Giant Left Ventricular Pseudoaneurysm Diagnosed using ...



Giant Left Ventricular Pseudoaneurysm Diagnosed using Microsphere Contrast Transthoracic Echocardiography - a case report

Christian Hamilton-Craig MBBS BMedSci(Hons) FRACP 1,2

Natalie Kelly, BExSci, AMS Cardiac2

David Platts MBBS MD FRACP FCSANZ FESC2

Matthew Pincus MBBS FRACP 1,2

1. Department of Cardiology, The Prince Charles Hospital, QLD

2. Echocardiography Laboratory, Cardiac Sciences Unit, Prince Charles Hospital, Qld.

Abbreviations:

PSA = Pseudoaneurysm

LV = left ventricle

TTE = trans-thoracic echocardiography

Introduction

Left ventricular pseudoaneurysm (PSA) is a rare mechanical complication following an acute myocardial infarction [1, 2]. Free intrapericardial rupture usually results in cardiac tamponade and sudden death. When, however, the rupture is contained by the pericardium or scar tissue an LV pseudoaneurysm (PSA) may develop [3]. Early diagnosis of this complication is imperative due to risk of further PSA rupture with very high mortality [6].

We report a case of a large PSA diagnosed using a perflutren microsphere contrast echocardiography agent (Definity®, Lantheus Medical Imaging), which is the only second-generation contrast agent currently licensed for clinical use in Australia.

Case Study

A 79 year-old male was transferred to our institution from a regional centre following late presentation infero-lateral ST segment elevation myocardial infarction (STEMI). An electrocardiogram (ECG) showed sinus rhythm with ST elevation in the inferior and lateral leads and two episodes of non-sustained ventricular tachycardia. Physical examination revealed a heart rate of 63bpm and a blood pressure of 117/66mmHg. Cardiac troponin I was 12 μg/mL.

Coronary angiography revealed two-vessel coronary artery disease. A large third obtuse marginal branch (OM3) of the circumflex coronary artery was subtotally occluded, with thrombus present (Figure 1), signifying the culprit lesion. This was treated with a bare metal stent, complicated by no-reflow and repeat balloon dilatation, resulting in TIMI-2 flow (incomplete perfusion). The proximal left anterior descending artery had an 80% heavily calcified stenosis (Figure S-1), which was unsuccessfully dilated. Limited transthoracic echocardiography (TTE) performed day 1 post procedure showed normal LV cavity size, an akinetic lateral wall with a LV ejection fraction (LVEF) of 40-45% and moderate mitral regurgitation. The patient discharged himself against medical advice during performance of the echocardiogram, limiting further assessment.

Seven days following self-discharge, the patient represented to the emergency department with symptomatic heart failure. An ECG showed lateral Q waves and persistent mild ST elevation in V5-V6. Repeat TTE demonstrated that the LV was at the upper limits of normal in size (137mls) with moderate segmentally impaired systolic function (LVEF of 39%). There were extensive LV regional wall motion abnormalities; the apical region was akinetic and the inferior and anterior wall segments were hypokinetic. Of particular note, the anterolateral and inferolateral wall segments were thin with poor endocardial definition (Figure S-2A, S3-A).

To improve imaging of the lateral and inferolateral segments, a contrast echocardiogram was performed using an intravenous microsphere contrast agent (Definity®, Lantheus Medical Imaging). Using contrast specific imaging, excellent opacification of the LV chamber and enhancement of the endocardial borders was achieved, revealing a giant lateral pseudoaneurysm almost equal in size to the native LV cavity. From the apical four chamber view, (Figure S-2B) this cavity measured 5.3cm at entry with a maximal diameter of 7.0cm and a radius measuring 3.7cm. From the apical long axis view, (Figure S-3B) the entry of the PSA measured 5.2cm, the maximal diameter was 6.7cm and the radius was 4.2cm. There was no evidence of mural thrombus lining the aneurysm cavity. Moderate aortic stenosis was present (mean gradient 30mmHg, aortic valve area 1.1cm2).

Cardiac MRI (GE Twinspeed 1.5T) was performed with cine steady state free precession and late gadolinium enhancement imaging. This confirmed the presence of a pseudoaneurysm, being a contained rupture of the left ventricle surrounded by a thin layer of parietal pericardium, as distinct from true aneurysm formation (Figure S-4).

The following day the patient was taken to surgery for PSA repair (Dor procedure), coronary artery bypass, aortic valve replacement and mitral valve repair (commissural plication). Aortic valve replacement was recommended as per the Duke criteria for patients with moderate aortic stenosis undergoing open-heart surgery [12]. The PSA was repaired by complete excision of the sac and approximation of the myocardial walls with Teflon-buttressed sutures. There were no post-operative complications and the patient was discharged on day 5 post-surgery on optimal medical therapy. Repeat echocardiography at 3 months showed significantly improved LV systolic function, with a LVEF of 46% and hypokinesis of the repaired lateral wall and normal prosthetic valve function.

Discussion

This case illustrates an important mechanical complication following STEMI and highlights the pivotal role of second generation contrast-enhanced echocardiography in providing incremental information over unenhanced echocardiography.

Pseudoaneurysm formation is most commonly caused by transmural myocardial infarction, followed by cardiac surgery, trauma and infective endocarditis [4,6,7]. Patients with normal coronary arteries have also been documented to develop a PSA secondary to coronary spasm or coronary thrombosis [7]. Transmural infarction has the potential to develop either a true aneurysm through ventricular remodeling, or more rarely a contained rupture occurs leading to PSA formation. Anterior myocardial infarctions more commonly lead to true aneurysm formation [8]. Inferior or infero-lateral myocardial infarctions account for the majority of PSA formation, possibly due to the altered wall mechanics in this area of the myocardium [7]. Unlike true aneurysms, PSAs contain no endocardium or myocardium, rather only pericardial and fibrous elements in its wall [3-6]. They are classically characterised by a narrow neck of communication between the LV and aneurysmal cavity [6, 11]. However some may display a wide neck [11] such as in the present case. It is common for both types of aneurysms to contain mural thrombi due to stasis of blood flow, having the potential for systemic embolus [6].

Differentiation of true aneurysm from pseudo-aneurysm is important due to the different potential for subsequent fatal rupture and the significantly different approaches to treatment (medical therapy versus urgent cardiac surgery). Untreated patients with PSA have a 30-45% risk of rupture and with medical therapy and a mortality of almost 50% [4, 6]. Notably, a PSA may not only rupture during the early stages but can also rupture late after the established fibrous stage is reached [6]. Consequently, surgery is recommended [4]. With current techniques the perioperative mortality is less than 10%, with those requiring mitral valve replacement for severe mitral regurgitation at increased risk [9,10].

Conclusion

This report illustrates an important complication of myocardial infarction, its detection by contrast echocardiography and successful surgical repair with good functional outcome. The case emphasises the incremental value of microsphere echo contrast agents in clinical practice in particular situations, as this post infarct complication was not be adequately visualised by conventional unenhanced transthoracic echocardiography.

References

1. Figueras, J; Cortadellas, J; Calvo, F; Soler-Soler, J. Relevance of delayed hospital admission on development of cardiac rupture during acute myocardial infarction: Study on 225 patients with free wall, septal or papillary muscle rupture. J Am Coll Cardiol. 1998; 32(1):135-139.

2. Reeder, G.S. Identification and treatment of complications of myocardial infarction. Mayo Clin Proc. 1995; 70(9):880-884.

3. Dachman, A.H; Spindola-Franco, H; Solomon, N. Left ventricular pseudoaneurysm: Its recognition and significance. JAMA. 1981; 246:1951-1953.

4. Frances, C; Romero, A; Grady, D. Left ventricular pseudoaneurysm. 1998; 32: 557-561.

5. Davutoglu, V; Soydinc, S; Sezen, Y; Aksoy, M. Unruptured giant left ventricular pseudoaneurysm complicating silent myocardial infarction in a diabetic young adult. Int J CV Imaging. 2005; 21: 231-234.

6. Vlodaver, Z; Coe, J.L; Edwards, J.E. True and false left ventricular aneurysms: Propensity for the latter to rupture. Circ. 1975; 51: 567-572.

7. Asha Mahilmaran, D.M; Pradeep, G; Nayar, D; Mukundan Sheshadri, M; Gurijala Sudarsana, D; Abraham, K. Left ventricular pseudoaneurysm caused by coronary spasm, myocardial infarction and myocardial rupture. Tex Heart Inst J. 2002; 29(2): 122-125.

8. Feigenbaum, H. Echocardiography. 5th ed. Lea and Febiger. Philadelphia; 1994.

9. Bolooki, H. Surgical treatment of complications of acute myocardial infarction. JAMA. 1990; 264: 1237-1240.

10. Komeda, M; David, T. Surgical treatment of postinfarction false aneurysm of the left ventricle. J Thorac Cardiovasc Surg. 1993; 106: 1189- 1191.

11. Oh, JK; Seward, J; Tajik, AJ. The Echo Manual. 3rd ed. Wolters Kluwer Health. Sydney: Lippincott, Williams and Wilkins; 2006.

12. Smith et al Aortic valve replacement for Moderate Aortic Stenosis at time of coronary artery bypass surgery. J Am Coll Cardiol. 2004 V44(6):1241-7.

13. Mulvagh SL, Rakowski H, Vannan MA, Abdelmoneim SS, Becher H et al. American Society of Echocardiography Consensus Statement on the Clinical Applications of Ultrasonic Contrast Agents in Echocardiography. J Am Soc Echo. 2008 Nov;21(11):1179-201

Supplementary Figure Legends:

Supplementary Figure S1. Coronary angiogram from RAO caudal view. A large OM3 of the circumflex artery showed an acutethrombotic occlusion (culprit lesion). The proximal LAD showed a severely calcified an 80% stenosis.

Supplementary Figure S2. Apical four chamber view a) conventional tissue harmonic 2-dimensional echocardiogram, b) perflutren microsphere contrast enhancement using power pulse inversion imaging. Note the suspicion of pseudoaneurysm on the standard 2D image in the basal lateral wall, and the marked difference in the appearance of the cavity size after contrast enhancement. (LV-Left Ventricle; LA-Left Atrium; RV-Right Ventricle; RA-Right Atrium; PSA-Pseudoaneurysm)

Supplementary Figure S3. Apical long axis view a) conventional tissue harmonic 2-dimensional echocardiogram, b) perflutren microsphere contrast enhancement using power pulse inversion imaging showing the giant PSA in the basal inferolateral wall (abbreviation as for figure S-2).

Supplementary Figure S4. Cardiac MRI: Steady state free precession images show the pseudoaneurysm cavity in the four chamber view (A) and the short axis view (B). Full thickness gadolinium delayed enhancement of the wall of the PSA is seen (C,D) which extends beyond the margins in continuity with the pericardium, confirming contained rupture and pseudoaneurysm formation.

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