You are in: eMedicine Specialties > Radiology > CARDIAC Ventricular AneurysmsArticle Last Updated: Jul 13, 2006AUTHOR AND EDITOR INFORMATIONAuthor: Vibhuti N Singh, MD, MPH, FACC, FSCAI, Director, Suncoast Cardiovascular Center; Chair, Cardiology Division and Cath Labs, Department of Medicine at Bayfront Medical Center; Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine Vibhuti N Singh is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Florida Medical Association Coauthor(s): Joel A Strom, MD, FACC, Professor of Medicine and Biomedical Engineering, University of South Florida; Consulting Staff, James A Haley Veterans Administration Hospital, H Lee Moffitt Cancer Hospital Editors: Justin D Pearlman, MD, PhD, ME, MA, Director of Dartmouth Advanced Imaging Center, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; David S Levey, MD, PhD, Orthopedic/Spine MRI TeleRadiologist, Radsource, LLC; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Eugene C Lin, MD, Consulting Staff, Department of Radiology, Virginia Mason Medical Center Author and Editor Disclosure Synonyms and related keywords: left ventricular aneurysms, LV aneurysm, dyskinetic left ventricle, ventricular true aneurysm, ventricular pseudoaneurysm, false aneurysm INTRODUCTIONBackgroundAn 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, and it consists of fibrous tissue with or without myocardial fibers. Aneurysms interfere with ventricular performance due to loss of contractile function and subtraction because they bulge outward when other sections contract. Aneurysms 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. PathophysiologyCell death impairs the ability of the wall to contract and resist expansive pressures. The wall of the true aneurysm is thinner than the rest of the LV, and 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, 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, patients any poorly collateralized left anterior descending coronary artery generally becomes totally occluded. An aneurysm is rarely seen with multivessel disease a nonoccluded left anterior descending artery or extensive collaterals 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, which may even become partially calcified after several years. True LV aneurysms (in contrast to pseudoaneurysms) have 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 can develop after a blunt chest injury, in which case the aneurysm is attributed to myocardial contusion or direct vascular damage that cause myocardial necrosis. In such cases, also look for pseudoaneurysms of adjacent structures (eg, aorta) for 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. 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. FrequencyUnited StatesThe frequency 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 left anterior descending coronary artery and are rare in other coronary distributions. About 88% of ventricular aneurysms result from an anterior infarction, and the remainder follow 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. 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 followed by 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. InternationalThe data are similar to those for the United States. Mortality/MorbidityMortality rates in patients with a LV 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 LV aneurysm patients is often sudden and predominantly related to the high incidence of ventricular tachyarrhythmias that occur with aneurysms. In rare cases, death is from rupture.
SexBefore menopause occurs in women, sizable infarcts leading to aneurysm are more common in men than in women. AgeAges mirror the incidence of MI. 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. AnatomyA true anatomic LV aneurysm protrudes during both systole and diastole, it has a mouth that is as wide as or wider than its maximal diameter, it has a wall that was formerly the wall of the LV, and it is composed of fibrous tissue with or without residual myocardial fibers. A true aneurysm may or may not contain thrombus and 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 of the aneurysm, 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, and it consists of fibrous tissue with or without myocardial fibers. Clinical DetailsTrue ventricular aneurysms do not rupture, and surgical excision may be performed just to improve function. However, angina, embolization, and life-threatening tachyarrhythmias can 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, ie, 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, which could result in the condition known as pigeon heart. An aneurysm is generally repaired by resecting the thinned-out aneurysmal wall and by leaving an approximately 3-cm rim of scar tissue to allow for reconstruction of the normal LV contour. An endoventricular patch of polyester fiber (Dacron) or pericardium may be used to help reconstruct the LV. Regarding associated surgical procedures, concurrent coronary bypass can be performed after the aneurysm is resected and closed in standard fashion. If moderate-to-severe mitral regurgitation is present, an Alfieri stitch approximating the middle of the anterior and posterior mitral leaflets, mitral valve reconstruction or replacement, and/or placement of a valvular ring to reduce the size of the annulus may be performed during 1 operation. Preferred ExaminationAneurysm can be noninvasively diagnosed by means of echocardiography, MRI, radionuclide ventriculography, or dynamic gated CT. It can 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, it sometimes misses the apex even when windows (access through lungs) appear to be good. MRI is good for imaging the apex because it enables accurate cardiac-oriented views not limited by the lungs. Typical indications for MRI are unexpected hypotension, unexpected severity of heart failure, a new murmur, or poor windows for echocardiography. MRI is also good for detecting the other complications of MI, which include ruptured chordae, septal defect, fistulae, and pericarditis. In addition, MRI can be performed 10-20 minutes after a double dose of gadolinium-based contrast material is intravenously administered to identify myocardial scarring by assessing delayed enhancement. This finding can help clarify a difficult case of pseudoaneurysm and evaluate tissue viability (scar less than one third of the wall thickness). In addition, MRI can 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 recently 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. Limitations of TechniquesSonography 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. DIFFERENTIALSCardiomyopathy, Dilated Myocardial Infarct, Acute Other Problems to Be ConsideredMyocardial rupture
RADIOGRAPHFindingsA characteristic bulge of the silhouette of the LV is frequently seen on chest radiographs. Marked calcification of the LV silhouette may be present. Deposition of calcium in myocardial tissue is related to the production of carbon dioxide in slowly metabolizing tissue. As a consequently, the development of relative alkalinity and reduced solubility of calcium leads to the deposition of soft tissue. True aneurysms Myocardial calcification most frequently occurs in true LV aneurysms localized to the apical and anterolateral aspects of the LV wall. The calcium deposits in LV aneurysms are usually curvilinear and in the periphery of the infarct or aneurysm. They are occasionally homogeneous when an entire infarcted area is calcified. False aneurysms A false LV aneurysm occurs when the chamber ruptures into the pericardium, where adhesions then contain the blood. False aneurysms usually occur along the posterolateral wall of the LV. Degree of ConfidenceWhen clear-cut, radiographic findings are relatively specific, but they have limited sensitivity. False Positives/NegativesFalse findings are frequent. CT SCANFindingsCT is a reliable and noninvasive technique to identify LV aneurysms and to screen for resectability. After an MI occurs, CT can be used to demonstrate regional wall thinning and complications of infarction, such as LV aneurysm and mural thrombus. Electron-beam CT (EBCT) demonstrates reduced wall thickening and wall motion as evidence of LV segmental dysfunction in ischemic heart disease. EBCT has also been used to monitor LV remodeling after acute MI. multidetector-row CT (MDCT), eg, CT simultaneously performed with 16-64 detectors has now replaced EBCT. Degree of ConfidenceCT is as accurate as 2-dimensional echocardiography. CT is fast and provides clear resolution of the LV, improving localization and estimation of the extent of wall thinning after infarction compared with projectional techniques, such as left ventriculography, and most scintigraphic techniques. However, the iodine-based contrast material may cause renal failure, and the x-ray exposure is greater with MDCT than with cardiac catheterization (eg, 13 Sv). Likewise, the site and extent of anterior and posterior aneurysms of the LV can be well demonstrated. CT-based differentiation of a true aneurysm from a pseudoaneurysm depends on the identification of the small ostium connecting the LV cavity and the aneurysm. False aneurysms are usually substantially larger than true aneurysms and frequently arise from the posterior or inferior wall of the LV. False Positives/NegativesFalse findings are infrequent. MRIFindingsMRI is a reliable noninvasive technique to identify LV aneurysms and to screen for resectability. In addition, dark-blood imaging can be performed to define the anatomy, as with CT. Dynamic bright-blood imaging helps in defining the blood pool motion and, in particular, delineates bulging of the aneurysm. MRI scar mapping with delayed enhancement shows the location and transmural extent of scar tissue. (Collagen retains the intravenously administered gadolinium-based contrast agent.) MRI strain mapping can be used to identify which units of myocardium retain contractile function versus tethering. MRI stripe tagging can depict pericardial adhesions. MRI T2* imaging helps in identifying thrombus; specific contrast agents can be used to define thrombi precisely.MRI can be performed to measure the model-independent ejection fraction and to estimate improvement after aneurysmectomy. MRI is the best technique for visualizing the pericardium. Degree of ConfidenceThe degree of confidence is high. False Positives/NegativesThe rate of false findings is high. ULTRASOUNDFindingsTwo-dimensional echocardiography often clearly demonstrates ventricular aneurysms and may assist in distinguishing between true and false aneurysms by demonstrating a narrow neck in relation to the size of the cavity. Color flow echocardiographic imaging is useful in identifying abnormal flow within the aneurysm, which may help in identifying a thrombus. Pulsed Doppler imaging can reveal a to-and-fro pattern of flow at the mouth of the aneurysm with characteristic respiratory variation in the peak systolic velocity. Tomographic 3-dimensional echocardiography allow for the calculation of LV volume and systolic function, comparable to MRI. Degree of ConfidenceThe degree of confidence is high. False Positives/NegativesSonographic studies can be unreliable in obese individuals and in patients with chronic lung disease because of attenuation of the transmitted sound waves. NUCLEAR MEDICINEFindingsRadionuclide ventriculography can demonstrate ventricular aneurysm. Degree of ConfidenceThe degree of confidence is good. False Positives/NegativesFalse findings are not uncommon. ANGIOGRAPHYFindingsBiplane left ventriculography is still the most widely used method for outlining a true LV aneurysm and for assessing septal motion. This study is performed in conjunction with selective coronary angiography to determine the extent of coronary disease. Although uncommon, the potentially high load of iodinated contrast agent may cause renal failure, especially in patients with diabetes. Therefore, noninvasive imaging is often performed in place of ventriculography. Degree of ConfidenceThe degree of confidence is high. False Positives/NegativesProjections of the mobile blood pool that do not show the wall may cause the reader to miss the distinction between some false and true aneurysms. A false aneurysm might be missed entirely if it is filled with thrombus. INTERVENTIONCoronary revascularization is frequently performed along with aneurysmectomy, especially in patients in whom angina accompanies heart failure. A large LV aneurysm in a patient with symptoms of heart failure may be an indication for surgery, particularly if angina pectoris is also present. The surgical mortality rate for simple LV aneurysmectomy is approximately 10% (range, 0-19%), with rates of 6% and 7.2% reported in recent series. No surgical mortality was reported in 26 patients who underwent endoventricular patchplasty between 1992 and 1994. The risk increases if valve surgery is also required. Angina pectoris instead of dyspnea as the dominant preoperative symptom decreases the surgical mortality rate. Surgery poses a particularly high risk in patients with severe heart failure, a low-output state, and/or akinesis of the interventricular septum, as assessed echocardiographically. Akinesis or dyskinesia of the posterior-basal segment of the LV and significant stenoses of the right coronary artery are additional risk factors. Risk factors for early death include poor LV function, recent MI, mitral regurgitation, and intractable ventricular arrhythmias. Pseudoaneurysms are associated with a high risk of sudden death and, therefore, should be resected on an urgent basis as soon as the diagnosis is established. Risk factors for late mortality if the patient survives surgery include incomplete revascularization, impaired systolic function of the basal segments of the ventricle and septum not involved by the aneurysm, a large aneurysm with a small quantity of residual viable myocardium, and severe cardiac failure as the initial feature. Surgical resection The surgical procedure for LV aneurysm requires CPB and standard anesthetic techniques and monitoring. A median sternotomy is performed, and CPB is started after the ascending aorta is cannulated and a double-stage venous cannula is placed in the right atrium. The LV is opened and carefully inspected, and any mural thrombus is removed. Cardioplegic solution is infused in an antegrade manner after the aorta is clamped. The LV aneurysm is repaired by resecting the thinned-out aneurysmal wall and leaving a rim of intervening scar tissue of approximately 3 cm to facilitate reconstruction of the normal LV contour. Care must be taken not to resect too much of the aneurysmal wall and to reduce the size of the cavity, problems that can result in low cardiac output and a high mortality rate. Anterior aneurysm defects are typically closed vertically between external strips of polytetrafluoroethylene (Teflon; DuPont, Wilmington, Del) felt. Large monofilament horizontal mattress sutures are used, and a second running layer of monofilament suture is applied for hemostasis. Improvement in LV function is reported in patients who survive resection of LV aneurysms complicated by cardiac failure. By removing the abnormal mechanical burden, LV aneurysmectomy can lead to late improvement in overall systolic function and improvement in the performance of regional nonischemic myocardium in zones remote from the LV aneurysm, in addition to improvement in measures of ventricular relaxation and cardiovascular neuroregulatory mechanisms. Concomitant improvement in exercise performance and clinical symptoms may also occur, particularly in patients who undergo complete revascularization. An early series of carefully selected patients demonstrated a 10-year survival rate of 69% among patients undergoing LV aneurysmectomy plus coronary revascularization compared with 57% in those undergoing aneurysmectomy alone. Patching New surgical approaches to the repair of LV aneurysms are designed to restore normal LV geometry by using an alternative method of epicardial closure and/or an endocardial patch to divide the area of the aneurysm from the rest of the ventricular cavity. Favorable clinical and hemodynamic results are reported after the use of these techniques, with 5-year survival rates of 73-87.5% and a corresponding improvement in hemodynamics and clinical symptoms. In 1 series, 88% of patients treated with the endoaneurysmorrhaphy technique had disease of New York Heart Association class I or II after a mean follow-up of approximately 3.5 years. Indications for the Dor procedure The Dor procedure is aneurysmal resection and endocardial patching for LV reconstruction. Indications include the following:
Surgical procedure A traditional incision of about 5-6 in. is made along the sternum. The heart is placed on heart-lung bypass. A small incision is made into the LV, and the exact location of the dead or scarred tissue is determined. Two or more rows of circular stitches are then placed around the border of the dead tissue to separate it from healthy myocardium. The stitches are then pulled together like a purse string to permanently separate the dead tissue from the rest of the heart. An area of scar tissue is sometimes removed before the stitches are pulled together. If a large amount of dead tissue must be removed and if the standard stitches are not enough to exclude the area, a patch must be placed. Lastly, the outside of the ventricle is reinforced with another row of stitches. Coronary artery bypass grafting (CABG) or valve surgery is performed if needed to improve cardiac function. The end result is a heart that is smaller and that it contracts more vigorously than before. Medical/Legal Pitfalls
MULTIMEDIA
REFERENCES
Article Last Updated: Jul 13, 2006 | |||||||||||||||||||||||||||||||||||||||||||||||||