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Ann Thorac Surg 2005;79:339-341
© 2005 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, St. Louis, Missouri, USA
b Department of Cardiothoracic Anesthesiology, Washington University School of Medicine, St. Louis, Missouri, USA
Accepted for publication August 19, 2003.
* Address reprint requests to Dr Lawton, Division of Cardiothoracic Surgery, Washington University in St. Louis, One Barnes Jewish Hospital Plaza, Queeny Tower, Ste 3108, St. Louis, MO, USA 63110
lawtonj{at}msnotes.wustl.edu
| Abstract |
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| Introduction |
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A 74-year-old woman was admitted with a myocardial infarction (troponin I, 20.0 ng/mL). Comorbidities included previous myocardial infarction, hypertension, diabetes mellitus, and peripheral vascular disease. Physical examination was unremarkable with the exception of obesity (weight, 117 kg).
Cardiac catheterization revealed a left main coronary artery stenosis of 70%, left anterior descending coronary artery (LAD) stenosis of 70%, right coronary artery (RCA) occlusion, an ejection fraction of 30%, and cardiomegaly. Echocardiogram demonstrated a dilated left ventricle, normal left atrial size (3.8 cm), anteroapical hypokinesis, mild mitral regurgitation, and a small pericardial effusion. There was no evidence of calcification of the mitral annulus. Electrocardiogram demonstrated a left bundle branch block. A roentgenogram demonstrated mild cardiomegaly (Fig 1). During the preoperative period, the patient required a transvenous pacemaker for an episode of symptomatic bradycardia.
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Postoperatively, the patient was kept on bed rest for 1 day, weaned from pressors, and extubated with complete neurologic recovery. Postoperative electrocardiogram demonstrated left bundle branch block, and myocardial injury was confirmed by elevation in troponin I levels with a peak of 30.9 ng/mL on postoperative day 1. Unfortunately, on postoperative day 4, heparin associated thrombocytopenia was diagnosed and confirmed by antibody testing. The patient was immediately placed on a thrombin inhibitor (Argatroban, Glaxo Smith Kline). She subsequently suffered massive pulmonary emboli and systemic emboli to both lower extremities. Transesophageal echocardiogram demonstrated moderate mitral regurgitation and a clot visible in the superior venae cava, the right atrium, the right ventricle, the main pulmonary artery, and in a patent foramen ovale. The patient ultimately expired on postoperative day 15 when support was withdrawn at the family's request.
| Comment |
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The atrioventricular groove provides a naturally weakened transitional area [4]. Embryologically, the atrial and ventricular myocardium begin to separate in fetal life at approximately 7 weeks of gestation and complete separation is seen at 12 weeks [5]. Conduction tissue provides the only muscular continuity between the atria and ventricle in adult life. This vulnerable area provided the pressure release for the patient's overdistended, anatomically manipulated heart.
Significant distortion of the mitral annulus with enlargement of the left atrium and pulmonary veins has been demonstrated during manipulation of the heart for off-pump CABG [6]. George and colleagues [6] reconstructed the mitral valve structure at end diastole during manipulation for off-pump CABG using transesophageal echocardiography. They noted that the greatest distortion of the valve occurred during manipulation of the heart to view the lateral wall. Three-dimensional reconstruction of the mitral valve demonstrated that the intracardiac structures were folded primarily at the atrioventricular groove. The greatest mean percent increase in left atrial pressure (66%) was documented using a left atrial catheter in 6 patients during manipulation to perform the left circumflex coronary artery graft. The left atrial pressure increased by only 13% during performance of the LAD graft and by 51% during the posterior descending artery graft construction. The increase in left atrial pressure was associated with an increase in left atrial dimension from 4 cm to 6 cm. The spontaneous atrioventricular groove tear in the patient reported is likely related to the heart manipulation that led to elevation in the left atrial pressure and size with resultant "pop-off" through the vulnerable atrioventricular groove.
Successful reports of repair of atrioventricular groove tears after mitral valve replacement have been accomplished using a pericardial patch with intracardiac as well as extracardiac repair and with complete explantation of the heart followed by repair and reimplantation [1, 4, 7]. Unlike previously described cases, our reported case began off pump. An attempt at repair of such a catastrophic injury should not be made while the heart is beating. A tension-free repair in normal, healthy tissue is paramount, and this can only be accomplished in the empty and arrested heart. In addition, in the case report we described, the risk of air embolus was extremely high while the heart was ejecting.
The postoperative findings of troponin elevation and moderate mitral regurgitation suggest that papillary muscle ischemia occurred as a result of deep repair sutures in the atrioventricular groove. Both branches of the left circumflex coronary artery were grafted in an attempt to minimize ischemia. The patient suffered no ill effects of coronary sinus ligation and no conduction disturbances as a result of the repair.
This case documents the successful repair of a spontaneous atrioventricular groove tear that occurred during off-pump CABG. This devastating complication requires immediate conversion to cardiopulmonary bypass and a tension-free repair. Caution should be exercised in the decision-making process regarding the use of off-pump CABG in patients with significant cardiomegaly and elevation of pulmonary artery pressure during heart manipulation.
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