Valvuloplasty for rheumatic mitral valve disease

J

THORAC CARDIOVASC SURG

1987;94:44-56

Valvuloplasty for rheumatic mitral valve disease A surgical challenge From January 1981 through February 1985,241 patients with rheumatic mitral valve disease (mean age 21.5 ± 11.8 years) were subjected to comprehensive mitral valvuloplasty. One hlDldred seven patients (44.4%) were 15 years or younger and 63 (26.1 %) were 12 years or younger. One hundred seventy five patients had pure or predominant regurgitation (mean age 19.3 ± 10.7 years) and 40 (16.6%) had active rheumatic carditis at the time of the operation. Almost all patients (229) were in New York Heart Association Functional Class ill or IV. The techniques used included shortening of anterior I~et chordae tendineae (136 patients), resection of secondary, tertiary, and basal posterior leaflet chordae (156 patients), commissurotomy (113 patients), and implantation of a Carpentier ring (164 patients~ Current operative mortality is 1.9%. The survivors were foUowed up for 576 patient-years (mean 2.64 ± 1.32 years). Late mortality was 2.60% per patient-year and was valve related in 1.04% per patient-year. Reoperation was required in 25 patients (4.34% per patient-year), mostly (72%) in the first year. There were only two cases (0.35 % per patient-year) of thromboembolism and three cases (0.52 % per patient-year) of infective endocarditis. Hence valve failure occurred at a linearized rate of 6.08 % per patient-year but was fatal in only 22 % of the patients. There was no relationship between valve failure and the type of lesion or procedure performed, but reoperation was required more frequently in patients aged 12 years or less (7.33 % per patient-year) than in those older than 12 years (3.29 % per patient-year) (p < O.~ Actuarial survival rate at 4 1/ 2 years was 90 %, and 82 % of the patients were free from valve-related complications. Valve function after valvuloplastywas assessed clinically. Eighty-four percent of the patients had a good immediate result, but this figure dropped to 69 % at the end of the foUow-up period (p < 0.05). The remainder had moderate valve dysfunction. However, 8S % of the patients remain in New York Heart Association Functional Class I. Mitral valvuloplastyis an exceUentalternative to valve replacement in young patients with rheumatic mitral valve disease. Persistent or reactivated rheumatic carditis may be a significant factor of valve failure, and penicillin prophylaxis is mandatory after operation.

Manuel J. Antunes, M.D., M.Med., Ph.D., F.A.C.C., Manuel P. Magalhaes, M.D., Peter R. Colsen, M.B., RCh., ER.C.S., and Robin H. Kinsley, M.R, RCh., EC.S., EA.C.C. Johannesburg, Republic of South Africa

h e complications of cardiac valve prostheses make conservation of the mitral valve desirable. However, From the Division of Cardiothoracic Surgery of the University of the Witwatersrand and the Johannesburg Group of Teaching Hospitals, Republic of South Africa This work forms part of a thesis submitted to the University of the Witwatersrand for the degree of doctor of philosophy. Received for publication June 25, 1986. Accepted for publication July 15, 1986. Address for correspondence: Professor M. J. Antunes, Division of Cardiothoracic Surgery, University of the Witwatersrand, Medical School, York Road, Parktown 2193, Republic of South Africa. No reprints available from the authors.

44

suture plication and other isolated annuloplastic techniques have not generally yielded good long-term results. I Understandably, comprehensive mitral valvuloplasty, as advocated by Carpentier and associates':' and designed to restore normal anatomy and function to all components of the mitral valve apparatus, rather than to the anulus alone, had considerable appeal. Valvuloplasty, when feasible, is now widely accepted as the best method of treatment of the diseased mitral valve.':' However, there is as yet insufficient information about the long-term durability of these procedures in young patients in the first three decades of life, where it can be influenced by persisting or recurrent rheumatic activity.

Volume 94 Number 1 July 1987

Valvuloplasty for rheumatic mitral disease

Table L Patients No. of patients Period Age (yr) (mean ± SD) Acute carditis (%) Atrial fibrillation (%) Cardiothoracic ratio Valve lesion (%) Pure stenosis Regurgitation Regurgitation + stenosis Associated valve procedures AVR/AVV AVR+TA

TA/TV

100' 241 January 1981 to February 1985 21.5 ± 11.8 16.6 21.6

45

SEX

-

[ill Male

D Female

80' -

0.67 ± 0.07

-

27.4

53.1

Mean 21.5!11.8

~

19.5

-

27

2 11

Legend: SO. Standard deviation. AVR. Aortic valve replacement. AVV. Aortic valvuloplasty. TA, Tricuspid annuloplasty. TV. Tricuspid valvuloplasty.

Cognizant of the high failure rate of the mechanical prostheses," tissue valves.t'? and annuloplasty,' we embarked on a program of repair of rheumatic mitral valves, whenever possible. The results obtained in a 5 year period in an underdeveloped population group are the subject of this report. Patients From January 1981 through February 1985, 241 patients with rheumatic mitral valve disease were subjected to comprehensive mitral valvuloplasty. The date of closure of the series was chosen to allow a minimum follow-up of 1 year. The clinical data on these patients are shown in Table I. Patients subjected to simple closed or open commissurotomy were not included. The study group comprises 35.5% of the patients subjected to isolated open mitral valve operations during the period. Although the need for aortic valve replacement did not, in principle, preclude mitral valvuloplasty, the surgeon was often biased toward mitral valve replacement whenever the aortic valve had to be replaced. Nevertheless, 26 patients had concomitant aortic valve replacement and one had an aortic valvuloplasty. Also, nine patients had tricuspid annuloplasty, two had tricuspid valvuloplasty, and another two had aortic valve replacement and tricuspid annuloplasty. Closure of an atrial septal defect, incidentally found at operation, was performed in two patients and one patient had closure of a ventricular septal defect. The distribution of the patients according to age and sex is shown in Fig. 1. There were 175 female and 66 male patients and the mean age was 21.5 ± 11.8 years. One hundred seven patients (44.4%) were 15 years old or younger and 63 (26.1%) were 12 years or less. The youngest was four years old. Because of the low mean

20

-

-

~:

tt~~~

::::::::::.

If! (10

IIIIIIIIII!

ID~

I~~I: ~jf~ f~ j

r--

w

~.

n

10-19 20-29 30-39 40-49 >50 AGE (years)

Fig. 1. Age and sex of the patients at operation.

age of the population, only 52 patients (21.6%) were in atrial fibrillation. Forty patients (16.6%) had confirmed active rheumatic carditis at the time of the operation. One hundred twenty-eight (53.1%) patients were operated on for isolated mitral regurgitation and 47 (19.5%) had mixed mitral valve disease, predominantly regurgitation but with significant stenosis. The remaining 66 patients (27.4%) had isolated or predominant mitral stenosis. The mean age of patients with isolated regurgitation was 19.3 ± 10.7 years and that of those with pure stenosis was 26.5 ± 12.4 years. The difference reflects the number of patients operated on in the first two decades of life, mainly with acute rheumatic carditis and regurgitant lesions. Only two of the patients who were operated on during the active phase had mitral stenosis. Preoperatively, the diagnosis was made clinically and confirmed by two-dimensional echocardiography in all cases. A small number of patients were subjected to cardiac catheterization to establish basal parameters of left ventricular function only. In none of these patients was the diagnosis or the management plan altered by the hemodynamic study. We believe that cardiac catheterization has very little role, if any, in the diagnosis and management of rheumatic mitral valve disease. All patients with mitral regurgitation were in New York Heart Association (NYHA) Functional Class III or IV before the operation, but 12 patients operated on for

The Journal of Thoracic and Cardiovascular Surgery

4 6 Antunes et al.

Table D. Intraoperative pathologic findings Valve disease MR (N= 128) No. Annular dilatation Leaflets Moderate thickening Marked thickening Redundant Fused commissures Calcium Chordae tendineae Elongated Ruptured Thickened/fused/shortened

%

No.

94.5

27

5

3.9

15 5

11.7 3.9

107 13 23

83.6 10.2 18.0

I

121

Table m. Intraoperative pressures (mean ± SD in mm Hg)

Mitral regurgitation LA mean v Wave RV systolic LA/LV gradient Mitral stenosis LA mean v Wave RV systolic LA/LV gradient

Before valvuloplasty

After valvuloplasty

25.0 ± 8.8 47.0 ± 16.3 50.0 ± 14.4

10.4 ± 2.1 13.0 ± 3.4 3.0 ± 1.9

22.2 ± 8.3 55.3 ± 23.1 14.9 ± 6.7

MR/MS (N

10.6 ± 2.5 13.8 ± 3.2 2.7 ± 2.2

Legend: LA, Left atrium. LV, Left ventricle. RV, Right ventricle.

mitral stenosis were in Class II. The mean cardiothoracic ratio was 0.67 ± 0.07. Intraoperative findings. The intraoperative pathologic findings are indicated in Table II. Annular dilatation was found in 94.5% of the patients with pure mitral regurgitation but was the isolated lesion in only 10.9%of the patients. Elongation of the chordae tendineae was the second most important cause of regurgitation and was present in 83.6% of patients. Rupture of chordae tendineae was found in 10.2% of all patients. In the majority of the patients two or more factors were involved. A single pathologic condition was encountered in only 15% of the patients with pure regurgitation. All patients with pure mitral stenosis had fusion of both commissures. Additionally, restriction of leaflet movement was the result of thickening of the leaflets in 63.6% of the patients and of shortened and/or matted chordae in 65.2%. The choice of valvuloplasty as the method of treatment influenced the relative frequency of the different types of lesion encountered. For example,

I

= 47) %

MS (N=66) No.

I

%

57.4

8

35 6

74.5 12.8

27 15

40.9 22.7

47 6

100.0 12.8

66 8

100.0 12.1

21 2 36

44.7 4.3 76.6

8

12.1

43

65.2

12.1

severely fibrosed and distorted valves had to be replaced and ruptured chordae tendineae of the anterior leaflet precluded valvuloplasty in most cases. Left atrial and ventricular chamber enlargement was invariably present with chronic valve regurgitation but usually was absent in acute carditis. Some patients had massive dilatation of the left atrium. The size of the left atrium was variable in patients with mitral stenosis but tended to be normal or only mildly dilated in the majority. In the absence of preoperative hemodynamic studies, intracavitary pressures were routinely measured intraoperatively, both before and after valvuloplasty. The mean values for patients with pure mitral regurgitation and stenosis are indicated in Table III. Markedly elevated left atrial mean and pulmonary artery pressures were the rule. There were significant v waves in patients with mitral regurgitation and large end-diastolic gradients in those with valve stenosis. Technique. The techniques used were those developed by Carpentier and associates,":" adapted or modified to suit the local spectrum of disease (Fig. 2).15.16 Their frequency is indicated in Table IV. Commissurotomies were performed in all 113 patients with valve stenosis, bilaterally in 93% of the patients. Tertiary and basal chordae tendineae were resected in almost all these patients, but in only about 40% of those with pure mitral regurgitation. As described elsewhere," secondary chordae tendineae inserting in the ventricular surface of the body of the anterior leaflet were often resected to improve the mobility of this leaflet. Fenestration of chordae tendineae was required in 37.8% of the patients with isolated mitral stenosis. Other procedures aimed at improving the mobility of the leaflets were performed in 12 patients. These procedures included resection of lumps of calcium and localized areas of fibrosis and

Volume 94 Number 1 July 1987

Valvuloplasty for rheumatic mitral disease

47

Fig. 2. Techniques used for valvuloplasty. a, Shortening of elongated chordae (ec) tendineae. b, Transposition of chordae to substitute ruptured chordae (rc) of the anterior leaflet. c, leaflet resection. The anterior leaflet (al) tolerates a much less resection (Ys of the free edge) than the posterior leaflet (pi); d, Resection of secondary chordae (sc) of the posterior leaflet. e, Commisurotomy. f, Incision of fused commissural chordae. g, Fenestration of fused free-edge chordae. h, Ring annuloplasty.

tangential shaving of the free edge of the leaflets, usually the posterior, Shortening of chordae tendineae was performed in 73.1% of all patients with regurgitation, but in 83.6% of those with pure regurgitation. In the majority, two or more groups of chordae were shortened. Initially, a papillary muscle sliding plastic procedure was preferred. More recently, a chordal shortening plastic operation was performed almost invariably. Readjustment of the length of the chordae was required in nearly 15% of the patients, mostly for excessive shortening. Leaflet resection was performed in 22 patients (9.1%), the posterior in 16 instances, the anterior leaflet in three, and both in another three. The resection was necessitated by ruptured chordae tendineae in eight patients. Elective posterior leaflet resection was performed in nine patients with redundancy of the leaflet" and as part of the technique of transposition of chordae tendineae in five patients with ruptured chordae of the anterior leaflet. A Carpentier ring was implanted in 164 patients

(68.0%), but in 90.6% of all patients with pure regurgitation. Exceptions included six patients younger than 10 years in whom the implantation of a small ring was impractical or thought to be contraindicated. In this series, all but 16 patients received size 30 to 34 nun rings (Table V). Sizes 30 and 32 nun are considered adequate in the female and 32 and 34 nun in the male adult patient. However, the size of the ring did not bear a significant direct relationship with the end-diastolic gradient between the left atrium and left ventricle after completion of the procedure; this gradient was 3.4 ± 2.8 nun Hg in patients with rings size 32 nun or greater and 2.3 ± 2.1 nun Hg in patients with smaller rings (p = NS*). The intracavitary pressures measured after discontinuation of bypass are indicated in Table III. The comparison of these values with those obtained preoperatively in the same patients has some value and demon*No significant difference.

The Journal of Thoracic and Cardiovascular Surgery

4 8 Antunes et al.

Table IV. Surgical technique MR (N= 128)

I

%

No.

107

83.6

51

39.8

5

3.9

20

15.6

No. Chordae tendineae Shortening one group = 31 two groups = 105 Resection (tertiary and basal) Fenestration Transposition Leaflets Commissurotomy Resection Anterior = 3 Posterior = 16 Anterior + posterior = 3 Excision calcium/fibrosis Anulus Carpentier ring Suture plication

MR/MS (N

116 4

90.6 3.1

= 47)

I

MS (N= 66)

I

%

No.

21

44.7

8

12.1

45 14

95.7 29.8

60 25

90.9 37.8

47 2

100.0 4.3

66

100.0

2

4.3

10

15.2

38 2

80.9 4.3

10

15.2

%

Legend: MR, Mitral regurgitation. MS, Mitral stenosis.

Table VI. Causes of late death

Table V. Size of Carpentier ring Size (mm)

No,

%

Cause

No.

%

%/pt-yr

28 30 32 34 36

9 40 73 35 7

5,5 24.4 44.5 21.3 4.3

Cardiac Valve related Non-valve related Noncardiac Sudden/unknown

6 2 I 6

40.0 13,3 6.7 40,0

0,35 0.17

Total

164

100,0

15

100,0

2.60

strates the immediate improvement in their hemodynamic condition. However, a decision to conserve or replace the value after completion of the repair was only rarely influenced by the pressures obtained. Furthermore, the amplitude of the v wave has not correlated well with the degree of mitral regurgitation assessed clinically in the immediate postoperative period. Inadequately repaired valves were immediately replaced in at least seven patients not included in the current series. It is possible that a few more patients had immediate valve replacement after initial attempts, but they did not exceed 5% of the total. Late follow-up. All patients under 30 years of age were given oral penicillin. As poor compliance had been previously demonstrated, a monthly intramuscular injection of penicillin was added in the past 3 years. All patients were expected to return monthly to our outpatient clinic or to their regional hospitals. The wide geographic distribution of the patients' residences made

Total

1.04 1.04

follow-up difficult, and a social worker traveled up to 500 km at a time to visit defaulters and require them to report to our outpatient clinic. Patients living in relatively inaccessible regions and foreign countries were contacted by letter, telegram, or telephone or through their assistant physicians. Despite these efforts, 20 patients (8.5% of survivors) were lost to follow-up. The remainder were followed up for 576 patient-years with a mean of 2.64 ± 1.32 years per patient (range I to 5 years). Methods of analysis. Linearized incidences (percent per patient-year) include all suspected or confirmed events. The actuarial curves were calculated excluding operative deaths, by the method described by Grunkemeier and Starr." Percentages were expressed as percent ± 1 standard error and means as mean ± 1 standard deviation for 68% confidence limits. Statistical significance was established by the x2 test with the aid of 2 by 2 contingency tables and Yates' correction for small numbers.

Volume 94 Number 1

Valvuloplasty for rheumatic mitral disease 4 9

July 1987

Results Perioperative mortality. There were no operative deaths but eight patients died within 1 to 40 days of operation.Thus the early mortality rate was 3.3%. Four of the eight deaths occurred among the first 30 patients operated on and only four in the last 211 patients (1.9%). Two patients died ofvalve-related causes. Early in the series, a 7-year-old boy with severe mitral regurgitation and acute rheumatic carditis required a cross-clamp time of 129 minutes for the valvuloplasty. Despite an obviously inadequate result, valve replacement was not undertaken immediately, because of the long bypass and cross-elamp times. He died 4 days after a rooperation performed 2 weeks later. Retrospectively, the mitral valve should have been replaced during the first procedure. The second patient died during emergency reoperation for replacement of a valve repaired 20 days earlier for mitral stenosis. Sudden regurgitation occurred because of rupture of a chorda after an ostensibly good initial result. One patient died 40 days after operation, of the neurologic sequelae of a respiratory arrest resulting from dislodgment of the endotracheal tube 4 hours after uncomplicated and successful valvuloplasty. One patient died of a pulmonary embolus 6 days after emergency operation. Two patients died of arrhythmias occurring within 48 hours of operation and the last two patients died of pneumonia, 15 and 25 days after discharge from hospital. There was no statistically significant difference among the early mortality rates of patients operated on for mitral regurgitation (3.9%), mitral stenosis (3.0%), and mixed disease (2.1%). Perioperativecomplications occurred in four patients. Two required reexploration for excessive mediastinal bleeding, and another two had significant early pericardial effusions necessitating drainage. All four survived. Late mortality. Fifteen patients (6.2%) died 1 to 38 (mean 10.5 ± 11.3) months after operation, for a linearized late mortality rate of 2.60% per patient-year. The incidence was 4.65% per patient-year for the first 30 patients and 2.32% per patient-year for the remainder (p < 0.05) at the same follow-up time. During this period, 4.5% of patients with mitral stenosis (three patients), 12.8% of those with mixed disease (seven patients), and 5.5% of those with mitral regurgitation (six patients) died (p < 0.10). The causes of late death are summarized in Table VI and were valve related in six patients (1.04% per patient-year). In four of these, death was presumably due to severe residual or recurrent mitral regurgitation, as judged from the reviewof the outpatient records. Two

MX I6V

4 1--,,'l---,-------iI

~1

5

....._ . J

2

MS~3 •

, patient reoperated on for I.E.

Fig. 3. Valve lesion at reoperation (right column) in relation to the original lesion (left column). MR, Mitral regurgitation. MX, Mixed mitral disease. MS, Mitral stenosis. IE, Infective endocarditis.

of them had refused rooperation. One patient, with mitral stenosis, died at rooperation and the other had infective endocarditis. Other causes of late death included a thrombosed aortic valve prosthesis, severe hemoptysis, and late pericardial effusion (one patient each). In the remaining six patients the cause of death could not be ascertained as consent for autopsy was not obtained. In these cases, the reveiw of the patients' records did not reveal any fact that could predict imminent death. Reoperation. Besides the three patients who died, another 25 patients (10.4% of the total or 12.7% of survivors) required rooperation for severe residual or recurrent valve dysfunction, for a linearized rate of 4.34% per patient-year. The mitral valve was replaced in all instances. All three patients who died underwent emergency rooperation. There were no deaths among patients having elective procedures. Rooperation was required in 6.1% of the patients with mitral stenosis (four patients), 10.2% of those with mitral valve regurgitation (13 patients), and 17.0% of those with mixed disease (eight patients) (p < 0.10). Rooperation was performed 1 to 39 months postoperatively (mean 9.9 ± 10.6 months), but 18 of the patients (72.0%) were rooperated on in the first year after the initial operation (mean 4.2 ± 3.0 months). The valve lesions at rooperation, in relation to the original lesion, are shown in Fig. 3. Mitral regurgitation (with a degree of stenosis in five

50

Antunes et al.

The Journal of Thoracic and Cardiovascular Surgery

Fig. 4. A, Ruptured chorda 3 months after valvuloplasty. B, Ventricular aspect of the excised valve showing complete endothelialization of the papillary muscle at the site of chordal shortening plastic incision. patients) was the cause for reoperation in all but two of the 25 patients. One patient had tight rigid mitral stenosis and another had infective endocarditis without significant valve dysfunction. At reoperation the most important anatomical causes for regurgitation were retraction of the leaflets and prolapse of the anterior leaflet. The former presumably resulted from progression or reactivation of the rheumatic process. Indeed, acute rheumatic carditis was present either at the initial procedure or at reoperation in eight of these patients. Prolapse of the anterior leaflet could have been caused by insufficient shortening of the chordae tendineae or recurrent elongation. As the initial shortening procedure was invariably found well consolidated by fibrosis and endothelialization of the papillary muscle incision, it seems logical to conclude that recurrent elongation was caused by either further disease of

the chordae tendineae or increased chordal strain. The same mechanism or mechanisms were probably responsible for the four cases of ruptured chordae tendineae (Fig. 4). In one instance, however, injury to the chordae tendineae may have been caused at the time of the valvuloplasty. In all, "technical errors" could have been responsible for 11 reoperations, including those of three patients who did not receive a ring and another three patients, originally with stenosis, in whom posterior leaflet holes were probably the result of overenthusiastic resection of secondary and basal chordae tendineae. Other complications. Major systemic emboli occurred in only two patients (0.35% per patient-year). Both patients had been operated on for pure mitral regurgitation and were in sinus rhythm. The first one, a 36-year-old woman, is well with only a minor neurologic

Volume 94 Number 1 July 1987

Valvuloplasty for rheumatic mitral disease 5 1

100

Table VII. Causes of valve failure Cause

No.

%/pt-yr

Valve-related mortality Reoperation Severe valve dysfunction Other

8 25 I

4.34

Total

35

lAO

90

0.17

g.s>

0.17

~

6.08

,,!!

...

~-.....-e90%

80

'<;1---0--0

70 deficit, and the other one, a 20-year-old man, had a hemiparesis and is currently lost to follow-up. Three patients (0.52% per patient-year) had infective endocarditis of the mitral valve involving the Carpentier ring. One' patient, aged 21 years, died of a Serratia marcescens infection, and the other two, aged 13 and 11 years, were successfully reoperated on with replacement of the valve. Valve failure. The causes of valve failure, defined as all valve-related complications resulting in the death or permanent disability of the patient or necessitating reoperation, and including one patient currently with severevalve dysfunction, are shown in Table VII. Valve failure occurred at a linearized rate of 6.08% per patient-year but was fatal in less than a quarter of the patients (1.40% per patient-year). The valve failed in 19.1% of the patients with mixed disease, 14.1% of those with isolated regurgitation, and 9.1% of those with pure stenosis, but these differences did not reach statistical significance. When analyzed against the type of procedure performed, valve failure appeared to be more frequent in patients who had commissurotomy together with shortening of chordae tendineae (mixed disease). Failure occurred in three of the six patients with regurgitation in whom a ring could not be inserted. There were no early failures among patients who had transposition of chordae tendineae. Good results were also obtained in other patients in whom this technique was more recently performed and who were not included in the series. Actuarial survival. The actuarial survival curves are shown in Figs. 5 and 6. At 4V2 years, 90% ± 4% of the patients were alive, 78% ± 8% of whom were free from reoperation or other complications. Thirty survivors entered the fifth year of follow-up. Freedom from valve-related mortality was 94% ± 4% and freedom from all valve-related complications including reoperation and death was 82% ± 7% after the same

period.

Valveperformance according to age groups. Sever-

al parameters of patient/valve performance were ana-

78%

0

~

.Total oFree from reoperation

I 4

I

I

3

2 Years

Fig. 5. Actuarial survival of the whole group.

100

- .............~....--- __-----l. 94 % 90

0 .z

...> 80

""0--0--0

:J

82%

If)

,,!! 0

70

• Free from VR Mortality o Free from VR Complications

234 Years

Fig. 6. Survival free from valve-related (VR) mortality and other valve-related complications.

lyzed for the following age groups: above and below 12 years and above and below 15 years (Table VIII). The mortality rates were lower in younger patients, probably reflecting better ventricular function. However, younger patients required reoperation more frequently, and the rate increases as one goes down the age scale, probably because of an increased incidence of acute carditis. Although we could not demonstrate any significant differences between the results of the acute and chronic rheumatic groups, it is likely that many of the patients included in the latter had subclinical activity that resulted in progressive fibrosis of the valve. The actuarial survival and complication-free survival curves for these age groups are shown in Figs, 7 and 8. Global survival was higher for younger patients, but more of the older patients were alive and complication free after the end of follow-up.

The Journal of Thoracic and Cardiovascular Surgery

Antunes et al.

52

Table VIII. Factors of patientfvalve performance <12 yr

>12 yr

p Value

<15 yr

>15 yr

p Value

1.33 7.33 8.00 96 73

3.05 3.29 4.69 88 81

<0.05 <0.05 NS <0.05 <0.10

1.56 5.86 6.64 93 77

3.44 3.13 4.38 88 78

<0.05 <0.10 NS NS NS

Late mortality (%/pt-yr) Reoperation (%/pt-yr) Valve failure (%/pt-yr) Actuarial survival (% at 4'h yr) Complication-free survival (% at 4\6 yr)

Legend: NS. Not significant.

Table IX. Late clinical assessment of valve function Residual valve dysfunction

Original lesion Stenosis" Regurgitation Mixed' Total

No.

No.

36 75 26

29 51 15

137

95

I

Severe

Moderate

None/mild %

No.

81 68 58

7 23 11

69

41

I

%

No.

19 31 42

o

I

%

1

o

30

'p < 0.05. stenosis versus mixed.

Table

x. Early clinical assessment of valve function * Residual valve dysfunction Moderate

None/mild Original lesion Stenosis Regurgitation Mixed Total

No.

No.

37 63 25

33 52 20

125

105

I

%

No.

89 83 80

4 11 4

84

19

I

Severe %

11 17 16

No.

o o 1

I

%

4

15

'p = NS among the three groups.

Valve function. Late valve function was assessed by retrospective analysis of the outpatient records of the 173 patients available for follow-up. Only clinical assessments made by a senior cardiologist or surgeon were considered. The records were reviewed at the end of the follow-up period (12 to 61 monhts) by an independent observer. Insufficient or inconsistent information did not permit classification of 36 patients, including 12 patients whose assessment, made outside the department, was not considered. The results in the remaining 137 patients are indicated in Table IX. The best late results were found in the mitral stenosis group and the worst in the mixed mitral valve disease group (p < 0.05). To obtain a better perspective of these results, an early assessment of the mitral valve function of 125 patients who had undergone valvuloplasty was conducted in the past 18 months by an independent senior cardiologist. This

assessment was purely clinical and was carried out blindly, i.e., without knowledge of the preoperative diagnosis or the technique used, 10 to 14 days after operation, before discharge from the hospital (Table X). A good result (no dysfunction or mild valve dysfunction) had been achieved in 84% of the patients and a satisfactory result (more than mild but not severe valve dysfunction) in 15%. One patient with a poor result (severe residual valve dysfunction) required early reoperation. There were no significant differences among the three groups of valve lesions. In the mixed disease group, there was a significant difference between the immediate postoperative and late valve function assessments (p < 0.05) (Fig. 9). A less significant difference (p < 0.10) between early and late results was found in the mitral regurgitation group and there was no difference in the stenosis group.

Volume 94 Number 1 July 1987

Valvuloplasty for rheumatic mitral disease 53

100

95

100

_

......-

...-

. .--4........-

...-.96"10

90

"0--0--0

.

'0---<;>--0 88"10

-.!!

....- 4 _. . .-.73"10

.....-

85

;!. 70

." 12 years 0) 12 years

I 2

I

3

60

I 4

0)12 years

Years

."12 years

Fig. 7. Actuarial survival for patients older and younger than 12 years.

Symptomatic status. The late symptomatic class (NYHA) in the 158 patients in whom adequate and consistent information was available was also analyzed and is shown in Fig. 10 and Table XI. Eighty-five percent of patients are in Class I and all but one of the remainder are in Class II (most patients are electively maintained on low-dose antifailure therapy). The absence of a significant difference among the three groups of valve lesions appears to indicate that the symptomatic status of the patient does not correlate well with the valve function after mitral valvuloplasty. Discussion Rheumatic valvular disease has almost been eradicated in developed countries. IS By contrast, rheumatic carditis is still seen in epidemic proportions in the underdeveloped, predominantly black population of South Africa and in many other poorly developed countries. The mitral valve is involved in 97% of the cases and mitral regurgitation is by far the commonest lesion. 19 Although valves that are functionally abnormal during acute rheumatic carditis may return to normal, especially when recurrences are prevented/D. 21 in most cases the lesions are progressive and eventually lead to severe disability of the patient. The natural history of the disease demonstrates that surgical treatment is the only effective method of achieving hemodynamic improvement in patients with severe valvular lesions." Since the introduction of the cardiac valvular prostheses in 1960, valve replacement has succeeded in providing relief to hundreds of thousands of patients affected by rheumatic valvular disease. However, the consequences of prosthetic mitral valve replacement were soon evident. Indeed, it

81"10

I

I

2

Years

I

3

4

Fig. 8. Survival free from complications for patients older and younger than 12 years.

c

.Q

U c

90 -

.2 80~

51 "8 o


DEarly

100'-

70' -

60-

50 -

Em Late -

,....--

,....--

JI

MR

MX

Original

I I

MS

lesion

Fig. 9. Percent of patients with good valve function (early and late) according to original valve lesion.

has been said that "valve replacement is simply exchanging one disease for another.'?' The early mechanical prostheses were plagued by an unacceptably high incidence of thromboembolic events and the bioprostheses had a prohibitive rate of biodegradation and calcification, especially in the younger age groups. Our own experience with these two types of prostheses confirmed their high failure rate in this population group. s.io Thrombotic obstruction of the Bjork-Shiley and other mechanical prostheses and degeneration of glutaraldehyde-preserved porcine xenografts constituted

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Antunes et al.

Table XI. Symptomatic status of patients at late follow-up*

%

100

NYHAfunctional class III III

80

Original lesion

.2 u

Class I No.

No.

No.

6 13 3

15 15 9

22

14

Stenosis

40

34

Regurgitation Mixed

86

72

32

29

85 84 91

.2

Total

158

135

85

«

40

I%

I%

60 ~ .Q

g

Class II

Class III No.

I%

o 1

o

*p = NS among the three groups.

I

>-

z

20

II

MR

MX Original

MS

lesion

Fig. 10. Percent of patients in different categories of NYHA functional class according to original valve lesion.

the two most common indications for reoperation of the mitral valve in our unit in the past 10 years." Despite the immense strides in the perfection of materials and design, the ideal valve remains elusive. Consequently, the attitude of preservation of the mitral valve whenever possible has gained in popularity. However, whereas open commissurotomy is now fairly generally accepted for the treatment of isolated mitral stenosis, a conservative surgical approach for mitral regurgitation has only had a limited adherence. Previously, we performed mitral valve annuloplasty in some patients with predominant or pure mitral regurgitation. The Reed asymmetrical measured anuloplasty" was used initially with poor late results. These were usually a consequence of redilatation of the segment of unprotected anulus between the two commissural plications. After rheumatic carditis, the mitral anulus dilates almost exclusively in the area of its posterior segment, which, apart from the leaflet itself, has limited fibrous tissue. Conversely, the anterior anulus, which is an integral part of the fibrous skeleton of the heart, is rarely affected. Hence a modified Paneth posterior plication annuloplasty suture" was introduced, and although the initial results appeared more encouraging, a similar high failure rate was experienced in the long term. 1 Why should suture annuloplasty have such poor results? The multifactorial pathology of mitral regurgitation was stressed by Carpentier and co-workers.":" Our experience confirmed that only in a mere 10% of

the patients is annular dilatation the sole cause of mitral regurgitation. Chordal abnormalities (thickening/shortening, elongation, or rupture) were observed in 94% of the patients and the leaflets were abnormal in 30%. A more complete valvuloplasty (as distinct from annuloplasty) had compelling logic. We adopted this approach in 1981. When the initial results were analyzed, a striking learning curve was demonstrated." Because of the large number of patients subjected to operation in a relatively short period of time, a more encouraging trend soon developed. Otherwise, our experience might have come to an abrupt halt, as many surgeons have been deterred by their early failures. In the process of learning, many aspects of the technique of valvuloplasty were adapted or modified to suit the characteristics of this population. Newer techniques were evolvedand others were used with indications different from those originally intended. As time has elapsed, it has become more evident to us that the scope for improvement is infinite. The compliance of the patient to medication must significantly influence the long-term results of mitral valvuloplasty. Rheumatic fever is endemic in this population and the possibilities of recurrence are endless, as most patients are in the susceptible age group. Over and above the effect of the postrheumatic healing process, persistence or recurrence of the rheumatic activity can only further scar and distort the valve structures, resulting in regurgitation. Therefore, it is essential that patients receive penicillin regularly after the operation. However, the influence of penicillin prophylaxis in improving the late results of valvuloplasty has yet to be confirmed. After our initial poorer results in patients with acute rheumatic carditis, valvuloplasty was abandoned for some time in these patients. Edema of the tissues compromised the holding of the sutures and resulted in early recurrence. Also, impaired pliability of the leaflets caused obstruction to ventricular filling and frequently necessitated immediate valve replacement.

Volume 94 Number 1 July 1987

More recently, however, patients with acute rheumatic carditis but without gross abnormality of the valve leaflets have been subjected to valvuloplasty. Only patients with "hyperacute" inflammatory signs are now excluded. Valvuloplasty was performed in over 90% of the patients with pure regurgitation in whom it was thought possible preoperatively, and in six percent of those with valves that had not been considered really suitable. Echocardiography was the most reliable method of predicting the possibility of conservation of the valve, and a pliable and large anterior leaflet was the most important determinant for an adequate valvuloplasty. Conversely, the identification of ruptured chordae tendineae and a rigid and small posterior leaflet are relatively adverse factors. The presence of severe dysfunction of the left ventricle did not preclude valvuloplasty, but often biased the surgeon toward valve replacement in our earlier experience. The potential benefits of valvuloplasty were thought to be offset by the poorer long-term outlook of patients with a low ejection fraction and the risk of a less than ideal result. However, the presence of severe left ventricular dysfunction may favor valvuloplasty, as our own observations (unpublished) appear to indicate that left ventricular function is better after valvuloplasty, where the subvalvular mechanism is preserved. On the other hand, poor left ventricular function increases the likelihood of embolism from the prosthetic valve. Hence we no longer consider a poor left ventricle to be a contraindication to valvuloplasty. The probability of valvuloplasty in patients with pure mitral stenosis is of the order of 60% and if favored by such echocardiographic signs as the pliability of the leaflets, especially the anterior, and the absence of gross involvement of the submitral apparatus and of extensive areas of calcification. However, the association of significant regurgitation and stenosis made conservation possible in less than 30% of the patients. In these patients, the decision to perform a valvuloplasty was always made exclusively intraoperatively and often implied a clear perception by the surgeon that the final result could be less than ideal. Thus the indication for valvuloplasty was influenced by factors such as the relative adequacy of the valve and a greater need for preservation, as in very young age or presumed noncompliance of the patient to postoperative follow-up and therapy. A ring annuloplasty was performed in all but 12 of the patients with pure or significant regurgitation. Among these were six patients aged less than 10 years in whom the implantation of a ring was impractical or thought to be contraindicated because of the small size of the anulus. The end result was unsatisfactory in five

Valvuloplasty for rheumatic mitral disease 5 5

of these patients, of whom three have already required valve replacement. We now believe that when an adequate size ring (at least 28 mm) cannot be im-: planted, valvuloplasty is probably contraindicated. However, the size of the ring did not bear a significant direct relationship to the end-diastolic gradient between the left atrium and left ventricle, measured after completion of the procedure. Larger transvalvular gradients were invariably measured in patients with thickened, relatively nonpliable leaflets. We can now consistently predict such gradients and confidently select the valves that can be satisfactorily repaired. Evaluation of valve function after valvuloplasty is difficult. Mild to moderate degrees of stenosis or regurgitation cannot be easily quantitated by echocardiography or cardiac catheterization. Clinical evaluation appears to be at least as sensitive as these methods. To the best of our knowledge, no previous report has addressed itself to an in-depth analysis of the clinical condition of patients after mitral valvuloplasty. In our view, the characterization of systolic murmurs alone does not accurately indicate valvular function. In this series, 84% of the patients had no dysfunction or very mild residual valve dysfunction immediately after valvuloplasty, which indicates successful reconstruction. As discussed earlier, we had often accepted less than ideal results, as assessed intraoperatively, to avoid the implantation of a prosthesis in children. Although all patients were symptomatically much improved after operation, some subsequently required valve replacement because of the severe and progressive nature of the dysfunction. Besides, some of those with a good result initially had moderate dysfunction at the time of the late clinical assessment. They appear to confirm the rule that "regurgitation begets regurgitation.'?" although in some cases moderate valve regurgitation remained unaltered after 3 to 4 years. Nevertheless, nearly 70% of the survivors continue to have good valve function at late follow-up. This figure compares well with those reported by Carpentier,' Lessana," and their colleagues, especially if the differences in age and in the incidence of acute rheumatic carditis are considered. As 85% of the patients remain asymptomatic, identical to the experience of other authors, the relative discrepancy in the number of patients with moderate valve dysfunction in our series may indicate an excessively critical assessment. Finally, the major advantage of mitral valvuloplasty versus valve replacement is the very low incidence of potentially lethal complications, such as thromboembolism and infective endocarditis. The linearized thromboembolic rate of 0.35% per patient-year is much lower

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Antunes et ai.

than that observed for mitral valve replacement with a mechanical prosthesis (3.92% per patient-year) in the same population group during the same period. Valvuloplasty is an excellent alternative to valve replacement even in a group affected exclusively by rheumatic mitral valve disease. Although a clear learning curve is attached, the techniques are reproducible and the results reasonably predictable. We remain confident of the prediction that satisfactory mitral valvuloplasty is possible in the majority of young patients with rheumatic heart disease. We are greatly indebted to Professor Alain Carpentier, who taught one of us (M.J.A.) these techniques, to Professor John Barlow for the early clinical assessment of the patients included in this study, and to Sister Monica Zimu for her efforts in conducting the follow-up of the patients. REFERENCES

I. Antunes MJ, Kinsley RH. Mitral valve anuloplasty: results in an underdeveloped population group. Thorax 1983;38:730-6. 2. Carpentier A, Deloche A, Dauptain J, et al. A new reconstructive operation for correction of mitral and tricuspid insufficiency. J THORAC CARDIOVASC SURG 1971;61:1-13. 3. Carpentier A. Cardiac valve surgery-the "French correction". J THORAC CARDIOVASC SURG 1983;86:323-37. 4. Carpentier A, Chauvaud S, Fabiani IN, et al. Reconstructive surgery of mitral valve incompetence: ten-year appraisal. J THORAC CARDIOVASC SURG 1980;79:338-48. 5. Bonchek LI. Correction of mitral valve disease without valve replacement. Am Heart J 1982;I04:865-8. 6. Spencer FC, Colvin SB, Culliford AT, Isom OW. Experience with the Carpentier techniques of mitral valve reconstruction in 103 patients (1980-1985). J THORAC CARDIOVASC SURG 1985;90:341-50. 7. Cosgrove DM, Chavez A, Lytle BW, Goormastic M, Borsh J, Loop FD. Results of mitral valve reconstruction [Abstract]. Circulation 1985;72(Pt 2):III21O. 8. Copans H, Lakier JB, Kinsley RH, Colsen PR, Fritz VU, Barlow JB. Thrombosed Bjork-Shiley mitral prosthesis. Circulation 1980;61:169-74. 9. Antunes MJ, Santos LP. Performance of glutaraldehydepreserved porcine bioprosthesis as a mitral valve substitute in a young population group. Ann Thorac Surg 1984; 37:387-92. 10. Antunes MJ. Bioprosthetic valve replacement in children: long-term follow-up of 135 isolated mitral valve implantations. Eur Heart J 1984;5:913-8. II. Carpentier A. La valvuloplastie reconstitutive. Une nouvelle technique de valvuloplastie mitrale. Presse Med 1969;77:251.

12. Carpentier A. Plastic and reconstructive mitral valve surgery. In: Kalmanson D, ed. The mitral valve. Acton, Massachusetts: Publishing Sciences Group, 1976;52740. 13. Carpentier A. Mitral valve reconstructive surgery. In: Robb C, Smith R, eds. Operative surgery. London: Butterworth, 1977:169-77. 14. Carpentier A, Reiland J, Deloche A, et al. Conservative management of the prolapsed mitral valve. Ann Thorac Surg 1978;26:294-302. 15. Antunes MJ. Mitral valve repair in an underdeveloped population group [Thesis]. Johannesburg, University of the Witwatersrand, 1986. 16. Antunes MJ, Colsen PR, Kinsley RH. Mitral valvuloplasty: a learning curve. Circulation 1983;68(Pt 2):1170-5. 17. Grunkemeier GL, Starr A. Actuarial analysis of surgical results: rationale and method. Ann Thorac Surg 1977; 24:404-8. 18. Sellers TF. An epidemiologic view of rheumatic fever. Prog Cardiovasc Dis 1973;16:303-7. 19. McLaren MJ, Hawkins OW, Koornhof HJ, et al. Epidemiology of rheumatic heart disease in black schoolchildren of Soweto, Johannesburg. Br Med J 1975;3:4748.

20. Bland EF, Jones TD. Rheumatic fever and rheumatic heart disease. Circulation 1951;4:836-43. 21. Tompkins DG, Boxerbaum B, Liebman J. Long term prognosis of rheumatic fever patients receiving regular intramuscular benzathine penicillin. Circulation 1972; 45:543-51. 22. Kinsley RH, Girdwood RW, Milner S. Surgical treatment during the acute phase of rheumatic carditis. In: Nyhus LM, ed. Surgery annual. New York; AppletonCentury-Crofts, 1981:299-323. 23. Kinsley RH. Valve replacement. Ann Life Ins Med 1980;6:185-201. 24. Antunes MJ, Magalhaes MP, Azevedo MG, Baptista AL, Kinsley RH. Reoperations of the mitral and aortic valves. Z Kardiol 1986;75:163-7. 25. Reed GE, Tice DA, Clauss RH. Asymmetrical exaggerated mitral annuloplasty: repair of mitral insufficiency with hemodynamic predictability. J THORAC CARDIOVASC SURG 1965;49:752-61. 26. Burr HB, Krayenbuhl C, Sutton MStJ, Paneth M. The mitral plication suture. J THORAC CARDIOVASC SURG 1977;73:589-95. 27. Edwards JE, Burchell HB. Endocardial and mitral lesions Get impact) as possible sites of origin of murmurs. Circulation 1958;18:946-60. 28. Lessana A, Viet IT, Ades F, et al. Mitral reconstructive operations: a series of 130 consecutive cases. J THORAC CARDIOVASC SURG 1983;86:553-61.