The Rapid Diagnosis of Pseudoaneurysm Formation in Left Ventricular Free Wall Rupture

Mechanical complications of an acute myocardial infarction (AMI) include rupture of the interventricular septum, papillary muscle or left ventricular free wall. These events constitute 4–24% of all complications. Ventricular free wall rupture is particularly important, because it is usually associated with sudden cardiac death due to hemopericardium and cardiac tamponade.1 Most ventricular free wall ruptures develop through the mid lateral wall and usually complicate inferoposterolateral infarction from occlusion of the left circumflex artery;2 it is unusual to develop a rupture at the apex. Risk factors for developing a post-MI cardiac rupture infarction include: sixth decade of life or later, female gender, pre-existing systemic hypertension, absence of previous angina pectoris or infarction, first transmural MI, symptoms of pericarditis, repetitive unprovoked emesis with restlessness and agitation, a deviation of the ST segment or T wave (or both) from the usual evolutionary pattern, peak MB creatine kinase >= to 150 IU/L, absence of mural thrombus, lack of coronary artery collateral vessels in the area of infarction, and thrombolytic treatment given more than 7 hours after onset of chest pain.3–5 Ventricular free wall rupture may lead to the formation of a pseudoaneurysm, which is contained by pericardium, organized thrombotic material and associated adhesions. Pseudoaneurysms are a rare complication of AMI with unknown prevalence. They are known to be unstable, with a high incidence of spontaneous and frequently fatal rupture. Consequently, immediate surgical repair is the treatment of choice in those patients suitable for aggressive therapy.6 We describe a patient with suspected myocardial rupture in whom the diagnosis was rapidly established with the novel use of contrast echocardiography in an emergency room setting. Case Report. A 58-year-old woman presented to the Emergency Department with sudden onset of anterior chest pain that radiated to both shoulders. The patient was in her usual state of excellent health until 2 months prior to this current presentation, when she presented to another institution with a 6-hour history of severe anterior chest discomfort. She was subsequently diagnosed with an anterior wall AMI, and underwent emergent cardiac catheterization with documentation of 100% occlusion of the proximal left anterior descending artery. She had successful percutaneous coronary intervention with stent placement in the proximal left anterior descending coronary artery. Despite the successful intervention, she developed Q-waves in the anterior precordial leads and had creatine kinase evaluated at > 5,000 IU. She was medically treated with a combination of aspirin, plavix, metoprolol, ACE inhibitor and a statin agent. The patient was discharged without complications. Four days later, she complained of mild shortness of breath with respiratory chest discomfort. She was diagnosed with Dressler’s Syndrome and started on high-dose steroids, with a gradual taper over the course of 12 days. Four days after discontinuing steroids, she again had the same chest discomfort with mild shortness of breath. She was presumed to have persistent Dressler’s syndrome and was re-started on high-dose steroids. She had no further symptoms for the next month until the night of presentation to our institution. Her chief complaint at this time was a sudden onset of chest pain radiating to both shoulders, associated with shortness of breath, diaphoresis and mild nausea. However, the patient stated that her chest discomfort was dissimilar to the CP during her MI. The patient’s blood pressure was 95/60 mmHg, heart rate was 112 bpm, and she appeared uncomfortable and slightly diaphoretic. Her physical exam was significant for a systolic murmur that was non-radiating and best heard at the apex. Her electrocardiogram, when compared to one performed 1 day after her AMI (6 weeks earlier), showed improved ST elevation in the anterior leads (Figure 1). Her Troponin I was 12.0 and a chest x-ray demonstrated an enlarged cardiac silhouette with a bulge in the left upper heart border (Figure 2). Based on her history, exam and chest x-ray findings, a mechanical complication was suspected and a transthoracic echocardiogram was performed. Initial images demonstrated a hypokinetic and thinned left ventricular (LV) apex, and a possible pseudoaneurysm or aneurysm (Figure 3). Based on the clinical suspicion of an LV pseudoaneurysm, we decided to confirm this diagnosis with a contrast injection. Following intravenous contrast injection (3 cc of undiluted Definity), the pseudoaneurysm was unequivocally demonstrated with visualization of blood flow from the LV apex into the pericardial cavity (Figure 4). Within 1 hour of her presentation at the emergency room, the diagnosis of LV apical rupture was established noninvasively. She was referred for emergent surgery on the evening of her admission. Intraoperatively, the patient was found to have a 2 x 2 cm apical perforation contained by adhesions at the perforation site. The rupture site had well-defined edges and the pericardium was used to close the rupture. As the lateral and anterior wall were friable in nature, an Onlay patch was placed on the entire anterolateral wall. A post-operative, two-dimensional echocardiogram demonstrated mildly reduced LV systolic function, with good contractility involving the anterobasal and inferobasal segments. There was apical hypokinesis corresponding to the site of the Onlay patch and ejection fraction was 40%. Subsequent electrocardiograms showed no changes and the Troponin I normalized. The elevated Troponin I was attributed to myocardial necrosis secondary to ventricular destruction. The patient had an uneventful recovery, and was transferred to a rehabilitation facility 10 days after surgery. Discussion. Our patient was at an increased risk of rupture since she apparently developed post-MI Dressler’s syndrome. Treatment with glucosteroids and non-steroidal anti-inflammatory agents has been recommended for the management of these patients.7 However, there have been case reports that steroid treatment after AMI increases the risk of ventricular rupture and subsequent formation of a pseudoaneurysm,8 possibly by inhibiting ventricular scar formation. The incidence of Dressler’s syndrome, originally thought to be 1–4%,9 has recently declined due to successful thrombolysis in AMI patients.10 As a result, pseudoaneurysm formation after Dressler’s syndrome treatment is a rare complication. As emergent surgery is the appropriate treatment of pseudoaneurysms; it is imperative that the diagnosis be established as rapidly as possible. Once a rupture is suspected (by history, physical exam, electrocardiogram and radiographic findings), the physician has a choice of imaging modalities to confirm the diagnosis. These modalities include contrast ventriculography, magnetic resonance imaging (MRI) and echocardiography. Ventricular angiography is considered the gold standard for diagnosing a pseudoaneurysm and distinguishing it from a true aneurysm.11 Characteristic features include a narrow-based neck connecting the ventricle to the pseudoaneurysm cavity, with the contrast medium remaining in the pseudoaneurysmal cavity for several beats after injection, consistent with stagnant flow in the pericardial sac. In contrast, a wide neck with more rapid flow is characteristic of a true aneurysm. In addition, unlike a true aneurysm, a pseudoaneurysm lies outside the epicardium and thus extends beyond the coronary arteries. Contrast ventriculography, however, is time-consuming and invasive, and can delay treatment of a potentially life-threatening condition. MRI has been described as a useful technique in identifying LV pseudoaneurysms.12–14 Advantages of MRI include its high spatial resolution and ability to image the entire heart. Accordingly, it is highly accurate in determining the size and location of the pseudoaneurysm. Additional advantages include the capability to distinguish between pericardium, thrombus and myocardium, as well as the potential to visualize disruption of the epicardial fat layer by the pseudoaneurysm. However, the primary limitations of MRI are its lack of portability, and the time required for scanning and interpretation. Transthoracic echocardiography is the most commonly used initial technique to detect pseudoaneurysm formation.15 The major advantages are the immediate interpretation and excellent visualization afforded by echocardiography. As in ventriculography, the narrow neck of a pseudoaneurysm is often seen on cross-sectional echocardiography. However, it has been reported that a definitive diagnosis was made in only 26% of patients using two-dimensional echocardiography.16 In the case of an LV apical rupture, this percentage might be lower, as it is often difficult to optimally visualize the LV apex with standard transthoracic echocardiography. To improve upon the sensitivity of planar echocardiography, Doppler flow techniques have been studied. The presence of turbulent flow detected by pulsed Doppler at the neck of a cavity, or within the cavity itself, suggests the possibility of a pseudoaneurysm.17 Color flow Doppler, which shows bidirectional flow between the pseudoaneurysmal cavity and the left ventricle, has been shown to be superior to both pulsed and continuous-wave Doppler in detecting flow into a pseudoaneurysm.18 Even with these advances, two-dimensional echocardiography remains limited in sensitivity because cardiac motion can create artifactual flow signals, and the velocity of flow can sometimes be slow due to adhesion and thrombus formation. In a patient with suspected LV free wall rupture, an ideal imaging modality is one that is portable, noninvasive and provides high sensitivity and specificity. In our patient’s case, contrast echocardiography satisfied both criteria. The quality of flow, the lining of the epicardium and adhesion formation were readily visualized with administration of contrast. In one case report, the injection of contrast was shown to clearly delineate the LV apex.19 In another, contrast echocardiography was used to follow the actual formation of a pseudoaneurysm from a sealed rupture to pericardial containment.20 To our knowledge, this is the first case report describing the rapid diagnosis of LV pseudoaneurysm using contrast echocardiography at the point of care, with bypass of the use of more time-consuming and invasive imaging modalities. In our patient, contrast echocardiography immediately confirmed the clinical diagnosis of a pseudoaneurysm, rather than a true aneurysm. The patient underwent successful emergent surgery, which prevented what almost certainly would have been a fatal complication of an AMI. Based on our experience, we believe that contrast echocardiography should be considered the first choice for patients suspected of having LV pseudoaneurysm, a potentially fatal but treatable complication of MI.

1. Bates RJ, Beutler S, Resnekov L, et al. Cardiac rupture — Challenge in diagnosis and management. Am J Cardiol 1977;40:429–437. 2. Hung M-J, Wang C-H, Cherng W-J. Unruptured left ventricular pseudoaneurysm following myocardial infarction. Heart 1998;80:94–97. 3. Pohjola-Sintonen S, Muller JE, Stone PH, et al. MILIS study group. Ventricular septal and free wall rupture complicating acute myocardial infarction: Experience in the multicenter investigation of limitation of infarct size. Am Heart J 1989;117:809–818. 4. Honan MB, Harrell FE, Reimer KA, et al. Cardiac rupture, mortality and timing of thrombolytic therapy: A metaanalysis. J Am Coll Cardiol 1990;16:359–367. 5. Oliva PB, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable complication of acute myocardial infarction: Report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 1993;22:720–726. 6. Brown SL, Gropler RJ, Harris KM. Distinguishing left ventricular aneurysm from pseudoaneurysm: A review of the literature. Chest 1997;111:1403–1409. 7. Kahn. Pericarditis of myocardial infarction: Review of the literature with case presentation. Am Heart J 1975;90:788–794. 8. Silverman HS, Pfeifer MP. Relation between use of anti-inflammatory agents and left ventricular free wall rupture during acute myocardial infarction. Am J Cardiol 1987;59:363–364. 9. Kahn. Pericarditis of myocardial infarction: Review of the literature with case presentation. Am Heart J 1975;90:788–794. 10. Shahar A, Hod H, Barabash GM, et al. Disappearance of a syndrome: Dressler's syndrome in the era of thrombolysis. Cardiology 1994;85:255–258. 11. Frances C, Romero A, Grady D. Left ventricular pseudoaneurysm. J Am Coll Cardiol 1998;32:557–561. 12. Harrity P, Patel A, Bianco J, et al. Improved diagnosis and characterization of postinfarction left ventricular pseudoaneurysm by cardiac magnetic resonance imaging. Clin Cardiol 1991;14:603–606. 13. Sorensen MB, Moat N, Mohiaddin RH. Images in cardiovascular medicine. False left ventricular aneurysm documented by magnetic resonance imaging. Circulation 2002;105:1734. 14. Frances CD, Shlipak MG, Grady D. Left ventricular pseudoaneurysm: Diagnosis by cine magnetic resonance imaging. Cardiology 1999;92:217–219. 15. Catherwood E, Mintz GS, Kotler MN, et al. Two-dimensional echocardiographic recognition of left ventricular pseudoaneurysm. Circulation 1980;62:294–303. 16. Frances C, Romero A, Grady D. Left ventricular pseudoaneurysm. J Am Coll Cardiol 1998;32:557–561. 17. Loperfido F, Pennestri F, Mazzari M, et al. Diagnosis of left ventricular pseudoaneurysm by pulsed Doppler echocardiography. Am Heart J 1985;110:1291–1293. 18. Roelandt JR, Sutherland GR, Yoshida K, et al. Improved diagnosis and characterization of left ventricular pseudoaneurysm by Doppler color flow imaging. J Am Coll Cardiol 1988;12:807–811. 19. Waggoner A, Williams G, Gaffron D, Schwarze, M. Potential utility of left heart contrast in diagnosis of myocardial rupture by 2-dimensional echocardiography. J Am Soc Echo 1999;12:272–274. 20. Harpaz D, Kriwisky M, Cohen A, et al. Unusual form of cardiac rupture: Sealed subacute left ventricular free wall rupture, evolving to intramyocardial dissecting hematoma and to pseudoaneurysm formation — A case report and review of the literature. J Am Soc Echo 2001;14:219–227.