Ann Thorac Surg 2004;77:1441-1443
© 2004 The Society of Thoracic Surgeons
Case report
Left ventricularcoronary sinus/right ventricular fistula late after mitral valve replacement
Luis Fernando López Almodóvar, MDa*,
Juan José Rufilanchas, MDa,
Fernando Enríquez, MDa,
Luis Maroto, MDa,
Enrique Pérez de la Sota, MDa,
José Cortina, MDa
a Department of Cardiac Surgery, 12 de Octubre University Hospital, Madrid, Spain
Accepted for publication May 29, 2003.
* Address reprint requests to Dr López Almodóvar, Department of Cardiac Surgery, 12 de Octubre University Hospital, Avda de Córdoba s, n, 28041 Madrid, Spain.
e-mail: lfla{at}telepolis.com
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Abstract
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Development of an intracardiac fistula is a rare complication after mitral valve replacement. In the literature we have found six cases of left ventricularcoronary sinus fistula and another one of left ventricularcoronary sinus and right atrial fistula. We report the history and course of a patient in whom a left ventricularcoronary sinus and right ventricular fistula developed late after mitral valve replacement. The current study examines this type of intracardiac shunt, and presents our report on a left ventricularcoronary sinus and right ventricular fistula complication.
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Introduction
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Mitral valve replacement has been associated with many complications, which include posterior left ventricular rupture, left ventricularright atrial fistula, circumflex artery injury, and cardiac rhythm disturbances, among others. The development of a left ventricularcoronary sinus and right ventricular fistula is a rare complication after mitral valve replacement, which has not been previously reported.
A 52-year-old woman had a history compatible with acute rheumatic fever during adolescence. She underwent closed mitral commissurotomy in 1963. She did well during 25 years after the operation until progressive symptoms of congestive heart failure appeared. At that time electrocardiogram revealed chronic atrial fibrillation with echocardiographic severe mitral stenosis. In July 1989 the mitral valve was replaced with a 29-mm Omnicarbon prosthesis in another hospital. The mitral valve was sclerosed and calcified but the operative report does not provide information about annulus calcification. She fully recovered, but in 1996 an echocardiogram suggested mild tricuspid regurgitation and a small ventricular septal defect. The patient was in New York Heart Association (NYHA) functional class I until March 1999, when symptomatic deterioration occurred with dyspnea and orthopnea. Transthoracic echocardiography demonstrated enlargement of left and right atria and severe tricuspid regurgitation with pulmonary hypertension, excluding prosthetic malfunction or periprosthetic leak. Doppler color-flow imaging displayed turbulent flow in right atrium and right ventricle Transesophageal echocardiography confirmed these findings, including tricuspid regurgitation, and suggested a left-to-right shunt in the membranous portion of the interventricular septum. Cardiac catheterization and left ventricular angiography confirmed severe pulmonary hypertension (70/3445 mm Hg) and left-to-right shunt, with flow ratio of 2.1 to 1. The ventriculogram demonstrated a severe dilated left ventricle and a small aneurysm in the interventricular septum near the posterior mitral annulus (Fig 1).
Right ventricular pressure was 75/020 mm Hg, left ventricular pressure 165/1028 mm Hg, and right atrial pressure 28/1020 mm Hg. Cardiac index was 3.17 L · min−1 · m−2. Left ventricular ejection fraction was 59%. With the diagnosis of interventricular septal defect and severe tricuspid regurgitation, the patient underwent surgery in December 1999. Through a right atriotomy the tricuspid valve was carefully explored, without finding significant tricuspid regurgitation nor dilatation or organic disease. The ventricular septal defect was sought in the membranous and muscular septum without success. Further exploration of the right atrium revealed a dilated coronary sinus. The left ventricle communicated directly into the coronary sinus by two fistulae near to the Eustachian valve (Fig 2)
and into the right ventricle by three fistulae below the septal tricuspid leaflet (Fig 3).
These defects were closed with sutures using 4-0 polypropylene, and the mitral prosthesis was not removed. An intraoperative transesophageal echocardiogram after repair did not indicate left-to-right shunt nor tricuspid regurgitation. No complications occurred in the postoperative period and the patient exhibited immediate symptomatic improvement. Three years after the operation the patient is in NYHA class I, without echocardiographic residual shunt, and with normal pulmonary artery pressure.

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Fig 1. Left ventriculogram demonstrating a severe dilated left ventricle and a small aneurysm in the superoposterior interventricular septum, near the posterior mitral annulus.
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Fig 2. The left ventricle communicated directly into the coronary sinus by two fistulae (white arrows) near the Eustachian valve. (CS = coronary sinus; PA = pulmonary artery; RV = right ventricle.)
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Fig 3. The left ventricle communicated into the right ventricle by three fistulae (white arrows) below the septal tricuspid leaflet. (LV = left ventricle; PA = pulmonary artery; RV = right ventricle.)
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Comment
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Left ventricularcoronary sinus fistula have been reported after reiterated mitral prosthesis replacement [13]. The danger of excessive debridement of the mitral annulus are widely recognized [4, 5], and hematoma in the posterior atrioventricular groove is a feared intraoperative complication. The time delay between the mitral valve replacement and the appearance of symptoms in our patient (10 years) suggests that direct trauma to the coronary sinus during prosthesis implantation did not occur [6]. An operative injury probably led to an intramural or intraseptal dissection or hematoma, which later ruptured into the coronary sinus and the right ventricle. A new systolic murmur with high cardiac output can suggest this complication, but can be misdiagnosed as tricuspid regurgitation, interventricular septal defect, or both, and the patient undergoes surgery without a correct diagnosis. Surgical treatment is recommended for these patients because of symptoms, left ventricular enlargement, or pulmonary hypertension. The choice of surgical approach is open to discussion. Access to the fistula should be better through the starting chamber than through the exit chamber. But in our patient we did not know for sure where the starting point was located. Access through the left atrium did not reveal the fistula and a complete exploration would require explantation of the mitral prosthesis, which was functioning well, and, consequently, prolonged aortic crossclamp. We elected a right atrial approach due to these considerations and in the belief that tricuspid valve repair was necessary. Closure of the multiple fistulae through the coronary sinus and right ventricle does not preclude that new fistulae could not develop over time if the inlet has not been closed. But, to date, the patient is asymptomatic and without new complications. The etiology in our patient remains unproved, and we can only speculate that excessive debridement or resection of mitral annulus led to this late complication. Even if these fistulae are not common, great care should be taken in the debridement of the mitral annulus at the posteromedial commissure to avoid damaging adjacent structures.
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References
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