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Acute thrombosis of Starr-Edwards aortic prosthesis
7 9 0 Brief communications
The Journal of Thoracic and Cardiovascular Surgery
It would seem most likely that the fistula in this patient is congenital and that she was able to tolerate the lesion because of the very small functional communication. This allowed minimal soilage and may have even become intermittently occluded with secretions or food particles, which would have permitted brief periods of relief of symptoms. She remains well 3 years after the operation. REFERENCES 1. Fitzgerald RH Jr, Bartles DM, Parker EF. Tracheoesophageal fistulas secondary to carcinoma of the esophagus. J THORAC CARDIOVASC SURG 1981;82:194-7. 2. Hutchin P, Lindskog GE. Acquired esophagobronchial fistula of infectious origin. J THORAC CARDIOVASC SURG 1964;48:1-12. 3. Antkowiak JG, Cohen ML, Kyllonen AS. Tracheoesophageal fistula following blunt trauma. Arch Surg 1974;109:529-31. 4. Halasz NA, Lindskog GE, Liebow AA. Esophagobronchial fistula and bronchopulmonary sequestration. Ann Surg 1962;55:215-20.
Fig. 1. View of the thrombosed valve from the aortic aspect.
Acute thrombosis of Starr-Edwards aortic prosthesis Cumaraswamy Sivathasan, FRCS, Chao Tzee Cheng, FRCPath, FRACP, and Tan Ngoh Chuan, AM, FRACS, Singapore From the Departments of Cardiothoracic Surgery and Pathology, Singapore General Hospital, Singapore. A case of acute valve thrombosis occurring in a Starr-Edwards aortic prosthesis during the immediate postoperative period is reported. This appears to be the first such case to be reported.
Acute thrombosis occurring in a Starr-Edwards aortic prosthesis during the immediate postoperative period has not been previously reported in the English literature. Such a complication occurring during the first 6 hours after aortic valve replacement is described in the following case report. Case hospital dyspnea dyspnea
report. A 56-year-old man was admitted to the in August 1985 with a history of progressive effort of 18 months' duration and paroxysmal nocturnal of 4 months' duration.
Address for reprints: C. Sivathasan, Department of Cardiothoracic Surgery, Singapore General Hospital, Outram Rd, Singapore 0316, Republic of Singapore.
Fig. 2. View of the thrombosed valve from the ventricular aspect. The clinical findings were compatible with a diagnosis of aortic stenosis and regurgitation. The cardiac catheterization study revealed aortic stenosis with a gradient of 126 mm Hg and a left ventricular systolic pressure of 238 mm Hg. The left ventricular end-diastolic pressure was 27 mm Hg with an ejection fraction of 39%. He had grade 3/4 aortic regurgitation. The coronary angiogram demonstrated significant stenoses of the left anterior descending coronary artery, first diagonal branch, and right coronary artery. A diagnosis of rheumatic aortic stenosis and aortic incompetence along with ischemic coronary artery disease was made. The operation was performed with intermittent infusion of crystalloid cold cardioplegic solution, topical cooling, and hypothermia, the temperature being maintained around 25° C. The diseased coronary arteries were bypassed with vein grafts. The aortic valve was replaced with a size 24 mm, Model 1260 Starr-Edwards prosthesis, which was attached with interrupted subannular 2-0 Dacron pledget-supported sutures. Because we believed that the tertiary orifice of the prosthesis could be obstructed by the rather narrow ascending aorta, the aortotomy was closed with a pericardial patch. The patient was weaned from cardiopulmonary bypass with good cardiac contraction.
Volume 94 Number 5 November 1987
On transfer to the intensive care unit he remained in stable condition with adequate cardiac output. The prosthetic clicks were clear. Because the myocardium had been compromised preoperatively, a dopamine infusion of 5 JLg/min/kg body weight was begun along with an infusion of sodium nitroprusside. However, during the first postoperative hour the urine output began to fail and the mean left atrial pressure rose to 23 mm Hg. Increasing dopamine support failed to maintain adequate output, and epinephrine infusion was commenced during the second postoperative hour. The cardiac output continued to fail, and intra-aortic balloon counterpulsation was begun during the third postoperative hour. He remained in a low perfusion state and finally died during the sixth postoperative hour. Autopsy revealed no evidence of cardiac tamponade. The vein grafts were patent and there was no evidence of recent myocardial infarction. Examination of the prosthetic valve revealed fibrin clot formation mounting on three sides of the metal struts and forming a tent. It was adherent to the silicone rubber ball and limited its movements (Fig. 1). When water was flushed from the side of the ventricle, none passed through the valve. There was also thrombus formation along the skirt of the valve (Fig. 2). There were no clots in the chambers of the heart.
Discussion The cause of valve thrombosis in this patient remains unexplained. The gradual fall in the
Brief communications
79 I
cardiac output resulting in relative stasis of the ball valve may explain the cause of thrombosis. However, we have not observed this phenomenon in the past, in patients dying under similar conditions. A narrow proximal ascending aorta can hinder the excursion of the ball valve and predispose to thrombosis, but autopsy did not reveal a prosthetic mismatch. Fuster and associates' studied the possible predisposing factors causing thromboembolism after prosthetic valve replacements and could not find a correlation between age, sex, severity of symptoms, and cardiomegaly. Thrombosis occurring on a Starr-Edwards prosthesis is well documented in the literature, but not during the immediate postoperative period. Hence this report appears to describe a unique case. REFERENCE 1. Fuster Y, Pumphrey CW, McGoon MD, Chesebro JH, Pluth JR, McGoon DC. Systemic thromboembolism in mitral and aortic Starr-Edwards prosthesis. Circulation 1982;66(Pt 2):1157-61.
The Journal of Thoracic and Cardiovascular Surgery
It would seem most likely that the fistula in this patient is congenital and that she was able to tolerate the lesion because of the very small functional communication. This allowed minimal soilage and may have even become intermittently occluded with secretions or food particles, which would have permitted brief periods of relief of symptoms. She remains well 3 years after the operation. REFERENCES 1. Fitzgerald RH Jr, Bartles DM, Parker EF. Tracheoesophageal fistulas secondary to carcinoma of the esophagus. J THORAC CARDIOVASC SURG 1981;82:194-7. 2. Hutchin P, Lindskog GE. Acquired esophagobronchial fistula of infectious origin. J THORAC CARDIOVASC SURG 1964;48:1-12. 3. Antkowiak JG, Cohen ML, Kyllonen AS. Tracheoesophageal fistula following blunt trauma. Arch Surg 1974;109:529-31. 4. Halasz NA, Lindskog GE, Liebow AA. Esophagobronchial fistula and bronchopulmonary sequestration. Ann Surg 1962;55:215-20.
Fig. 1. View of the thrombosed valve from the aortic aspect.
Acute thrombosis of Starr-Edwards aortic prosthesis Cumaraswamy Sivathasan, FRCS, Chao Tzee Cheng, FRCPath, FRACP, and Tan Ngoh Chuan, AM, FRACS, Singapore From the Departments of Cardiothoracic Surgery and Pathology, Singapore General Hospital, Singapore. A case of acute valve thrombosis occurring in a Starr-Edwards aortic prosthesis during the immediate postoperative period is reported. This appears to be the first such case to be reported.
Acute thrombosis occurring in a Starr-Edwards aortic prosthesis during the immediate postoperative period has not been previously reported in the English literature. Such a complication occurring during the first 6 hours after aortic valve replacement is described in the following case report. Case hospital dyspnea dyspnea
report. A 56-year-old man was admitted to the in August 1985 with a history of progressive effort of 18 months' duration and paroxysmal nocturnal of 4 months' duration.
Address for reprints: C. Sivathasan, Department of Cardiothoracic Surgery, Singapore General Hospital, Outram Rd, Singapore 0316, Republic of Singapore.
Fig. 2. View of the thrombosed valve from the ventricular aspect. The clinical findings were compatible with a diagnosis of aortic stenosis and regurgitation. The cardiac catheterization study revealed aortic stenosis with a gradient of 126 mm Hg and a left ventricular systolic pressure of 238 mm Hg. The left ventricular end-diastolic pressure was 27 mm Hg with an ejection fraction of 39%. He had grade 3/4 aortic regurgitation. The coronary angiogram demonstrated significant stenoses of the left anterior descending coronary artery, first diagonal branch, and right coronary artery. A diagnosis of rheumatic aortic stenosis and aortic incompetence along with ischemic coronary artery disease was made. The operation was performed with intermittent infusion of crystalloid cold cardioplegic solution, topical cooling, and hypothermia, the temperature being maintained around 25° C. The diseased coronary arteries were bypassed with vein grafts. The aortic valve was replaced with a size 24 mm, Model 1260 Starr-Edwards prosthesis, which was attached with interrupted subannular 2-0 Dacron pledget-supported sutures. Because we believed that the tertiary orifice of the prosthesis could be obstructed by the rather narrow ascending aorta, the aortotomy was closed with a pericardial patch. The patient was weaned from cardiopulmonary bypass with good cardiac contraction.
Volume 94 Number 5 November 1987
On transfer to the intensive care unit he remained in stable condition with adequate cardiac output. The prosthetic clicks were clear. Because the myocardium had been compromised preoperatively, a dopamine infusion of 5 JLg/min/kg body weight was begun along with an infusion of sodium nitroprusside. However, during the first postoperative hour the urine output began to fail and the mean left atrial pressure rose to 23 mm Hg. Increasing dopamine support failed to maintain adequate output, and epinephrine infusion was commenced during the second postoperative hour. The cardiac output continued to fail, and intra-aortic balloon counterpulsation was begun during the third postoperative hour. He remained in a low perfusion state and finally died during the sixth postoperative hour. Autopsy revealed no evidence of cardiac tamponade. The vein grafts were patent and there was no evidence of recent myocardial infarction. Examination of the prosthetic valve revealed fibrin clot formation mounting on three sides of the metal struts and forming a tent. It was adherent to the silicone rubber ball and limited its movements (Fig. 1). When water was flushed from the side of the ventricle, none passed through the valve. There was also thrombus formation along the skirt of the valve (Fig. 2). There were no clots in the chambers of the heart.
Discussion The cause of valve thrombosis in this patient remains unexplained. The gradual fall in the
Brief communications
79 I
cardiac output resulting in relative stasis of the ball valve may explain the cause of thrombosis. However, we have not observed this phenomenon in the past, in patients dying under similar conditions. A narrow proximal ascending aorta can hinder the excursion of the ball valve and predispose to thrombosis, but autopsy did not reveal a prosthetic mismatch. Fuster and associates' studied the possible predisposing factors causing thromboembolism after prosthetic valve replacements and could not find a correlation between age, sex, severity of symptoms, and cardiomegaly. Thrombosis occurring on a Starr-Edwards prosthesis is well documented in the literature, but not during the immediate postoperative period. Hence this report appears to describe a unique case. REFERENCE 1. Fuster Y, Pumphrey CW, McGoon MD, Chesebro JH, Pluth JR, McGoon DC. Systemic thromboembolism in mitral and aortic Starr-Edwards prosthesis. Circulation 1982;66(Pt 2):1157-61.