Left ventricular pseudoaneurysm is a rare disease; it is defined as a ventricular rupture contained by epicardium, pericardial adhesions, or both. It most frequently occurs as a complication of acute myocardial infarction. Surgical treatment is recommended for pseudoaneurysms that are large or symptomatic and for those discovered less than 3 months after myocardial infarction.
We report our experience with 2 patients who had left ventricular pseudoaneurysms discovered less than a week after inferior myocardial infarction. Both patients were middle-aged men with right coronary occlusion in whom the diagnoses were established by echocardiography during the first week after infarction. Because both patients were clinically stable, we opted to defer surgery until scarring could facilitate correction; this decision was based on a review of the literature showing that in-hospital mortality is higher with early surgery. The patients were monitored closely in the intensive care unit and were prescribed β-blockers and vasodilators. Both patients underwent left ventricular patch reconstruction with exclusion of the pseudoaneurysm and posterior septum; both received moderate inotropic support and prophylactic intra-aortic balloon pump assistance. Their postoperative courses were uneventful.
In 5 prior reports describing 45 patients (13 with acute pseudoaneurysm [≤2 wk after infarction] and 32 with nonacute pseudoaneurysm), in-hospital mortality was 61.5% for patients in the acute group and 15.6% for the nonacute group (P = .0066).
We recommend that clinicians consider deferring surgery for patients with stable acute left ventricular pseudoaneurysm to reduce the risks associated with early repair.
Left ventricular pseudoaneurysm (LVPA) is a rare condition; it is defined as a rupture of the free wall of the left ventricle that is contained by pericardial adhesions, epicardium, or both. Most frequently, the condition arises after acute myocardial infarction (AMI), but it can also be a complication of cardiac surgery, trauma, or infection.1 Postinfarction LVPA can be acute (<2 wk after AMI), subacute, or chronic (>3 mo after AMI).2 Because the condition is rare, knowledge of it is still incomplete. Most researchers recommend surgical treatment of LVPA, especially when it is discovered in the first 3 months after AMI, when it is symptomatic, and when it is expanding or large (>3 cm).2 In the era of routine echocardiographic monitoring of patients with AMI, early diagnosis of LVPA is more frequent; however, choosing the proper time for surgery in these patients poses a difficult dilemma. Surgeons must balance the risk of death from LVPA rupture with the risks of an emergency operation performed in the acute phase of a myocardial infarction (the latter, presumably, are similar to the risks associated with other mechanical complications of AMI).
Here, we describe our experience with 2 patients who had LVPA discovered within 1 week of an AMI. In both patients, we deferred surgery until at least 3 weeks after the AMI. We decided on this approach based on a review of the literature and an assessment of the early results of LVPA repair, focusing on the relationship between in-hospital mortality and time between infarction and surgery.
Patient 1 was a 54-year-old man who was referred to our institution 7 days after an inferior AMI with a partially thrombosed LVPA and a moderate pericardial effusion without signs of tamponade. Echocardiography showed an LVPA, measuring 5 × 3 cm, with the neck located between the mitral annulus and posterior papillary muscle. There was mild mitral regurgitation and good left ventricular ejection fraction (50%). Coronary angiography revealed an occlusion of the right coronary artery (RCA) and 70% stenosis of the left anterior descending artery. Because this patient was clinically stable, we chose to defer repair to allow scarring to strengthen the tissue and facilitate correction. He was monitored continuously in the intensive care unit, with clopidogrel discontinued and β-blockers and vasodilators added to his regimen.
At surgery, performed 4 weeks after the AMI, we performed pericardiolysis and then were able to visualize the LVPA surrounded by extensive pericardial adhesions (Fig. 1A). After aortic cross-clamping we opened the LVPA, extracted the thrombus, and reconstructed the left ventricle using a large Dacron patch (Fig. 1B). We also performed a left internal mammary artery bypass to the left anterior descending artery. The infarction had already been replaced by suture-facilitating fibrous tissue. Postoperative hemodynamics were stable under transient prophylactic balloon-pump assistance and moderate inotropic support. The patient was discharged on postoperative day 9 and was alive and well at the time of latest follow-up, 6 years after surgery.
Patient 2, a 48-year-old man, was referred to our institution 5 days after an inferior AMI for assessment of an RCA occlusion. Echocardiography showed a small posteroinferior LVPA measuring 2 × 3 cm. The left ventricular ejection fraction was 40%, and there was mild mitral regurgitation. Because he was clinically stable, we deferred surgical treatment. He was monitored closely, with 2 echocardiographic assessments per day. We discontinued clopidogrel to be ready for surgery at any moment, and prescribed β-blockers and vasodilators. Although the patient remained stable, serial echocardiography revealed progressive LVPA dilation. On the 21st day after his AMI, the LVPA reached a size of 3 × 4 cm, and surgery was indicated. At surgery, the LVPA wall consisted only of transparent, thin epicardium, with no adhesions (Fig. 2A). The infarcted tissue was friable, and scarification was incomplete. We performed a bovine pericardial patch reconstruction of the left ventricle, excluding the necrotic septum (Fig. 2B). The RCA was not suitable for grafting. Postoperatively, the patient required 2 days of prophylactic balloon-pump assistance and moderate inotropic support. He was discharged on postoperative day 10 and was alive and well at the time of latest follow-up, 2 years after surgery.
Because LVPA is rare, most reports describe only a single patient or a small case series; larger series usually combine patients with different causes of LVPA1–4 or with acute and chronic forms of postinfarction LVPA.5,6 Regarding the natural history of postinfarction LVPA, little can be added to the statement made by Treasure7 more than 2 decades ago: “All that can be said is that rupture is a risk, but its true frequency is unknown.” With conservative treatment, LVPA rupture is thought to occur in up to 45% of patients.1,8 The risk for rupture is highest in the first week after AMI and sharply decreases thereafter.1
By the time the diagnosis was confirmed and coagulation had normalized after clopidogrel withdrawal, both our patients were past the high-risk first week and were stable and only mildly symptomatic. Although the indication for surgery was clear, choosing when to operate presented a dilemma: should the patients undergo surgery immediately, or would it be better to wait and allow infarct healing to facilitate suturing, thus decreasing the surgical risk?
To answer this question, we reviewed the literature for early results of LVPA surgery. From the PubMed database, we selected reports that included at least 5 surgical patients with postinfarction LVPA (13 reports); 9 of these reports included acute LVPA, but only 5 included both surgical outcome and time from surgery to infarction. These 5 reports included 45 patients; 13 underwent surgery in the acute phase, defined as within 2 weeks after AMI (Table I).2,4–6,9–17 The in-hospital mortality rate after LVPA repair was significantly higher (61.5%) in patients who underwent surgery within 2 weeks of AMI than in patients who had later surgery (15.6%; χ2 test with Yates correction, P = .0066). We determined therefore that surgeons should consider delaying repair of acute LVPA in stable patients until adequate infarction healing has occurred; this healing facilitates repair and may reduce surgical risk. We noted in our patients that the myocardial tissue was much stronger in the repair performed 4 weeks after AMI than in the repair performed at 3 weeks.
Deferring surgery for LVPA discovered early after AMI does have some drawbacks. Fatal rupture remains a threat during the waiting period, and the cost of treatment may increase because this strategy requires a prolonged stay in the intensive care unit with close hemodynamic and echocardiographic monitoring (multiple exams per day) to detect any signs of impending rupture (eg, enlarging LVPA, growing pericardial collection). It is imperative that emergency cardiac surgery be available on site at all times.
In principle, aneurysmectomy is associated with concomitant revascularization of severely stenotic coronary arteries (including the culprit artery). In our patients, poor graftability prevented RCA revascularization. For Patient 1, we were able to surgically bypass a significantly stenosed left anterior descending artery without apparent effect on his postoperative course.
Our report describes only 2 patients, and the available literature on LVPA is limited. Because of nonuniform presentation of data, we were not able to adjust for patient characteristics during statistical analysis.
Because surgery during the acute phase of LVPA incurs a high mortality rate, surgeons should consider deferring repair for 3 to 4 weeks after AMI for patients who are in stable condition but have early discovery of an LVPA. Surgery should only be deferred if intensive monitoring can be implemented and cardiac surgery is available at all times. An LVPA registry would be helpful in establishing optimal management for early LVPA after AMI.
Conflict of Interest Disclosures: None