eMedicine Specialties > Radiology > Cardiac

Ventricular Aneurysms

Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI, Director, Suncoast Cardiovascular Center; Chair, Cardiology Division and Cath Labs, Department of Medicine, Bayfront Medical Center; Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine
Coauthor(s): Joel A Strom, MD, ME, Professor of Internal Medicine, Chemical and Biomedical Engineering, and Honors College, University of South Florida
Contributor Information and Disclosures

Updated: Dec 2, 2008

Introduction

Background

An aneurysm is a section of defective wall that bulges outward. A ventricular aneurysm is a defect in the left (or right) ventricle of the heart, usually produced by transmural infarction.

The 2 types of aneurysms are true and false. A true aneurysm is made of damaged myocardial wall. A false aneurysm is actually a rupture, whereby the wall of the aneurysm is not myocardium but rather an external containing boundary (eg, pericardium). A functional left ventricular (LV) aneurysm, a forme fruste variant of a true aneurysm, protrudes during ventricular systole but not during diastole; it consists of fibrous tissue, with or without myocardial fibers.

Aneurysms bulge outward when other sections contract; they interfere with ventricular performance by diminishing contractile function and subtraction. Aneurysms that are largely made up of a mixture of scar tissue and viable myocardium or thin scar tissue alone impair LV function by causing paradoxical expansion and loss of effective contraction.

False aneurysms represent localized myocardial rupture in which pericardial adhesions limit the hemorrhage. False aneurysms usually have a mouth that is considerably smaller than its maximal diameter. True and false aneurysms may coexist, though the combination is rare.^1,2,3

Related eMedicine topics:
Aneurysm, Thoracic
Thoracic Aortic Aneurysm

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Pathophysiology

Cell death impairs the ability of the wall to contract and to resist expansive pressures. The wall of the true aneurysm is thinner than the rest of the LV. It is usually composed of fibrous tissue and necrotic muscle. It is occasionally mixed with viable myocardium. Aneurysm formation occurs when intraventricular tension stretches the noncontracting infarcted heart muscle, producing infarct expansion and fibrous tissue that bulges with each cardiac contraction. With time, the wall of the aneurysm becomes densely fibrotic, but it typically continues to bulge with systole, thereby reducing the effectiveness of ventricular contraction. The impaired motion in the aneurysm predisposes the area to clot formation (mural thrombus).

When an aneurysm is present after an anterior myocardial infarction (MI) occurs, any poorly collateralized left anterior descending coronary artery generally becomes totally occluded. An aneurysm is rarely seen with multivessel disease; in the presence of a nonoccluded left anterior descending artery; or when extensive collateral arteries are present.

Ventricular aneurysms are usually 1-8 cm in diameter. They occur approximately 4 times more often at the apex and in the anterior wall than in the inferoposterior wall. The overlying pericardium is usually densely adherent to the wall of the aneurysm; after several years, the aneurysm may even become partially calcified. True LV aneurysms (in contrast to pseudoaneurysms) are associated with a low and decreasing risk of rupture as the density of fibrous tissue increases over time.

True and false LV aneurysms frequently occur in the areas of a healed MI. LV aneurysms may develop after a blunt chest injury, in which case the aneurysm is attributed to myocardial contusion or direct vascular damage, resulting in myocardial necrosis. In such cases, a search should be made for pseudoaneurysms of adjacent structures (eg, aorta); for a dissecting hematoma in an arterial wall; and for traumatic valve disease. Death from rupture of a false aneurysm caused by nonpenetrating chest trauma has been described.

With the loss of contraction from the area of the aneurysm, the rest of the ventricle must become hyperkinetic to compensate. With relatively large aneurysms, complete compensation is impossible. Either the stroke volume decreases, or it is maintained at the expense of an increase in end-diastolic volume, which in turn increases wall tension and myocardial oxygen demand. Heart failure may ensue, and angina may appear or worsen.^4,5,6

Frequency

United States

The incidence of ventricular aneurysms depends on the incidence of transmural MI and congestive heart failure in the population studied.

True LV aneurysms develop in less than 10% of all patients with occlusion of the left anterior descending coronary artery; they are rarely found in association with other coronary conditions. About 88% of ventricular aneurysms result from an anterior infarction; the remainder occur after an inferior infarction (involving a dominant right coronary artery).

The rate of LV aneurysm in patients with acute MI was 7.6% in the Coronary Artery Surgery Study (CASS). However, this rate is declining because of aggressive early intervention with thrombolytics and revascularization after acute MI. The open-artery hypothesis suggests that revascularization improves remodeling of an infarct and is therefore worthwhile even when it is too late to preserve viability of the affected muscle.

The incidence of LV aneurysms and the need for aneurysmectomy have declined dramatically during the past 5-10 years in concert with the expanded use of acute repair of the infarct-related artery and subsequent complete revascularization.

More than 80% of LV aneurysms are located at or near the apex (<80% lateral). They are often associated with total occlusion of the left anterior descending coronary artery and a poor collateral blood supply.

Approximately 5-10% of aneurysms are posterior. Three fourths of patients with aneurysms have multivessel coronary artery disease.

International

The incidence of ventricular aneurysms internationally is similar to that in the United States.

Mortality/Morbidity

Mortality rates in patients with a left ventricular aneurysm, in the setting of acute MI, are approximately 6 times higher than those in patients without aneurysms, even when LV ejection fractions are comparable. Death in patients with LV aneurysm is often sudden; death is predominately related to the high incidence of ventricular tachyarrhythmias that occur with aneurysms. In rare cases, death is from rupture.

• Almost 50% of patients with moderate or large aneurysms have symptoms of heart failure (with or without associated angina); a third have severe angina; and approximately 15% have symptomatic ventricular arrhythmias that may be intractable and life threatening.
• Mural thrombi are found in about 50% of patients with chronic LV aneurysms. Half of the thrombi are detected during angiography or 2-dimensional echocardiography; MRI is twice as accurate as these modalities for the detection of thrombi. Systemic embolic events in patients with thrombi and LV aneurysm tend to occur early after MI. In a Mayo Clinic study involving patients who were confirmed to have chronic LV aneurysm at least 1 mo after having had an infarction, subsequent systemic emboli were extremely uncommon (0.35 case per 100 patient-years in patients not receiving anticoagulants).

Sex

Sizable infarcts that lead to ventricular aneurysms are more common in men than in premenopausal women.

Age

The incidence of MI increases with increasing age. In the absence of predispositions, patients are typically older than 40 years. However, ventricular aneurysms also occur in young patients with hypertrophic cardiomyopathy, Chagas disease, sarcoid, myocarditis, trauma, glycogen storage disease, or right ventricular dysplasia.

Anatomy

A true anatomic left ventricular aneurysm protrudes during both systole and diastole. It has a mouth that is as wide as or wider than its maximal diameter. The wall of an LV aneurysm was formerly the wall of the LV; it is composed of fibrous tissue, with or without residual myocardial fibers.

A true aneurysm may or may not contain thrombus; it almost never ruptures after the wall heals.

A false anatomic LV aneurysm protrudes during both systole and diastole. It has a mouth that is considerably smaller than its maximal diameter. It represents a myocardial rupture site. It has a wall made up of parietal pericardium. It virtually always contains thrombus, and it often ruptures.

A functional LV aneurysm, a forme fruste variant of a true aneurysm, protrudes during ventricular systole but not during diastole. It consists of fibrous tissue, with or without myocardial fibers.

Presentation

True ventricular aneurysms do not rupture. Surgical excision may be performed just to improve function. However, angina, embolization, and life-threatening tachyarrhythmias may occur.

Persistent ST-segment elevations may be observed on the resting ECG in the absence of chest pain.

Aggressive management of acute MI, including coronary thrombolysis, may diminish the incidence of ventricular aneurysms.

The surgical procedure for LV aneurysm — aneurysmectomy or the more extensive Dor procedure (LV reconstructive surgery) — requires cardiopulmonary bypass (CPB). Surgical aneurysmectomy is generally successful only if the remaining heart is not too small for normal cardiac output; if aneurysmectomy is performed in a patient whose heart is too small, it could result in the condition known as pigeon heart.

An aneurysm is generally repaired by resecting the thinned-out aneurysmal wall and by leaving a rim of scar tissue of approximately 3 cm, to allow for reconstruction of the normal LV contour.

An endoventricular patch of polyester fiber (Dacron) or pericardium may be used to help in the reconstruction of the LV.

Coronary bypass may be performed as a concurrent procedure, after the aneurysm is resected. Closure is performed in the standard fashion. If moderate to severe mitral regurgitation is present, the following procedures may be performed, either separately or in combination, during a single operation: an Alfieri stitch, approximating the middle of the anterior and posterior mitral leaflets; mitral valve reconstruction or replacement; and placement of a valvular ring, to reduce the size of the annulus.^7,8,9,10,11

Preferred Examination

A ventricular aneurysm may be noninvasively diagnosed by means of echocardiography, MRI, radionuclide ventriculography, or dynamic gated CT. It may also be recognized during cardiac catheterization by means of left ventriculography. Echocardiography is commonly performed after MI to assess the patient's cardiac status; however, with echocardiography, the apex is sometimes missed, even when windows (access through lungs) appear to be good.

MRI is good for imaging the apex because it enables accurate cardiac-oriented views that are not limited by the lungs. Typical indications for MRI are unexpected hypotension; heart failure of unexpected severity; a new murmur; or poor windows for echocardiography. MRI is also good for detecting other complications of MI, including ruptured chordae, septal defect, fistulae, and pericarditis. In addition, MRI may be used to evaluate myocardial scarring. In this application, a double dose of gadolinium-based contrast material is administered, and MRI is performed 10-20 minutes later to assess delayed enhancement. Findings may be helpful in clarifying a difficult case of pseudoaneurysm and in evaluating tissue viability (scar less than one third of the wall thickness). MRI may also be used to compute the volume of ventricle after the aneurysm is excised.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic, Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans.

NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Limitations of Techniques

Sonography is limited by the availability of a good window. In obese patients and in those with chronic emphysema, transthoracic echocardiography may fail to provide details. In addition, echocardiography may fail to distinguish layered thrombus from myocardium.

Differential Diagnoses

Cardiomyopathy, Dilated
Myocardial Infarct, Acute

Other Problems to Be Considered

Myocardial rupture
Cardiomyopathy
Takotsubo disease
Chagas disease
Sarcoid
Myocarditis
Paracardiac cyst
Cor triatriatum
Aortic sinus aneurysm or windsock

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