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Ann Thorac Surg 1996;62:1506-1507
© 1996 The Society of Thoracic Surgeons
Departments of Cardiovascular and Thoracic Surgery and Pathology, Seth G.S. Medical College and King Edward VII Memorial Hospital, Bombay, India
Accepted for publication May 10, 1996.
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| Introduction |
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A 14-year-old male patient with tetrology of Fallot was admitted to our hospital for intracardiac repair. Chest roentgenogram and electrocardiogram were in accordance with the clinical diagnosis. Echocardiography and cardiac catheterization showed single subaortic ventricular septal defect with right-to-left shunt, infundibular and valvar pulmonary stenosis, and dilated CS with persistent left superior vena cava (SVC) draining into it. The relevant preoperative test results were as follows: hemoglobin level, 16.5 g/dL; packed cell volume, 47%; platelet count, 80,000/µL; and clotting time, 18 minutes.
The patient was taken on elective basis for intracardiac repair under conventional bypass using a Polystan Safe II oxygenator (Polystan A/S, Denmark). The right SVC and inferior vena cava were cannulated with Polystan right-angled 5-mm and 7-mm cannulas, respectively. In addition, the left SVC was cannulated with a 5-mm straight Polystan cannula by a closed technique, through a pursestring suture on the right atrial free wall, via the CS. This cannulation was done on an empty heart on cardiopulmonary bypass and was uneventful. The right SVC and IVC were snugged directly. The left SVC was also snugged outside the heart. On cardiopulmonary bypass, circulating packed cell volume was maintained between 26% and 30%. Total correction was carried out by a transventricular approach with antegrade blood cardioplegia with a cardiac anoxia time of 48 minutes and a cardiopulmonary bypass time of 120 minutes. The patient required ionotropic support of 5 µgkg-1min-1 of dobutamine and 3 µgkg-1min-1 of dopamine for the first 36 hours. The central line was removed postoperatively after 48 hours. The patient was hemodynamically stable with no evidence of congestive cardiac failure. Postoperative test results were as follows: hemoglobin level, 12.2 g/dL; packed cell volume, 37%; platelet count, 1,00,000/µL; and clotting time, 12 minutes. The patient received 12 units of platelet transfusion during and after the operation. There was no evidence of arrhythmia on electrocardiograms taken on the second and fifth postoperative days. On the sixth postoperative day, the patient had sudden cardiac arrest with no premonitory signs and could not be resuscitated.
Gross examination of the heart showed the coronary sinus ostium and sinus occluded completely by an adherent thrombus (Fig 1
). Thrombus extended into the left SVC. The coronary veins draining into the sinus were free of thrombus but engorged. The coronary arteries were normal and patent. There was no gross evidence of trauma to the CS endothelium.
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Histologic examination showed that the CS contained antemortem thrombus within its lumen attached to its endothelium. Myocardium in the left posterior ventricular wall showed areas of ischemic injury. The lungs were unremarkable.
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Coronary sinus thrombosis is an unusual complication after cardiopulmonary bypass. Although in a case report it was reported after mitral valve replacement, the cause was CS trauma due to a catheter, a pacemaker, or during a mitral valve operation [8]. Persistent left SVC has been cannulated through the right atrium during cardiopulmonary bypass in our unit for the last 18 years. Coronary sinus thrombosis usually does not usually occur in this situation, possibly because bypass is conducted after heparinization, with low packed cell volumes, and under constant flow rates. In this case the central venous catheter was positioned in the right SVC, which was confirmed on the operating table and on the postoperative roentgenogram. Additional factors such as right ventricular failure and endocarditis were also absent. As spontaneous CS thrombosis is not a known entity, it is possible that in this case microscopic trauma to CS endothelium during cannulation led to CS thrombosis.
Venous stasis in the coronary sinus system due to thrombosis may not cause venous myocardial infarction, due to the presence of an adequate collateral circulation with anterior cardiac veins and thebesian veins [5]. It may also be detected incidentally [8]. This may not always be the case, as CS thrombosis has led to myocardial infarction in a few cases [4, 5]. It is also known to be a source of pulmonary embolus [3] and has caused cardiac tamponade [2]. In this case CS thrombosis led to myocardial infarction, which led to sudden deterioration and a fatal outcome.
This case of CS thrombosis after left SVC cannulation through the CS during cardiopulmonary bypass is very unusual, although procedures where foreign bodies are in contact with the CS are a recognized cause [15, 8]. We conclude that although CS thrombosis is excessively rare, it should be considered as a cause for sudden deterioration in patients after left SVC cannulation during cardiopulmonary bypass.
| Acknowledgments |
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This article has been cited by other articles:
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J. Stevenhagen, A. Meijer, F. A. Bracke, and B. M. van Gelder Coronary sinus atresia and persistent left superior vena cava with the presence of thrombus complicating implantation of a left ventricular pacing lead Europace, March 1, 2008; 10(3): 384 - 387. [Abstract] [Full Text] [PDF] |
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E. Neri, A. Tripodi, E. Tucci, G. Capannini, and C. Sassi Dramatic improvement of LV function after coronary sinus thromboembolectomy Ann. Thorac. Surg., September 1, 2000; 70(3): 961 - 963. [Abstract] [Full Text] [PDF] |
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