| Abstract|| |
A 65-year-old woman presented with a history of dyspnea and atypical chest pain. She was diagnosed with a non-ST-segment elevation myocardial infarction due to a giant right coronary artery aneurysm. After a failed percutaneous embolization, she was scheduled for right coronary artery aneurysm resection, posterior descending artery revascularization and mitral valve repair. During the induction of anesthesia and institution of mechanical ventilation, the patient suffered cardiovascular collapse. The transesophageal echocardiographic examination revealed tamponade physiology owing to compression of the cardiac chambers by the unruptured aneurysm, which resolved with the sternotomy. The surgery was carried out uneventfully.
Keywords: Intraoperative transesophageal echocardiography, Right coronary artery aneurysm, Tamponade
|How to cite this article:|
Orozco DM, Abello M, Osorio J, Melgarejo I. Giant right coronary artery aneurysm with unusual physiology: Role of intraoperative transesophageal echocardiography. Ann Card Anaesth 2012;15:240-3
|How to cite this URL:|
Orozco DM, Abello M, Osorio J, Melgarejo I. Giant right coronary artery aneurysm with unusual physiology: Role of intraoperative transesophageal echocardiography. Ann Card Anaesth [serial online] 2012 [cited 2021 Jun 20];15:240-3. Available from: https://www.annals.in/text.asp?2012/15/3/240/97982
| Introduction|| |
Coronary artery aneurysms are localized dilations of the coronary artery, with a frequency of 1.5% in postmortem studies.  However, giant aneurysm are rare lesions, whose true incidence is unknown, because they tend to be asymptomatic. A myriad of presentations have been reported in the literature such as acute coronary syndromes,  heart failure,  superior vena cava syndrome,  right ventricular outflow obstruction,  cardiac compression,  sudden death  and cardiac tamponade  due to rupture of the aneurysmal sac and hemopericardium. We describe tamponade physiology in an unruptured giant right coronary artery (RCA) aneurysm. A literature search in BioMedCentral, PubMed and EMBASE, suggest that this report may be the first one in the literature. An intraoperative transesophageal echocardiography (TEE) imaging allowed us to document the correlation between the hemodynamic parameters and echocardiographic data to set a basis to the diagnosis of cardiac tamponade.
| Case Report|| |
A 65 -year-old female presented with a history of exertional fatigue that progressed to dyspnea at rest, which was accompanied by atypical chest pain. Her prior medical history was unremarkable. She was diagnosed with a non-ST-segment elevation myocardial infarction exhibiting Q waves on the inferior leads of her electrocardiogram. On catheterization, a RCA aneurysm with anterograde supply through the RCA and a moderate mitral regurgitation (MR) were found. It was decided to embolize the aneurysm percutaneously. The patient developed heart failure 72 h after embolization which was considered due to inferior wall myocardial ischemia. A transthoracic echocardiogram was performed in which a new regional wall motion abnormality (RWMA) in the inferior wall and a worsening of the MR were documented. The mechanism of the MR was RWMA causing tethering of the posterior mitral valve leaflet that prevented coaptation. Catheterization revealed aneurysm enlargement and partial thrombosis; the aneurysm showed retrograde flow through the left circulation. It was then decided for resection of the aneurysm, inferior territory revascularization and mitral valve repair.
During induction of anesthesia and mechanical ventilation, the patient suffered hemodynamic instability that rapidly progressed to cardiovascular collapse with profound hypotension refractory to high doses of vasopressors and inotropes. A pulmonary artery (PA) catheter was placed that revealed the following hemodynamic data: cardiac index 1.1 L/min/m 2 , central venous pressure (CVP) 21 mmHg, PA pressure 43/22 mmHg and pulmonary artery wedge pressure PAWP 22 mmHg.
A Matrix 3D TEE probe (Philips Healthcare, Andover, MA, USA) was placed, which showed the following:
- A giant mass on the right atrioventricular groove, 5 cm x 6 cm with echodensities corresponding to thrombotic formations, which was compressing the right atrium [Figure 1].
|Figure 1: (a) Partial mid-esophageal four-chamber view with a focus on the right side of the heart demonstrating right coronary artery (RCA) aneurysm causing compression of the right atrium. RA - right atrium; RV - right ventricle; LA - left atrium; LV - left ventricle. The arrow points at the RCA aneurysm. (b) Live 3D of the giant RCA aneurysm compressing the RA|
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- Exaggerated respiratory spectrum was found upon Doppler examination of the tricuspid, mitral and aortic valves.
- Severe left atrial dilation and Severe MR due to restriction of the posterior mitral valve leaflet owing to a dyskinetic left ventricular inferior wall. [Figure 2] a and b.
|Figure 2: (a) Mid-esophageal two-chamber view demonstrating severe mitral regurgitation with a thick jet toward the posterior aspect of the left atrium. The arrow points at the hypokinetic inferior left ventricular wall. LA - left atrium; LV - left ventricle. (b) 3D en face view of the mitral valve with the posterior mitral leaflet (PML) at the top and the anterior mitral leaflet (AML) at the bottom; the arrow points at the lack of coaptation due to the restriction of the PML. AML; LAA - left atrial appendage; AV - aortic valve|
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- Left ventricle with moderate systolic dysfunction and ejection fraction of 40%, dyskinetic inferior wall.
- Moderate dilation of the right ventricle.
The findings - giant mass compressing the right atrium and exaggerated Doppler spectrum across tricuspid, mitral and aortic valves during respiratory excursion are consistent with cardiac tamponade. The patient underwent urgent sternotomy and pericardiotomy, which relieved the extracardiac compression. Immediately, the hemodynamics improved and the inotropes and vasopressors were gradually tapered off. The hemodynamic data recorded from PA catheter showed cardiac index 2.5 L/min/m 2 , CVP 16 mmHg, PA 37/18 mmHg and PAWP 14 mmHg.
Aneurysm resection, mitral valve repair and posterior descending artery revascularization were performed during a 105-min pump run. During the postbypass echocardiographic examination, there was adequate resection of the mass, no mitral insufficiency and no change in ventricular function. The remaining postoperative period was uneventful and the patient was discharged after 15 days from admission.
| Discussion|| |
A coronary artery aneurysm is an area of localized arterial dilation more than twice the diameter of the adjacent normal segment; when its diameter is greater than 2 cm, it is called a giant coronary artery aneurysm.  Although the most common etiology of coronary artery aneurysm is arteriosclerosis, other etiologies such as congenital malformations, posttraumatic, postsyphilitic and connective tissue diseases like Marfan's or Kawasaki's disease have also been described.  The previous reports on tamponade due to coronary aneurysms were always a consequence of their rupture and subsequent hemopericardium. ,, In our patient, the aneurysmal sac was intact, but the mass was large enough to restrict the right atrial and right ventricular filling producing low cardiac output as a consequence.
The cardiovascular collapse that occurred on induction of anesthesia and mechanical ventilation deserves more discussion. Perhaps, our patient was on the verge of hemodynamic collapse and the combined effects of the intravenous anesthetics (fentanyl and midazolam) on the vascular tone and inotropism and the restriction of the ventricular filling posed by the mechanical ventilation precipitated acute decrease in venous return, low cardiac output and hemodynamic collapse.
The positive pressure because of giant aneurysm compresses the adjacent cardiac chambers. The right heart chambers, because of their low pressures, are the first to be affected. Ventricular filling in cardiac tamponade is a complex phenomenon and depends highly on the respiratory pattern. The rise in the end diastolic pressure of both the ventricles result in systemic and pulmonary venous hypertension that maintain the ventricular filling, the fall in the intrathoracic pressure during inspiration enhances the inflow to the atria in an exaggerated manner in the spontaneously breathing patient. The reversal of the intrathoracic pressures during controlled ventilation decreases the venous return to the right atrium, which, combined with the increment of the right ventricular afterload because of pulmonary hypertension secondary to MR resulted in decreased right ventricular stroke volume. Considering these pathophysiological effects, it appears that the intravenous anesthetics, fentanyl and midazolam, were a poor choice, In this situation, Etomidate or ketamine would have been a better choice to maintain hemodynamic stability. It also appears that spontaneous ventilation should have been maintained until the pericardium was dissected. However, we were not aware of the tamponade physiology at the time of the induction of anesthesia and, therefore, these precautions were not taken.
The intraoperative TEE imaging was the key factor in defining the hemodynamic status of our patient, as we documented gross compression of the right atrium and exaggerated respiratory shifts consistent with tamponade physiology on the Doppler examination of the tricuspid, mitral and aortic valves.  The genesis of these phenomena is ventricular interdependence posed by the tamponade, in which a fall in the right ventricular stroke volume combined with the shift of the septum to the left during the inspiratory phase of a positive-pressure ventilation result in decreased left ventricular stroke volume during the expiratory phase. These cyclic changes in the left ventricular or right ventricular filling can be accurately tracked by pulsed Doppler interrogation of mitral and tricuspid valve. The sternotomy and dissection of the pericardium improved the hemodynamics, so that the vasopressors and inotropes could be discontinued. The data obtained by the PA catheter showed a dramatic reduction in cardiac filling pressures, and normalization of the cardiac index which further confirmed the tamponade physiology. It is possible that heart failure that developed after the coronary embolization was a summation of several events: the myocardial ischemia caused by the occlusion of the RCA, the worsening MR and the restricted filling due to enlarging aneurysm.
To summarize, Our report shows that the rupture of a coronary aneurysm is not the only mechanism responsible for tamponade physiology, but rather the compression imposed by an extracardiac mass could eventually lead to this condition.
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David M Orozco
Fundación Clínica Shaio, Diagonal 115A N 70c 75, Department of Anaesthesia, Bogotá
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2]