Diagnosis and surgical treatment of post-infarction left ventricular pseudoaneurysm (2009)

Left ventricular pseudoaneurysm (LVPA) is a rare clinical entity that could be life-threatening. It could be of congenital and acquired origin.1,2 Among the acquired LVPA, post-infarction LVPA constitutes most of the cases. LVPA always occurs after acute myocardial infarction (MI) and develops chronically. Reliable diagnosis and early surgical intervention are vital for the patients' recovery. Here we present 7 cases of LVPA in Anzhen Hospital between May 1993 to March 2007, focusing on the evaluation of diagnosis methods and treatment efficiency of LVPA. CLINICAL DATA Patients Of the 7 cases of post-infarction LVPA, there were 4 males and 3 females with an age range of 47 to 63 (54.5±6.7)years. One case was acute LVPA, and the other 6 cases were chronic. Four cases were in NYHA functional class III or IV, while three others were in NYHA functional class I or II. A dual phase murmur ranged from 2 to 4 grades over six grades could be heard in precordial area in 5 cases, and a systolic murmur could be heard in the other case. Rale in both basis pulmonis was present in 2 cases. The electrocardiogram showed an old inferior wall MI in 3 cases, an old extensive anteroseptal wall MI in 2 cases, an old lateral wall MI in one case, and an acute anteroseptal wall MI in one case. Chest roentgenography showed plethoric lung field in one case, congestive lung field in 4 cases, and the cardiothoracic ratio ranged from 0.57 to 0.69. Three cases had received thrombolytic treatment. The pre-procedure coronary angiogram demonstrated coronary stenosis in three branches in 4 cases, and in two coronary branches in the other 3 cases. The pre-procedure echocardiography revealed a left ventricular ejection fraction ranged from 26% to 50% with a mean of (37±12)%, and a severe mitral regurgitation in one case, a mild to moderate mitral regurgitation in one case. The 7 cases of LVPA were diagnosed by echocardio-graphy, left ventriculography, and CT/MRI scan to explore their location, size, and the neck diameter. One case with acute LVPA was diagnosed three days after the acute MI. This patient has a true aneurysm of left ventricular and a ventricular septal rupture accompanied with the acute pseudoaneurysm (Figure). Among the 6 chronic LVPA, one was misdiagnosed preoperatively and confirmed during the coronary artery bypass grafting (CABG) procedure. The other 5 cases were diagnosed 3 months to 2 years after acute MI, in which LVPA was found to be located in the anteroseptal, inferior, or lateral myocardial wall by echocardiography. The diameter of the chronic LVPA ranged from 12 mm×25 mm to 45 mm×65 mm, and the neck of the LVPA ranged from 8 to 28 mm. The endocardium was detached completely from the myocardium. Four cases underwent left ventriculography, which showed the LVPA pouched outward and formed a dumbbell-like structure with a narrow neck, and with contrast came back and forth across the neck. In two cases, multi-sliced CT scan demonstrated the out pouching LVPA, which constituted only with epicardium as its aneurysm body. The chest roentgenography revealed enlarged silhouette in two cases, and gradual cardiomegaly with prominence of the left fourth arch in one case.Figure.: Echocardiography of one case with acute LVPA, and a true aneurysm of left ventricular and a ventricular septal rupture. PSEUDO, pseudoaneurysm. ANEU, true aneurysm. FENES, septal perforation. LV, left ventricle. RV, right ventricle.Surgical procedures One patient died from rupture of the LVPA without operation and the other 6 patients were operated on under general anesthesia and cardiopulmonary bypass with cardiac arrest. One patient underwent emergent surgery due to high risk of rupture of the LVPA, and the other 5 procedures were elective (Table). For the Case 1 of chronic LVPA, the pseudoaneurysm was incised and the incision was closed through a polytetrafluoroetylene (PTFE) patching with running suture, then lined with the remnant wall of the pseudoaneurysm. For the Case 2 with the acute LVPA, the coexisted septal perforation was closed with a Dacron patching and the LVPA was corrected through a Dor procedure using two teflon felts reinforced in the both sides of the incision. For the Case 3 with a simple anterior-septal wall LVPA, a Dor procedure was also adopted. For the Case 4 with an anteroseptal LVPA and a pseudoaneurysm extended into anterior myocardium, a Dor procedure was performed and the anterior myocardium was resected at the same time. For the Case 5 of a lateral wall LVPA with a narrow neck of 8 mm in diameter, a direct closure procedure was made using the teflon felt and mattress 2-0 Prolene suture. For the Case 6 of an inferior wall LVPA complicated by papillary muscle rupture, a patching procedure and a mitral valve repair procedure were carried out. For all of the 6 operated patients, thrombus evacuation was made in three cases, and 15 coronary arterial bypasses were completed with a mean of 2.5 in each patient. The cardiopulmonary bypass duration ranged from 89 to 176 (142±37) minutes, and the clamping time ranged from 68 to 132 (94±28) minutes.Table: Pathology and the surgical procedures of 7 cases of post infarction LVPARESULTS One patient died before surgery due to acute LVPA rupture and cardiac tamponade, while the other six patients were surgically treated through direct closing, cut and patching, or cut and sandwiching procedure (Dor procedure) along with CABG procedure. There was no operative death, but intra-aortic balloon pump (IABP) supports after the procedure was used in two cases, and dialysis due to renal failure was adopted in one case. Four cases had an uneventful recovery. No brain or other organ embolization occurred in all of the operative patients. The pathological results showed that the acute LVPA constituted only with epicardium and remnant myocardium, but the 5 chronic LVPA constituted with epicardium and organized thrombus and granulated tissue. During a follow-up period of 2 months to 13 years, 1 case died from cardiac rupture and acute pericardial tamponade 4 years after the repair procedure. Among the other 5 survivors, the ejection fraction measured with echocardiography ranged from 42% to 53%, and there was no relapse of LVPA by echocardiography evaluation. The heart function was in NYHA functional class I for three cases and was in NYHA functional class II for two cases. DISCUSSION The diagnosis and differential diagnosis of the LVPA LVPA is an unusual complication of myocardial infarction, cardiac surgery, trauma, infection, or inflammation. LVPA is also the result of cardiac wall rupture contained by overlying, adherent pericardium, or scar tissue.3 The post-infarction LVPA constitute about 55% of the entity. As to the location of LVPA, according to Frances et al,4 inferior wall LVPA was most often to be discovered, contributing about 40% of the cases. LVPA can be classified as acute (onset 2 weeks within the acute MI), sub-acute (onset between 2 weeks and 3 months), and chronic (onset after 3 months after acute MI).5,6 The chronic LVPA is always a large pseudoaneurysm. LVPA requires early diagnosis and subsequent surgical correction, because it tends to rupture even in the chronic phase regardless of its size. However, patients are often asymptomatic, and the LVPA is always found incidentally upon imaging study. A high degree of suspicion is needed to avoid missing the diagnosis.7 Of the 7 cases of post-infarction LVPA in this series, one was misdiagnosed and was discovered during the CABG procedure incidentally. What distinguishes the LVPA from the LV true aneurysm is the sharp discontinuity of the myocardium around the aneurismal cavity. The presence of a neck smaller than the cavity is strongly suggestive of pseudoaneurysm, thus left ventriculography is the best tool to establish the diagnosis.8 But echocardiography is the simplest and easy way to diagnose LVPA, so transthoracic echocardiography (TTE) is a reasonable first diagnostic tool, and TTE can reveal a back and forth blood flow across the pseudoaneurismal neck. TTE and left ventriculography can often reveal a pseudoaneurysm with only epicardium.9 Coronary angiography is usually necessary before surgery to evaluate the need for concomitant bypass grafting. MRI has the merit of non-invasive assessment of LVPA for comprehensive structural and cardiac function.10,11 Although left ventriculography is the gold standard for LVPA, its positive rate is only 54%, whereas the positive rate for echocardiography is as high as 97%.12 The characteristics of LVPA revealed through echocardiography are as follows: (1) a left ventricular wall rupture in M mode of echocardiography; (2) the two dimensional echo can show a rupture in left ventricular endocardium and a narrow neck connecting the pseudoaneurysm with the left ventricle, and the neck is of less than 50% of the pseudoaneurysm in diameter; (3) pulsed wave Doppler (PW) and color Doppler flow imaging (CDFI) can show a blood flow going back and forth across the aneurismal neck; (4) TTE can accurately diagnose the posterior wall LVPA.13 Although the differentiation of LVPA from a true aneurysm may be difficult, the presence of a narrow neck on either color-flow Doppler echocardiography or left ventriculography is strongly indicative of LVPA. Characteristic features of the LVPA are a narrow neck at the site of rupture with an abrupt transition from normal myocardium to aneurysm, and the diameter of the neck is less than 50% of the maximum diameter of the aneurysm itself.14 LVPA should be differentiated with the true aneurysm after acute MI. Unlike a true aneurysm, the wall of the LVPA is formed by thrombi and enveloping pericardial tissue with a narrow neck.15 The wall of LVPA lacks myocardial elements. Although heart failure is rare following high lateral wall MI, it is not an uncommon clinical outcome in pseudoaneurysm cases. LVPA should be recognized and distinguished from left ventricular true aneurysm,16 because it has a propensity to rupture, and may cause symptoms of heart failure. LVPA has been reported to originate usually at the posterior basal and rarely at the apical segment of the left ventricle after occlusion of the right coronary or left anterior descending artery.17-19 Procedure choice and the timing of the surgical treatment Surgical repair is considered as an optimum treatment for LVPA because untreated pseudoaneurysm has an approximately 30% to 45% risk of rupture. Patients with LVPA have a mortality as high as 23% if treated surgically and 48% if treated medically. The prognosis of LVPA is poor. Without surgical intervention, most of the LVPA will rupture and patients die from pericardial tamponade or circulation collapse. So, surgical procedure is imperative. Timing of surgery is important in determining the outcomes. Due to tissue fragility and edema, the acute pseudoaneurysm should not be resected until mature hyalinized fibrous tissue becomes tough enough to anchor sutures after 4 weeks following acute MI. The Case 2 in our study was an acute LVPA and was supported by mechanical ventilation and IABP to live through the acute phase. This patient received operation 45 days after the acute MI when infarcted myocardium could sustain the LVPA and septal rupture could be obliterated. The timing of surgical intervention depends on the characteristics of the LVPA. For example, asymptomatic pseudoaneurysms that occur a few days after acute MI or surgery are extremely unstable and tend to rupture. Although the natural history of the post infarction LVPA is not known completely, large LVPA rupture more easily than the small and chronic ones. A few case series have reported that the surgical risk on chronic lesions is still very high. The timing of surgery depends also on the age of the myocardial infarction. It is highly recommended that an emergency procedure should be conducted for LVPA found within the first 2 to 3 months after myocardial infarction, since onset of rupture is unpredictable.20 For LVPA found years after myocardial infarction, the urgency and even the need for operation are determined by symptoms rather than by risk of rupture. About 10% to 20% of chronic LVPA are discovered incidentally.4 The outcome of this entity treated conservatively is very poor with a mortality rate of around 50% at 2 years.21 Because of the uncertainties in its natural history, and the relative safety of surgical intervention in this subset, operation should be superior to conservative management in the cases of large or expanding pseudoaneurysms. The surgical technique for correcting the LVPA mainly depends on the location and the neck diameter of LVPA. For the LVPA located in inferior wall, it is feasible to patch the neck of the LVPA directly with bovine pericardium or PTFE patch, then reinforce with autologous pseudoaneurismal wall, as for the Cases 1 and 6 in our series. For the LVPA located in lateral wall and with narrow neck, it is very easy to adopt direct closure procedure with mattress suture, as for the Case 5. For the LVPA located in anteroseptal wall, Dor procedure is an effective way to correct the attenuated and thin pseudoaneurysm wall, as for the Cases 2, 3, and 4. The comorbidities, such as septal perforation, coronary artery stenosis, and myocardium dissection, et al, should also be treated accordingly.