CASE REPORT
A iant pseudoaneurysm becoming apparent after cardiac resynchronisation therapy
M. Scheffer, B.M. van Gelder, R. van Mechelen z
A 57-year-old male patient with coronary artery disease developed a pseudoaneurysm after an inferior infarct in 1997. He underwent coronary bypass surgery and retion of the pseudoaneurysm located at the inferior wall. Unfortunately, the pseudoaneurysm recurred due to dehiscence of the patch, necessitating a second surgical intervention. After six years he developed progressive heart failure due to severe left ventricular dysfimction. He was referred to our institution for cardiac resynchronisation therapy (CRT) because of drug refractory heart failure which was associated with a left bundle branch block, ejection fraction of 12%, and a NYHA class IV status. After successful implantation of a biventricular pacemaker, a remarkable clinical recovery was observed. Left ventricular function improved and echocardiography now demonstrated that the pseudoaneurysm at the inferior wall had recurred for the third time. This diagnosis could not be established by preoperative
echocardiography. (NethHeartJ2005;13:366-9.) Key words: cardiac resynchronisation therapy, coronary artery disease, pseudoaneurysm
Lft ventricular pseudoaneurysm is a very rare omplication of acute myocardial infarction in which a free wall rupture is contained by overlying adherent pericardium or scar tissue.' Other causes are cardiac surgery, trauma and infection.2 M. Scheffer
Department of Cardiology, R,jnmond-Zuid Medical Centre, Rotterdam B.M. van Gelder Department of Cardiology, Catharina Hospital, Eindhoven R. van Mechelen Department of Cardiology, St. Franciscus Hospital, Rotterdam Correspondence to: M. Scheffer Department of Cardiology, MCRZ, location St. Clara Hospital, Olympiaweg 350, 3068 HT Rotterdam E-mail: [email protected]
366
The first report describing this phenomenon was from Corvisart in 1797.3 Since then the literature is composed of case reports or small series which makes the natural history and the risk for rupture unknown; even a large review of 290 patients was unable to determine the best therapeutic strategy.4 The most frequently reported symptom is heart failure, but over 10% of patients with a pseudoaneurysm are asymptomatic.' Cardiac resynchronisation is a new option in the treatment of patients with severe heart failure on top of optimal medical therapy.67 In this manuscript we describe a patient in whom a biventricular pacemaker was implanted because of severe heart failure after two operations for a pseudoaneurysm. Only after initiation of resynchronisation therapy did a huge pseudoaneurysm become apparent by transthoracic echocardiography. This diagnosis ofpseudoaneurysm could not be made by preoperative echocardiography. Case report A 57-year-old male had an inferior myocardial infarction in 1997 with rupture of the left ventricular wall and formation of a left ventricular pseudoaneurysm at the inferior wall. He underwent aortocoronary saphenous vein bypass grafting to the obtuse marginal artery and the left internal mammary artery was used for revascularisation of a large anterolateral branch. The pseudoaneurysm was resected and repaired with a Gelseal patch. Six months later the pseudoaneurysm recurred due to dehiscence of the Gelseal patch and a surgical redo was performed. After this operation the patient was free of symptoms until 2003 when he developed progressive dyspnoea and was admitted with severe left heart failure due to left ventricular dys-
function. Echocardiography revealed an ejection fraction of 12% and global hypokinesia to akinesia of all left ventricular walls with dyskinesia of the inferior wall with adjacent thrombus. The left ventricular enddiastolic dimension measured 105 mm, and the endsystolic dimension was 95 mm. Doppler echocardiography showed an aortic velocity time integral (VTI Ao) of 12.8 cm and minimal mitral regurgitation. Right ventricular pressure measured by tricuspid Nedherlands Heart Journal, Volume 13, Number 10, October 2005
A giant pseudoaneurysm becoming apparent after cardiac resynchronisation therapy
Figure 1. Preimplantation transthoracal echocardiogram. Parasternal long-axis view of the left ventricle. LV=left ventricle, LA=left atrium, PA=pseudoaneurysm; AO=aorta, IVS=interventricular septum, amvl, pmvl=anterior and posterior mitral valve leaflet.
insufficiency was normal. Tissue Doppler myocardial imaging, tissue tracking and strain all showed asynchrony of the lateral ventricular wall. Despite optimal medical therapy, the patient was refractory to treatment resulting in NYHA class IV. The electrocardiogram showed sinus rhythm with a left bundle branch block. The LV ejection fraction was 12%.7 Echocardiography demonstrated LV asynchrony. Subsequently, cardiac resynchronisation therapy was initiated. The right ventricular lead was positioned in the right ventricular outflow tract and the left ventricular lead in a posterior tributary ofthe coronary sinus at the apical level of the left ventricle. Because the patient's history revealed paroxysmal atrial fibrillation, the atrial lead was implanted in the low interatrial septum above the coronary sinus ostium. A satisfactory threshold for pacing and sensing was achieved for all leads. A Medtronic 8042 Insync III pacemaker was used, with programmable AV and interventricular (V-V) delays. One day after implantation a remarkable clinical improvement was observed employing the standard setting ofthe pacemaker. Subsequently tissue tracking and strain imaging was used for further optimisation ofthe AV and V-V intervals, according to the method described by Sogaard et al.8 After optimisation the echocardiogram showed improved left ventricular function and, surprisingly, due to enhanced contraction of the apical region of the inferior and posterior walls a clear huge pseudoaneurysm of the infero-postero-basal wall was visualised (figures 1 and 2). Through a large hole in the inferior wall, spontaneous contrast again opacified the pseudoaneurysm. A thick layer of thrombus formation was present at the wall of the aneurysm. Doppler echocardiography showed no mitral regurgitation and the VTI Ao was raised to 21.5 cm.
Netherlands Heart Journal, Volume 13, Number 10, October 2005
Figure 2. Transoesophageal echocardiogram of the left ventricle (LV), left atrium (LA) and a giant pseudoaneurysm (PA), showing spontaneous contrast (arrow).
Left ventricular angiography confirmed the presence of a giant pseudoaneurysm (figure 3), with a good residual left ventricular function without mitral regurgitation. Coronary angiography revealed a normal right coronary artery, occluded left circumflex artery, which was distally filled from the aortosapheneous vein graft. The left anterior descending artery showed a severe stenosis but good distal filling from the left internal mammary artery. To make a better delineation of the pseudoaneurysm and its surroundings after two surgical procedures a multislice
Figure 3. Left ventricular (LV) angiography, RAO view showing agiantpseudoaneurysm (PA) located at the inferior wall.
367
A giant pseudoaneurysm becoming apparent after cardiac resynchronisation therapy
Figure 4. Multislice CTpicture ofthe left ventricle (LV) with the giant pseudoaeurysm (PA).
CT scan was performed (figure 4), with 3D reconstruction (figure 5). Subsequently, the patient was referred for cardiac surgery to repair the pseudoaneurysm.
Discussion Cardiac rupture of the free wall of the left ventricle may be a fatal complication of myocardial infarction, occurring in approximately 4 to 23% of patients with acute myocardial infarction.9 In the majority of cases it is associated with sudden cardiac death due to haemopericardium and cardiac tamponade.10 Occasionally, cardiac rupture may be confined by a portion of pericardium or scar tissue leading to the formation of a pseudoaneurysm. Pseudoaneurysms do not contain endocardium or myocardium tissue as a true left ventricular aneurysm does, and are prone to rupture.1' Other complications are congestive heart failure, embolic events or arrhythmias.'2 Patients with left ventricular pseudoaneurysm usually present with symptoms of chest pain, dyspnoea and heart failure, which are also common in patients with coronary heart disease, making a differential diagnosis complicated. Over 10% of the patients with pseudoaneurysm are asymptomatic or have nonspecific symptoms leading to incidental findings on imaging tests.4 For an accurate diagnosis and proper surgical strategy noninvasive techniques such as transthoracic echocardiography, colour Doppler imaging or transoesophageal echocardiography, multislice CT or MRI must be performed.13-15
368
Figure 5. 3D reconstruction of the left ventricle (LV) and the pseudoaneurysm (PA) located inferior of the heart. The dimensions of the pseudoaneurysm exceed those ofthe left ventricle.
In this particular case, the patient was referred for implantation of a biventricular pacemaker, because he fulfilled all criteria for CRT.7 Echocardiography preimplant showed a severely dilated almost noncontracting left ventricle. After CRT, echocardiography showed improvement in contraction of the anterior and septal wall and inferoposteroapical region of the left ventricle. Due to the increase in contractility ofthe left ventricle, spontaneous contrast visualised a large hole located at the inferior wall. What seemed to be a very large and dilated left ventricle with dyskinesia of the inferior wall before CRT, appeared to be a normal left ventricle qua dimension, with a giant pseudoaneurysm situated at the inferoposterior wall after initialising CRT. Although CRT is not the therapeutic treatment of choice in patients with a pseudoaneurysm, in this case it led to the discovery of the third recurrence of the pseudoaneurysm. CRT initiated a remarkable clinical recovery in this patient, which made him suitable for resection of this pseudoaneurysm, because of its propensity to rupture. Conclusion A pseudoaneurysm may be difficult to diagnose by transthoracic echocardiography when there is poor contractile function of the residual part of the left ventricle. Diagnostic techniques as multislice CT or MRI should be considered in those patients with extremely large left ventricles showing akinetic regions with transthoracic echocardiography.
Netherlands Heart Journal, Volume 13, Number 10, October 2005
pc
A giant pseudoaneurysm becoming apparent after cardiac resynchronisation therapy
CRT, however, can be considered in patients with pseudoaneurysm and a poor residual left ventricular function with asynchrony fulfilling all other selection criteria for CRT. Application of CRT may lead to clinical improvement, thus facilitating the option of surgical repair of the pseudoaneurysm.c References 1 2
3 4
5 6 7
Roberts WC, Morrow AG. Pseudo aneurysm of the left ventricle: an unusual sequel of myocardial infarction and rupture of the heart. Am JMed 1967;43:639-44. Stewart S, Huddle R, Stuard I, Schreiner BF, DeWeese JA. False aneurysm and pseudo-false aneurysm ofthe left ventricle: etiology, pathology, diagnosis and operative management. Ann Thorac Surg 1981;31:259-65. Corvisart JN. An essay on the organic diseases and lesions of the heart and great vessels (translated by Gates J). Boston: Bradford & Read, 1812. Frances C, Romero A, Grady D. Left ventricular pseudo aneurysm. JAm Coll Cardiol 1988;32:557-61. Brown SL, Gropler RJ, Harris KM. Distinguishing left ventricular aneurysm from pseudoaneurysm. A review ofthe literature. Chest 1997;111:1403-9. Cazeau S, Leclercq C, Lavergne T, et al. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. NEnglJMed 2001;344:873-80. Abraham WT, Fisher WG, Smith AL, et al. MIRACLE Study Group. Multicenter Insync Randomized Clinical Evaluation. Cardiac resynchronization in chronic heart failure. NEnglJMed
8
9 10 11
12
13 14
15
Sogaard P, Egleblad H, Pederson AK, et al. Sequential versus simultaneous biventricular resynchronisation for severe heart failure: evaluation by tissue Doppler imaging. Circulation 2002; 106:2078-84. Pollak H, Nobis H, Miczoch J. Frequency of left ventricular wall rupture complicating acute myocardial infarction since the advent of thrombolysis. AmjCardiol 1994;74:184-6. Bates RJ, Beutler S, Resnekov L. Cardiac rupture challenge in diagnosis and management. Am J Cardiol 1977;40:429-37. March KL, Sawada SG, Tarver KA, Kesler KA, Armstrong WF. Current concepts of left ventricular pseudo aneurysm: pathophysiology, therapy and diagnostic imaging methods. Clin Cardiol 1989;12:531-40. Moreno R, Gordillo E, Zamorano J, Garcia-Rubira JC, FernandezOrtiz A, Macaya C. Long term outcome of patients with postinfarction left ventricular pseudo aneurysm. Heart2003;89:11446. Sutherland GR, Smyllie JH, Roelandt JR. Advantages ofcolor flow imaging in the diagnosis of left ventricular pseudoaneurysm. Br HeartJ 1989;61:59-64. Burns CA, Paulsen W, Arrowood JA. Improved identification of posterior left ventricular pseudo aneurysm by transoesophageal echocardiography. Am HeartJ 1992;124:796-9. Duvernoy 0, Wikstrom G, Mannting F, Larsson SG, Andren B, Dubiel T. Pre- and postoperative CT and MRin pseudo aneurysms of the heart. JComputAssist Tomogr 1992;16:401-9.
2002;346:1845-53.
IC
Netherlands Heart Journal, Volume 13, Number 10, October 2005
369
A iant pseudoaneurysm becoming apparent after cardiac resynchronisation therapy
M. Scheffer, B.M. van Gelder, R. van Mechelen z
A 57-year-old male patient with coronary artery disease developed a pseudoaneurysm after an inferior infarct in 1997. He underwent coronary bypass surgery and retion of the pseudoaneurysm located at the inferior wall. Unfortunately, the pseudoaneurysm recurred due to dehiscence of the patch, necessitating a second surgical intervention. After six years he developed progressive heart failure due to severe left ventricular dysfimction. He was referred to our institution for cardiac resynchronisation therapy (CRT) because of drug refractory heart failure which was associated with a left bundle branch block, ejection fraction of 12%, and a NYHA class IV status. After successful implantation of a biventricular pacemaker, a remarkable clinical recovery was observed. Left ventricular function improved and echocardiography now demonstrated that the pseudoaneurysm at the inferior wall had recurred for the third time. This diagnosis could not be established by preoperative
echocardiography. (NethHeartJ2005;13:366-9.) Key words: cardiac resynchronisation therapy, coronary artery disease, pseudoaneurysm
Lft ventricular pseudoaneurysm is a very rare omplication of acute myocardial infarction in which a free wall rupture is contained by overlying adherent pericardium or scar tissue.' Other causes are cardiac surgery, trauma and infection.2 M. Scheffer
Department of Cardiology, R,jnmond-Zuid Medical Centre, Rotterdam B.M. van Gelder Department of Cardiology, Catharina Hospital, Eindhoven R. van Mechelen Department of Cardiology, St. Franciscus Hospital, Rotterdam Correspondence to: M. Scheffer Department of Cardiology, MCRZ, location St. Clara Hospital, Olympiaweg 350, 3068 HT Rotterdam E-mail: [email protected]
366
The first report describing this phenomenon was from Corvisart in 1797.3 Since then the literature is composed of case reports or small series which makes the natural history and the risk for rupture unknown; even a large review of 290 patients was unable to determine the best therapeutic strategy.4 The most frequently reported symptom is heart failure, but over 10% of patients with a pseudoaneurysm are asymptomatic.' Cardiac resynchronisation is a new option in the treatment of patients with severe heart failure on top of optimal medical therapy.67 In this manuscript we describe a patient in whom a biventricular pacemaker was implanted because of severe heart failure after two operations for a pseudoaneurysm. Only after initiation of resynchronisation therapy did a huge pseudoaneurysm become apparent by transthoracic echocardiography. This diagnosis ofpseudoaneurysm could not be made by preoperative echocardiography. Case report A 57-year-old male had an inferior myocardial infarction in 1997 with rupture of the left ventricular wall and formation of a left ventricular pseudoaneurysm at the inferior wall. He underwent aortocoronary saphenous vein bypass grafting to the obtuse marginal artery and the left internal mammary artery was used for revascularisation of a large anterolateral branch. The pseudoaneurysm was resected and repaired with a Gelseal patch. Six months later the pseudoaneurysm recurred due to dehiscence of the Gelseal patch and a surgical redo was performed. After this operation the patient was free of symptoms until 2003 when he developed progressive dyspnoea and was admitted with severe left heart failure due to left ventricular dys-
function. Echocardiography revealed an ejection fraction of 12% and global hypokinesia to akinesia of all left ventricular walls with dyskinesia of the inferior wall with adjacent thrombus. The left ventricular enddiastolic dimension measured 105 mm, and the endsystolic dimension was 95 mm. Doppler echocardiography showed an aortic velocity time integral (VTI Ao) of 12.8 cm and minimal mitral regurgitation. Right ventricular pressure measured by tricuspid Nedherlands Heart Journal, Volume 13, Number 10, October 2005
A giant pseudoaneurysm becoming apparent after cardiac resynchronisation therapy
Figure 1. Preimplantation transthoracal echocardiogram. Parasternal long-axis view of the left ventricle. LV=left ventricle, LA=left atrium, PA=pseudoaneurysm; AO=aorta, IVS=interventricular septum, amvl, pmvl=anterior and posterior mitral valve leaflet.
insufficiency was normal. Tissue Doppler myocardial imaging, tissue tracking and strain all showed asynchrony of the lateral ventricular wall. Despite optimal medical therapy, the patient was refractory to treatment resulting in NYHA class IV. The electrocardiogram showed sinus rhythm with a left bundle branch block. The LV ejection fraction was 12%.7 Echocardiography demonstrated LV asynchrony. Subsequently, cardiac resynchronisation therapy was initiated. The right ventricular lead was positioned in the right ventricular outflow tract and the left ventricular lead in a posterior tributary ofthe coronary sinus at the apical level of the left ventricle. Because the patient's history revealed paroxysmal atrial fibrillation, the atrial lead was implanted in the low interatrial septum above the coronary sinus ostium. A satisfactory threshold for pacing and sensing was achieved for all leads. A Medtronic 8042 Insync III pacemaker was used, with programmable AV and interventricular (V-V) delays. One day after implantation a remarkable clinical improvement was observed employing the standard setting ofthe pacemaker. Subsequently tissue tracking and strain imaging was used for further optimisation ofthe AV and V-V intervals, according to the method described by Sogaard et al.8 After optimisation the echocardiogram showed improved left ventricular function and, surprisingly, due to enhanced contraction of the apical region of the inferior and posterior walls a clear huge pseudoaneurysm of the infero-postero-basal wall was visualised (figures 1 and 2). Through a large hole in the inferior wall, spontaneous contrast again opacified the pseudoaneurysm. A thick layer of thrombus formation was present at the wall of the aneurysm. Doppler echocardiography showed no mitral regurgitation and the VTI Ao was raised to 21.5 cm.
Netherlands Heart Journal, Volume 13, Number 10, October 2005
Figure 2. Transoesophageal echocardiogram of the left ventricle (LV), left atrium (LA) and a giant pseudoaneurysm (PA), showing spontaneous contrast (arrow).
Left ventricular angiography confirmed the presence of a giant pseudoaneurysm (figure 3), with a good residual left ventricular function without mitral regurgitation. Coronary angiography revealed a normal right coronary artery, occluded left circumflex artery, which was distally filled from the aortosapheneous vein graft. The left anterior descending artery showed a severe stenosis but good distal filling from the left internal mammary artery. To make a better delineation of the pseudoaneurysm and its surroundings after two surgical procedures a multislice
Figure 3. Left ventricular (LV) angiography, RAO view showing agiantpseudoaneurysm (PA) located at the inferior wall.
367
A giant pseudoaneurysm becoming apparent after cardiac resynchronisation therapy
Figure 4. Multislice CTpicture ofthe left ventricle (LV) with the giant pseudoaeurysm (PA).
CT scan was performed (figure 4), with 3D reconstruction (figure 5). Subsequently, the patient was referred for cardiac surgery to repair the pseudoaneurysm.
Discussion Cardiac rupture of the free wall of the left ventricle may be a fatal complication of myocardial infarction, occurring in approximately 4 to 23% of patients with acute myocardial infarction.9 In the majority of cases it is associated with sudden cardiac death due to haemopericardium and cardiac tamponade.10 Occasionally, cardiac rupture may be confined by a portion of pericardium or scar tissue leading to the formation of a pseudoaneurysm. Pseudoaneurysms do not contain endocardium or myocardium tissue as a true left ventricular aneurysm does, and are prone to rupture.1' Other complications are congestive heart failure, embolic events or arrhythmias.'2 Patients with left ventricular pseudoaneurysm usually present with symptoms of chest pain, dyspnoea and heart failure, which are also common in patients with coronary heart disease, making a differential diagnosis complicated. Over 10% of the patients with pseudoaneurysm are asymptomatic or have nonspecific symptoms leading to incidental findings on imaging tests.4 For an accurate diagnosis and proper surgical strategy noninvasive techniques such as transthoracic echocardiography, colour Doppler imaging or transoesophageal echocardiography, multislice CT or MRI must be performed.13-15
368
Figure 5. 3D reconstruction of the left ventricle (LV) and the pseudoaneurysm (PA) located inferior of the heart. The dimensions of the pseudoaneurysm exceed those ofthe left ventricle.
In this particular case, the patient was referred for implantation of a biventricular pacemaker, because he fulfilled all criteria for CRT.7 Echocardiography preimplant showed a severely dilated almost noncontracting left ventricle. After CRT, echocardiography showed improvement in contraction of the anterior and septal wall and inferoposteroapical region of the left ventricle. Due to the increase in contractility ofthe left ventricle, spontaneous contrast visualised a large hole located at the inferior wall. What seemed to be a very large and dilated left ventricle with dyskinesia of the inferior wall before CRT, appeared to be a normal left ventricle qua dimension, with a giant pseudoaneurysm situated at the inferoposterior wall after initialising CRT. Although CRT is not the therapeutic treatment of choice in patients with a pseudoaneurysm, in this case it led to the discovery of the third recurrence of the pseudoaneurysm. CRT initiated a remarkable clinical recovery in this patient, which made him suitable for resection of this pseudoaneurysm, because of its propensity to rupture. Conclusion A pseudoaneurysm may be difficult to diagnose by transthoracic echocardiography when there is poor contractile function of the residual part of the left ventricle. Diagnostic techniques as multislice CT or MRI should be considered in those patients with extremely large left ventricles showing akinetic regions with transthoracic echocardiography.
Netherlands Heart Journal, Volume 13, Number 10, October 2005
pc
A giant pseudoaneurysm becoming apparent after cardiac resynchronisation therapy
CRT, however, can be considered in patients with pseudoaneurysm and a poor residual left ventricular function with asynchrony fulfilling all other selection criteria for CRT. Application of CRT may lead to clinical improvement, thus facilitating the option of surgical repair of the pseudoaneurysm.c References 1 2
3 4
5 6 7
Roberts WC, Morrow AG. Pseudo aneurysm of the left ventricle: an unusual sequel of myocardial infarction and rupture of the heart. Am JMed 1967;43:639-44. Stewart S, Huddle R, Stuard I, Schreiner BF, DeWeese JA. False aneurysm and pseudo-false aneurysm ofthe left ventricle: etiology, pathology, diagnosis and operative management. Ann Thorac Surg 1981;31:259-65. Corvisart JN. An essay on the organic diseases and lesions of the heart and great vessels (translated by Gates J). Boston: Bradford & Read, 1812. Frances C, Romero A, Grady D. Left ventricular pseudo aneurysm. JAm Coll Cardiol 1988;32:557-61. Brown SL, Gropler RJ, Harris KM. Distinguishing left ventricular aneurysm from pseudoaneurysm. A review ofthe literature. Chest 1997;111:1403-9. Cazeau S, Leclercq C, Lavergne T, et al. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. NEnglJMed 2001;344:873-80. Abraham WT, Fisher WG, Smith AL, et al. MIRACLE Study Group. Multicenter Insync Randomized Clinical Evaluation. Cardiac resynchronization in chronic heart failure. NEnglJMed
8
9 10 11
12
13 14
15
Sogaard P, Egleblad H, Pederson AK, et al. Sequential versus simultaneous biventricular resynchronisation for severe heart failure: evaluation by tissue Doppler imaging. Circulation 2002; 106:2078-84. Pollak H, Nobis H, Miczoch J. Frequency of left ventricular wall rupture complicating acute myocardial infarction since the advent of thrombolysis. AmjCardiol 1994;74:184-6. Bates RJ, Beutler S, Resnekov L. Cardiac rupture challenge in diagnosis and management. Am J Cardiol 1977;40:429-37. March KL, Sawada SG, Tarver KA, Kesler KA, Armstrong WF. Current concepts of left ventricular pseudo aneurysm: pathophysiology, therapy and diagnostic imaging methods. Clin Cardiol 1989;12:531-40. Moreno R, Gordillo E, Zamorano J, Garcia-Rubira JC, FernandezOrtiz A, Macaya C. Long term outcome of patients with postinfarction left ventricular pseudo aneurysm. Heart2003;89:11446. Sutherland GR, Smyllie JH, Roelandt JR. Advantages ofcolor flow imaging in the diagnosis of left ventricular pseudoaneurysm. Br HeartJ 1989;61:59-64. Burns CA, Paulsen W, Arrowood JA. Improved identification of posterior left ventricular pseudo aneurysm by transoesophageal echocardiography. Am HeartJ 1992;124:796-9. Duvernoy 0, Wikstrom G, Mannting F, Larsson SG, Andren B, Dubiel T. Pre- and postoperative CT and MRin pseudo aneurysms of the heart. JComputAssist Tomogr 1992;16:401-9.
2002;346:1845-53.
IC
Netherlands Heart Journal, Volume 13, Number 10, October 2005
369
