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Transient cerebral ischemic attacks associated with worn porcine heterograft prosthesis
Transient cerebral ischemic attacks associated with worn porcine heterograft prosthesis Case report Details are reviewed of a case (if transient cerebral ischemic attacks which probably resulted from thromboembolism from a Hancock porcine heterograft prosthesis. Cause (if the embolism probably was thrombus formation on the worn cloth covering of the supporting valve stent . Technical and anatomic factors which assure precise seating of the prosthesis in the mitral anulus without contacting the ventricular wall appear to be important in preventing this complication.
Fred Stahrnann, M.D.,* Hurley W. Knott, M.D.,** and Donald B. Doty, M.D., Iowa City, Iowa
Since its introduction by Carpentier and associates 1 in 1969, the glutaraldehyde-preserved porcine aortic homograft valve has been increasingly utilized for mitral valve replacement. The popularity of this valve is due to its low incidence of thromboembolism, so that longterm anticoagulation is not required. Nevertheless, a low incidence of embolic episodes associated with this valve has been reported." 3 This report reviews a case of probable embolization from a Hancock bioprosthesis causing transient cerebral ischemic attacks. The source of emboli appeared to be the cloth covering of the supporting valve stent, which was worn owing to contact between one strut of the valve and the ventricular septum, with thrombus formation on the denuded strut.
Case report A 64-year-old white woman had been followed at The University of Iowa Hospitals and Clinics since 1949, when she first presented with symptoms and signs of congestive From the Division of Thoracic and CardiovascularSurgery. Department of Surgery, The University of Iowa Hospitals and Clinics, Iowa City, Iowa 52242. Received for publication Nov. 13, 1978. Accepted for publication Dec. 14, 1978. Address for reprints: Donald B. Doty, M.D., Professor, Division of Thoracic and Cardiovascular Surgery, Department of Surgery, The University of Iowa Hospitals and Clinics, Iowa City, Iowa 52242. *Allending Surgeon, The Lexington Clinic, Lexington, Ky. **Attending Surgeon, Baptist-Montclaire Hospital, Birmingham, Ala.
872
heart failure. Treatment with digitalis and diuretics provided relief of symptoms until 1967, when she returned with a Grade 5/6 pansystolic murmur at the cardiac apex radiating to the left axilla, hepatomegaly, and marked ankle edema. Electrocardiogram showed right bundle branch block and left axis deviation. Cardiac catheterization revealed a partial atrioventricular canal defect with marked mitral valve incompetence. An operation was performed with repair of the cleft mitral valve and closure of the atrial septal defect with a Teflon patch. Postoperative course was uncomplicated. She did well for 2 years but then began to have signs of cardiomegaly and hepatomegaly. Heart failure was stabilized with medical therapy until November, 1975, when failure rapidly worsened. Cardiac catheterization showed severe mitral valve incompetence and significant tricuspid valve incompetence. At operation, the anterior leaflet of the mitral valve was scarred and fused to the septum and the previously placed Teflon patch. The mitral valve was excised and replaced with a 27 mm. porcine heterograft prosthesis.* The valve was sutured to the scarred anulus at its junction with the Teflon patch. Sutures were taken through the patch to close a small leak at the lower edge of the patch. After the operation, heart failure persisted but gradually responded to vigorous medical therapy. By April, 1976, heart failure and signs of tricuspid valve incompetence prompted cardiac catheterization, which showed moderate tricuspid valve incompetence, severe mitral paravalvular leak, and an 8 mm. Hg gradient across the mitral prosthesis. The patient would not consent to reoperation. In August, 1976, the patient had severe heart failure with exertional and paroxysmal nocturnal dyspnea. She had gained 27 pounds and exhibited ascites, ankle edema, marked cardiomegaly, and hepatomegaly. Heart failure did not respond to medical therapy. Three transient cerebral ischemic attacks then occurred. These episodes were characterized by transient *Hancock Laboratories, Inc., Tustin, Calif.
0022-5223/79/060872+03$00.30/0 © 1979 The C. V. Mosby Co.
Volume 77 Number 6 June, 1979
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loss of speech and weakness of the right upper extremity. No permanent neurologic deficit occurred. Noninvasive examination of the extracranial vascular system (Doppler) showed no abnormalities. At operation in September, 1976, the prosthesis was found dehisced at the junction of the mitral anulus with the Teflon patch closing the atrial septal defect. Otherwise, the atrial aspect of the prosthesis was well healed and covered with thin, glistening neointima. The Dacron cloth covering of the supporting strut of the prosthetic stent, which abutted against the ventricular septum anteriorly, had become completely worn through. At this location there was a fibrin clot on the prosthesis (Fig. I), and the endocardium of the septum was calcified where the prosthesis was in juxtaposition. The Hancock mitral prosthesis and the tricuspid valve, which was scarred and contracted, were replaced with Bjork-Shiley prostheses. She was discharged much improved 14 days after the operation. No further cerebral symptoms have been noted during a 16 month follow-up period.
Comment
In this case, contact occurred between one of the struts of the valve and the ventricular septum and resulted in wearing away of the Dacron cloth covering. This worn area served as a site for thrombus formation, which was probably' the source of emboli for three transient ischemic attacks. This mechanism of thrombus formation has not been reported previously and should not be expected to occur when the prosthetic valve is seated in a normal anatomic position. When the prosthetic valve is seated with the anulus in a normal anatomic position, the struts will project into the ventricular chamber away from the septum, and no contact should take place. In this case, dehiscence of the septal portion of the valve from the anulus, causing para valvular leak, may have resulted in sufficient motion of the prosthesis to bring it into contact with the septum. Also, the relationship of the mitral anulus to the septum may have been distorted by the primary anomaly of partial atrioventricular canal. Prior closure of the atrial septal defect with a Teflon patch along with dense fibrous scarring may have displaced the septal portion of the anulus. In addition, during the initial mitral valve replacement, suture placement incorporated the patch material along the septum, which may have caused the septal portion of the valve to seat higher than intended or at an angle allowing strut contact with the ventricular septum. The exact mechanism responsible for contact between the septum and the valve strut, however, was not precisely determined in this case. Porcine heterograft prostheses are generally considered to be "low profile" valves. However, the atrioventricular porcine heterograft prosthesis reported here has a significant profile length ranging from 19 to 26 mm. depending on the size of prosthesis employed.
Fig. I. Thrombus is present on the strut of the valve at the point at which the Dacron covering has been worn away.
This is related to the height of the porcine aortic valve commissures and the slightly greater length of stent support required. Most reported embolic episodes from porcine heterograft valves in the mitral position have occurred in patients in whom systemic conditions existed which predisposed to thrombus formation. Low cardiac output," atrial fibrillation," chronic renal failure with dialysis, and estrogen therapy" have been associated with embolic phenomena. In this case, thrombus formation occurred because of an abnormal anatomic relationship which allowed one strut of the valve to come into contact with the ventricular septum and resulted in cloth wear and subsequent thrombus formation. The patient had three transient episodes of cerebral ischemia which, fortunately, left no permanent neurologic injury. These transient ischemic attacks probably were related to emboli from the thrombus on the damaged prosthesis, because the episodes ceased once the prosthesis was removed and have not recurred during a long follow-up period. In this case, however, it must be recognized that cerebrovascular angiography was not performed to rule out other sources of emboli or other causes of cerebral ischemic attacks. The status of the cerebrovascular system was evaluated by noninvasive Doppler studies, which did not absolutely exclude ulcerative plaques in the carotid system. Therefore, a cause and effect relationship between the prosthetic valve and embolic phenomena has not been unequivocally established. Nevertheless, cloth wear on a
The Journal of
874 Stahmann, Knott, Doty
Thoracic and Cardiovascular Surgery
porcine heterograft prosthesis was associated with thrombus formation, a clinical setting in which embolic cerebral ischemic attacks would likely be associated. This case report underscores the importance of technical and anatomic factors which must be considered in precise seating of this prosthesis into the mitral anulus so that contact of the struts with the ventricular wall is prevented. REFERENCES Carpentier A, Lemaigre G, Robert L, Carpentier S, Dubost C: Biological factors affecting long-term results of valvular heterografts. J THORAC CARDIOVASC SURG 58:467-483, 1969 2 Cevese PG, Gallucci V, Morea M, et al: Heart valve replacement with the Hancock bioprosthesis. Analysis of long-term results. Cardiovasc Surg 17:Suppl 2: 111-116, 1976
3 Salomon NW, Stinson EB, Griepp RB, et al: Mitral valve replacement. Long-term evaluation of prosthesis-related mortality and morbidity. Circulation 56:Suppl 2:94-101, 1977 4 Spray TL, Roberts WC: Structural changes in porcine xenografts used as substitute cardiac valves. Gross and histologic observations in 51 glutaraldehyde-preserved Hancock valves in 41 patients. Am J Cardiol 40:319-330, 1977 5 Horowitz MS, Goodman DJ, Fogarty TJ, Harrison DC: Mitral valve replacement with the glutaraldehyde-preserved porcine heterograft. Clinical, hemodynamic, and pathological correlations. J THORAC CARDIOVASC SURG 67:885-895, 1974 6 Fishbein MC, Gissen SA, Collins JJ Jr, et al: Pathologic findings after cardiac valve replacement with glutaraldehyde-fixed porcine valves. Am J Cardiol 40:331-337, 1977
Copyright information The appearance of a code at the bottom of the first page of an original article in this journal indicates the copyright owner's consent that copies of the article may be made for personal or internal use, or for the personal or internal use of specific clients. This consent is given on the condition, however, that the copier pay the stated per copy fee through the Copyright Clearance Center, Inc., P.O. Box 765, Schenectady, N. Y. 12301,518-3744430, for copying beyond that permitted by Sections 107 or 108 of the U. S. Copyright Law. This consent does not extend to other kinds of copying, such as copying for general distribution, for advertising or promotional purposes, for creating new collective works, or for resale.
Fred Stahrnann, M.D.,* Hurley W. Knott, M.D.,** and Donald B. Doty, M.D., Iowa City, Iowa
Since its introduction by Carpentier and associates 1 in 1969, the glutaraldehyde-preserved porcine aortic homograft valve has been increasingly utilized for mitral valve replacement. The popularity of this valve is due to its low incidence of thromboembolism, so that longterm anticoagulation is not required. Nevertheless, a low incidence of embolic episodes associated with this valve has been reported." 3 This report reviews a case of probable embolization from a Hancock bioprosthesis causing transient cerebral ischemic attacks. The source of emboli appeared to be the cloth covering of the supporting valve stent, which was worn owing to contact between one strut of the valve and the ventricular septum, with thrombus formation on the denuded strut.
Case report A 64-year-old white woman had been followed at The University of Iowa Hospitals and Clinics since 1949, when she first presented with symptoms and signs of congestive From the Division of Thoracic and CardiovascularSurgery. Department of Surgery, The University of Iowa Hospitals and Clinics, Iowa City, Iowa 52242. Received for publication Nov. 13, 1978. Accepted for publication Dec. 14, 1978. Address for reprints: Donald B. Doty, M.D., Professor, Division of Thoracic and Cardiovascular Surgery, Department of Surgery, The University of Iowa Hospitals and Clinics, Iowa City, Iowa 52242. *Allending Surgeon, The Lexington Clinic, Lexington, Ky. **Attending Surgeon, Baptist-Montclaire Hospital, Birmingham, Ala.
872
heart failure. Treatment with digitalis and diuretics provided relief of symptoms until 1967, when she returned with a Grade 5/6 pansystolic murmur at the cardiac apex radiating to the left axilla, hepatomegaly, and marked ankle edema. Electrocardiogram showed right bundle branch block and left axis deviation. Cardiac catheterization revealed a partial atrioventricular canal defect with marked mitral valve incompetence. An operation was performed with repair of the cleft mitral valve and closure of the atrial septal defect with a Teflon patch. Postoperative course was uncomplicated. She did well for 2 years but then began to have signs of cardiomegaly and hepatomegaly. Heart failure was stabilized with medical therapy until November, 1975, when failure rapidly worsened. Cardiac catheterization showed severe mitral valve incompetence and significant tricuspid valve incompetence. At operation, the anterior leaflet of the mitral valve was scarred and fused to the septum and the previously placed Teflon patch. The mitral valve was excised and replaced with a 27 mm. porcine heterograft prosthesis.* The valve was sutured to the scarred anulus at its junction with the Teflon patch. Sutures were taken through the patch to close a small leak at the lower edge of the patch. After the operation, heart failure persisted but gradually responded to vigorous medical therapy. By April, 1976, heart failure and signs of tricuspid valve incompetence prompted cardiac catheterization, which showed moderate tricuspid valve incompetence, severe mitral paravalvular leak, and an 8 mm. Hg gradient across the mitral prosthesis. The patient would not consent to reoperation. In August, 1976, the patient had severe heart failure with exertional and paroxysmal nocturnal dyspnea. She had gained 27 pounds and exhibited ascites, ankle edema, marked cardiomegaly, and hepatomegaly. Heart failure did not respond to medical therapy. Three transient cerebral ischemic attacks then occurred. These episodes were characterized by transient *Hancock Laboratories, Inc., Tustin, Calif.
0022-5223/79/060872+03$00.30/0 © 1979 The C. V. Mosby Co.
Volume 77 Number 6 June, 1979
Porcine heterograft prosthesis
873
loss of speech and weakness of the right upper extremity. No permanent neurologic deficit occurred. Noninvasive examination of the extracranial vascular system (Doppler) showed no abnormalities. At operation in September, 1976, the prosthesis was found dehisced at the junction of the mitral anulus with the Teflon patch closing the atrial septal defect. Otherwise, the atrial aspect of the prosthesis was well healed and covered with thin, glistening neointima. The Dacron cloth covering of the supporting strut of the prosthetic stent, which abutted against the ventricular septum anteriorly, had become completely worn through. At this location there was a fibrin clot on the prosthesis (Fig. I), and the endocardium of the septum was calcified where the prosthesis was in juxtaposition. The Hancock mitral prosthesis and the tricuspid valve, which was scarred and contracted, were replaced with Bjork-Shiley prostheses. She was discharged much improved 14 days after the operation. No further cerebral symptoms have been noted during a 16 month follow-up period.
Comment
In this case, contact occurred between one of the struts of the valve and the ventricular septum and resulted in wearing away of the Dacron cloth covering. This worn area served as a site for thrombus formation, which was probably' the source of emboli for three transient ischemic attacks. This mechanism of thrombus formation has not been reported previously and should not be expected to occur when the prosthetic valve is seated in a normal anatomic position. When the prosthetic valve is seated with the anulus in a normal anatomic position, the struts will project into the ventricular chamber away from the septum, and no contact should take place. In this case, dehiscence of the septal portion of the valve from the anulus, causing para valvular leak, may have resulted in sufficient motion of the prosthesis to bring it into contact with the septum. Also, the relationship of the mitral anulus to the septum may have been distorted by the primary anomaly of partial atrioventricular canal. Prior closure of the atrial septal defect with a Teflon patch along with dense fibrous scarring may have displaced the septal portion of the anulus. In addition, during the initial mitral valve replacement, suture placement incorporated the patch material along the septum, which may have caused the septal portion of the valve to seat higher than intended or at an angle allowing strut contact with the ventricular septum. The exact mechanism responsible for contact between the septum and the valve strut, however, was not precisely determined in this case. Porcine heterograft prostheses are generally considered to be "low profile" valves. However, the atrioventricular porcine heterograft prosthesis reported here has a significant profile length ranging from 19 to 26 mm. depending on the size of prosthesis employed.
Fig. I. Thrombus is present on the strut of the valve at the point at which the Dacron covering has been worn away.
This is related to the height of the porcine aortic valve commissures and the slightly greater length of stent support required. Most reported embolic episodes from porcine heterograft valves in the mitral position have occurred in patients in whom systemic conditions existed which predisposed to thrombus formation. Low cardiac output," atrial fibrillation," chronic renal failure with dialysis, and estrogen therapy" have been associated with embolic phenomena. In this case, thrombus formation occurred because of an abnormal anatomic relationship which allowed one strut of the valve to come into contact with the ventricular septum and resulted in cloth wear and subsequent thrombus formation. The patient had three transient episodes of cerebral ischemia which, fortunately, left no permanent neurologic injury. These transient ischemic attacks probably were related to emboli from the thrombus on the damaged prosthesis, because the episodes ceased once the prosthesis was removed and have not recurred during a long follow-up period. In this case, however, it must be recognized that cerebrovascular angiography was not performed to rule out other sources of emboli or other causes of cerebral ischemic attacks. The status of the cerebrovascular system was evaluated by noninvasive Doppler studies, which did not absolutely exclude ulcerative plaques in the carotid system. Therefore, a cause and effect relationship between the prosthetic valve and embolic phenomena has not been unequivocally established. Nevertheless, cloth wear on a
The Journal of
874 Stahmann, Knott, Doty
Thoracic and Cardiovascular Surgery
porcine heterograft prosthesis was associated with thrombus formation, a clinical setting in which embolic cerebral ischemic attacks would likely be associated. This case report underscores the importance of technical and anatomic factors which must be considered in precise seating of this prosthesis into the mitral anulus so that contact of the struts with the ventricular wall is prevented. REFERENCES Carpentier A, Lemaigre G, Robert L, Carpentier S, Dubost C: Biological factors affecting long-term results of valvular heterografts. J THORAC CARDIOVASC SURG 58:467-483, 1969 2 Cevese PG, Gallucci V, Morea M, et al: Heart valve replacement with the Hancock bioprosthesis. Analysis of long-term results. Cardiovasc Surg 17:Suppl 2: 111-116, 1976
3 Salomon NW, Stinson EB, Griepp RB, et al: Mitral valve replacement. Long-term evaluation of prosthesis-related mortality and morbidity. Circulation 56:Suppl 2:94-101, 1977 4 Spray TL, Roberts WC: Structural changes in porcine xenografts used as substitute cardiac valves. Gross and histologic observations in 51 glutaraldehyde-preserved Hancock valves in 41 patients. Am J Cardiol 40:319-330, 1977 5 Horowitz MS, Goodman DJ, Fogarty TJ, Harrison DC: Mitral valve replacement with the glutaraldehyde-preserved porcine heterograft. Clinical, hemodynamic, and pathological correlations. J THORAC CARDIOVASC SURG 67:885-895, 1974 6 Fishbein MC, Gissen SA, Collins JJ Jr, et al: Pathologic findings after cardiac valve replacement with glutaraldehyde-fixed porcine valves. Am J Cardiol 40:331-337, 1977
Copyright information The appearance of a code at the bottom of the first page of an original article in this journal indicates the copyright owner's consent that copies of the article may be made for personal or internal use, or for the personal or internal use of specific clients. This consent is given on the condition, however, that the copier pay the stated per copy fee through the Copyright Clearance Center, Inc., P.O. Box 765, Schenectady, N. Y. 12301,518-3744430, for copying beyond that permitted by Sections 107 or 108 of the U. S. Copyright Law. This consent does not extend to other kinds of copying, such as copying for general distribution, for advertising or promotional purposes, for creating new collective works, or for resale.