wave MI, but there has been a significant decrease following improvements in the management of patients with acute MI.^[1] Currently, it is estimated that true left ventricular aneurysms develop in less than 5% of all patients with STEMI.^[2] The use of thrombolytic agents has decreased the incidence of LV aneurysm from 18.8% to 7.2%.^[2]

There is no data regarding the age predominance in LV aneurysm formation but it is assumed that elderly patients are more prone to develop it.

There is no data regarding racial predominance in developing LV aneurysm.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

The common risk factors for developing LV aneurysm include ST elevation MI, hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), advanced age, and hypertension.

The most potent risk factor for the development of the LV aneurysm is ST elevation MI. Other risk factors include:^[1][2][3][4]

• Hypertrophic cardiomyopathy (HCM)
• Dilated cardiomyopathy (DCM)
• Advanced age
• Hypertension
• Use of corticosteroids

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

The clue to the diagnosis of LV aneurysm after an MI is a persistent ST elevation without chest pain, and there is no recommendation for screening patients for LV aneurysm.

According to 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction, screening for LV aneurysm is not recommended.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Heart failure, ventricular arrhythmia, mural thrombosis, and ventricular rupture, are complications of LV aneurysm that may develop despite proper treatment of the underlying myocardial event. The overall prognosis is dependent on the size of the aneurysm, the presence of akinesia, and the extent of the underlying cardiac event.

If left untreated, it may lead to heart failure and persistent anginal pain. For false aneurysms, rupture and hemodynamic compromise are the usual outcomes if left untreated. Improvements in STEMI management, control of hypertension, and avoidance of corticosteroids in STEMI have led to a better prognosis and decreased mortality.^[1]

It occurs in almost 50% of patients and can be detected by angiography or echocardiography.^[1]

Paradoxical movement in the aneurysmal portion of the LV wall reduces the efficiency of the ventricular contraction, and compromises the stroke volume. It may lead to LV dilation and an increase in LV end-diastolic pressure, this may be accompanied by chest pain.^[2][3]

Approximately 15% have symptomatic ventricular arrhythmias that may be intractable and life-threatening.^[4]

Unlike false aneurysms, a mature true LV aneurysm rarely ruptures.^[5]

Depending on the size of the aneurysm, the extent of the underlying cardiac event, the presence of complications, and the promptness of medical intervention, the prognosis may vary. However, the overall prognosis is improved by modern treatment and advanced management.

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