Correspondence *8-Bond Wing, St Michael's Hospital, 30 Bond Street, Toronto, ON M5B 1W8, Canada

Email latterd@smh.toronto.on.ca

The case

A 77-year-old man presented at a hospital with non-ST-segment elevation myocardial infarction, congestive heart failure and cardiogenic shock. In the coronary care unit, the patient was initially stabilized by diuresis with furosemide and afterload reduction with captopril. Echocardiography revealed moderate mitral regurgitation (MR), apical displacement of the papillary muscles, substantial tenting of the mitral valve leaflets and blunting of systolic flow in the pulmonary vein. A posterolateral pseudoaneurysm was also identified in the wall of the left ventricle (Figure 1 A–C). The patient had a left ventricular end-systolic dimension of 79.7 mm and an end-diastolic dimension of 88 mm. His left ventricular ejection fraction was 20–40% and his right ventricular systolic pressure was 42 mmHg (normal value 5–30 mmHg). Coronary angiography revealed triple vessel disease and complete occlusion of the left anterior descending artery and distal right coronary artery, a left ventricular end-diastolic pressure of 25 mmHg (normal value 5–8 mmHg), a large posterolateral aneurysm and moderate to severe MR.

Figure 1 Transesophageal echocardiograms of a 77-year-old man with a non-ST-segment elevation myocardial infarction, congestive heart failure and cardiogenic shock.

(A) Echocardiography revealed severe tenting of the mitral valve leaflets and lack of leaflet coaptation. The area of tenting can be defined as the region between the plane of the mitral annulus and the valve leaflets. This area increases with progressive apical displacement of the papillary muscles. (B) A large pseudoaneurysm is evident in the posterior wall of the left ventricle. There is free communication between the psuedoaneurysm and the cavity of the left ventricle. (C) Before repair of the pseudoaneurysm, severe regurgitation of flow is evident across the valve from the left ventricle to the left atrium during systole. LA, left atrium; LV, left ventricle; MA, plane of the mitral annulus; PA, psuedoaneurysm; PMVL, posterior mitral valve leaflet.

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Six months before hospital admission, the patient had experienced an episode of severe dyspnea, orthopnea and chest heaviness, which might have been the first signs of the inciting myocardial infarction that led to the formation of a pseudoaneurysm. After further diuretic treatment and medical stabilization, he underwent coronary artery bypass grafting and ventricular remodeling without mitral annuloplasty.

Median sternotomy and intrapericardial dissection were performed on the patient without complication. The posterior dissection was not completed until full cardiopulmonary bypass with the heart arrested and the aorta cross-clamp, to avoid embolization of intraventricular debris to the brain and body, were in place (Figure 2). An area (4 cm 8 cm) was resected from the pseudoaneurysm wall and a thrombus removed from the left ventricle. It was evident that the pseudoaneurysm had distorted the mitral valve apparatus and was the underlying cause of MR, since the posterior (ventricular) aspect of the mitral valve was visible from the annulus to the point of papillary muscle attachment (Figure 3). A 3 cm 6 cm bovine pericardial patch was applied to the resected area of the left ventricle, with remodeling of the ventricular chamber (Figure 4). The left internal thoracic artery and saphenous vein were used to bypass the left anterior descending artery and the circumflex artery; the distal right coronary artery could not be grafted because the vessel was too small.

Figure 2 Median sternotomy and pericardial dissection.

Anterior dissection was carried out in the plane between the pseudoaneurysm capsule and the edge of the pericardium. The location of the pseudoaneurysm in relation to the left anterior descending artery and first diagonal coronary artery is evident. D1, first diagonal coronary artery; LAD, left anterior descending artery; PAC, pseudoaneurysm capsule; PE, pericardial edge.

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Figure 3 An intraoperative view of the left ventricle.

After resection of the pseudoaneurysm capsule and removal of a large thrombus, the subvalvular apparatus could be seen. Scarring of the endocardium and base of the posteromedial papillary muscle was also evident. AMVL, anterial mitral valve leaflet; ES, endocardial scar; PAC, pseudoaneurysm capsule; PMPM, posteromedial papillary muscle; PMVL, posterior mitral valve leaflet.

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Figure 4 Repair of the resected pseudoaneurysm wall using a bovine pericardial patch.

Closure of the pseudoaneurysm capsule using a pericardial patch and Teflon^® (du Pont de Nemours and Company, Wilmington, DE) felt strip reduced the distance between the papillary muscles. PAC, pseudoaneurysm capsule; PP, pericadial patch; TFS, Teflon^® felt strip.

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Aortic cross-clamping time lasted 1 h 45 mins and cardiopulmonary bypass support for 1 h 55 mins in total. Myocardial protection was achieved with intermittent antegrade cold blood cardioplegia, and a terminal hot shot was delivered before removal of the aortic cross-clamp. After completion of the repair, the patient was weaned from cardiopulmonary bypass support with intravenous dopamine, epinephrine, norepinephrine and vasopressin.

Transesophageal echocardiography during and after surgery showed that tethering and tenting of the mitral valve leaflets had reduced with improved coaptation (Figure 5). The patient's left ventricular ejection fraction had increased to 40% and his MR had disappeared. Six months after surgery, the patient continues to do well clinically, without MR symptoms.

Figure 5 Transesophageal echocardiography after repair of the pseudoaneurysm.

This echocardiogram shows the absence of regurgitation after repair of the pseudoaneurysm. LA, left atrium; LV, left ventricle.

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Discussion of diagnosis

The mitral valve has a complex anatomy, and optimum function depends on synchronization of its components (i.e. the mitral valve leaflets, annulus, subvalvular apparatus and left ventricle). Chronic ischemic MR occurs when ventricular remodeling and dilatation after myocardial infarction lead to valve apparatus dysfunction. Annular dilatation in particular can increase the septolateral dimension, thereby reducing coaptation of the mitral valve leaflets. Displacement of the papillary muscles as the left ventricle dilates also causes valve tethering and tenting, which can reduce leaflet mobility and coaptation.¹

Left ventricular pseudoaneurysms are rare entities that can occur after myocardial infarction. Unlike true aneurysms, which are regions of dilated ventricle encompassing all the layers (i.e. the endocardium, myocardium and epicardium), ventricular pseudoaneurysms affect only the epicardium and are often contained by the serosal layer of the pericardium. These pseudoaneurysms occur most commonly after myocardial infarction, but can develop after mitral valve replacement surgery as a consequence of contained atrioventricular separation. Sometimes, ventricular pseudoaneurysms are associated with closure of a ventriculotomy and, in rare cases, they have been reported after infectious pericarditis or trauma.^{2, 3}

Enlargement of a pseudoaneurysm can lead to congestive heart failure by reducing forward ejection fractions and elevating end-diastolic pressure and ventricular volumes. Mitral valve dysfunction can also develop, causing MR and potentially heart failure. In the case described here, the patient presented with congestive heart failure, which is a typical presentation of a late ventricular pseudoaneurysm.

Left ventricular free wall rupture occurs in up to 6% of patients after MI. This complication is often fatal, usually as a result of acute hemopericardium and cardiac tamponade. Patients sometimes survive if the free wall rupture has been contained by the epicardium or by adhesions surrounding the site of rupture in the pericardial space. Although the exact cause of these adhesions is unknown, they are likely to form in the period following a transmural infarct and before the ventricular free wall rupture.

Treatment and management

Many surgical procedures have been used to relieve MR symptoms and most have focused on reconstruction of the mitral valve leaflets or annulus. Because ischemic MR is predominantly associated with left ventricle dysfunction, these approaches have led to recurrent ischemic MR and poor short-term and long-term patient outcomes.^{4, 5} Experimental work in laboratory models has shown that ventricular reshaping or altering the geometry of the subvalvular apparatus can substantially reduce MR associated with ischemic myocardial infarction.^{6, 7, 8}

In the case presented here, a bovine pericardial patch was used to reshape the left ventricular cavity and subvalvular mitral apparatus. A bovine patch was chosen because it has a smoother surface than other types of patch and might be associated with a reduced risk of thrombus formation.

The main concept behind this repair technique is that MR symptoms in patients with ischemic cardiomyopathy are caused primarily by defects in the left ventricle and papillary muscles, rather than in the annulus or valve leaflets. Application of the pericardial patch reduced the overall size of the left ventricle. As a result, the papillary muscles were also repositioned to an approximately normal location. Furthermore, by shortening the distance between the papillary muscles and the annulus, the degree of valve tethering was reduced, thereby increasing the surface area available for leaflet coaptation and decreasing valve regurgitation. Suture of fibrous tissue from the pseudoaneurysm wall over the pericardial patch also helped to remodel the left ventricle and achieve hemostasis.

Although surgical repair of ischemic MR by ventricular remodeling is a less reproducible operation than annular or leaflet-based approaches such as mitral valve replacement, it obviates the need for a separate atrial incision. This less-complicated procedure is likely to improve the patient's chance of survival by shortening the overall surgery time. In this case, the patient's ischemia was alleviated with coronary artery bypass surgery. Provided the grafts continue to function and the patient remains free of ischemia, he has a good prognosis.

Deciding whether or not to operate on a patient with a pseudoaneurysm following myocardial infarction depends on the timing and the mode of presentation. The patient described here was admitted to an intensive care unit with congestive heart failure and ongoing ischemia. Indications for surgery were triple vessel coronary disease, decreased ventricular function, congestive heart failure and severe MR. In general, patients with evidence of a pseudoaneurysm within 2 weeks of myocardial infarction should be operated on emergently. Since there is a risk of complications associated with surgical intervention, however, this might not be the best option for patients with chronic psuedoaneurysm of the left ventricle. Indications for surgery include congestive heart failure, an aneurysm with a diameter of greater than 3 cm and evidence of aneurysm expansion or rupture. In less severe cases, such as those associated with scarring after myocardial infarction or akinetic posterolateral ventricle, heart surgery can be avoided.⁹ A stable pseudoaneurysm less than 3 cm in diameter can be monitored using echocardiography and managed with medical therapy.^{10, 11}

After an initial assessment 1 month after being discharged from hospital, ventricular and valvular function of the patient in this case will be evaluated by echocardiography every 6 months. Continued absence of heart failure symptoms, preserved ventricular function and the absence of valvular regurgitation will establish the long-term success of this operation.

Conclusion

Although a rare clinical entity, left ventricular pseudoaneurysms can cause mitral valve dysfunction leading to MR and potential heart failure. In this case, MR symptoms were eliminated using a bovine pericardial patch to remodel the subvalvular apparatus and left ventricular components of the mitral valve, thereby avoiding reconstruction of the annulus or mitral valve leaflets.

References

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