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Results of valve replacement with the Lillehei-Kaster disc prosthesis
Results of valve replacement w i t h the Lillehei Kaster disc prosthesis Robert Forman, M.B., Ch.B. (Cape Town), F.C.P. (S.A.) Walter Beck, M.Med. (Cape Town), F.R.C.P. (London), F.A.C.C. Christiaan N. Barnard, M.Med., M.D., D.Sc. (Cape Town), M.S. (Minn.), F.A.C.S., F.A.C.C. Cape Town, South
Africa
The choice of a prosthesis for replacement of a diseased cardiac valve is based on its mechanical efficiency, low incidence of complications, and ease of insertion. Caged prostheses may cause significant valvar obstruction'' - and may be difficult to insert in patients with small aortic roots. They may malfunction or cause arrhythmias when inserted in the mitral position in patients with small ventricular cavities.' The Lillehei-Kaster aortic and mitral valves were designed with the objective of eliminating these problems.^ They are low profile valves which have a pivoting disc with central flow to reduce transvalvar gradients and thrombus formation. The disc tilts eccentrically with fourfifths of the flow passing through the larger orifice and one-fifth through the smaller. The disc is made of thrombo-resistant Pyrolite. The titanium base and retaining struts are bare while the outer annulus is covered with knitted Teflon. The reported functional and hemodynamic advantages^ •' prompted us to submit these valves to critical trial in our clinic. This report deals with the results of aortic and mitral valve replacement in a series of 150 patients. Subjects and methods
An unselected total of 150 patients underwent valve replacement surgery with Lillehei-Kaster From the Cardiac Clinic, Groote Schuur Hos{Jital, and the Departments of Medicine and Cardiac Surgery, University of Cape Town, Cape Town, South Africa. This work was supported by a Grant-in-Aid from the Cape Town City Council, Cape Town, South Africa. Received for publication Apr. 29, 1976. Accepted for publication June 22, 1976. Reprint requests: Dr. Robert Forman, Cardiac Clinic, Groote Schuur Hospital, Cape Town, 8001, South Africa.
282
prostheses during the period July, 1972, to December, 1973. These may be grouped as follows: Aortic valve replacement: 71 patients (72 operations). All these patients were symptomatic: 53 were in Class III or IV (N.Y. Heart Association) and 12 in Class II, five had embolism from previous aortic valve replacement and two had aortic insufficiency following treatment for infected prosthetic valves. Infective endocarditis was present at the time of operation in five patients. Mitral valve replacement: 62 patients (63 operations). Fifty-nine were in Class III or IV at the time of surgery and four were in Class II. Double and triple valve replacement: 17 patients. All these patients were in Class III or IV. Warfarin therapy was administered postoperatively to 120 of the 137 surviving patients with the objective of controlling the Quick prothrombin time between 22 and 30 seconds. In 17 patients it was withheld because distance to be travelled made it impractical, specific contraindications were present, or patients were unreliable. Followup extended from 18 to 40 months. We examined 103 of the patients at our outpatient clinic at three-monthly intervals except those living at a long distance, where information was obtained by letter from these patients and their physicians. Five patients were lost to follow-up. The results were analyzed using actuarial methods described by Anderson and co-workers." Only occurrences of definite embolism or valve thrombosis were included in analyses. Episodes of dizziness, transient visual disturbances, or emboli from infected prosthetic valves were not analyzed. Cerebral
September, 1977, Vol. 94, No. 3, pp. 282-286
Lillehei-Raster
emboli were termed "major" if permanent neurological deficit resulted and "transient" if the patient recovered completely. Results
disc
prosthesis
100
u 80
Aortic valve replacement.
Operative mortality and postoperative disability. Six intra-operative or hospital deaths occurred (8% mortality). Prosthetic valve malfunction was not implicated in any of these deaths. Of the 65 survivors, 9 patients had Class II or more disability. Four of these patients had infective endocarditis at time of surgery. Late deaths. Fourteen patients died after discharge from hospital: two from infective endocarditis, two from thromboembolism, two from cardiac failure, and three from non-cardiac disease; two had diffuse coronary artery disease incompletely revascularized with aortic coronary bypass grafts. Three patients died suddenly and unexpectedly. The cause of death was not evident at autopsy in two of the latter patients. Thromboembolism. Six of the surviving patients (9 per cent) developed thromboembolic complications. Two of these patients who were not receiving anticoagulants died: one had a minor and a major cerebral embolus, and the other had a thrombosed prosthetic valve (proved at postmortem). In the other four patients, all receiving anticoagulants, there were three transient and one major cerebral embolic episodes. Actuarial analysis of deaths and thromboembolism is shown in Fig. 1. The cummulative thromboembolic-free rate three years following aortic valve replacement was 89 per cent. Mechanical problems. No instance of mechanical malfunction of prostheses apart from thrombosis was recorded. One patient with infective endocarditis at the time of surgery developed significant paravalvar leak and underwent reoperation. Specific investigations to detect minor degrees of hemolysis were not undertaken, but overt hemolytic anemia was not observed. Valve sounds and murmurs. An opening sound was audible in only two patients. It was soft and could have been easily missed. Phonocardiograms were recorded in 31 patients and opening sounds were noted in five. An ejection systolic murmur was recorded in 28 patients. Mitral valve replacement.
Operative mortality and postoperative disability. Seven operative or hospital deaths occurred
American Heart Journal
60
o 40
20
1/12
1
2
3
Fig. 1. Actuarial survival and thromboembolic incidence in 71 patients (72 operations) given Lillehei-Kaster aortic prostheses. Solid circles = per cent survival, open circles = per cent thromboembolic-free patients. Vertical bars denote standard errors.
(11 per cent mortality rate). No deaths were attributed to prosthetic valve malfunction. Eighteen of the surviving 55 patients had Grade II or more disability. Late deaths. Seven late deaths occurred: one from a thrombosed valve, one from infective endocarditis, one from intracerebral hemorrhage related to anticoagulant therapy, one from noncardiac disease and three from cardiac failure (one of these had a normal prosthetic valve function at recatheterization; the other two developed their symptoms acutely and were not recatheterized or examined postmortem). Thromboembolism. Seven of the surviving patients (13 per cent), all of whom received Warfarin therapy, developed thromboembolic episodes. One patient had a transient cerebral episode and another required a femoral embolectomy. Five patients had a total of 6 episodes of valvar thrombosis with acute or subacute left heart failure. Emergency valve replacement was successfully undertaken in three of these patients (one patient thrombosed two successive LilleheiKaster mitral prostheses). The other two patients died: one from valvar thrombosis which was present at postmortem, the other following emergency surgery. Two patients had multiple peripheral emboli prior to valve thrombosis. The angiogram of a thrombosed valve with its opera-
283
Forman, Beck, and Barnard
f
i*-^
B
1-76
'5
Fig. 2A and B. A, Left ventricular angiogram in a patient with thrombosed Lillehei-Kaster mitral prosthesis (R.A.O,). The thrombus produces a translucent contrast-free area on the ventricular side of the prosthesis. The left atrium is filled with contrast medium due to prosthetic valvar insufficiency. B, The operative specimen.
tive specimen is illustrated in Fig. 2. In five patients the thrombus involved the bare titanium base and spread to the metal retaining struts, and occluded the smaller of the two mitral orifices. Actuarial analysis of deaths and thromboembolism is shown in Fig. 3. The cummulative thromboembolic-free rate three years following mitral valve replacement was 78 per cent. Mechanical problems. No instance of mechanical malfunction of prostheses (other than thrombosis) or overt hemolytic anemia was detected. Two patients developed mitral incompetence in the early postoperative period and were reoperated upon using Starr-Edwards prostheses. Both these patients had extensive calcification of the mitral annulus which made suturing difficult. Valve sounds and murmurs. Phonocardiograms were recorded in 34 patients postoperatively. Apical mid-diastolic murmurs were observed in 21 patients (62 per cent). A mitral systolic murmur was not recorded in any patient with a normally functioning prothesis. A soft mitral opening sound was audible in two patients and phonocardiographically recorded in five (15 per cent). Multiple valve replacement. There were no operative deaths. Four late deaths occurred: two from thromboembolism, one from infective endocarditis and one patient, who was recatheterized postoperatively and had normal prosthetic aortic and mitral valve function, died with low cardiac output. Three patients (18 per cent) had thromboembolic episodes: one who was not receiving
284
anticoagulants died of a cerebral embolus, one died of a thrombosed prosthesis confirmed at postmortem, and one had a transient cerebral episode. One patient developed severe hemolytic anemia with a hemoglobin of 7 Gm. per cent, corrected reticulocyte count 7,5 per cent, serum bilirubin 2.5 mg. per cent, haptoglobin under 20 mg. per cent and LDH 1324u. Hemosiderin was present in the urine. Following oral iron therapy, this patient has maintained a normal hematocrit. Discussion
In a series of 68 patients alternately given Lillehei-Kaster and Bjork-Shiley disc aortic prostheses, Nitter-Hauge and colleagues^ clinically assessed the Lillehei-Kaster valve to be satisfactory and no different from the Bjork-Shiley prosthesis. No thromboembolic episodes were recorded during a one year follow-up period. Lillehei and associates* recorded two transient thromboembolic episodes during a two year follow-up of 75 patients with aortic or mitral valve replacement. In their series anticoagulant therapy was given only to patients with more advanced preoperative cardiac disease. They reported there was no evidence of significant postoperative intravascular hemolysis. In the present series of 150 patients the results have been analyzed by actuarial methods. The operative mortality rate, which was partly due to the patients' poor preoperative state, was not attributed to the prosthesis itself in any instance.
September,
1977, Vol. 94, No. 3
Lillehei-Kaster
A serious thromboembolic rate occurred particularly in patients with mitral prostheses, despite anticoagulant therapy. Patients with obstructed prostheses had extensive thrombus formation on the bare metallic base extending to the metallic struts. We believe this bare metal to be a nidus for thrombus formation and possibly a serious defect in valve design. Only rarely were opening sounds of aortic and mitral prostheses audible or phonocardiographically recordable. This series confirms the report by Gibson and co-workers' of low intensity and infrequency of recorded mitral openings sounds and the frequent occurrence of mid-diastolic murmurs, but contrary to that report, in our patients mitral systolic murmurs were not recorded with normally functioning prostheses. In our series early detection of significant mitral valve obstruction by auscultation and phonocardiography was difficult because a mid-diastolic murmur and absence of an opening sound was frequently encountered in apparently normally functioning valves. Valvar obstruction was suspected when sudden left heart failure occurred. In non-thrombosed aortic and mitral prostheses in our series, the hemodynamic results have been satisfactory on clinical assessnient. We attributed postoperative effort intolerance and cardiac decompensation to residual cardiac disease. In a separate report to be published on the results of postoperative recatheterization of our patients we document that the mitral and larger aortic prostheses have a satisfactory calculated functional valve area whereas the smaller aortic valves produced significant valve obstruction. No instance of prosthetic malfunction, excluding valvar thrombosis, was detected. One patient with an aortic and mitral prosthesis developed overt intravascular hemolysis. Our conclusion is that Lillehei-Kaster aortic and mitral valve prostheses have not been satisfactory in our series of patients. A significant thromboembolic rate has been encountered and has discouraged us from continuing to use these prostheses in our institution.
disc
prosthesis
100
80
< a. 60
< 40
20
1/12 YEARS
Fig. 3. Actuarial survival and thromboembolic incidence in 62 patients (63 operations) given Lillehei-Kaster mitral prostheses. Symbols as in Fig. 1.
tive thromboembolic-free rate three years following mitral valve replacement and 89 per cent following aortic valve replacement. Five patients had a total of six episodes of mitral valve thrombosis despite anticoagulant therapy. Early detection of mitral valve obstruction was difficult because a mid-diastolic murmur and absence of an opening sound was frequently encountered in normally functioning prostheses. Hemodynamic results assessed clinically in patients with nonthrombosed prostheses were satisfactory. Addendum
A recent report has indicated t h a t rapid washout of angiographic dye in the aorta was observed only on the larger opening side of the Lillehei-Kaster disc valve whereas turbulence and persistence of contrast medium with delayed washout occurred on the smaller orifice side." We believe this to possibly be an explanation for our observation that the thrombus formation was always in the smaller of the two orifices of thrombosed prostheses.
Summary
The results of valve replacement in 150 patients with Lillehei-Kaster aortic and mitral prostheses followed for 20 to 40 months are reviewed. Actuarial analysis showed 78 per cent cummula-
American Heart Journal
REFERENCES
1. 2.
Bjork, V. O., and Olin, C : The hydrodynamic performance of the pediatric Bjork-Shiley disc valve prosthesis, Scand. J. Thorac. Cardiovasc. Surg. 6:1, 1972. Stenseth, J. H., Danielson, G. K., and McGoon, D. C :
285
Forman, Beck, and Barnard
Pericardial patch enlargement of aortic outflow tract, J. Thorac. Cardiovasc. Surg. 62:442, 1971. Roberts, W. C , Bulkley, B. H., and Morrow, A. G.: Pathologic anatomy of cardiac valve replacement. A study of 224 necropsy patients, Progr. Cardiovasc. Dis. 6:539, 1973. Lillehei, C. W., Raster, R. L., Coleman, M., and Bloch, J. H.: Heart valve replacement with Lillehei-Kaster pivoting disk prosthesis, N. Y. State J. Med. 74:1426, 1974. Nitter-Hauge, S., Hall, K.-V., Froysaker, T., and Efskind, L.: Aortic valve replacement. One year results with Lillehei-Kaster and Bjork-Shiley disc prostheses, A M .
Anderson, R. P., Boncheck, L. I., Grunkemeier, G. L., Lambert, L. E., and Starr, A.: The analysis and presentation of surgical results by actuarial methods, J. Surg. Res. 16:224, 1974. Gibson, T. C , Starek, P. J. K., Moos, S., and Craige, B.: Echocardiographic and phonocardiographic characteristics of the Lillehei-Kaster mitral valve prosthesis. Circulation 49:434, 1974. Sigwart, U., Schmidt, H., Gleichmann, U., and Borst, H. G.: In vivo evaluation of the Lillehei-Kaster heart valve prosthesis, Ann. Thorac. Surg. 22:213, 1976.
H E A R T J. 88:23, 1974.
286
September, 1977, Vol. 94, No. 3
Africa
The choice of a prosthesis for replacement of a diseased cardiac valve is based on its mechanical efficiency, low incidence of complications, and ease of insertion. Caged prostheses may cause significant valvar obstruction'' - and may be difficult to insert in patients with small aortic roots. They may malfunction or cause arrhythmias when inserted in the mitral position in patients with small ventricular cavities.' The Lillehei-Kaster aortic and mitral valves were designed with the objective of eliminating these problems.^ They are low profile valves which have a pivoting disc with central flow to reduce transvalvar gradients and thrombus formation. The disc tilts eccentrically with fourfifths of the flow passing through the larger orifice and one-fifth through the smaller. The disc is made of thrombo-resistant Pyrolite. The titanium base and retaining struts are bare while the outer annulus is covered with knitted Teflon. The reported functional and hemodynamic advantages^ •' prompted us to submit these valves to critical trial in our clinic. This report deals with the results of aortic and mitral valve replacement in a series of 150 patients. Subjects and methods
An unselected total of 150 patients underwent valve replacement surgery with Lillehei-Kaster From the Cardiac Clinic, Groote Schuur Hos{Jital, and the Departments of Medicine and Cardiac Surgery, University of Cape Town, Cape Town, South Africa. This work was supported by a Grant-in-Aid from the Cape Town City Council, Cape Town, South Africa. Received for publication Apr. 29, 1976. Accepted for publication June 22, 1976. Reprint requests: Dr. Robert Forman, Cardiac Clinic, Groote Schuur Hospital, Cape Town, 8001, South Africa.
282
prostheses during the period July, 1972, to December, 1973. These may be grouped as follows: Aortic valve replacement: 71 patients (72 operations). All these patients were symptomatic: 53 were in Class III or IV (N.Y. Heart Association) and 12 in Class II, five had embolism from previous aortic valve replacement and two had aortic insufficiency following treatment for infected prosthetic valves. Infective endocarditis was present at the time of operation in five patients. Mitral valve replacement: 62 patients (63 operations). Fifty-nine were in Class III or IV at the time of surgery and four were in Class II. Double and triple valve replacement: 17 patients. All these patients were in Class III or IV. Warfarin therapy was administered postoperatively to 120 of the 137 surviving patients with the objective of controlling the Quick prothrombin time between 22 and 30 seconds. In 17 patients it was withheld because distance to be travelled made it impractical, specific contraindications were present, or patients were unreliable. Followup extended from 18 to 40 months. We examined 103 of the patients at our outpatient clinic at three-monthly intervals except those living at a long distance, where information was obtained by letter from these patients and their physicians. Five patients were lost to follow-up. The results were analyzed using actuarial methods described by Anderson and co-workers." Only occurrences of definite embolism or valve thrombosis were included in analyses. Episodes of dizziness, transient visual disturbances, or emboli from infected prosthetic valves were not analyzed. Cerebral
September, 1977, Vol. 94, No. 3, pp. 282-286
Lillehei-Raster
emboli were termed "major" if permanent neurological deficit resulted and "transient" if the patient recovered completely. Results
disc
prosthesis
100
u 80
Aortic valve replacement.
Operative mortality and postoperative disability. Six intra-operative or hospital deaths occurred (8% mortality). Prosthetic valve malfunction was not implicated in any of these deaths. Of the 65 survivors, 9 patients had Class II or more disability. Four of these patients had infective endocarditis at time of surgery. Late deaths. Fourteen patients died after discharge from hospital: two from infective endocarditis, two from thromboembolism, two from cardiac failure, and three from non-cardiac disease; two had diffuse coronary artery disease incompletely revascularized with aortic coronary bypass grafts. Three patients died suddenly and unexpectedly. The cause of death was not evident at autopsy in two of the latter patients. Thromboembolism. Six of the surviving patients (9 per cent) developed thromboembolic complications. Two of these patients who were not receiving anticoagulants died: one had a minor and a major cerebral embolus, and the other had a thrombosed prosthetic valve (proved at postmortem). In the other four patients, all receiving anticoagulants, there were three transient and one major cerebral embolic episodes. Actuarial analysis of deaths and thromboembolism is shown in Fig. 1. The cummulative thromboembolic-free rate three years following aortic valve replacement was 89 per cent. Mechanical problems. No instance of mechanical malfunction of prostheses apart from thrombosis was recorded. One patient with infective endocarditis at the time of surgery developed significant paravalvar leak and underwent reoperation. Specific investigations to detect minor degrees of hemolysis were not undertaken, but overt hemolytic anemia was not observed. Valve sounds and murmurs. An opening sound was audible in only two patients. It was soft and could have been easily missed. Phonocardiograms were recorded in 31 patients and opening sounds were noted in five. An ejection systolic murmur was recorded in 28 patients. Mitral valve replacement.
Operative mortality and postoperative disability. Seven operative or hospital deaths occurred
American Heart Journal
60
o 40
20
1/12
1
2
3
Fig. 1. Actuarial survival and thromboembolic incidence in 71 patients (72 operations) given Lillehei-Kaster aortic prostheses. Solid circles = per cent survival, open circles = per cent thromboembolic-free patients. Vertical bars denote standard errors.
(11 per cent mortality rate). No deaths were attributed to prosthetic valve malfunction. Eighteen of the surviving 55 patients had Grade II or more disability. Late deaths. Seven late deaths occurred: one from a thrombosed valve, one from infective endocarditis, one from intracerebral hemorrhage related to anticoagulant therapy, one from noncardiac disease and three from cardiac failure (one of these had a normal prosthetic valve function at recatheterization; the other two developed their symptoms acutely and were not recatheterized or examined postmortem). Thromboembolism. Seven of the surviving patients (13 per cent), all of whom received Warfarin therapy, developed thromboembolic episodes. One patient had a transient cerebral episode and another required a femoral embolectomy. Five patients had a total of 6 episodes of valvar thrombosis with acute or subacute left heart failure. Emergency valve replacement was successfully undertaken in three of these patients (one patient thrombosed two successive LilleheiKaster mitral prostheses). The other two patients died: one from valvar thrombosis which was present at postmortem, the other following emergency surgery. Two patients had multiple peripheral emboli prior to valve thrombosis. The angiogram of a thrombosed valve with its opera-
283
Forman, Beck, and Barnard
f
i*-^
B
1-76
'5
Fig. 2A and B. A, Left ventricular angiogram in a patient with thrombosed Lillehei-Kaster mitral prosthesis (R.A.O,). The thrombus produces a translucent contrast-free area on the ventricular side of the prosthesis. The left atrium is filled with contrast medium due to prosthetic valvar insufficiency. B, The operative specimen.
tive specimen is illustrated in Fig. 2. In five patients the thrombus involved the bare titanium base and spread to the metal retaining struts, and occluded the smaller of the two mitral orifices. Actuarial analysis of deaths and thromboembolism is shown in Fig. 3. The cummulative thromboembolic-free rate three years following mitral valve replacement was 78 per cent. Mechanical problems. No instance of mechanical malfunction of prostheses (other than thrombosis) or overt hemolytic anemia was detected. Two patients developed mitral incompetence in the early postoperative period and were reoperated upon using Starr-Edwards prostheses. Both these patients had extensive calcification of the mitral annulus which made suturing difficult. Valve sounds and murmurs. Phonocardiograms were recorded in 34 patients postoperatively. Apical mid-diastolic murmurs were observed in 21 patients (62 per cent). A mitral systolic murmur was not recorded in any patient with a normally functioning prothesis. A soft mitral opening sound was audible in two patients and phonocardiographically recorded in five (15 per cent). Multiple valve replacement. There were no operative deaths. Four late deaths occurred: two from thromboembolism, one from infective endocarditis and one patient, who was recatheterized postoperatively and had normal prosthetic aortic and mitral valve function, died with low cardiac output. Three patients (18 per cent) had thromboembolic episodes: one who was not receiving
284
anticoagulants died of a cerebral embolus, one died of a thrombosed prosthesis confirmed at postmortem, and one had a transient cerebral episode. One patient developed severe hemolytic anemia with a hemoglobin of 7 Gm. per cent, corrected reticulocyte count 7,5 per cent, serum bilirubin 2.5 mg. per cent, haptoglobin under 20 mg. per cent and LDH 1324u. Hemosiderin was present in the urine. Following oral iron therapy, this patient has maintained a normal hematocrit. Discussion
In a series of 68 patients alternately given Lillehei-Kaster and Bjork-Shiley disc aortic prostheses, Nitter-Hauge and colleagues^ clinically assessed the Lillehei-Kaster valve to be satisfactory and no different from the Bjork-Shiley prosthesis. No thromboembolic episodes were recorded during a one year follow-up period. Lillehei and associates* recorded two transient thromboembolic episodes during a two year follow-up of 75 patients with aortic or mitral valve replacement. In their series anticoagulant therapy was given only to patients with more advanced preoperative cardiac disease. They reported there was no evidence of significant postoperative intravascular hemolysis. In the present series of 150 patients the results have been analyzed by actuarial methods. The operative mortality rate, which was partly due to the patients' poor preoperative state, was not attributed to the prosthesis itself in any instance.
September,
1977, Vol. 94, No. 3
Lillehei-Kaster
A serious thromboembolic rate occurred particularly in patients with mitral prostheses, despite anticoagulant therapy. Patients with obstructed prostheses had extensive thrombus formation on the bare metallic base extending to the metallic struts. We believe this bare metal to be a nidus for thrombus formation and possibly a serious defect in valve design. Only rarely were opening sounds of aortic and mitral prostheses audible or phonocardiographically recordable. This series confirms the report by Gibson and co-workers' of low intensity and infrequency of recorded mitral openings sounds and the frequent occurrence of mid-diastolic murmurs, but contrary to that report, in our patients mitral systolic murmurs were not recorded with normally functioning prostheses. In our series early detection of significant mitral valve obstruction by auscultation and phonocardiography was difficult because a mid-diastolic murmur and absence of an opening sound was frequently encountered in apparently normally functioning valves. Valvar obstruction was suspected when sudden left heart failure occurred. In non-thrombosed aortic and mitral prostheses in our series, the hemodynamic results have been satisfactory on clinical assessnient. We attributed postoperative effort intolerance and cardiac decompensation to residual cardiac disease. In a separate report to be published on the results of postoperative recatheterization of our patients we document that the mitral and larger aortic prostheses have a satisfactory calculated functional valve area whereas the smaller aortic valves produced significant valve obstruction. No instance of prosthetic malfunction, excluding valvar thrombosis, was detected. One patient with an aortic and mitral prosthesis developed overt intravascular hemolysis. Our conclusion is that Lillehei-Kaster aortic and mitral valve prostheses have not been satisfactory in our series of patients. A significant thromboembolic rate has been encountered and has discouraged us from continuing to use these prostheses in our institution.
disc
prosthesis
100
80
< a. 60
< 40
20
1/12 YEARS
Fig. 3. Actuarial survival and thromboembolic incidence in 62 patients (63 operations) given Lillehei-Kaster mitral prostheses. Symbols as in Fig. 1.
tive thromboembolic-free rate three years following mitral valve replacement and 89 per cent following aortic valve replacement. Five patients had a total of six episodes of mitral valve thrombosis despite anticoagulant therapy. Early detection of mitral valve obstruction was difficult because a mid-diastolic murmur and absence of an opening sound was frequently encountered in normally functioning prostheses. Hemodynamic results assessed clinically in patients with nonthrombosed prostheses were satisfactory. Addendum
A recent report has indicated t h a t rapid washout of angiographic dye in the aorta was observed only on the larger opening side of the Lillehei-Kaster disc valve whereas turbulence and persistence of contrast medium with delayed washout occurred on the smaller orifice side." We believe this to possibly be an explanation for our observation that the thrombus formation was always in the smaller of the two orifices of thrombosed prostheses.
Summary
The results of valve replacement in 150 patients with Lillehei-Kaster aortic and mitral prostheses followed for 20 to 40 months are reviewed. Actuarial analysis showed 78 per cent cummula-
American Heart Journal
REFERENCES
1. 2.
Bjork, V. O., and Olin, C : The hydrodynamic performance of the pediatric Bjork-Shiley disc valve prosthesis, Scand. J. Thorac. Cardiovasc. Surg. 6:1, 1972. Stenseth, J. H., Danielson, G. K., and McGoon, D. C :
285
Forman, Beck, and Barnard
Pericardial patch enlargement of aortic outflow tract, J. Thorac. Cardiovasc. Surg. 62:442, 1971. Roberts, W. C , Bulkley, B. H., and Morrow, A. G.: Pathologic anatomy of cardiac valve replacement. A study of 224 necropsy patients, Progr. Cardiovasc. Dis. 6:539, 1973. Lillehei, C. W., Raster, R. L., Coleman, M., and Bloch, J. H.: Heart valve replacement with Lillehei-Kaster pivoting disk prosthesis, N. Y. State J. Med. 74:1426, 1974. Nitter-Hauge, S., Hall, K.-V., Froysaker, T., and Efskind, L.: Aortic valve replacement. One year results with Lillehei-Kaster and Bjork-Shiley disc prostheses, A M .
Anderson, R. P., Boncheck, L. I., Grunkemeier, G. L., Lambert, L. E., and Starr, A.: The analysis and presentation of surgical results by actuarial methods, J. Surg. Res. 16:224, 1974. Gibson, T. C , Starek, P. J. K., Moos, S., and Craige, B.: Echocardiographic and phonocardiographic characteristics of the Lillehei-Kaster mitral valve prosthesis. Circulation 49:434, 1974. Sigwart, U., Schmidt, H., Gleichmann, U., and Borst, H. G.: In vivo evaluation of the Lillehei-Kaster heart valve prosthesis, Ann. Thorac. Surg. 22:213, 1976.
H E A R T J. 88:23, 1974.
286
September, 1977, Vol. 94, No. 3