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ORIGINAL ARTICLE |
Department of Cardiovascular Surgery, Kartal Kosuyolu Yuksek Ihtisas Training and Research Hospital Istanbul, Turkey
Ali Fedakar, MD, Tel: +90 216 4594041, Fax: +90 216 4596321, Email: alfdkr67{at}hotmail.com, Department of Cardiovascular Surgery, Kartal Kosuyolu Yuksek Ihtisas Training and Research Hospital, 34846 Kartal, Istanbul, Turkey.
ABSTRACT
The outcomes of 3 different methods of repair of left ventricular pseudoaneurysm after myocardial infarction were analyzed retrospectively. The operations were carried out in 22 patients between 1985 and 2008. Repair procedures included primary closure with Teflon-pledgeted sutures, and Dacron or pericardial patches. Overall hospital mortality was 27.3% (2 patients had primary closure, 3 had a Dacron patch, and 1 had a pericardial patch). Mean postoperative bleeding was 885 mL (range, 200–4,800 mL). Mean preoperative and postoperative ejection fractions were 40% (30%–47%) and 48% (30%–65%), respectively. The overall incidence of arrhythmia was 36.4% (8 patients). The incidence of arrhythmia was lowest in the pericardial patch group, but this was not statistically significant. No significant differences in postoperative ejection fraction or hemorrhage were found among the study groups. Mean survival was 61.9 ±41.4 months in the 16 hospital survivors. Although the 3 techniques gave similar results, repair with an autologous pericardial patch may offer an advantage in terms of less postoperative arrhythmias.
Key Words: Aneurysm • False • Cardiac Surgical Procedures • Heart Rupture • Post-Infarction • Myocardial Infarction
INTRODUCTION
Pseudoaneurysm of the left ventricle (LV) usually develops following ventricular rupture due to transmural myocardial infarction (MI).1 In addition, it may be associated with mitral valve replacement, previous unsuccessful ventriculotomy, trauma, inflammation, tumor invasion, and apical venting.2–5 LV rupture after transmural MI advances from the endocardium to the pericardium. The incidence of LV free wall rupture following MI is 2%.6 Free wall rupture causes fatal pericardial tamponade in most cases, but in some, the thrombus becomes organized within the limitation of the surrounding tissues and pericardium, and becomes a cavity that results in pseudoaneurysm formation.7 Although David and colleagues8 reported that the probability of rupture is higher in lateral wall infarctions, pseudoaneurysms are also frequently encountered in the inferior and posterobasal walls. Because of the high risk of rupture, treatment of LV pseudoaneurysms should be surgical. However, surgical repair of chronic lesions still carries a high risk of mortality. Primary repair with Teflon-pledgeted sutures or secondary closure using synthetic (Teflon or Dacron) patches are the preferred surgical repair procedures.1,9,10 In this study, we also used glutaraldehyde-treated autologous pericardium to repair LV pseudoaneurysms in 6 appropriate patients. The aim of this retrospective review was to analyze the results of LV pseudoaneurysm repair by the 3 different techniques.
PATIENTS AND METHODS
Between February 1985 and September 2008, 22 patients were operated on for LV pseudoaneurysm at Kosuyolu Heart and Research Hospital in Istanbul. The study was approved by the local ethical committee, and consent was obtained from all patients. We did not included true LV aneurysms in this study. All of these pseudoaneurysms were a consequence of transmural MI. Those identified within the first 2 weeks after MI were deemed early pseudoaneurysms. Table 1
shows the clinical features of the patients and the surgical techniques. Of the 22 patients included in this study, 17 were male, and the mean age was 64.0 ±8.7 years. Pseudoaneurysm diameter was estimated by transthoracic echocardiography in 16 patients, by contrast left ventriculography in 3, and intraoperatively in 3. The mean pseudoaneurysm diameter was 5.0 ±0.4 cm. The time from MI to diagnosis was 68.5 ±50.7 days (range, 3–158 days; 86.4 ±43.2 days in the late presenting group, and 7.4 ±3.4 days in the early presenting group). Four acute pseudoaneurysms were found incidentally at echocardiography after MI, and 16 were diagnosed during investigation for cardiac symptoms of heart failure, arrhythmias, and stable angina pectoris. The preoperative mean LV ejection fraction was 40%. Preoperative coronary angiography was performed in all patients. There was 3-vessel disease in 15 patients, 2-vessel in 5, and 1-vessel in 2.
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and 2). An echocardiogram on the 1st postoperative day in a patient who received a pericardial patch is shown in Figure 3. Follow-up information was obtained from all 16 discharged patients in November 2008, by telephone in 4 and during hospital visits in 12. Postoperative hemorrhage, ejection fraction, and incidence of ventricular arrhythmia were compared between the autologous pericardial patch group and the other 2 groups.
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RESULTS
Overall early postoperative mortality was 27.3%. Hospital deaths occurred in 2/9 (22.2%) patients in the primary closure group, 3/7 (42.9%) in the Dacron patch group, and 1/6 (16.7%) in the pericardial patch group (Table 1
). Two of these 6 deaths were after repair of acute pseudoaneurysms and 4 after repair of chronic pseudoaneurysms; 3 deaths were caused by low cardiac output syndrome leading to multiple organ failure, 1 was due to pneumonia on postoperative day 17, one occurred after peptic ulcer perforation on postoperative day 17, and one was related to a neurological event on postoperative day 18 (Table 1). During follow-up of the surviving patients, one died due to stomach cancer. The hospital survivors exhibited considerable improvements in their general capacity during the follow-up period (New York Heart Association class I/II) compared to their preoperative state. Mean survival was 61.9 ±41.4 months in all discharged patients. Mean survival was 84±41.7 months in the primary closure group, 80 ±45.3 months in the Dacron patch group, and 32.5 ±30.3 months in the autologous pericardial patch group. Table 2 summarizes variables related to the surgical repair techniques. No significant differences were found among the 3 groups of patients in terms of postoperative bleeding and ejection fraction. The overall incidence of arrhythmias was 36.4%: they were detected in 5/9 (55.6%) patients in the primary closure group, 2/7 (28.6%) in the Dacron patch group, and 1/6 (16.7%) in the autologous pericardial patch group; however, this difference was not significant (p = 0.183), probably due to the small sample size.
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Ventricular rupture following transmural MI is responsible for 8% of deaths caused by infarction.10 Rupture is unpredictable and can occur at any time.10 Some believe that the risk of rupture is similar regardless of whether the pseudoaneurysm is large or small.11 Because of its rarity, the natural history of LV pseudoaneurysm is unknown. Although ventricular pseudoaneurysms are reported to be frequently localized to the inferobasal and posterobasal segments of the LV (and rarely, apical segments), involvement of the inferior wall of the right ventricle and the lateral wall of the LV have also been reported as unusual cases.12–15 David and colleagues8 suggested that lateral wall infarctions are more likely to rupture compared to those located on the anterior and inferior walls. In our study, 17 of the 22 patients had inferior and posterobasal lesions. LV pseudoaneurysms are mostly asymptomatic and may be detected by echocardiography during post-infarction follow-up or investigations for congestive heart failure, arrhythmia, embolism, or angina. Pseudoaneurysms can be diagnosed preoperatively by echocardiography, computed tomography, ventriculography, color-flow echocardiography, and cardiac magnetic resonance imaging.3,4 Currently, echocardiography (transthoracic or transesophageal) is the diagnostic standard.10 Intraoperative diagnosis is possible on inspection during coronary artery bypass grafting. In our cases, preoperative diagnoses were established by echocardiography or ventriculography, and 3 were found incidentally during coronary artery bypass grafting.
The general consensus is that surgery is indicated for all patients as soon as the diagnosis is established, unless the surgical risk is prohibitive. If a pseudoaneurysm is diagnosed within 2 to 3 months after MI, emergency surgery should be performed because of the high risk of rupture. If the diagnosis is made years after MI, the necessity and urgency of surgery depends on the symptoms.1 Small chronic pseudoaneurysms diagnosed incidentally seem to have a more stable course. Pretre and colleagues9 suggested that chronic asymptomatic pseudoaneurysms < 3 cm in diameter and without evidence of expansion could be treated conservatively. Moreno and colleagues16 reported 1-year survival of 90% and 4-year survival of 74% in 10 patients treated conservatively; only one patient died from cardiac causes, but 3 suffered ischemic stroke during this period. In another series, the 2-year mortality was reported to be 50% in patients with chronic LV pseudoaneurysms monitored without intervention.17 As an alternative to conservative monitoring, advances in technology now allow the option of percutaneous closure of pseudoaneurysms.17
Before opening the sternum, it may preferable to cannulate the femoral vessels, establish cardiopulmonary bypass, and institute hypothermic circulatory arrest. We did not perform femoral cannulation, but rather used ascending aorta and double-venous or 2-stage venous cannulation. In patients with preoperatively diagnosed pseudoaneurysms, the heart should be gently dissected subsequent to cannulation, and aortic crossclamping should be performed to prevent preoperative thromboembolism and rupture. Various techniques have been used to obliterate the neck of the pseudoaneurysm. The choice of the technique is based on the extent of the defect and the status of the myocardium. Fibrotic margins, which can be found in the neck of aneurysms, may aid direct closure in chronic cases. In our study, primary closure was performed in 9/22 patients.
Unfortunately, primary repair carries a higher risk of arrhythmias because pressure is exerted on the LV. Patch closure of necrotic myocardial tissue is more effective than primary closure in acute cases and large LV pseudoaneurysms. The materials used for these patches include synthetic substances such as Dacron, bovine pericardium, and autologous pericardium.1,10,12 Pericardium is an excellent material for surgical repair of certain acquired defects, including all parts of the LV outflow tract. Pericardium has also been used to repair the LV in patients with post-infarction ventricular septal defect. Atik and colleagues10 described fresh pericardial patch closure for repair of 3 LV pseudoaneurysms, and 2 such cases were reported by Daglar and colleagues.18 Our intentions in using glutaraldehyde-treated autologous pericardial patches were to decrease the risk of infection by avoiding synthetic material, to provide a more appropriate configuration with biological tissue, and to make the procedure more cost-effective. No significant differences were found between cases treated with pericardial patches and those with Dacron patches or primary closure, but a tendency for fewer postoperative arrhythmias was noted in the autologous pericardial patch group. The mean survival time was lower in the autologous pericardial patch group, most likely because such patches have only been used in the last 10 years.
Study limitations include the small sample size, which was not sufficient to reach a meaningful statistical conclusion. However, LV pseudoaneurysm in 22 patients is a large number from a single institution, due to the rarity of this lesion. Furthermore, these patients were operated on over a period of almost 25 years during which there have been many changes in medication, anesthesia, extracorporeal circulation management, anticoagulation and antiaggregation therapy.
Although LV pseudoaneurysms are infrequent, there is a high risk of death when conservative monitoring is used. Pseudoaneurysms can be repaired surgically, with acceptable mortality, until a more appropriate method becomes available.
REFERENCES
Asian Cardiovasc Thorac Ann 2010;
18:39-43
© 2010 by SAGE Publications
DOI: 10.1177/0218492309353988
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