Fundamentals
of clinical
Mitral
for
valve
repair
cardiology
significant
mitral
insufficiency
Jerome Harold Kay, M.D. Pablo Zubiate, M.D. Michael A. Mendez, M.D. Neal Vanstrom, M.D. Taro Yokoyama, M.D. Los An&es,
Calif.
Prior to the article by Starr and Edwards in 1961’ on mitral valve replacement, it was necessary to repair the abnormally functioning mitral valve at the time of surgery, since a prosthetic mitral valve was not available. With the introduction of prosthetic valves, it has been technically easier for surgeons to replace the valve than attempt repair. Our first repair for pure mitral insufficiency was performed in 1959, and except for brief periods, this has remained our method of choice for surgery for significant mitral insufficiency for the past 18 years. Rc;pair has not been popular with surgeons, however, since repair is more difficult and takes greater thought than excising a valve and replacing it with a prosthesis. With 15 years clinical and experimental experience with various prosthetic devices, it is our strong conviction that a mitral prosthesis of any variety or a porcine valve should be inserted only if repair cannot be accomplished. With short- and long-term results of mitral valve replacement being published not only with the Starr-Edwards valve but also the Hancock porcine valve, it would appear of interest to compare these results to the results with repair of the insufficient mitral valve. The following is a report of two groups of patients: 145 patients with From The Los Angeles Heart Institute Center. Los Angeles, and The University of Medicine Los Angeles.
at The St. Vincent of Southern California
Aided by a grant Foundation.
Thoracic
Received Reprint Street.
from
The Los Angeles
for publication requests: Jerome Los Angeles, Calif.
000%8703/78/0296-0253$01.00/O
Dec.
and
Medical School
Cardiovascular
12, 1977.
Harold 900.57.
Kay,
M.D.,
0 1978
123
The
South
Alvarado
C. V. Mosby
Co.
pure mitral insufficiency in whom mitral repair was performed from 1959 to 1977, and 55 patients with mitral insufficiency and coronary artery disease in whom repair was performed at the time of myocardial revascularization from 1970 to 1977. Although the basic principle is the same for repair of the insufficient mitral valve for all patients, the data from the two groups of patients is presented separately in this art,icle. Since 1970 myocardial revascularization has been performed in all but one patient with mitral insufficiency and coronary artery disease requiring mitral valve surgery when significant coronary artery disease was present. In this patient revascularization was not needed nor possible since the vessel obstructed led t.o an area of infarct and the other two vessels had only minimal disease. These patients comprise Group II. There were 14 patients operated upon prior to 1970 with mitral insufficiency and coronary artery disease, but myocardial revascularization was not combined with repair or replacement by us until 1970. These patients are included in the first group of patients with pure mitral insufficiency. There may be other patients in Group I who had coronary artery disease and whose mitral insufficiency was due to or associated with the coronary artery disease and were operated upon for their mitral insufficiency during the years from 1959. If so, the coronary artery disease was not proven even though suspected, since coronary arteriography was not performed in these patients. In order to better understand our approach to
American
Heari
Journal
253
Kay
et
al.
P iapitlary
mug.
Fig. 1. The area of the leaflet involved with stretched or torn chordae tendineae or torn repaired by placing interrupted figure-of-eight sutures of 2-O Tevdek through the head of muscle and then bringing this suture up through the leading edge of the involved area of the separate sutures are used at each area. For ease of exposure, all sutures are placed prior to
Fig. 2. In in size. This bringing it upon. The
order to obliterate the insufficiency, the greatly dilated sagging mural annulus is decreased considerably must be accomplished by decreasing the length of the mural annulus to about % of its size and thereby up into apposition with the anterior leaflet. The annulus of the anterior leaflet cannot be encroached repair is accomplished with No. 2 silk sutures as illustrated.
the repair of the mitral valve, it is important to be familiar with our thinking as to the development of mitral insufficiency. Whether the patient began with mitral valve prolapse without significant insufficiency and over the years developed wide-open mitral insufficiency, or whether the patient had myocarditis and developed mitral insufficiency secondary to this, the progression is similar. With mitral valve prolapse, the annulus is large and the leaflets meet only at their edges. With myocarditis, the left ventricle enlarges, thereby enlarging the annulus, and the mitral leaflets do not coapt. Because the leaflets meet only at their edges or not at all, there is
254
papillary muscle is the nearer papillary leaflet. Usually two tying.
significant tension on the leaflets each time the heart contracts. This creates tension on the chordae tendineae as well. With time the leaflets stretch and enlarge as do the chordae tendineae. In many patients, the chordae tendineae tear. The leaflets are usually thickened and reveal fibromyxoid degeneration. This fibromyxoid degeneration in the leaflets is secondary to the trauma produced by the pressure of the blood on the unsupported leaflets during systole. With mitral insufficiency secondary to coronary artery disease, the mitral insufficiency may be due to tearing of infarcted papillary muscle or
August,
1978, Vol. 96, No. 2
Mitrnl
o-o
\
80%
A GROUP
‘ON “\h,
valve repair
II
-4 70
\
61.5%
--o-o
GROUP
50
o Group A Group
I -Repair II- Repair 1
2
4
TIME 3. Actuarial Program BMDllS.
Fig.
curves:
Mitral
repair
results
17 year Follow up S.E. f 5.5% and Revascularization 7 year Follow up SE. f 6% I I I 1 I
6
8
chordae tendineae because of infarcted papillary muscle. With these patients there is always secondary annular dilatation due to enlargement of the left ventricle. In other patients with coronary artery disease, the infarct may involve the muscle near the annulus with resultant dilatation of the annulus and failure of coaptation of the leaflets. In some patients with a massive infarct the annulus may be stretched due to enlargement of the left ventricle. No matter what the etiology of the mitral insufficiency, it is always necessary to decrease the size of the annulus and this part of the repair is almost always performed in the same manner. This consists of decreasing the length of the mural annulus and not the annulus of the anterior leaflet. The trigona fibrosa cordis prevents the annulus of the anterior leaflet of the mitral valve from stretching. The mural leaflet portion of the annulus does not have a similar support and therefore the mitral annulus dilates at the area of the mural annulus but not the area of the anterior annulus. It is important to remember that the mural annulus only is stretched in all patients with mitral insufficiency. The majority of patients with mitral insufficiency not secondary to coronary artery disease will have torn chordae tendineae and/or stretched chordae tendineae. The patient with mitral insufficiency secondary to myocardial infarction may or may not have torn chordae
American
Heart
Journal
10
INTERVAL for Group
in mifr/rl
12
I
60
-50
I
14
16
II patients
using
(YEARS)
I and
Group
Biomedical
Computer
tendineae or torn papillary muscle, but they will not have associated stretched chordae tendineae unless the insufficiency is of many years’ duration. Technique
The technique of repair is as follows. After opening the left atrium, a careful search is made to determine if there are torn or stretched chordae tendineae or torn papillary muscle. If there are significantly stretched chordae tendineae, torn chordae tendineae or torn papillary muscle, this area of the valve is sutured down to the nearest papillary muscle head (Fig. 1). New chordae are not constructed. The anterolateral, posteromedial, midportion, or all three areas of the mural leaflet may require suturing to the nearest papillary muscle. If there are torn or stretched chordae tendineae of the anterior leaflet, this area is sutured to the head of the papillary muscle involved. If all of the chordae tendineae of the anterior leaflet are stretched, then either the anterolateral or posteromedial portion of the anterior leaflet is sutured to the head of the nearest area involved (Fig. 1). This allows the remaining portion of the anterior leaflet to billow and close against the mural leaflet. It is important for the anterior leaflet to billow in order to abut against the mural leaflet, otherwise the insufficiency will not be corrected. Except for minor variations in individual
255
Kay
et al.
I. Mitral
Table
I
insufficiency without
I
Patient No. 1.
I
I
Age at first surgery
Date of first surgery
R. F. 36
8/11/59
myocardial revascularization-repair
Initial cause of mitral insufficiency
Cause of failure
Torn chordae tendineae of anterior leaflet
Torn chordae not repaired at initial operation
10/l/63
Thrombosis of Starr valve
g/27/74
2.
G. P. 37
g/2/60
Dilated annulus prolapsed anterior leaflet with stretched chordae tendineae
Stenosis with calcification of area of previous repair
7/11/74
3.
M. P. 48
10/31/61
Gross dilatation due to stretched C.T., mural & anterior leaflet
12/10/70
4.
J. P. 37
5/19/64
Dilated annulus with calcification slightly stretched C.T.
Torn C.T. anterior leaflet; greatly dilated tricuspid annulus with insufficiency Stenosis due to calcification of both leaflets
5.
P. c. 39
7/29/66
Torn C.T., leaflet
mural
Recurrence of torn chordae tendineae
l/17/68
6.
T. D. A. 47
g/8/67
Torn C.T., leaflet
mural
Repair of mural leaflet intact. Torn CT. occurred at anterior leaflet
10/8/73
patients, the remaining part of the mitral valve repair is now the same for all patients and consists of decreasing the annulus of the mitral valve by doing away with approximately 65 per cent to 70 per cent of the annulus of the mural leaflet. The annulus is decreased mainly at the posteromedial commissural area, where usually two interrupted figure-of-eight sutures of No. 2 silk are placed and tied to do away with 40 per cent or 45 per cent of the annulus. The same
256
Date of subsequent surgery
9/9/76
failures
Procedure Replacement with No. 3 Starr-Edwards Ball valve 4 yrs. later Replacement with No. 31 Hancock glutaraldehyde porcine valve 11 yrs. later Replacement with No. 29 Hancock, glutaraldehyde porcine valve 14 yrs. later Second repair of mitral valve and primary repair of tricuspid valve 9 yrs. later Replacement with No. 31 Hancock glutaraldehyde porcine valve 12 yrs. Iater Replacement with No. 4 Kay-Shiley disc valve Tricuspid annuloplasty 2 yrs. later Replacement with No. 7 Kay-Shiley disc valve with muscle guard 6 yrs. later
Outcome Ball valve replaced 11 years later for valve thrombosis Living and well on Coumadin 3 yrs.
CVA 3 yrs after insertion of porcine valve. Living and well 3 yrs. on Coumadin Living and well 7 yrs., no murmurs or medication
Living and well 1 year, on Coumadin
Living and well 9.5 years, on Coumadin
Hosp. death, Bronchial pneumonia, probable myocardial in-
procedure is used to decrease the mural annulus of the anterolateral commissural area for another 20 per cent or 25 per cent. The sutures placed at the anterolateral commissural area should not be deep so that the circumflex coronary artery is encircled. When the annuloplasty is completed, approximately 30 per cent or 35 per cent of the mural annulus remains and there is a snug twofingerbreadth opening (Fig. 2). It is important not to encroach on the annulus of the anterior leaflet;
August,
1978,
Vol.
96, No.
2
Mitral
rlaltvz
repair
in mittwl
I., continued
Table
- --
Age at first surgery
Date of first surgery
M. T. 61
10/l/68
8.
J. G. 66
11/26/68
9.
?I. G. 59
10.
G. B.
Patient NO. 7.
Initial cause of mitral insufficiency
Cause of failure
5/ 10176
l/9/69
Torn C.T., leaflet
mural
Mitral insuff. through center of repaired valve
“/“O/69
7114171
Torn C.T., leaflet
mural
Mitral insuf. due to tear of suture line
10/i/71
Torn C.T., mural leaflet; stretched C.T., anterior leaflet; S.B.E. 6 yrs. prior to surgery Dilated annulus with stretched C.T.; coarctation & aortic aneurysmectomy 20 years previously
Torn C.T., anterior leaflet
6/16/7.5
Mitral insuf. due to prolapsed anterior leaflet
4/3/75
E. I,. 57
6/24/74
12.
D. c. 62
12/g/74
otherwise mitral stenosis may be produced without correcting the insufficiency. This technique was first described in 1961 and in subsequent publications.‘-“’ Material Group I-Mitral insufficiency without myocardial revascularization. Between 1959 and 1977,
216 patients were operated upon with significant pure mitral insufficiency. The majority of these patients had mitral valve prolapse with severe insufficiency and without coronary artery disease. Mitral valve repair was performed in 145 patients (67 per cent) and replacement was performed in 71 (33 per cent). Ages varied from 17 to 76 years in these patients. There were 80 men
Journal
fhctcome
Procedure -.-
Mitral insuff. due to large anterior leaflet with stretched C.T Prolapse of anterior leaflet due to stretched C.T.
11.
Heart
Date of subseyuent surger,v
Calcification mural leaflet: Prolapse of both leaflets Torn C.T., mural leaflet
47
American
insuficirncy
S/27/69
Second mitral valve repair vrs. later
H
Replacement with No. 8 Kay-Shiley disc valve with muscle guard 1 \‘I’. later Replacemenl with No. 8 Kay-Shiley dis(, vaive with mus. cle guard I month later Replacement with No. 7 Kay-Shiley disc valve with mus. clr guard Replacement with No. 31 Hancock glutaraldehyde porcine valve 1 vr. later Replacement with No. 31 Hancock glutaraldehyde par. tine valve 4 months late)
Living and well 6 i-ears, on Couinadin
On Coumadin & .qirin. Emboli ausing temp. hlindness after valve replaced Iiving 2 years Living and well 2 vears, on Counadin
and 65 women followed from 6 months to 17 years after surgery. Thirty-eight were in New York Heart Association Class IV and 107 were in Class III. Nine patients (6 per cent) had a myocardial infarct 15 days to 84 months (mean 18 months) before surgery. Six of these nine patients had angina at the time of surgery. Five more patients (3 per cent) had angina preoperatively but had not had an infarct. In 68 patients (47 per cent) a history of rheumatic heart disease and in 10 patients (47 per cent) a history of subacute bacterial endocarditis had been noted. The heart size as demonstrated by x-ray ranged from Grade 2/6 to 5/6 enlarged with a mean of 3/6. Seventythree patients had torn chordae tendineae and 15 had a ruptured, infarcted, or necrotic head of a
257
Kay
et al.
papillary muscle. In 26 patients there were stretched chordae tendineae, and in the remaining 31 patients the operative report mentioned only a dilated annulus. Prior to performing repair, a portion of the valve was removed for biopsy in 29 patients. Fibromyxoid degeneration of the mitral leaflet was noted in 19 patients, inactive rheumatic changes in seven patients and valvulitis of the valve with calcification in three patients. These pathological findings were essentially the same as in those patients in whom the excised valve was replaced. Group II-Mitral revascularization.
insufficiency
and
myocardial
From 1970 to 1977 67 patients were operated upon with myocardial revascularization and mitral repair of replacement. In 57 patients, mitral insufficiency occurred secondary to coronary artery disease,and in 10, the patient’s knowledge of mitral insufficiency antedated the history of coronary artery disease, Repair was feasible in 55 of these patients (82 per cent). Of these 55 patients undergoing repair, 19 were women and 36 were men between 42 and 72 years of age (mean 59). Twenty-seven patients were in New York Heart Association Class III and 28 were in Class IV. The patients were classified on the basis of fatigue, dyspnea, and congestive heart failure. These symptoms were accompanied by angina in 46 patients, but severity of angina was not used for classification. Eleven patients had Grade II/VI, 26 had Grade III/VI, and 18 Grade IV/VI mitral insufficiency. The amount of insufficiency was determined as follows. The cardiac output was obtained by the Fick Principle. The stroke volume of the left ventricle was determined by radiographic means with injection of 76 per cent Renografin into the left ventricle. If the amount of blood ejected into the left atrium equaled that ejected into the aorta, then this was graded as II/VI. If the blood ejected into the left atrium was two times the amount ejected into the aorta, this was Grade IV/VI. If the amount ejected into the left atrium was three times the amount ejected into the aorta, this was graded as VI/VI. The pulmonary artery pressure was measured prior to left ventriculography and coronary arteriography in 27 patients. These varied from a normal of 24/13 to a high of 119/61 with 16 patients (59 per cent) having a pulmonary artery systolic pressure of 50 mm. Hg or more. The left
258
ventricular end-diastolic pressure prior to radiopaque studies was measured in 35 patients and varied from 7 mm. Hg to 38. Twenty-nine patients (83 per cent) had an end-diastolic pressure of 15 mm. Hg (mean 22.6) or greater. The ejection fraction was also measured prior to coronary arteriography and ranged from 0.15 to 0.7 in these 55 patients. Thirty-three patients had a ruptured or infarcted papillary muscle or torn chordae tendineae with secondary annular dilatation. Twenty-two patients had a dilated annulus only. At operation 92 vein grafts and six left internal mammary arteries were employed for myocardial revascularization. Results Group I. There were 7 hospital deaths (5 per cent) in the 145 patients with mitral valve repair. Repair failed in 12 patients (8 per cent) from 1 month to 14 years (mean 4.6 years) after the initial operation, Table I. Two of these patients had a second repair 7% and 8% years after the first operation, and both are doing well without a murmur 1 and 7 years following the second operation. In one of these two patients, tricuspid repair as described in 196511,I? was also successfully performed at the time of the second operation. Of the 10 patients with subsequent valve replacement, seven patients are alive 9 months to 9% years after mitral valve replacement. There were 30 (20 per cent) late deaths from 3 months to 10 years (mean 5 years) after mitral valve repair, Table II. Two of the 30 late deaths were due to hepatitis, 12 were due to myocardial infarction, and six deaths were due to carcinoma or leukemia. Thromboembolic events occurred in four patients followed for a total of 922 years, 0.4 per cent per patient year. These four emboli resulted in the hospital death in one patient and late death in two patients. The fourth patient had a cerebral vascular accident 2% years after mitral repair from which he recovered completely but died 6% years later. The autopsy reveaIed a recent myocardial infarct with pulmonary emboli. Change in the New York Heart Association classification as judged by a physician is noted in Table III. The actuarial curve revealed a survivability of 61.5% ( k 5.5%) at 17 years (Fig. 3). Of the 10 patients with subsequent valve replacement, one is lost to follow-up and seven patients are
August,
1978, Vol. 96, No. 2
II. Mitral insufficiency without myocardial revascularization-late deaths Table
No.
of
Cause
patients 1 1
12 1 2
2 2 1 2 1 1 4
of death
Serum hepatitis Infectious hepatitis Myocardial infarction Suicide Lung carcinoma Stroke &-east carcinoma Int.estinal cancer I’ulmonarg embolus (1 myocardial inf.) Ventricular fibrillation Leukemia lrnknown
Time postoperatively 5 mos. 2 yrs. 3 mos. to 9% yrs.
I I I. Mitral insufficiency without myocardial revascularization-NYHA functional classification of 96 surviving patients --____ Table
To postopernh
Preoperativr
1 yr.
1?4 and 10 yrs. 1% and 5 yrs. 8 and 12 yrs. 7 yrs. 3% and 6% yrs.
class
IV III II I
IV. Preoperative ejection fraction as related to mortality in patients with mitral repair and myocardial revascularization Table
1% yr. 5 yrs. 4 yrs. to 9 yrs.
Ejection
alive from 1 to 9% years with a survivability of 73.6 per cent ( + 16%) at 9 years. Group II. There were two (4 per cent) hospital deaths in these 55 patients. One patient with an ejection fraction of 0.2 died of bacterial endocarditis 37 days following surgery, and one patient with an ejection fraction of 0.4 died 8 days after surgery of a pulmonary embolus. Table IV reveals the hospital deaths and late deaths as related to the ejection fraction and Table V lists the cause of the six late deaths. Table VI reveals the postoperative change in New York Heart Association Classification of the 47 surviving patients. The survivability at 7 years is 80% ? 6% (Fig. 3). There was one peripheral embolic event resulting in hemiplegia in the 55 patients with repair followed for a total of 164 years, or 0.6 per cent per patient year. One patient with repair died from cerebral hemorrhage 7 months after surgery; however, this patient was continued on sodium warfarin by her family physician for 7 months, at which time she had a cerebral hemorrhage with the prothrombin time at 10 per cent. Anticoagulant therapy is advised for only 3 months following mitral repair, with the prothrombin time maintained at 20 per cent. Discussion
Patients with mitral insufficiency should be operated upon if with adequate medical therapy their symptoms prevent them from performing their daily duties in a manner satisfactory to the
American
Hrart
Journal
,c’ ~~luss
0.15-0.20 Total patients Hospital deaths Late deaths Total deaths
4
I 2 3 (75%)
f&c/ion
(J.2.S0.40 24
1 I 2 (8%)
0.45-0.70 27
0 iI 3 (11%)
patient. Because of the increased morbidity with mitral valve prostheses it is imperative that mitral valve repair be considered before replacement. Few surgeons, however, are presently prepared to attempt repair for mitral insufficiency. In 1976 Salomon, Stinson, Criepp. and Shumway” reported on 66 patients with pure mitral insufficiency without coronary artery disease. This group of patients is similar to our 145 patients with pure mitral insufficiency in whom repair was performed. The mitral valve was replaced in their 66 patients. Starr-Edwards Model 6120 valves were used in :38 patients, porcine aortic valve Xenografts (Hancock) in 20, and stented aortic valve allografts in eight. The operative mortality rate was 6 per cent. The overall survival rate, calculated by the actuarial method, was 50 per cent i 8 per cent at five years. Ten of their 38 operative patients with the Starr-Edwards valve inserted in the mitral area had systemic thromboembolic episodes with two deaths from the emboli. Two of their eight patients with an allograft in the mit,ral area had systemic thromboembolic episodes. None of the patients with the porcine valve had systemic thromboembolic episodes at the time of this
259
Kay
et al.
V. Mitral insufficiency repair and myocardial revascularization-late deaths Table
Ejection fraction 0.60
0.18 0.46 0.35 0.68 0.15
Cause of death Cerebral hemorrhage (on sodium warfarin/prothrombin time 10%) Cardiac arrest Pulmonary emboli Mediastinitis Unknown Died in sleep
Months postop.
VI. Mitral repair and myocardial revascularization NYHA functional classification of 47 surviving patients Table
I
To postoperative
7
Preoperative class IV 8 3 3 18 11
report; however, a subsequent article by Shumway revealed a significant incidence of cerebral emboli with the Hancock glutaraldehyde-treated porcine valve. In our 145 patients with pure mitral insufficiency who had a mitral annuloplasty performed from 1959 through 1976, there were seven hospital deaths and 30 late deaths. A peripheral embolus occurred in only four of these 145 patients with mitral valve repair followed for a total of 922 years, or 0.4 per cent per patient year. The overall survival rate calculated by the actuarial method at 17 years is 61.5 per cent (t5.5 per cent) for repair alone. This does not include the remaining seven of 10 patients still alive after subsequent valve replacement. Of the original 145 patients with repair there are 96 alive with mitral repair and seven more alive after subsequent replacement, for a total of 103 living (71 per cent). Of the 30 late deaths two died of hepatitis, six died of cancer, and 12 patients died of myocardial infaretion. Approximately % of the deaths were unrelated to the mitral repair. Two patients with repair and one with subsequent replacement are lost to follow-up and these are counted as dead. There would appear to be a significant difference in results with the group of patients reported by Salomon, Stinson, Griepp and Shumway with replacement for pure mitral insufficiency. Our patient group included 14 patients with a history of angina and infarction, a subset with a poorer prognosis because revascularization was not performed for these patients prior to 1970. Our patient group also included a subset of 68 patients with pure mitral insufficiency with a history of rheumatic fever. However, neither at surgery by visualizing the valve or myocardium or in longterm longevity could one detect any difference in
III II-
class
IV
III
II
I
-
2 1 -
14 11 -
5 14 -
-
-
-
I-
this subset or the subset with mitral valve prolapse with pure mitral insufficiency without a prior history of rheumatic fever. In 1976 Starr and colleagues” reported on 290 patients who had isolated mitral valve replacement for single mitral valve disease with their currently used prostheses. These were the noncloth-covered Model 6120 prosthesis, and the cloth-covered-composite seat Model 6310-6320 prosthesis inserted between 1965 and 1975. There was a 6.6 per cent combined operative mortality rate. There was a 58 per cent observed survival at 10 years for operative survivors only, so that the observed survival is closer to 51 per cent at 10 years if one includes the operative mortality rate. They stated that for operative survivors, “At 6 years, the chance to be embolus-free is 85 per cent with the cloth-covered prosthesis and 66 per cent with the non-cloth-covered prosthesis. The chance to be embolus-free at 10 years with the non-cloth-covered prosthesis is 51 per cent”-obviously a high incidence of peripheral embolization compared to repair. Buch and associates’” reported in 1975 on mitral valve replacement with the Hancock stabilized gluteraldehyde valve. The predicted survival of 87 patients without coronary artery disease or prior prosthetic valve replacements was 87.5 per cent at 2 years and 77.5 per cent at 4 years. There were four thromboembolic episodes, a rate of 2.4 per cent per patient year. In 1977 Stinson and associates’” reported on the long-term experience with the Hancock porcine valve in the mitral area. There were 243 patients with isolated replacement of the mitral valve. The operative mortality rate was 7.8 per cent. Actuarial analysis at 4.4 years revealed a survival rate of 78 per cent. At this same interval 92 per cent of the patients with mitral replacement with
August,
1978, Vol. 96, No. 2
a Hancock porcine valve were free of emboli. They furthermore stated that there was a linearized thromboembolism rate of 5.2 per cent per patient year-a very high rate for the Hancock glutaraldehyde porcine valve at first thought to be emboli-free. There is a paucity of reports of the results for patients operated upon with mitral replacement with glutaraldehyde-treated porcine valves with concomitant coronary artery disease or where the mitral insufficiency was secondary to coronary artery disease. The reports include very few patients and are as follows: Horowitz and coworkers’: reported one death among 23 patients who had isolated mitral valve replacement with the Hancock glutaraldehyde-preserved porcine heterograft without revascularization and two operative deaths among the remaining nine patients who had additional valve surgery or coronary artery grafting. In the report by Buch and associates, noted previously, they reported on 120 patients undergoing mitral valve replacement with the Hancock “stabilized gIutaraldehyde process” porcine xenograft from March, 1971, through April, 1975. There was a group of 23 patients who had mitral valve diseasewith coronary artery disease. Twelve of these had rheumatic valvular disease and coronary artery disease and the other 11 had coronary artery disease and nonrheumatic mitral regurgitation. Six of these 23 patients (26 per cent) died within the first 30 days following replacement of the patient’s mitral valve with a porcine valve. Three more patients died after discharge from the hospital so that there were nine deaths in this group of 23 patients with mitral replacement and coronary artery disease. Fourteen of these 23 patients had aorto-coronary bypass grafts. In the report of Stinson and colleagues quoted previously, they reported in 1977 on 243 patients with isolated replacement of the mitral valve with the Hancock glutaraldehyde-preserved porcine aortic valve xenografts. They stated that “Mitral valve patients with associated coronary artery disease accounted for a substantial portion of both early and late deaths. For example, in 54 patients the diagnosis of coronary artery disease was established by coronary angiography, electrocardiographic evidence of previous myocardial infarction, or postmortem examination within one year after operation. Operative mortality rate
American
Heart
,Journal
in this group was 18.5 per cent, and the survival rate of 2 years was only 56 ( i 7.8) per cent. Patients undergoing simultaneous coronary artery bypass grafting for angiographically defined coronary artery lesions fared similar!v.““~ In our 55 patients with mitral vul::e repair for significant mitral insufficiency and myocardial revascularization there were two i 1 per cent) operative deaths and six late deaths ( I 1 per cent ). The operative and long-term results were fairly similar for the patients with an ejection fraction of 0.45 to 0.70 and for the patients with an ejection fraction of 0.25 to 0.40. For the former, there were no operative deaths for 27 patients and three late deaths, for a tot,al of threr deaths ( 11 per cent) and for the latt.er, one operative death in 24 patients and one late death, for R total of two deaths (8 per cent). For patients with nn ejection fraction of 0.1 to 0.2, there was one operative deat.h in four patients operated uptm, however only one long-term survival. By actuarial methods the 7-year survival for the ,55 patients with repair and revascularization, including the operative mortality rate of 4 per cent, ~~a.480 per cent & 6 per cent. Fig. 3 reveals the actuarial curve of our two groups of pat,ients undergoing repair at 17 years for Group I and 7 years for Group II. There was one peripheral thromboembolic episode in the 55 patients with repail, followed for a total of 164 years, for a 0.6 per c’ent rate per year. There is again a significant difYt>rence in the results of the patients with repair ami revascularization compared to those series with replacement with a prosthesis or glutaraldehyde I)orcine valve and revascularization. Although the use of the porcine valve for mitral valve replacement may have redut,ed the incidence of peripheral embolization c>ompared to other prostheses, the number of emboii with this valve is still unacceptably high. The uncert.ain long-term durability of porcine valves also continues to be of great concern to most physicians and surgeons. If t,he experienct, of ours and others with homografts is a logical hasis for this concern, then the use of glutaraldehyde-treated porcine valves as well as other prostheses must be restricted to the minority of patient:- with mit.ral insufficiency in whom valve repair is not feasible. We would agree completely with Hurch and Giles” that the physician should not consider the patient “cured” once he has undergone cardiac
261
Kay
et al.
valve replacement, but rather should consider him to be the subject of meticulous long-term medical care. We would also go one step further to urge the surgeon to do his best to repair the mitral valve before considering replacement with any type of valve presently available.
5.
6.
7.
Summary
There has been skepticism since the early days of open heart surgery that good long-term or even short-term results were possible with repair for pure mitral insufficiency. The authors report 145 patients in whom a markedly insufficient mitral valve was repaired 6 months to 17 years previously and another 55 patients in whom repair of the insufficient mitral valve was performed along with myocardial revascularization from 6 months to 7 years previously, Comparative data with other published work reveals superior results with repair than with replacement with Starr-Edwards and Hancock glutaraldehyde-treated porcine valves and with far less emboli. Conservatism is urged in operating upon patients with mitral insufficiency. Repair of the valve rather than replacement is stressed for those patients requiring surgery.
8.
9.
10.
11. 12.
13.
14.
15.
REFERENCES Starr, A., and Edwards, M. L.: Mitral replacement: Clinical experience with a ball-valve prosthesis, Ann. Surg. 154:726,1961. Kay, J. H., Magidson, O., Meihaus, J. E., Lewis, R., Egerton, W. S., Zubiate, P., and Lefevre, T.: Mitral insufficiency and mitral stenosis: Surgical treatment using the heart-lung machine, Calif. Med. 95:382, 1961. Kay, J. H., and Egerton, W. S.: The repair of mitral insufficiency associated with ruptured chordae tendineae, Ann. Surg. 157:315, 1963. Kay, J. H., Maselli-Campagna, G., and Tsuji, H. K.: Surgical treatment of mitral insufficiency, West. J. Surg., Obstet. Gynecol. 72:149, 1964.
262
16.
17.
18.
Kay, J. H., Tsuji, H. K., and Redington, J. V.: The surgical treatment of mitral insufficiency associated with torn chordae tendineae, Ann. Thorac. Surg. 1:269, 1965. Kay, J. H., Tsuji, H. K., Redington, J. V., and Yokoyama, T.: Surgical treatment of mitral insufficiency, Calif. Med. 107:311,1967. Kay, J. H., Tsuji, H. K., Redington, J. V., and Mendez, A. M.: The surgical treatment of mitral insufficiency associated with torn chordae tendineae, Vast. Surg. 2:189, 1968. Mori, T., Zubiate, P., Mendez, A. M., and Kay, J. H.: Results of surgery for mitral insufficiency due to coronary artery disease, Israel J. Med. Sci. 11:245, 1975. Kay, J. H., Zubiate, P., Mendez, A. M., and Dunne, E. F.: Myocardial revascularization and mitral repair or replacement for mitral insufficiency due to coronary artery disease, Circulation 54(Suppl. 111):94, 1976. Kay, J. H., Zubiate, P., Mendez, A. M., Carpena, C., Watanabe. K.. and Maaidson. 0.: Mitral valve renair for patients with’ pure ml&al insufficiency: l- to is-year follow-up, J.A.M.A. 236:1584, 1976. Kay, J. H., and Tsuji, H. K.: Surgical treatment of tricuspid insufficiency, Ann. Surg. 162:53, 1965. Kav. J. H.. Mendez. A. M.. and Zubiate. P.: A further look at tricuspid annuloplasty, Ann. ‘Thorac. Surg. 22:498, 1976. Salomon, N. W., Stinson, E. B., Griepp, R. B., and Shumway, N. E.: Surgical treatment of degenerative mitral regurgitation, Am. J. Cardiol. 38:463, 1976. Starr, A., Grunkemeier, G., Lambert, L., Okies, J. E., and Thomas, D.: Mitral valve replacement: A lo-year followup of non-cloth-covered vs. cloth-covered caged-ball prostheses, Circulation 54 (Suppl. 111):47, 1976. Buch, W. S., Pipkin, R. D., Hancock, W. D., and Fogarty, T. J.: Mitral valve replacement with the Hancock stabilized glutaraldehyde valve: Clinical and laboratory evaluation, Arch. Surg. 110:1408, 1975. Stinson, E. B., Griepp, R. B., Oyer, P. E., and Shumway, R. E.: Long-term experience with porcine aortic valve xenografts, J. Thorac. Cardiovasc. Surg. 73:54, 1977. Horowitz, M. S., Goodman, D. J., Fogarty, T. J., and Harrison, D. C.: Mitral valve replacement with the glutaraldehyde-preserved porcine heterograft: Clinical, hemodynamic, and pathological correlations, J. Thorac. Cardiovasc. Surg. 67:885, 1974. Burch. G. E.. and Giles. T. D.: Clinical evaluation of aortic ‘and mitral valve prostheses, AM. HEART J. 92:2, 245, 1976.
August,
1978, Vol. 96, No. 2
of clinical
Mitral
for
valve
repair
cardiology
significant
mitral
insufficiency
Jerome Harold Kay, M.D. Pablo Zubiate, M.D. Michael A. Mendez, M.D. Neal Vanstrom, M.D. Taro Yokoyama, M.D. Los An&es,
Calif.
Prior to the article by Starr and Edwards in 1961’ on mitral valve replacement, it was necessary to repair the abnormally functioning mitral valve at the time of surgery, since a prosthetic mitral valve was not available. With the introduction of prosthetic valves, it has been technically easier for surgeons to replace the valve than attempt repair. Our first repair for pure mitral insufficiency was performed in 1959, and except for brief periods, this has remained our method of choice for surgery for significant mitral insufficiency for the past 18 years. Rc;pair has not been popular with surgeons, however, since repair is more difficult and takes greater thought than excising a valve and replacing it with a prosthesis. With 15 years clinical and experimental experience with various prosthetic devices, it is our strong conviction that a mitral prosthesis of any variety or a porcine valve should be inserted only if repair cannot be accomplished. With short- and long-term results of mitral valve replacement being published not only with the Starr-Edwards valve but also the Hancock porcine valve, it would appear of interest to compare these results to the results with repair of the insufficient mitral valve. The following is a report of two groups of patients: 145 patients with From The Los Angeles Heart Institute Center. Los Angeles, and The University of Medicine Los Angeles.
at The St. Vincent of Southern California
Aided by a grant Foundation.
Thoracic
Received Reprint Street.
from
The Los Angeles
for publication requests: Jerome Los Angeles, Calif.
000%8703/78/0296-0253$01.00/O
Dec.
and
Medical School
Cardiovascular
12, 1977.
Harold 900.57.
Kay,
M.D.,
0 1978
123
The
South
Alvarado
C. V. Mosby
Co.
pure mitral insufficiency in whom mitral repair was performed from 1959 to 1977, and 55 patients with mitral insufficiency and coronary artery disease in whom repair was performed at the time of myocardial revascularization from 1970 to 1977. Although the basic principle is the same for repair of the insufficient mitral valve for all patients, the data from the two groups of patients is presented separately in this art,icle. Since 1970 myocardial revascularization has been performed in all but one patient with mitral insufficiency and coronary artery disease requiring mitral valve surgery when significant coronary artery disease was present. In this patient revascularization was not needed nor possible since the vessel obstructed led t.o an area of infarct and the other two vessels had only minimal disease. These patients comprise Group II. There were 14 patients operated upon prior to 1970 with mitral insufficiency and coronary artery disease, but myocardial revascularization was not combined with repair or replacement by us until 1970. These patients are included in the first group of patients with pure mitral insufficiency. There may be other patients in Group I who had coronary artery disease and whose mitral insufficiency was due to or associated with the coronary artery disease and were operated upon for their mitral insufficiency during the years from 1959. If so, the coronary artery disease was not proven even though suspected, since coronary arteriography was not performed in these patients. In order to better understand our approach to
American
Heari
Journal
253
Kay
et
al.
P iapitlary
mug.
Fig. 1. The area of the leaflet involved with stretched or torn chordae tendineae or torn repaired by placing interrupted figure-of-eight sutures of 2-O Tevdek through the head of muscle and then bringing this suture up through the leading edge of the involved area of the separate sutures are used at each area. For ease of exposure, all sutures are placed prior to
Fig. 2. In in size. This bringing it upon. The
order to obliterate the insufficiency, the greatly dilated sagging mural annulus is decreased considerably must be accomplished by decreasing the length of the mural annulus to about % of its size and thereby up into apposition with the anterior leaflet. The annulus of the anterior leaflet cannot be encroached repair is accomplished with No. 2 silk sutures as illustrated.
the repair of the mitral valve, it is important to be familiar with our thinking as to the development of mitral insufficiency. Whether the patient began with mitral valve prolapse without significant insufficiency and over the years developed wide-open mitral insufficiency, or whether the patient had myocarditis and developed mitral insufficiency secondary to this, the progression is similar. With mitral valve prolapse, the annulus is large and the leaflets meet only at their edges. With myocarditis, the left ventricle enlarges, thereby enlarging the annulus, and the mitral leaflets do not coapt. Because the leaflets meet only at their edges or not at all, there is
254
papillary muscle is the nearer papillary leaflet. Usually two tying.
significant tension on the leaflets each time the heart contracts. This creates tension on the chordae tendineae as well. With time the leaflets stretch and enlarge as do the chordae tendineae. In many patients, the chordae tendineae tear. The leaflets are usually thickened and reveal fibromyxoid degeneration. This fibromyxoid degeneration in the leaflets is secondary to the trauma produced by the pressure of the blood on the unsupported leaflets during systole. With mitral insufficiency secondary to coronary artery disease, the mitral insufficiency may be due to tearing of infarcted papillary muscle or
August,
1978, Vol. 96, No. 2
Mitrnl
o-o
\
80%
A GROUP
‘ON “\h,
valve repair
II
-4 70
\
61.5%
--o-o
GROUP
50
o Group A Group
I -Repair II- Repair 1
2
4
TIME 3. Actuarial Program BMDllS.
Fig.
curves:
Mitral
repair
results
17 year Follow up S.E. f 5.5% and Revascularization 7 year Follow up SE. f 6% I I I 1 I
6
8
chordae tendineae because of infarcted papillary muscle. With these patients there is always secondary annular dilatation due to enlargement of the left ventricle. In other patients with coronary artery disease, the infarct may involve the muscle near the annulus with resultant dilatation of the annulus and failure of coaptation of the leaflets. In some patients with a massive infarct the annulus may be stretched due to enlargement of the left ventricle. No matter what the etiology of the mitral insufficiency, it is always necessary to decrease the size of the annulus and this part of the repair is almost always performed in the same manner. This consists of decreasing the length of the mural annulus and not the annulus of the anterior leaflet. The trigona fibrosa cordis prevents the annulus of the anterior leaflet of the mitral valve from stretching. The mural leaflet portion of the annulus does not have a similar support and therefore the mitral annulus dilates at the area of the mural annulus but not the area of the anterior annulus. It is important to remember that the mural annulus only is stretched in all patients with mitral insufficiency. The majority of patients with mitral insufficiency not secondary to coronary artery disease will have torn chordae tendineae and/or stretched chordae tendineae. The patient with mitral insufficiency secondary to myocardial infarction may or may not have torn chordae
American
Heart
Journal
10
INTERVAL for Group
in mifr/rl
12
I
60
-50
I
14
16
II patients
using
(YEARS)
I and
Group
Biomedical
Computer
tendineae or torn papillary muscle, but they will not have associated stretched chordae tendineae unless the insufficiency is of many years’ duration. Technique
The technique of repair is as follows. After opening the left atrium, a careful search is made to determine if there are torn or stretched chordae tendineae or torn papillary muscle. If there are significantly stretched chordae tendineae, torn chordae tendineae or torn papillary muscle, this area of the valve is sutured down to the nearest papillary muscle head (Fig. 1). New chordae are not constructed. The anterolateral, posteromedial, midportion, or all three areas of the mural leaflet may require suturing to the nearest papillary muscle. If there are torn or stretched chordae tendineae of the anterior leaflet, this area is sutured to the head of the papillary muscle involved. If all of the chordae tendineae of the anterior leaflet are stretched, then either the anterolateral or posteromedial portion of the anterior leaflet is sutured to the head of the nearest area involved (Fig. 1). This allows the remaining portion of the anterior leaflet to billow and close against the mural leaflet. It is important for the anterior leaflet to billow in order to abut against the mural leaflet, otherwise the insufficiency will not be corrected. Except for minor variations in individual
255
Kay
et al.
I. Mitral
Table
I
insufficiency without
I
Patient No. 1.
I
I
Age at first surgery
Date of first surgery
R. F. 36
8/11/59
myocardial revascularization-repair
Initial cause of mitral insufficiency
Cause of failure
Torn chordae tendineae of anterior leaflet
Torn chordae not repaired at initial operation
10/l/63
Thrombosis of Starr valve
g/27/74
2.
G. P. 37
g/2/60
Dilated annulus prolapsed anterior leaflet with stretched chordae tendineae
Stenosis with calcification of area of previous repair
7/11/74
3.
M. P. 48
10/31/61
Gross dilatation due to stretched C.T., mural & anterior leaflet
12/10/70
4.
J. P. 37
5/19/64
Dilated annulus with calcification slightly stretched C.T.
Torn C.T. anterior leaflet; greatly dilated tricuspid annulus with insufficiency Stenosis due to calcification of both leaflets
5.
P. c. 39
7/29/66
Torn C.T., leaflet
mural
Recurrence of torn chordae tendineae
l/17/68
6.
T. D. A. 47
g/8/67
Torn C.T., leaflet
mural
Repair of mural leaflet intact. Torn CT. occurred at anterior leaflet
10/8/73
patients, the remaining part of the mitral valve repair is now the same for all patients and consists of decreasing the annulus of the mitral valve by doing away with approximately 65 per cent to 70 per cent of the annulus of the mural leaflet. The annulus is decreased mainly at the posteromedial commissural area, where usually two interrupted figure-of-eight sutures of No. 2 silk are placed and tied to do away with 40 per cent or 45 per cent of the annulus. The same
256
Date of subsequent surgery
9/9/76
failures
Procedure Replacement with No. 3 Starr-Edwards Ball valve 4 yrs. later Replacement with No. 31 Hancock glutaraldehyde porcine valve 11 yrs. later Replacement with No. 29 Hancock, glutaraldehyde porcine valve 14 yrs. later Second repair of mitral valve and primary repair of tricuspid valve 9 yrs. later Replacement with No. 31 Hancock glutaraldehyde porcine valve 12 yrs. Iater Replacement with No. 4 Kay-Shiley disc valve Tricuspid annuloplasty 2 yrs. later Replacement with No. 7 Kay-Shiley disc valve with muscle guard 6 yrs. later
Outcome Ball valve replaced 11 years later for valve thrombosis Living and well on Coumadin 3 yrs.
CVA 3 yrs after insertion of porcine valve. Living and well 3 yrs. on Coumadin Living and well 7 yrs., no murmurs or medication
Living and well 1 year, on Coumadin
Living and well 9.5 years, on Coumadin
Hosp. death, Bronchial pneumonia, probable myocardial in-
procedure is used to decrease the mural annulus of the anterolateral commissural area for another 20 per cent or 25 per cent. The sutures placed at the anterolateral commissural area should not be deep so that the circumflex coronary artery is encircled. When the annuloplasty is completed, approximately 30 per cent or 35 per cent of the mural annulus remains and there is a snug twofingerbreadth opening (Fig. 2). It is important not to encroach on the annulus of the anterior leaflet;
August,
1978,
Vol.
96, No.
2
Mitral
rlaltvz
repair
in mittwl
I., continued
Table
- --
Age at first surgery
Date of first surgery
M. T. 61
10/l/68
8.
J. G. 66
11/26/68
9.
?I. G. 59
10.
G. B.
Patient NO. 7.
Initial cause of mitral insufficiency
Cause of failure
5/ 10176
l/9/69
Torn C.T., leaflet
mural
Mitral insuff. through center of repaired valve
“/“O/69
7114171
Torn C.T., leaflet
mural
Mitral insuf. due to tear of suture line
10/i/71
Torn C.T., mural leaflet; stretched C.T., anterior leaflet; S.B.E. 6 yrs. prior to surgery Dilated annulus with stretched C.T.; coarctation & aortic aneurysmectomy 20 years previously
Torn C.T., anterior leaflet
6/16/7.5
Mitral insuf. due to prolapsed anterior leaflet
4/3/75
E. I,. 57
6/24/74
12.
D. c. 62
12/g/74
otherwise mitral stenosis may be produced without correcting the insufficiency. This technique was first described in 1961 and in subsequent publications.‘-“’ Material Group I-Mitral insufficiency without myocardial revascularization. Between 1959 and 1977,
216 patients were operated upon with significant pure mitral insufficiency. The majority of these patients had mitral valve prolapse with severe insufficiency and without coronary artery disease. Mitral valve repair was performed in 145 patients (67 per cent) and replacement was performed in 71 (33 per cent). Ages varied from 17 to 76 years in these patients. There were 80 men
Journal
fhctcome
Procedure -.-
Mitral insuff. due to large anterior leaflet with stretched C.T Prolapse of anterior leaflet due to stretched C.T.
11.
Heart
Date of subseyuent surger,v
Calcification mural leaflet: Prolapse of both leaflets Torn C.T., mural leaflet
47
American
insuficirncy
S/27/69
Second mitral valve repair vrs. later
H
Replacement with No. 8 Kay-Shiley disc valve with muscle guard 1 \‘I’. later Replacemenl with No. 8 Kay-Shiley dis(, vaive with mus. cle guard I month later Replacement with No. 7 Kay-Shiley disc valve with mus. clr guard Replacement with No. 31 Hancock glutaraldehyde porcine valve 1 vr. later Replacement with No. 31 Hancock glutaraldehyde par. tine valve 4 months late)
Living and well 6 i-ears, on Couinadin
On Coumadin & .qirin. Emboli ausing temp. hlindness after valve replaced Iiving 2 years Living and well 2 vears, on Counadin
and 65 women followed from 6 months to 17 years after surgery. Thirty-eight were in New York Heart Association Class IV and 107 were in Class III. Nine patients (6 per cent) had a myocardial infarct 15 days to 84 months (mean 18 months) before surgery. Six of these nine patients had angina at the time of surgery. Five more patients (3 per cent) had angina preoperatively but had not had an infarct. In 68 patients (47 per cent) a history of rheumatic heart disease and in 10 patients (47 per cent) a history of subacute bacterial endocarditis had been noted. The heart size as demonstrated by x-ray ranged from Grade 2/6 to 5/6 enlarged with a mean of 3/6. Seventythree patients had torn chordae tendineae and 15 had a ruptured, infarcted, or necrotic head of a
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Kay
et al.
papillary muscle. In 26 patients there were stretched chordae tendineae, and in the remaining 31 patients the operative report mentioned only a dilated annulus. Prior to performing repair, a portion of the valve was removed for biopsy in 29 patients. Fibromyxoid degeneration of the mitral leaflet was noted in 19 patients, inactive rheumatic changes in seven patients and valvulitis of the valve with calcification in three patients. These pathological findings were essentially the same as in those patients in whom the excised valve was replaced. Group II-Mitral revascularization.
insufficiency
and
myocardial
From 1970 to 1977 67 patients were operated upon with myocardial revascularization and mitral repair of replacement. In 57 patients, mitral insufficiency occurred secondary to coronary artery disease,and in 10, the patient’s knowledge of mitral insufficiency antedated the history of coronary artery disease, Repair was feasible in 55 of these patients (82 per cent). Of these 55 patients undergoing repair, 19 were women and 36 were men between 42 and 72 years of age (mean 59). Twenty-seven patients were in New York Heart Association Class III and 28 were in Class IV. The patients were classified on the basis of fatigue, dyspnea, and congestive heart failure. These symptoms were accompanied by angina in 46 patients, but severity of angina was not used for classification. Eleven patients had Grade II/VI, 26 had Grade III/VI, and 18 Grade IV/VI mitral insufficiency. The amount of insufficiency was determined as follows. The cardiac output was obtained by the Fick Principle. The stroke volume of the left ventricle was determined by radiographic means with injection of 76 per cent Renografin into the left ventricle. If the amount of blood ejected into the left atrium equaled that ejected into the aorta, then this was graded as II/VI. If the blood ejected into the left atrium was two times the amount ejected into the aorta, this was Grade IV/VI. If the amount ejected into the left atrium was three times the amount ejected into the aorta, this was graded as VI/VI. The pulmonary artery pressure was measured prior to left ventriculography and coronary arteriography in 27 patients. These varied from a normal of 24/13 to a high of 119/61 with 16 patients (59 per cent) having a pulmonary artery systolic pressure of 50 mm. Hg or more. The left
258
ventricular end-diastolic pressure prior to radiopaque studies was measured in 35 patients and varied from 7 mm. Hg to 38. Twenty-nine patients (83 per cent) had an end-diastolic pressure of 15 mm. Hg (mean 22.6) or greater. The ejection fraction was also measured prior to coronary arteriography and ranged from 0.15 to 0.7 in these 55 patients. Thirty-three patients had a ruptured or infarcted papillary muscle or torn chordae tendineae with secondary annular dilatation. Twenty-two patients had a dilated annulus only. At operation 92 vein grafts and six left internal mammary arteries were employed for myocardial revascularization. Results Group I. There were 7 hospital deaths (5 per cent) in the 145 patients with mitral valve repair. Repair failed in 12 patients (8 per cent) from 1 month to 14 years (mean 4.6 years) after the initial operation, Table I. Two of these patients had a second repair 7% and 8% years after the first operation, and both are doing well without a murmur 1 and 7 years following the second operation. In one of these two patients, tricuspid repair as described in 196511,I? was also successfully performed at the time of the second operation. Of the 10 patients with subsequent valve replacement, seven patients are alive 9 months to 9% years after mitral valve replacement. There were 30 (20 per cent) late deaths from 3 months to 10 years (mean 5 years) after mitral valve repair, Table II. Two of the 30 late deaths were due to hepatitis, 12 were due to myocardial infarction, and six deaths were due to carcinoma or leukemia. Thromboembolic events occurred in four patients followed for a total of 922 years, 0.4 per cent per patient year. These four emboli resulted in the hospital death in one patient and late death in two patients. The fourth patient had a cerebral vascular accident 2% years after mitral repair from which he recovered completely but died 6% years later. The autopsy reveaIed a recent myocardial infarct with pulmonary emboli. Change in the New York Heart Association classification as judged by a physician is noted in Table III. The actuarial curve revealed a survivability of 61.5% ( k 5.5%) at 17 years (Fig. 3). Of the 10 patients with subsequent valve replacement, one is lost to follow-up and seven patients are
August,
1978, Vol. 96, No. 2
II. Mitral insufficiency without myocardial revascularization-late deaths Table
No.
of
Cause
patients 1 1
12 1 2
2 2 1 2 1 1 4
of death
Serum hepatitis Infectious hepatitis Myocardial infarction Suicide Lung carcinoma Stroke &-east carcinoma Int.estinal cancer I’ulmonarg embolus (1 myocardial inf.) Ventricular fibrillation Leukemia lrnknown
Time postoperatively 5 mos. 2 yrs. 3 mos. to 9% yrs.
I I I. Mitral insufficiency without myocardial revascularization-NYHA functional classification of 96 surviving patients --____ Table
To postopernh
Preoperativr
1 yr.
1?4 and 10 yrs. 1% and 5 yrs. 8 and 12 yrs. 7 yrs. 3% and 6% yrs.
class
IV III II I
IV. Preoperative ejection fraction as related to mortality in patients with mitral repair and myocardial revascularization Table
1% yr. 5 yrs. 4 yrs. to 9 yrs.
Ejection
alive from 1 to 9% years with a survivability of 73.6 per cent ( + 16%) at 9 years. Group II. There were two (4 per cent) hospital deaths in these 55 patients. One patient with an ejection fraction of 0.2 died of bacterial endocarditis 37 days following surgery, and one patient with an ejection fraction of 0.4 died 8 days after surgery of a pulmonary embolus. Table IV reveals the hospital deaths and late deaths as related to the ejection fraction and Table V lists the cause of the six late deaths. Table VI reveals the postoperative change in New York Heart Association Classification of the 47 surviving patients. The survivability at 7 years is 80% ? 6% (Fig. 3). There was one peripheral embolic event resulting in hemiplegia in the 55 patients with repair followed for a total of 164 years, or 0.6 per cent per patient year. One patient with repair died from cerebral hemorrhage 7 months after surgery; however, this patient was continued on sodium warfarin by her family physician for 7 months, at which time she had a cerebral hemorrhage with the prothrombin time at 10 per cent. Anticoagulant therapy is advised for only 3 months following mitral repair, with the prothrombin time maintained at 20 per cent. Discussion
Patients with mitral insufficiency should be operated upon if with adequate medical therapy their symptoms prevent them from performing their daily duties in a manner satisfactory to the
American
Hrart
Journal
,c’ ~~luss
0.15-0.20 Total patients Hospital deaths Late deaths Total deaths
4
I 2 3 (75%)
f&c/ion
(J.2.S0.40 24
1 I 2 (8%)
0.45-0.70 27
0 iI 3 (11%)
patient. Because of the increased morbidity with mitral valve prostheses it is imperative that mitral valve repair be considered before replacement. Few surgeons, however, are presently prepared to attempt repair for mitral insufficiency. In 1976 Salomon, Stinson, Criepp. and Shumway” reported on 66 patients with pure mitral insufficiency without coronary artery disease. This group of patients is similar to our 145 patients with pure mitral insufficiency in whom repair was performed. The mitral valve was replaced in their 66 patients. Starr-Edwards Model 6120 valves were used in :38 patients, porcine aortic valve Xenografts (Hancock) in 20, and stented aortic valve allografts in eight. The operative mortality rate was 6 per cent. The overall survival rate, calculated by the actuarial method, was 50 per cent i 8 per cent at five years. Ten of their 38 operative patients with the Starr-Edwards valve inserted in the mitral area had systemic thromboembolic episodes with two deaths from the emboli. Two of their eight patients with an allograft in the mit,ral area had systemic thromboembolic episodes. None of the patients with the porcine valve had systemic thromboembolic episodes at the time of this
259
Kay
et al.
V. Mitral insufficiency repair and myocardial revascularization-late deaths Table
Ejection fraction 0.60
0.18 0.46 0.35 0.68 0.15
Cause of death Cerebral hemorrhage (on sodium warfarin/prothrombin time 10%) Cardiac arrest Pulmonary emboli Mediastinitis Unknown Died in sleep
Months postop.
VI. Mitral repair and myocardial revascularization NYHA functional classification of 47 surviving patients Table
I
To postoperative
7
Preoperative class IV 8 3 3 18 11
report; however, a subsequent article by Shumway revealed a significant incidence of cerebral emboli with the Hancock glutaraldehyde-treated porcine valve. In our 145 patients with pure mitral insufficiency who had a mitral annuloplasty performed from 1959 through 1976, there were seven hospital deaths and 30 late deaths. A peripheral embolus occurred in only four of these 145 patients with mitral valve repair followed for a total of 922 years, or 0.4 per cent per patient year. The overall survival rate calculated by the actuarial method at 17 years is 61.5 per cent (t5.5 per cent) for repair alone. This does not include the remaining seven of 10 patients still alive after subsequent valve replacement. Of the original 145 patients with repair there are 96 alive with mitral repair and seven more alive after subsequent replacement, for a total of 103 living (71 per cent). Of the 30 late deaths two died of hepatitis, six died of cancer, and 12 patients died of myocardial infaretion. Approximately % of the deaths were unrelated to the mitral repair. Two patients with repair and one with subsequent replacement are lost to follow-up and these are counted as dead. There would appear to be a significant difference in results with the group of patients reported by Salomon, Stinson, Griepp and Shumway with replacement for pure mitral insufficiency. Our patient group included 14 patients with a history of angina and infarction, a subset with a poorer prognosis because revascularization was not performed for these patients prior to 1970. Our patient group also included a subset of 68 patients with pure mitral insufficiency with a history of rheumatic fever. However, neither at surgery by visualizing the valve or myocardium or in longterm longevity could one detect any difference in
III II-
class
IV
III
II
I
-
2 1 -
14 11 -
5 14 -
-
-
-
I-
this subset or the subset with mitral valve prolapse with pure mitral insufficiency without a prior history of rheumatic fever. In 1976 Starr and colleagues” reported on 290 patients who had isolated mitral valve replacement for single mitral valve disease with their currently used prostheses. These were the noncloth-covered Model 6120 prosthesis, and the cloth-covered-composite seat Model 6310-6320 prosthesis inserted between 1965 and 1975. There was a 6.6 per cent combined operative mortality rate. There was a 58 per cent observed survival at 10 years for operative survivors only, so that the observed survival is closer to 51 per cent at 10 years if one includes the operative mortality rate. They stated that for operative survivors, “At 6 years, the chance to be embolus-free is 85 per cent with the cloth-covered prosthesis and 66 per cent with the non-cloth-covered prosthesis. The chance to be embolus-free at 10 years with the non-cloth-covered prosthesis is 51 per cent”-obviously a high incidence of peripheral embolization compared to repair. Buch and associates’” reported in 1975 on mitral valve replacement with the Hancock stabilized gluteraldehyde valve. The predicted survival of 87 patients without coronary artery disease or prior prosthetic valve replacements was 87.5 per cent at 2 years and 77.5 per cent at 4 years. There were four thromboembolic episodes, a rate of 2.4 per cent per patient year. In 1977 Stinson and associates’” reported on the long-term experience with the Hancock porcine valve in the mitral area. There were 243 patients with isolated replacement of the mitral valve. The operative mortality rate was 7.8 per cent. Actuarial analysis at 4.4 years revealed a survival rate of 78 per cent. At this same interval 92 per cent of the patients with mitral replacement with
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1978, Vol. 96, No. 2
a Hancock porcine valve were free of emboli. They furthermore stated that there was a linearized thromboembolism rate of 5.2 per cent per patient year-a very high rate for the Hancock glutaraldehyde porcine valve at first thought to be emboli-free. There is a paucity of reports of the results for patients operated upon with mitral replacement with glutaraldehyde-treated porcine valves with concomitant coronary artery disease or where the mitral insufficiency was secondary to coronary artery disease. The reports include very few patients and are as follows: Horowitz and coworkers’: reported one death among 23 patients who had isolated mitral valve replacement with the Hancock glutaraldehyde-preserved porcine heterograft without revascularization and two operative deaths among the remaining nine patients who had additional valve surgery or coronary artery grafting. In the report by Buch and associates, noted previously, they reported on 120 patients undergoing mitral valve replacement with the Hancock “stabilized gIutaraldehyde process” porcine xenograft from March, 1971, through April, 1975. There was a group of 23 patients who had mitral valve diseasewith coronary artery disease. Twelve of these had rheumatic valvular disease and coronary artery disease and the other 11 had coronary artery disease and nonrheumatic mitral regurgitation. Six of these 23 patients (26 per cent) died within the first 30 days following replacement of the patient’s mitral valve with a porcine valve. Three more patients died after discharge from the hospital so that there were nine deaths in this group of 23 patients with mitral replacement and coronary artery disease. Fourteen of these 23 patients had aorto-coronary bypass grafts. In the report of Stinson and colleagues quoted previously, they reported in 1977 on 243 patients with isolated replacement of the mitral valve with the Hancock glutaraldehyde-preserved porcine aortic valve xenografts. They stated that “Mitral valve patients with associated coronary artery disease accounted for a substantial portion of both early and late deaths. For example, in 54 patients the diagnosis of coronary artery disease was established by coronary angiography, electrocardiographic evidence of previous myocardial infarction, or postmortem examination within one year after operation. Operative mortality rate
American
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in this group was 18.5 per cent, and the survival rate of 2 years was only 56 ( i 7.8) per cent. Patients undergoing simultaneous coronary artery bypass grafting for angiographically defined coronary artery lesions fared similar!v.““~ In our 55 patients with mitral vul::e repair for significant mitral insufficiency and myocardial revascularization there were two i 1 per cent) operative deaths and six late deaths ( I 1 per cent ). The operative and long-term results were fairly similar for the patients with an ejection fraction of 0.45 to 0.70 and for the patients with an ejection fraction of 0.25 to 0.40. For the former, there were no operative deaths for 27 patients and three late deaths, for a tot,al of threr deaths ( 11 per cent) and for the latt.er, one operative death in 24 patients and one late death, for R total of two deaths (8 per cent). For patients with nn ejection fraction of 0.1 to 0.2, there was one operative deat.h in four patients operated uptm, however only one long-term survival. By actuarial methods the 7-year survival for the ,55 patients with repair and revascularization, including the operative mortality rate of 4 per cent, ~~a.480 per cent & 6 per cent. Fig. 3 reveals the actuarial curve of our two groups of pat,ients undergoing repair at 17 years for Group I and 7 years for Group II. There was one peripheral thromboembolic episode in the 55 patients with repail, followed for a total of 164 years, for a 0.6 per c’ent rate per year. There is again a significant difYt>rence in the results of the patients with repair ami revascularization compared to those series with replacement with a prosthesis or glutaraldehyde I)orcine valve and revascularization. Although the use of the porcine valve for mitral valve replacement may have redut,ed the incidence of peripheral embolization c>ompared to other prostheses, the number of emboii with this valve is still unacceptably high. The uncert.ain long-term durability of porcine valves also continues to be of great concern to most physicians and surgeons. If t,he experienct, of ours and others with homografts is a logical hasis for this concern, then the use of glutaraldehyde-treated porcine valves as well as other prostheses must be restricted to the minority of patient:- with mit.ral insufficiency in whom valve repair is not feasible. We would agree completely with Hurch and Giles” that the physician should not consider the patient “cured” once he has undergone cardiac
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valve replacement, but rather should consider him to be the subject of meticulous long-term medical care. We would also go one step further to urge the surgeon to do his best to repair the mitral valve before considering replacement with any type of valve presently available.
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Summary
There has been skepticism since the early days of open heart surgery that good long-term or even short-term results were possible with repair for pure mitral insufficiency. The authors report 145 patients in whom a markedly insufficient mitral valve was repaired 6 months to 17 years previously and another 55 patients in whom repair of the insufficient mitral valve was performed along with myocardial revascularization from 6 months to 7 years previously, Comparative data with other published work reveals superior results with repair than with replacement with Starr-Edwards and Hancock glutaraldehyde-treated porcine valves and with far less emboli. Conservatism is urged in operating upon patients with mitral insufficiency. Repair of the valve rather than replacement is stressed for those patients requiring surgery.
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REFERENCES Starr, A., and Edwards, M. L.: Mitral replacement: Clinical experience with a ball-valve prosthesis, Ann. Surg. 154:726,1961. Kay, J. H., Magidson, O., Meihaus, J. E., Lewis, R., Egerton, W. S., Zubiate, P., and Lefevre, T.: Mitral insufficiency and mitral stenosis: Surgical treatment using the heart-lung machine, Calif. Med. 95:382, 1961. Kay, J. H., and Egerton, W. S.: The repair of mitral insufficiency associated with ruptured chordae tendineae, Ann. Surg. 157:315, 1963. Kay, J. H., Maselli-Campagna, G., and Tsuji, H. K.: Surgical treatment of mitral insufficiency, West. J. Surg., Obstet. Gynecol. 72:149, 1964.
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Kay, J. H., Tsuji, H. K., and Redington, J. V.: The surgical treatment of mitral insufficiency associated with torn chordae tendineae, Ann. Thorac. Surg. 1:269, 1965. Kay, J. H., Tsuji, H. K., Redington, J. V., and Yokoyama, T.: Surgical treatment of mitral insufficiency, Calif. Med. 107:311,1967. Kay, J. H., Tsuji, H. K., Redington, J. V., and Mendez, A. M.: The surgical treatment of mitral insufficiency associated with torn chordae tendineae, Vast. Surg. 2:189, 1968. Mori, T., Zubiate, P., Mendez, A. M., and Kay, J. H.: Results of surgery for mitral insufficiency due to coronary artery disease, Israel J. Med. Sci. 11:245, 1975. Kay, J. H., Zubiate, P., Mendez, A. M., and Dunne, E. F.: Myocardial revascularization and mitral repair or replacement for mitral insufficiency due to coronary artery disease, Circulation 54(Suppl. 111):94, 1976. Kay, J. H., Zubiate, P., Mendez, A. M., Carpena, C., Watanabe. K.. and Maaidson. 0.: Mitral valve renair for patients with’ pure ml&al insufficiency: l- to is-year follow-up, J.A.M.A. 236:1584, 1976. Kay, J. H., and Tsuji, H. K.: Surgical treatment of tricuspid insufficiency, Ann. Surg. 162:53, 1965. Kav. J. H.. Mendez. A. M.. and Zubiate. P.: A further look at tricuspid annuloplasty, Ann. ‘Thorac. Surg. 22:498, 1976. Salomon, N. W., Stinson, E. B., Griepp, R. B., and Shumway, N. E.: Surgical treatment of degenerative mitral regurgitation, Am. J. Cardiol. 38:463, 1976. Starr, A., Grunkemeier, G., Lambert, L., Okies, J. E., and Thomas, D.: Mitral valve replacement: A lo-year followup of non-cloth-covered vs. cloth-covered caged-ball prostheses, Circulation 54 (Suppl. 111):47, 1976. Buch, W. S., Pipkin, R. D., Hancock, W. D., and Fogarty, T. J.: Mitral valve replacement with the Hancock stabilized glutaraldehyde valve: Clinical and laboratory evaluation, Arch. Surg. 110:1408, 1975. Stinson, E. B., Griepp, R. B., Oyer, P. E., and Shumway, R. E.: Long-term experience with porcine aortic valve xenografts, J. Thorac. Cardiovasc. Surg. 73:54, 1977. Horowitz, M. S., Goodman, D. J., Fogarty, T. J., and Harrison, D. C.: Mitral valve replacement with the glutaraldehyde-preserved porcine heterograft: Clinical, hemodynamic, and pathological correlations, J. Thorac. Cardiovasc. Surg. 67:885, 1974. Burch. G. E.. and Giles. T. D.: Clinical evaluation of aortic ‘and mitral valve prostheses, AM. HEART J. 92:2, 245, 1976.
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1978, Vol. 96, No. 2
