INTRODUCTION — Left ventricular aneurysms (LVAs) and pseudoaneurysms are two complications of myocardial infarction (MI) that can lead to death or serious morbidity.
An LVA is most commonly the result of MI, usually involving the anterior wall. Other causes of LVA include hypertrophic cardiomyopathy and Chagas disease, both of which can lead to the formation of an apical aneurysm. The aneurysm may be asymptomatic or present as heart failure, sustained ventricular tachyarrhythmias, or arterial embolism (image 1A-B). (See "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis" and "Hypertrophic cardiomyopathy: Morphologic variants and the pathophysiology of left ventricular outflow tract obstruction", section on 'Midcavity obstructive HCM'.)
A pseudoaneurysm, or false aneurysm, develops after an acute MI that is complicated by a ventricular free wall rupture that is contained by localized pericardial adhesions. As described below, the contained cavity is characterized by a narrow neck communicating freely to the left ventricle and a tendency to expand and rupture (image 2). These features are distinctly uncommon with a true LVA, which generally does not rupture after it forms. Other rare causes of pseudoaneurysms include trauma, postoperative, endocarditis, and idiopathic (image 3).
LEFT VENTRICULAR ANEURYSM — The definition of a left ventricular aneurysm (LVA) remains controversial. For the purpose of this topic review, a true LVA is defined as a well delineated, thin, scarred, or fibrotic wall (image 4), devoid of muscle or containing necrotic muscle, that is a result of a healed transmural myocardial infarction (MI). The involved wall segment is either akinetic (without movement) or dyskinetic (with paradoxical ballooning) during systole (image 5), and collapses inward when the ventricle is fully vented during surgery. Aneurysms of the apex and anterior wall are more than four times as common as those of the inferior or inferoposterior walls.
Incidence — It was previously estimated that LVA develops in up to 30 to 35 percent of patients with Q wave MI [1,2]. However, the incidence of this complication is decreasing, and currently is about 8 to 15 percent in such patients [3]. This change is related to the introduction of major improvements in the management of patients with acute MI. (See "Overview of the acute management of ST-elevation myocardial infarction".)
The most important improvements are the use of thrombolytic agents and/or percutaneous coronary intervention to produce an open "culprit" vessel, and the administration of afterload reducing agents. In one report, the incidence of LVA among 350 consecutive patients with ST elevation MI treated with thrombolytic therapy was significantly lower in those with a patent infarct-related artery (7.2 versus 18.8 percent) [4]. Total occlusion of the left anterior descending coronary artery and absence of a patent infarct-related artery were the major independent risk factors for LVA.
Pathology — Approximately 70 to 85 percent of LVAs are located in the anterior or apical walls due, in most cases, to total occlusion of the left anterior descending coronary artery and the absence of collateralization (image 6 and image 7) [5-8]. Only 10 to 15 percent involve the inferior-basal walls due to right coronary artery occlusion (image 8 and image 9). Lateral LVA secondary to left circumflex occlusion is exceedingly rare (figure 1) [5-8]. Among patients with multivessel disease, aneurysms are uncommon if there is extensive collateralization or a nonoccluded left anterior descending artery.
Although the size of an aneurysm varies widely, most are between 1 and 8 cm in diameter. The wall of the aneurysm typically consists of a white fibrous scar and is very thin. The endocardial surface is smooth and nontrabeculated (image 10) [6]. The aneurysm is filled with organized clot in over 50 percent of cases (image 11 and image 12). The mural thrombus may calcify over time and the aneurysmal wall may itself become calcified (image 13 and image 14). Dense adhesions between the aneurysm and the overlying pericardium are common [6,7].
In the early phase, the ventricular wall histologically is characterized by muscle necrosis and an intense inflammatory reaction. This is gradually replaced with scar tissue formation, and a mature aneurysm consists mostly of hyalinized fibrous tissue [6-8]. The "border zone" (between the aneurysm and the normal myocardium) is characterized by patchy fibrosis and abnormal alignment of the muscle fibers [6-8].
History and physical examination — A history of MI is invariably present in patients with an LVA not associated with hypertrophic cardiomyopathy or Chagas disease. The physical examination may reveal one or more of the following findings:
●Cardiac enlargement with a diffuse apical impulse that is displaced to the left of the midclavicular line. (See "Examination of the precordial pulsation".)
●An area of dyskinesis can occasionally be appreciated with palpation of the apex or left lateral chest wall, in the area of the anterior wall of the left ventricle.
●A third and/or fourth heart sound is often heard, indicating blood flow into a dilated and stiffened left ventricular chamber. (See "Auscultation of heart sounds".)
●A systolic murmur of mitral regurgitation may be appreciated due to the distortion of left ventricular geometry that results in the absence of leaflet apposition, papillary muscle dysfunction, and/or annular dilatation. (See "Auscultation of cardiac murmurs in adults".)
Complications — There are a number of serious complications that can occur as a consequence of LVA, particularly heart failure, ventricular arrhythmias, and thromboembolism (image 1A and image 1B).
Heart failure and angina — During systole, the paradoxical bulging of the aneurysmal segment results in "stealing" part of the LV stroke volume, thereby decreasing the effective cardiac output and inducing LV volume overload. The LV dilates, the wall stiffens, and LV end-diastolic pressure rises [9-11].
According to La Place's law, there is an obligatory increase in wall tension with enlargement of the LV cavity. This increase in LV dimension results in increased circumferential wall stress and therefore increased oxygen demand [12]. In the presence of coronary artery disease, the increase in oxygen demand may lead to relative or absolute myocardial ischemia and the occurrence of angina. (See "Angina pectoris: Chest pain caused by fixed epicardial coronary artery obstruction".)
The end-result of long-standing volume overload and prolonged ischemia is a globally dilated, failing left ventricle.
Ventricular arrhythmias — Ventricular arrhythmias, which can lead to sudden cardiac death, are common in patients with an LVA. Two principal mechanisms appear to contribute:
●Myocardial ischemia and increased myocardial stretch can lead to enhanced automaticity or triggered activity [13]. (See "Enhanced cardiac automaticity".)
●The myocardium located at the border zone is heterogeneous, consisting of a mix of fibrotic tissue, inflammatory cells, and damaged and disorganized muscle fibers [14]. A reentrant tachycardia may develop when two or more electrically heterogeneous pathways having different conduction velocities and refractoriness are connected proximally and distally [13,15]. (See "Reentry and the development of cardiac arrhythmias".)
Systemic embolization — A mural thrombus is identified in autopsy or surgery in more than 50 percent of patients with LVA [7,14,16]. Two factors contribute to clot formation in this setting:
●Stasis of flow in the aneurysm cavity [17,18]
●Contact of blood with potentially procoagulant fibrous tissue in an LVA rather than normal endocardium.
Systemic embolization can occur and carries the risk of stroke [19,20]. The efficacy of and indications for anticoagulation in patients with LV thrombus are discussed separately. (See "Left ventricular thrombus after acute myocardial infarction".)
Ventricular rupture — LVAs may enlarge over time. However, unlike false aneurysms, a mature true LVA rarely ruptures because of the dense fibrosis in its wall [21].
Diagnosis — The possible presence of an LVA should be suspected in a patient with a large, usually anterior MI develops one of the complications described in the preceding section. The electrocardiogram usually reveals evidence of a large anterior MI. There may be persistent elevation of the ST segment; however, this finding is usually the result of a large area of scar and does not necessarily imply an aneurysm (waveform 1).
The presence of an LVA may be suspected from the chest radiography (image 9 and image 6 and image 7), but the diagnosis of an LVA is definitively made with imaging techniques. A simple definition of an LVA on imaging is a dyskinetic wall motion abnormality with the feature of diastolic deformity.
Two-dimensional echocardiography is the first imaging study obtained in most patients (movie 1 and movie 2) [22,23]. Cardiac computerized tomographic angiography has become the standard imaging test and can confirm the diagnosis in patients where two-dimensional echocardiography is not diagnostic (figure 1). Radionuclide ventriculography (image 15) or contrast ventriculography (image 16) at the time of cardiac catheterization are alternatives. Three-dimensional echocardiography and magnetic resonance imaging (image 17) are newer modalities that are increasingly used for diagnosis, measurement of left ventricular volume, and postoperative follow-up. These modalities are also useful to distinguish between a true and pseudoaneurysm. Magnetic resonance imaging (MRI) can be useful to assess myocardial viability, particularly in patients with akinetic segments [24-28]. Data are more limited on the use of cardiovascular MRI [24,25].
Natural history — The natural history of patients with LVA continues to be a matter of controversy. In an older study of 102 patients with pathologically proven LVA, the three- and five-year survival rates were 27 and 12 percent, respectively [14]. Other studies published in the 1970s noted similar [29] or somewhat better results (47 and 18 percent survival at 5 and 10 years, respectively) [30]. In contrast, the five-year survival in the subset of patients with LVA from the Coronary Artery Surgery Study (CASS) was much better at 71 percent [31].
Such a wide variation in outcomes can be attributed to differences in several major patient variables including the size of the aneurysm, whether the aneurysmal segment is dyskinetic or akinetic, the extent of coronary disease (single versus multivessel), and the function of the nonaneurysmal part of the left ventricle.
An important limitation is that all of the above studies were performed before the institution of current medical therapies with the widespread use of primary percutaneous coronary intervention or thrombolytic therapy. As a result, they cannot be used as absolute markers against which surgical results should be compared.
Treatment — Treatment of an LVA consists of medical therapy of the complications that can occur and consideration of aneurysmectomy.
Medical therapy — Small to moderate size asymptomatic aneurysms can be safely treated medically with an anticipated five-year survival of up to 90 percent [32]. Therapy consists of afterload reduction for LV enlargement, usually with an angiotensin converting enzyme inhibitor, antiischemic medications for angina, and anticoagulation if there is significant LV dysfunction or evidence of thrombus within the aneurysm or LV. (See "Antithrombotic therapy in patients with heart failure" and "Acute coronary syndrome: Oral anticoagulation in medically treated patients" and "Left ventricular thrombus after acute myocardial infarction".)
The optimal approach to the patient with a large, asymptomatic LVA remains a clinical dilemma. Concomitant repair of the aneurysm has been advocated when coronary artery bypass surgery (CABG) or valve surgery is performed [33]. In the absence of such indications for surgery, these patients should otherwise be treated with the same regimen as those with a small LVA; they should also be followed closely for progressive left ventricular dilation.
Similar to other settings of chronic volume overload, such as mitral regurgitation, a progressive increase in LV diameter and/or decrease in LV ejection fraction (LVEF) is an indication for surgery even before the development of overt heart failure or other symptoms [33]. (See "Management of chronic primary mitral regurgitation".)
Oral anticoagulation — The identification of a mural thrombus in patients with a postinfarction LVA warrants consideration of oral anticoagulation to prevent embolization. Our approach to anticoagulation in such patients is presented elsewhere.
In contrast to patients with a recently formed LVA, the risk of embolism appears to be low with a chronic aneurysm diagnosed at least one month after an MI even though mural thrombus is frequently seen. In one report of 76 such patients diagnosed a median of 11 months after infarction, the incidence of clinical embolization at a median follow-up of five years was 0.35 percent per year [34]. These thrombi have presumably organized or been endothelialized and appear to rarely embolize. As a result, anticoagulation may not be warranted in such patients [19,34].
Indications for surgical repair — The 2004 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on ST elevation MI concluded that it is reasonable (class IIa recommendation) to consider aneurysmectomy, accompanied by CABG, in patients with an LVA who have intractable ventricular arrhythmias and/or heart failure unresponsive to medical and catheter-based therapy [35]. No changes to this approach were made in the 2007 focused update of the 2004 ACC/AHA guidelines for the management of patients with ST-elevation MI [36]. A similar level of recommendation for surgical repair of LVA in patients with intractable heart failure and recurrent ventricular arrhythmias was included in the summary of the 2017 European Society of Cardiology Taskforce on Acute ST Elevation MI [37].
Other possible indications include refractory angina, which is an indication for intervention in the absence of an LVA, and systemic embolization in patients who cannot take chronic warfarin therapy or cannot be well controlled.
Surgical repair should be considered for symptomatic patients with either akinetic or dyskinetic segments, as they represent variants in the spectrum of the same disease [38,39].
Surgical repair of an LVA is very effective, and results in a significant improvement in patient survival, symptoms and functional class compared to medical treatment. Furthermore, a marked decrease in operative mortality has been achieved in the past two decades, resulting in an expansion of indications for surgery.
Surgical considerations — The majority of the operations for repair of an LVA are performed via a median sternotomy incision using cardiopulmonary bypass [1,2,40]. However, in unusual circumstances, the operation can be performed via a left thoracotomy, particularly for posterior aneurysms [41]. An alternative approach to inferior-basal aneurysms is via the left atrium [42]. This endocavitary approach avoids ventriculotomy and is particularly useful when concomitant mitral valve repair or replacement is indicated for mitral regurgitation. The two surgical techniques most commonly used are the linear repair and the ventricular endoaneurysmorrhaphy. (See "Treatment of ischemic cardiomyopathy".)
Concurrent myocardial revascularization is indicated in most patients. Incomplete revascularization appears to be an independent predictor of increased long-term mortality [1,2,43]. Thus, every attempt should be made to achieve complete revascularization, particularly of the nonaneurysmal walls [1,2,33,40].
Mitral valve repair or replacement is sometimes required because of significant mitral regurgitation. This procedure can be performed conventionally through the left atrium or through the ventriculotomy.
Endocardial mapping followed by endocardial resection and/or cryoablation are performed in patients with malignant ventricular arrhythmias. Non-guided endocardectomy also may be an effective approach. In a review of 106 patients with LVA and spontaneous or inducible ventricular tachycardia (VT) who underwent this procedure, no patient had spontaneous VT at late follow-up and only 11 percent had inducible VT [44].
The STICH trial compared CABG alone to CABG with left ventricular reconstruction in patients with ischemic cardiomyopathy. The results of STICH are presented separately. (See "Treatment of ischemic cardiomyopathy".)
In-hospital outcome of surgical repair — Thirty-day hospital mortality following repair of LVA ranges from 0 to 19 percent [1,2,33,40,43,45-63]. Mortality rates have been consistently decreasing over time, probably related to improved anesthesia, myocardial preservation, newer surgical techniques, improved perioperative care, and more aggressive revascularization.
Mortality rates associated with the "plastic" reconstructive type of repair (average 4.3 percent, range 0 to 7.4 percent) [33,46-57] appear to be lower than those associated with linear repair (average 8.1 percent, range 0 to 19 percent) [43,58-63]. However, only a few observational studies have directly compared the two techniques [46,51,52,63-67]. We found no difference in operative or five-year mortality, but patients treated with "plastic repair," also called endoaneurysmorrhaphy, were more likely to be in New York Heart Association class I or II at a mean 41 month follow-up (88 versus 53 percent) [46].
With multivariate analyses, independent predictors of increased early mortality include [1,2,33,40,43,46,52,55,58-63]:
●Operation performed in an earlier decade
●Operation within 30 days of MI
●Preoperative need for intraaortic balloon pump support
●Cardiogenic shock
●Advanced age
●Operation for heart failure or arrhythmia (versus angina or embolism)
●Advanced New York Heart Association functional class
●Poor function of the nonaneurysmal walls
●Significant mitral regurgitation
●Preoperative renal failure
One report suggested that operation on akinetic scars was associated with a higher early and late mortality and less evident hemodynamic effect than surgery on a dyskinetic aneurysm [62]. However, in a later series, the clinical and hemodynamic results after repair of both types of aneurysms were similar. The size of the scar seems to play a role in terms of outcome, being worse in patients with large scars [57].
Both methods of repair result in a significant improvement in hemodynamics. Postoperatively cardiac index and LVEF are markedly increased and left ventricular end-diastolic volume and pressure are substantially lower [33,46-51,56,57,59]. The magnitude of these changes seems to be greater following the "plastic" type of repair, and patients undergoing left ventricular reconstruction have more favorable postoperative hemodynamics. These hemodynamic changes translate into a significant improvement in functional class.
Long-term results of surgical repair — Survival after LVA repair at 1, 5 and 10 years is in the range of 85 to 90 percent, 56 to 69 percent, and 51 to 73 percent, respectively [1,2,33,40,43,45,46,49-52,55,58-63]. These figures represent a substantial improvement when compared to medically treated patients in historical series [14,29,30].
However, most of the reports on medically-treated LVAs do not reflect modern treatment options. As a result, the comparisons probably overestimate the magnitude of benefit, and it is possible that there is no benefit.
In multivariate analyses, independent predictors of long-term mortality include [1,2,33,40,43,46,47,52,58-60,62,63]:
●Operation performed in an earlier decade
●Operation performed for heart failure or arrhythmia
●Incomplete coronary revascularization
●Low LVEF
●Advanced age
●Left main coronary artery disease
●Poor function of the nonaneurysmal wall, particularly the basal septum
Improvement in hemodynamic parameters, LVEF, and New York Heart Association functional class seen in the early postoperative period persist at late follow-up.
Long-term control of malignant ventricular arrhythmias is excellent when aneurysmectomy is combined with left ventricular reconstruction and endocardial resection, with or without cryoablation [44,53]. (See "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis", section on 'Surgical therapy'.)
LEFT VENTRICULAR PSEUDOANEURYSM — A left ventricular pseudoaneurysm or false aneurysm forms when cardiac rupture is contained by adherent pericardium or scar tissue [68]. Unlike a true aneurysm, a pseudoaneurysm contains no endocardium or myocardium. The diagnosis needs to be established early, since these aneurysms are prone to rupture [21].
Etiology — In a literature review of 253 patients with a pseudoaneurysm in whom the cause was reported, 55 percent were related to myocardial infarction (MI), particularly of the inferior wall, which was twice as common as anterior infarction [69]. The second most common cause was surgery, which was responsible for 33 percent of cases. The most common types of surgery were mitral valve replacement, which has been mostly described in case reports, and aneurysmectomy itself. Trauma accounted for 7 percent of cases.
The site of pseudoaneurysm varies with etiology. This was illustrated in a review of 52 patients seen at the Mayo Clinic [70]. Pseudoaneurysms were primarily seen in the inferior or posterolateral wall after MI, which is consistent with inferior infarction, in the right ventricular outflow tract after congenital heart surgery, in the posterior subannular region of the mitral valve after mitral valve replacement, and in the subaortic region after aortic valve replacement.
Clinical presentation — In the above literature review, the most frequent symptoms associated with left ventricular pseudoaneurysm were chest pain and dyspnea [69]. Sudden cardiac death was the presenting manifestation in about 3 percent, while 12 percent of patients were asymptomatic.
However, the distribution of presenting manifestations was different in the analysis of 52 patients from the Mayo Clinic, which permitted access to more complete patient information than the literature review [70]. Twenty-five patients (48 percent) were asymptomatic. The remaining patients with acute myocardial infarction, tamponade, heart failure, chest pain, syncope or arrhythmia, or systemic embolism.
Murmurs are present in about two-thirds of patients [69]. The murmur is often to-and-fro, but may be indistinguishable from that of mitral regurgitation. More than 95 percent of patients have ECG changes, including ST segment elevation in 20 percent and nonspecific changes in the remainder. Evidence of a mass on chest x-ray is seen in more than one-half of patients.
Diagnosis — The most reliable method for diagnosis of a pseudoaneurysm is angiography, which demonstrates a narrow orifice leading to a saccular aneurysm and lack of surrounding coronary arteries [71]. In the literature review, left ventricular angiography resulted in a definitive diagnosis in over 85 percent of patients, with only 2 percent having a normal examination [69].
Transthoracic echocardiogram is a reasonable first step, but a definitive diagnosis is made in only 26 percent of patients [72]. Transesophageal echocardiography has a diagnostic accuracy of more than 75 percent compared to angiography, but data about its use are limited. We use transthoracic echocardiography followed by contrast cineventriculography as initial studies. Transesophageal echocardiography is added when better assessment of the mitral valve is indicated. Cardiac computerized tomography and magnetic resonance imaging are increasingly used to define anatomy, measure left ventricular volume, and assess myocardial viability.
Echocardiography can usually distinguish a pseudoaneurysm from a true aneurysm by the appearance of the connection between the aneurysm and ventricular cavity (image 18). Only small ruptures of the ventricular wall are compatible with survival. As a result, pseudoaneurysms have a narrow neck, typically less than 40 percent of the maximal aneurysm diameter, that causes an abrupt interruption in the ventricular wall contour. In contrast, true aneurysms are nearly as wide at the neck as they are at the apex (movie 1 and movie 2).
Cardiovascular computerized tomography and magnetic resonance imaging are an alternative to angiography or echocardiography that may be useful in order to distinguish a pseudoaneurysm from a true aneurysm [24,73]. In a retrospective review of four cases of pseudoaneurysm and 18 cases of true aneurysm, which were pathologically confirmed, marked delayed enhancement of the pericardium was seen in all of the former, but only one of the latter [24]. Other discriminatory characteristics, such as the ratio between the maximal internal width of the orifice to the maximal parallel internal diameter, were also present with cardiac magnetic resonance imaging. (See "Clinical utility of cardiovascular magnetic resonance imaging".)
Treatment — Untreated pseudoaneurysms have a 30 to 45 percent risk of rupture and, with medical therapy, a mortality of almost 50 percent [21,69]. Thus, surgery is the preferred therapeutic option. With current techniques, the perioperative mortality is less than 10 percent; the risk is greater among patients with severe mitral regurgitation requiring concomitant mitral valve replacement [74,75]. Percutaneous transcatheter device closure of left ventricular pseudoaneurysm should be considered as an alternative to conventional surgery in high-risk patients, particularly if concomitant coronary revascularization is not indicated [76].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Non-ST-elevation acute coronary syndromes (non-ST-elevation myocardial infarction)" and "Society guideline links: ST-elevation myocardial infarction (STEMI)".)
SUMMARY AND RECOMMENDATIONS
●Left ventricular aneurysms (LVAs) and pseudoaneurysms are two complications of myocardial infarction that can lead to death or serious morbidity. (See 'Left ventricular aneurysm' above and 'Long-term results of surgical repair' above.)
●Transthoracic echocardiography is a reasonable starting point for diagnosis in patients suspected of having either LVA or pseudoaneurysm. Cardiac magnetic resonance imaging or LV angiography may be necessary in patients with suspected LV pseudoaneurysm. (See 'Diagnosis' above and 'Diagnosis' above.)
●Small to moderate size asymptomatic aneurysms can be treated medically with an anticipated five-year survival of up to 90 percent. Therapy of LVAs consists of afterload reduction, usually with an angiotensin converting enzyme inhibitor, and anticoagulation if there is significant LV dysfunction or evidence of thrombus within the aneurysm or LV. (See 'Treatment' above.)
●Aneurysmectomy accompanied by coronary artery bypass graft surgery should be considered in patients with an LVA who have intractable ventricular arrhythmias and/or heart failure unresponsive to medical and catheter-based therapy. (See 'Surgical considerations' above.)
●LV pseudoaneurysms have a 30 to 45 percent risk of rupture and, with medical therapy, a mortality of almost 50 percent. Surgery is the preferred therapeutic option. (See 'Treatment' above.)
