The International Journal of Cardiovascular Imaging (2006) 22: 205–212 DOI 10.1007/s10554-005-9013-3

Ó Springer 2005

Case Report

A giant inferoposterior true aneurysm of the left ventricle mimicking a pseudoaneurysm Oguz Yavuzgil1, Cemil Gu¨rgu¨n1, Anıl Apaydın2, Cahide Soydas C¸ınar1, Alper Yu¨ksel3 & Hakan Ku¨ltu¨rsay1 1

Ege University Medical Faculty, Department of Cardiology, Bornova, Izmir, Turkey; 2Ege University Medical Faculty, Department of Cardiovascular Surgery, Bornova, Izmir, Turkey; 3Kent Hospital, Department of Radiology, Cigli, Izmir, Turkey

Received 19 May 2005; accepted in revised form 25 June 2005

Key words:

coronary arteriosclerosis, myocardial infarction, heart aneurysm

Abstract A left ventricular aneurysm (LVA) is most commonly the result of myocardial infarction, usually involving the anterior wall. A left ventricular pseudoaneurysm (LVPSA) or false aneurysm forms when cardiac rupture is contained by adherent pericardium or scar tissue. The accurate diagnosis, although difficult to establish, is an important one to make because these aneurysms are prone to rupture. In this article, we report a challenging case of a cardiac aneurysm a year after a coronary bypass operation which could not be definitively diagnosed despite of imaging with different techniques including echocardiography, coronary angiography, left ventriculography and magnetic resonance imaging (MRI). The patient underwent a second cardiac surgery, the aneurysm was resected, the mitral valve was replaced and the defect in the ventricular wall was repaired. Because of the combined diagnostic capabilities like detailed and functional pathoanatomy and aneurysmal wall characterization, MRI seems to have multiple advantages in differential diagnosis. Introduction Left ventricular pseudoaneurysm (LVPSA) occurs when a rupture of the ventricular free wall is contained by overlying, adherent pericardium after a myocardial infarction. In contrast a true postinfarction left ventricular aneurysm (LVA) is caused by scar formation resulting in thinning of the infarcted myocardium [1]. In contrast to LVPSAs, only about 4% of true LVAs are located at the posterolateral or diaphragmatic surface [2]. The diagnosis, although difficult to establish, is an important one to make because these aneurysms

are prone to rupture [3]. In this article, we report an case of true inferoposterior LVA mimicking a LVPSA which was diagnosed during surgery despite of various imaging modalities including echocardiography, venticulography and magnetic resonance imaging (MRI). Case report A 75-year-old male patient with a history of coronary artery disease presented with symptoms of progressive palpitation and abdominal pain for 3 months. He had an history of inferior myocardial

206 infarction 1 year ago and had been given streptokinase on the 7th hour but because of the postinfarction angina, a coronary angiography had been performed on his 10th day. Because of severe 3vessel disease, left anterior descending (LAD), first diagonal (D) branch and first obtuse marginal (OM) branch had been grafted with three saphenous vein grafts on the 17th day after infarction. Left internal mammarian artery could not be used because of its weak flow and posterior descending artery could not be bypassed because of the lack of a graftable lumen. He had been discharged and did well for 9 months after surgery. On this second admission, nearly a year after CABG, his physical examination showed a moderate cachexia, signs of decompansated heart failure and tachycardia. ECG showed an atrial flutter with an 2:1 block, Q waves and ST elevations in inferior leads. On telecardiogram his cardiothorasic index was increased and there were significant signs of congestive heart failure. There was a prominent bulging of the left heart border in chest X-ray suggesting a large cardiac aneurysm. Transthorasic echocardiogram (TTE) revealed a huge inferoposterior left ventricular (LV) aneurysm with a narrow neck and an organized thrombus (Figure 1a and b), severe mitral regurgitation on color flow Doppler mapping (the maximal jet area was 11.6 cm2 and maximal jet area/left atrial area was 67%), and moderate LV systolic dysfunction with an ejection fraction of 40%. Diameters of the aneurysm were 9.26.5 cm and the neck was 4.4 cm. A cardiac smoke was seen in the aneurysmal sac and the color Doppler evaluation revealed the presence of bidirectional flow. Both 2-D and 3-D TTE images were suggesting a huge LVPSA. Abdominal ultrasound examination showed aneurysmatic dilatations of the abdominal aorta in both suprarenal and infrarenal segments with a maximum diameter of 4 cm. Coronary angiogram revealed patent bypass grafts with multivessel disease and a large inferoposterobasal LV aneurysm. Any part of the coronary arteries could not be demonstrated over the aneurysmal sac but this finding was not so useful for the differential diagnosis because the distal part of the right coronary artery could not be visible even in the first angiogram which had been done a year

ago. Presurgical evaluation with MRI measured the dimensions of cardiac aneurysm as 9.76.710.87.4 cm (Figure 2a and b). MRI could be able to measure the size of the neck more reliably which was larger then measured in TTE (4.67.4 cm). There was no epicardial fat at the orifice of the aneurysm. After IV administration of the gadopentate dimeglumine, delayed enhancement of the myocardium showed the thin scar tissue in the aneurysmal wall suggesting a true LVA (Figure 2b). But even after the full cardiac MRI investigation the definitive diagnosis was not possible. MRI of the aorta was consistent with the ultrasound findings and conservative treatment was decided. The patient underwent a second cardiac surgery with a possible diagnosis of cardiac pseudoaneurysm under the transesophageal echocardiography (TEE) guidance. TEE images were consistent with other imaging techniques and confirmed severe mitral regurgitation which seemed to have an unsuitable anatomy for the valve repair. After the exploration of the heart, a true inferoposterior LV aneurysm was diagnosed. There were no pericardial adhesions or hematoma. The aneurysm was resected, the mitral valve was replaced and the defect in the ventricular wall was closed by using a dacron patch. Intraoperative and pathologic examination revealed that it was a true LVA (Figure 3a and b). The patient was symptom free at the 4th month of follow-up. Discussion A LVA is most commonly the result of myocardial infarction, usually involving the anterior wall. It may be asymptomatic, but can be the cause of heart failure, sustained ventricular tachyarrhythmias, and arterial embolism. Although the exact definition of a LVA remains controversial, generally a true LVA is defined as a well delineated, thin, scarred or fibrotic wall, devoid of muscle or containing necrotic muscle, that is a result of a healed transmural myocardial infarction (MI). The involved wall segment is either akinetic or dyskinetic during systole, and collapses inwards when the ventricle is fully vented during surgery. It was previously estimated that LVA develops in up to

207

Figure 1. (a) Modified apical 4 chamber view of 2-D transthorasic echocardiography shows the large posterolateral LV aneurysm (A). Arrows indicates the thrombus. (b) Modified long axis view of live 3-D transthorasic echocardiography (Philips, SONOS 7500) shows the large posterolateral LV aneurysm (A). T: thrombus, (*): papillary muscles.

30–35% of patients with Q wave MI [4, 5]. However, the incidence of this complication is clearly decreasing, and currently it occurs in about 8–15% of patients [6] which is related to the introduction of major improvements in the management of

patients with acute MI like the use of thrombolytic agents and/or angioplasty to produce an open ‘culprit’ vessel, and the administration of afterload reducing agents [4, 5, 7]. Most of LVAs are located in the anterior or apical walls, a result of total

208

Figure 2. (a) The 2 chamber view of cine-MRI shows the large inferoposterolateral LV aneurysm (A). LV: left ventricle, LA: left atrium, T:thrombus. (b) Basal short axis view of cine-MRI. The hyper-enhancement of gadolinium (arrows), 15 min after injection, was consistent with previously infarcted areas and scar tissue in the aneurysmal wall. A: aneurysm, T: thrombus , LV: left ventricle, RV: right ventricle.

209

Figure 3. Intraoperative view of the aneurysm before (a) and after (b) the incision. LV: left ventricle, A: aneurysm, T: thrombus, Arrows: aneurysmal wall.

occlusion of the LAD coronary artery and the absence of collateralization [8–11]. Only 10–15% involve the inferior-basal walls due to right coronary artery occlusion. Lateral LVA secondary to left circumflex occlusion is exceedingly rare.

A LVPSA or false aneurysm forms when cardiac rupture is contained by adherent pericardium or scar tissue [1]. Unlike a true aneurysm, it contains no endocardium or myocardium. The diagnosis, although difficult to establish, is an important one

210 to make because these aneurysms are prone to rupture [2]. Most of them are related to a MI, particularly of the inferior wall which is twice as common as anterior infarction [12]. This is in contrast to true aneurysms which more commonly involve the anterior wall with only 10–15% located in the inferior wall. Previous cardiac surgery, most often mitral valve replacement, accounts for one-third of cases of LVPSA [12, 13]. Heart failure, chest pain, and dyspnea, are the most frequent symptoms similar and sudden death is the presenting symptom in about 3% of patients [12]. Approximately 10% of patients are asymptomatic. Murmurs, ECG changes, including ST segment elevation and evidence of a mass on chest X-ray are often like in our patient. Transthoracic echocardiogram is a reasonable first step, but a definitive diagnosis is made in only 26% of patients [13]. Echocardiography can usually distinguish a LVPSA from a true LVA by the appearance of the connection between the aneurysm and ventricular cavity. Only small ruptures of the ventricular wall are compatible with survival. As a result, LVPSAs have a narrow neck, typically less than 40% of the maximal aneurysm diameter, that causes an abrupt interruption in the ventricular wall contour. In contrast, true LVAs are nearly as wide at the neck as they are at the apex. Catherwood et al., using 2-D TTE, compared findings in five patients with LVPSA to a control group with true aneurysm [14]. TTE demonstrated a globular pseudoaneurysmal cavity in four of the five patients, with clot within the cavity in three of these four. In all four, the orifice of the pseudoaneurysmal cavity could be seen as a distinct discontinuity in the ventricular wall. Based on echocardiographic results, the mean ratio of orifice to cavity diameter was 0.37 for LVPSAs and 1.0 for LVAs, and the ratio of orifice to cavity perimeter was 0.17 for LVPSAs and 0.48 for LVAs. In another echocardiographic series, Gatewood and Nanda showed that the ratio of the maximum diameter of the orifice to the maximum internal diameter of the cavity had a ratio of 0.25– 0.50 for LVPSAs, while the range was 0.90–1.0 ratios for true LVAs [15] . The presence of turbulent flow by pulsed Doppler at the neck of a cavity or within the cavity itself suggests a LVPSA

[16]. Roelandt et al. described the presence of bidirectional color flow Doppler between an extracardiac echo-free space and the left ventricle that allowed distinction between a simple pericardial effusion and a LVPSA [17]. Sutherland et al. reported a series of cases in which color Doppler imaging was superior to both pulsed and continuous wave Doppler in detecting flow into a LVPSA [18]. It seems likely that the turbulence and size of a jet in the presence of a pseudoaneurysm would be quite different from the flow seen with a true aneurysm, but this distinction has not been confirmed. Three-dimensional TTE is also a new method for both imaging the ventricular geometry and measuring the ventricular volumes using a rotational approach in left ventricular aneurysms [19]. TEE is another safely applicable test that is ideal for use in the ICU or in the operation in the evaluation of the mechanical complications of myocardial infarction. A small number of cases have been described in which TEE provided more accurate information than TTE in the evaluation of posterior LVPSAs [20, 21]. One of the most reliable method for diagnosis of a LVPSA is coronary angiography and ventriculography which demonstrates a narrow orifice leading to a saccular aneurysm and the lack of surrounding coronary arteries [22]. In our case, ventriculography could not provide an accurate information about the aneurysmal wall and the lack of surrounding coronary arteries was not useful for the diagnosis because of the occluded posterior descending artery. Magnetic resonance imaging is another alternative for diagnosing a pseudoaneurysm. MRI can clearly localize the site of the aneurysm [23]. Additional advantages include the capability to distinguish between pericardium, thrombus, and myocardium, which are not easily distinguished by ventriculography. Viability MRI of the myocardium uses a delayed contrast-enhanced imaging technique to accurately delineate the infarct size and its extent. In the case of a true aneurysm, the tissue making up the wall of the aneurysm will show delayed enhancement, indicating scar tissue as a result of infarcted myocardium. Because the wall of the LVPSA is

211 composed only of pericardium, it does not show delayed enhancement in the sac; however, the border of the aneurysm will show enhancement, indicating a perianeurysmal infarcted area [24]. Enhancement of the pericardium related to a LVPSA has not been previously reported. However even the delayed enhancement of the myocardium is not specific for a myocardial scar. For example, tumors and inflammatory disease have also been reported to show delayed myocardial enhancement [24]. Loss of epicardial fat at the orifice of the LVPSA may be seen, but distinction from a true LVA may be difficult [25, 26]. Cine MRI may provide additional diagnostic help as blood flow turbulence in the cardiac chambers is a hemodynamic feature of LVPSA. In this case, MRI helped us for the measurement of the aneurysmal sac from different views and revealed that a larger neck then it was seen in TTE. Because of the different diameters from different views in MRI we thought that the ratios of orifice to cavity diameter or perimeter were not useful for differential diagnosis in any imaging modality in a case like this. There was no epicardial fat at the orifice of the aneurysm suggesting a LVPSA but cine images were consistent with a true LVA. Additionally viability MRI of the myocardium showed the scar tissue as a result of infarcted myocardial muscle. We thought that this was the most important clue for the accurate diagnosis. In summary, we present a case of giant true inferoposterior LVA mimicking a LVPSA that demonstrates the difficulties of an accurate diagnosis with using the conventional imaging techniques. This case report emphasizes the role of cardiac MRI for improving confidence in the differential diagnosis of cardiac aneurysms.

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