Ventricular Pseudoaneurysm Definition
A cardiac panel showed normal levels of troponin T and creatine kinase MB. An electrocardiogram (ECG) showed sinus rhythm. He then underwent cardiac catheterization due to refractory chest pain. The left anterior oblique view of the right coronary artery skull was negative for significant obstruction (Figure 1). A left anterior oblique caudal view of the left coronary artery also ruled out stenosis (Figure 2). Left ventriculography revealed no abnormalities in wall movement (Figure 3). Two months ago, the ischemic reassessment was completed. His 2-dimensional transthoracic echocardiography revealed normal basal to distal anterolateral and inferoseptal walls of the left ventricle (LV) without pocket or aneurysm (Figure 4). The short-axis parasternal view over the BT 2 months ago also showed normal walls (Figure 5). The pharmacological nuclear stress test before renal transplantation was also inconclusive for a perfusion defect in the insteroidal wall (Figure 6). Therefore, a plan was developed to repeat cardiac imaging and follow-up in a few weeks.
In this one, the 2-chamber apical view of transthoracic echocardiography showed a rupture or pseudoaneurysm included with a narrow neck of the basal wall of the inferoseptal LV (Figure 7). The short-axis parasternal view above the LV showed relaxation of the inferoseptal and lower walls (Figure 8). This is a new result compared to the deep cardiac imaging performed 2 months ago. Active surgical treatment of PVG with patch closure or primary occlusion is a highly recommended first choice, especially in patients with symptomatic and acute disease.3 PVL is thought to increase the risk of rupture to 48% when treated with medical treatment alone.19 Although few reports have shown 1 month of uneventful medical treatment, it is unclear whether surgical treatment should be performed for chronic PVL that are detected by chance.7 Post-IM LVPs benefit most from surgical occlusion of pseudoaneurysms if surgery is performed within 2 to 3 months of the episode.20 However, future research should aim to stratify the risks and indications of surgery in PVL patients. The preoperative diagnosis was a LV aneurysm. Therefore, the LV aneuryss was the intended operation. The patient was pretreated with ranitidine 150 mg tablet and Etizolam 0.5 mg tablet in the evening and morning of surgery. Anaesthesia was induced by injection midazolam 0.05 mg/kg, fentanyl injection 10 mcg/kg, etomidate injection 0.3 mg/kg and vecuronium injection 0.2 mg/kg. Standard monitoring techniques and transesophageal echocardiography (TEE) were used.
The intraoperative ET showed a large oval pouch (8.2 cm × 6.9 cm) of the posterolateral appearance of the LV, which communicated with the LV chamber through a passage of 2.7 cm [Figures [Figures 22 and 3].3]. VG function was good, but with hypokinesia in the side wall. The wall of the cystic cavity was akinetic. After cardiopulmonary bypass surgery and administration of cardioplegia, the cyst wall adhering to the pericardial cavity was dissected and opened [Figure 4]. The wall of the cystic cavity did not show myocardium. The redundant pseudoaneurysm was cut out and the defect was closed on the LV wall with promised Teflon. The duration of cardiopulmonary bypass surgery and aortic cross pliers was 108 and 74 minutes, respectively. Post-bypass TEE showed hypokinesia of the BT sidewall and good function of the BT. He was discharged from hospital under medical treatment in stable condition.
The patient was informed of vigilant monitoring of his condition and the importance of regular follow-up. At 6 months follow-up, repeated 2-dimensional transthoracic echocardiography ruled out pseudoaneurysm progression, as the lesion had the same dimensions. He sometimes experienced intermittent atypical chest pain, but was willing to undergo medical treatment on his own. Intraoperative image with the transmural hole of pseudoaneurysm Dor V, Saab M, Coste P, Kornaszewska M, Montiglio F: Left ventricular aneurysm: a new surgical approach. Thorac Cardiovasc Surg. 1989, 37: 11-19. 10.1055/S-2007-1013899. Medical treatment has always been advocated for patients with incidental signs of PVG and for patients at higher risk of morbidity and mortality after surgery.
More recently, the preference for pharmacotherapy has been emphasized for chronic GVPs, particularly lesions smaller than 3 mm.4,15 The primary goal of therapy is to reduce the enlargement of the pseudoaneurysm. In addition, reducing ventricular wall load by reducing afterload and reducing the risk of thromboembolism are important. Given the high rate of surgical mortality (23% in the systemic examination of 290 patients1 and 28% in a current case series of 30 patients6), critical decision-making is warranted given the advantages and disadvantages of a surgical approach. The exact pathogenesis of LVP has not yet been determined. These lesions usually occur when a small, weak portion of the heart wall, usually a transmural infarction, ruptures and, over a relatively long period of time, a narrow opening forms that connects the ventricular cavity to the potential space under the pericardium.9 Blood flows back and forth through the narrow opening and eventually accumulates under the roof of the pericardium or pericardial adhesions. Due to this accumulation, a bite occurs on the affected area. Since weak protrusion of the heart wall is also observed in true ventricular aneurysms and the clinical outcomes of these two pathologies are not specific, differentiation is a diagnostic challenge. In a series of cases, it has been shown that the location of a pseudoaneurysm is related to etiology. The most common site for the development of a pseudoaneurysm was the lower or posterolateral wall after MI (in 82% of MI patients).7 A pseudoaneurysm of the right ventricular flow pathways was observed in 87% of patients undergoing congenital heart surgery.7 All patients undergoing mitral valve and aortic valve replacement had the disease in the posterior subannular region of the mitral valve and region subaortic. 7,9 The patient in the present study had none of these abnormalities.
Since the formation of a pseudoaneurysm occurred without prior MI (normal coronary angiography), we assume that it was caused by an indolent infection after the start of immunosuppressive therapy after transplantation, which was suppressed by antibiotics. This infection led to a delay in the formation of a pseudoaneurysm, which caused chest pain, which our patient had initially imagined with. Bolooki H, DeMarchena E, Mallon SM, Katariya K, Barron M, Bolooki HM, Thurer RJ, Novak S, Duncan RC: factors influencing late survival after surgical remodeling of the left ventricular aneurysm. J Thorac Cardiovasc Surg. 2003, 126 (2): 374-85. 10.1016/S0022-5223(03)00023-0. MRI usually shows a dyskinetic segment with a focal bulge of the pericardium. Mural thrombus is also commonly observed. In some cases, delayed intensification of pseudoaneurysm may be observed 4. Ando S, Kadokami T, Momii H, Hironaga K, Kawamura N, Fukuiama T, Minato M: False pseudo- and left ventricular pseudoaneurysm: serial observations using cardiac magnetic resonance imaging.