Left Ventricular Pseudoaneurysm Found after Mitral Valve Replacement Performed 30 Years Earlier

ABSTRACT: Pseudoaneurysm of the left ventricle (LV) is a rare cardiac disease that occurs after myocardial infarction or cardiac surgery. Because patients frequently present with nonspecific symptoms, a high index of suspicion is needed to make the diagnosis. This report describes an unusual case demonstrating a large LV pseudoaneurysm after mitral valve replacement performed 30 years earlier. J INVASIVE CARDIOL 2010;22:E40–E41 Case Report. Pseudoaneurysm of the left ventricle (LV) is a rare cardiac disease that occurs after myocardial infarction or cardiac surgery. This report describes an unusual case demonstrating a large LV pseudoaneurysm after mitral valve replacement performed 30 years earlier. A 77-year-old female was admitted to the hospital for investigation of progressive dyspnea and chest pain which began 6 months earlier. She had a medical history of mitral valve replacement and tricuspid annuloplasty 30 years earlier at another hospital because of rheumatic valve disease. According to the medical chart obtained from that hospital, mitral valve replacement with a Björk number 22 prosthesis and tricuspid annuloplasty was carried out under cardiopulmonary bypass with transapical cannulation of the LV for arterial inflow. Her postoperative course was uneventful, and no infection was observed. She had been asymptomatic since surgery and routine studies were satisfactory during these years. However, 2 years earlier, she began to experience progressive dyspnea. The physical end blood tests were normal. Chest X-rays showed mild cardiomegaly. Transthoracic echocardiography (TTE) showed a mitral mechanical prosthesis with a normal gradient, mild tricuspid regurgitation, and progressive aortic stenosis with normal LV function and concentric remodeling of LV. Cardiac catheterization was performed prior to possible aortic valve replacement. Angiography revealed normal coronary arteries and moderate aortic stenosis was confirmed. Nevertheless, left ventriculography showed a large pseudoaneurysm of the inferior wall of the LV (Figure 1). No data on this large pseudoaneurysm were registered in previous studies after mitral valve replacement. A new TTE was achieved to detect a LV pseudoaneurysm of 36.7 mm x 40.3 mm, without apparent thrombus in the cavity, although the apex was not well visualized (Figure 2A). The LV end-diastole diameter (without pseudoaneurysm) was 52 mm, the LV end-systolic diameter (without pseudoaneurysm) was 28 mm and left atrium volume was above normal. Subsequently, 64 slice spiral computed tomography with intravenous contrast confirmed these findings (Figure 2B). The case was presented to the Cardiac Surgery Department. Due to the fact that the patient is asymptomatic, it was decided to pursue conservative management. Discussion. LV pseudoaneurysm is seen infrequently. It usually develops after myocardial infarction (MI) (particularly inferior wall MI). Furthermore, one-third of LV pseudoaneurysms result from cardiac surgery, most often mitral valve replacement (MVR). Spellberg and O’Reilly first reported a pseudoaneurysm after MVR that was diagnosed using left ventriculography.1 Karlson et al classified the rupture of the LV wall according to the timing of rupture. Early rupture is defined as occurring in the operating room any time after discontinuation of cardiopulmonary bypass. Delayed rupture occurs in the recovery room usually hours to days postoperatively. Late rupture occurs days to years after the valve replacement and presents as a pseudoaneurysm. In patients with late rupture, or in those with delayed rupture, a thin layer of heart wall — usually the epicardium with fibrosed pericardium — withstands the pressure load of the beating heart and escapes rupture.2 A wide variety of presentations for these structures has been reported such as embolic myocardial infarction, hemoptysis, compression of thoracic issues, etc. In addition, no specific symptoms of LV pseudoaneurysms have been described. Congestive heart failure, chest pain and dyspnea are the most frequently reported symptoms, but more than 10% of patients may be asymptomatic. Because patients frequently present with nonspecific symptoms, a high index of suspicion is needed to make the diagnosis. The diagnosis of a LV pseudoaneurysm is usually made by echocardiography and/or left ventriculography, but confirming the diagnosis can be difficult. A study by Hirose et al3 showed that 10% of LV aneurysms were diagnosed incidentally. Left ventriculography is the gold-standard tool which provides a definitive diagnosis in more than 85% of patients and is also useful in planning surgery. Transesophageal echocardiography can be an alternative method with a diagnostic accuracy of 75%.3 In contrast, diagnosis is often difficult with TTE, as in this case. In such a setting, cardiac magnetic resonance imaging and computed tomographic scanning could be considered an alternative, noninvasive modality for diagnosis. Although a pseudoaneurysm is asymptomatic when small, it usually grows rapidly and is prone to rupture. A large pseudoaneurysmal sac or its expansion can compromise the lumen of the circumflex artery and cause myocardial infarction. Other potential lethal complications of pseudoaneurysm include LV failure, thrombus embolization or rupture of the aneurysm and death. For appropriate candidates, for instance those with a pseudoaneurysm due to myocardial infarction and acute wall rupture, surgery is considered the treatment of choice. The principle of surgical treatment is closure of the ventricular wall defect. Direct closure or patch repair including ventriculoplasty of Dor are the most common surgical procedures reported, but several surgical approaches to its repair have been described in the literature. Although patients with LV pseudoaneurysms have high mortality rates regardless of treatment, prolonged survival has been observed even in some patients who do not undergo surgery. Regarding the mechanism of LV rupture in the present case, it is possible that a silent myocardial infarction of the inferior wall caused the pseudoaneurysm, but the patient’s coronary arteries were normal. It is reported that untethering of the LV occurs after MVR, and this promotes increased longitudinal stress in the LV. In this case, the cardiopulmonary bypass that performed in valve replacement surgery 30 years prior was performed with transapical cannulation of the LV for arterial inflow. This technique was first described by Zwart et al in 1950, and it was used in type A aortic dissections and sometimes in valve replacement. LV pseudoaneurysm has been described as a complication of this technique in some cases. Our case, therefore, highlights an unusual example of silent presentation of a large pseudoaneurysm due to transapical cannulation of the LV. Today, transapical cannulation has returned to be being used in transapical aortic valve replacement with the Edward-SAPIENS prosthesis. The present case serves to remind us that this entity could appear as a complication of these new techniques.

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From the Servicio de Cardiologia, Hospital Clinico Universitario, Zaragoza, Spain; and *Hospital Obispo Polanco, Teruel, Spain. The authors report no conflicts of interest regarding the content herein. Manuscript submitted April 1, 2009, provisional acceptance given May 18, 2009, final version accepted September 22, 2009. Address for correspondence: Dr. E. Castilla, Servicio de Cardiología, Hospital Clínico Universitario, Avda. San Juan Bosco, 15. 50009. Zaragoza. Spain. E-mail: elena_castilla@hotmail.com

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References

1. Spellberg RD, O’Belly RJ. Pseudoaneurysm of left ventricle following mitral valve replacement. Chest 1982;62:115–117. 2. Karlson KJ, Ashraf MM, Berger RL. Rupture of left ventricle following mitral valve replacement. Ann Thorac Surg 1965;46:590–597. 3. Hirose H, Matsunaga I, Strong M. Left Ventricular Pseudoaneurysm Found by CT Scan. The Open Cardiovascular Medicine Journal 2008;2:26–27.

1. Spellberg RD, O’Belly RJ. Pseudoaneurysm of left ventricle following mitral valve replacement. Chest 1982;62:115–117.