Mitral valve repair: results and the decision-making process in reconstruction. Report of 275 cases.

From January 1975 to June 1988, 275 patients underwent mitral valve repair for mitral regurgitation, pure (148 patients) or associated with mitral stenosis (127 patients). Patients with pure mitral stenosis were excluded from this study. The cause of mitral regurgitation was rheumatic in 180 patients (aged 28.6 +/- 1.2 years, mean +/- standard error of the mean) and degenerative in 84 patients (aged 54.7 +/- 1.5 years). Fifty-nine percent of the patients were in New York Heart Association classes III and IV before the operation. Intraoperative assessment of the mitral valve led us to identify four major mechanisms of mitral regurgitation: (1) restriction of leaflet motion by fibrosis (group I, 63 patients); (2) enhancement of leaflet motion by leaflet and chordal extension and prolapse (group II, 139 patients), (3) combination of both (group III, 64 patients); and (4) isolated dilatation of the anulus (group IV, 10 patients). One hundred sixty-one patients had isolated mitral disease and 114 had associated aortic or tricuspid valve disease, or both. The hospital mortality rate was 4.0%. Follow-up was 96% complete and totaled 1247.47 patient-years. At 13 years' follow-up, the survival rate was 93.0% +/- 6.8% in group I, 90.0% +/- 6.0% in group II, and 96.6% +/- 4.6% in group III. Freedom from reoperation was 78.1% +/- 21.0%, 83.2% +/- 18.9%, and 79.6% +/- 16.2%, respectively. Freedom from embolism was 94.7% for the whole series. In patients with isolated mitral valve repair, the cumulative morbidity was significantly higher in groups I (6.3 +/- 2.0%/pt-yr) and III 6.3% +/- 1.7%/pt-yr) than in group II (2.5% +/- 0.9%/pt-yr, p less than 0.05). Multivariate analysis identified age and associated tricuspid valve disease as significant predictors of reoperation (p less than 0.01 for both factors). These results suggest that conservative surgery should be used with caution in group I and III patients. In contrast, indications for mitral valve repair should be extended in group II patients. This observation has important clinical implications since, in Western countries, valve prolapse tends to be a major cause of mitral regurgitation.

[Role of peri-operative treatment in the surgery of advanced valvular cardiopathies]. / Rôle du traitement péri-opératoire dans la chirurgie des cardiopathies valvulaires évoluées.

Between January 1981 and October 1982, 100 consecutive patients with valvular heart disease (49 p. 100 polyvalvular disease) underwent surgery. All had severe lesions; Class III or IV of the NYHA classification; cardiomegaly with an average cardio-thoracic ratio of 59 +/- 7.7 p. 100; a cardiac index of less than 2.5 1/min/m2 in 70 p. 100 of cases; pulmonary hypertension (mean PAP : 31.93 +/- 12.17 mmHg) in 89 p. 100 of cases. Half the patients were in atrial fibrillation and all had been on chronic digitalo-diuretic therapy before surgery. Thirty of the 41 patients given preoperative venous vasodilator therapy had significant reductions of their cardiothoracic ratios (63 +/- 1.5 p. 100 vs 59.1 +/- 1.6 p. 100, p less than 0.001). Conservative surgical procedures were possible in 58 cases of mitral valvuloplasty and 5 aortic valvuloplasties. Correction of functional tricuspid regurgitation (34 p. 100) was systematic. Tricuspid regurgitation masked by salt and water depletion was detected by digital palpation after clamping the pulmonary artery. In 8 cases the aortic ring had to be enlarged. The low hospital mortality (6 p. 100) and the lack of postoperative complications (assisted ventilation for less than 24 hours in 92 p. 100 of cases) compare favourably with other reported series.

[Aortic valve replacement by bioprosthesis with enlargement of the aortic ring]. / Remplacement valvulaire aortique par bioprothèse avec élargissement de l'anneau aortique.

Small diameter aortic valve bioprostheses are associated with resting ventriculo-aortic pressure gradients of 10 to 35 mmHg. In order to avoid this factor favouring degradation of left ventricular function and early deterioration of the bioprosthesis, we enlarged the aortic ring when the diameter was less than 23 mm in patients considered unsuitable for long-term anticoagulation. The surgical technique involved incising the annulus from the postero-lateral commissure to the anterior mitral leaflet and implanting a Dacron patch lined with pericardium. Nine patients aged from 10 to 70 years (average 22 years) underwent aortic valve replacement with a Carpentier-Edwards bioprosthesis associated with enlargement of the aortic ring, between June 1979 and December 1981. The mean follow-up period is now 18 months (range 9 to 39 months). One patient has been lost to follow-up. Before surgery, 6 patients were in Stage III and 3 patients in Stage IV of the NYHA classification. There were 4 patients with pure aortic regurgitation with valve prolapse, 1 patient with aortic regurgitation due to endocarditis, and 4 patients with mixed aortic valve disease. The underlying disease was rheumatic in 6 cases, congenital in 2 cases and infective endocarditis in 1 case. The mean diameter of the aortic ring before enlargement was 19 mm. After the procedure, it increased to 23,8 mm, so enabling the implantation of no 23 and no 25 bioprostheses. Three patients had associated mitral regurgitation, 3 patients had mixed mitral valve disease, 1 patient had a membranous VSD with infundibular stenosis, and 1 patient had subvalvular aortic stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Mitral reconstructive operations. A series of 130 consecutive cases.

Between January, 1975, and January, 1982, 130 patients underwent mitral valvuloplasty for pure or predominant mitral insufficiency. Mean age at operation was 30 +/- 17 years. Twenty-five patients were under 15 years of age. Mitral insufficiency was mainly (112/130) due to rheumatic disease. Fifty-nine patients (45.4%) had another diseased valve which necessitated a surgical correction (tricuspid in 36 and aortic in 23). Surgical technique for mitral valvuloplasty varied according to the lesions. Three patients died in the first month after operation (2.3%). Five patients are lost to follow-up. The mean follow-up period for the 122 remaining patients is 38 +/- 27 months. Seven patients required reoperation and three of them died. An additional patient died without reoperation. Therefore, the late mortality was 3.1% (4/122). Almost all (116/118) of the remaining patients are in Class I (105) or II (11) of the New York Heart Association. Mean cardiothoracic ratio decreased from 60.6% +/- 7.7% preoperatively to 53.7% +/- 6.2% postoperatively (p less than 0.001). Thromboembolic episodes were noted in four patients, all of them in atrial fibrillation. Actuarial curves including hospital mortality showed a 92.0% survival rate at 7 years for the overall series (1.0% +/- 0.5%/patient-year), 93.7% +/- 4.9% at 7 years for isolated mitral reconstruction and 89.9% +/- 5.6% for mitral-tricuspid valvuloplasty at 5 years. The embolism-free rate at 7 years was 91.2%, with a rate of thromboembolic episodes of 1.0 +/- 0.5%/patient-year. Eighty-eight percent were free of reoperation at 7 years, with a rate of reoperation of 1.7 +/- 0.7%/patient-year. This system of mitral repair can provide stable functional results, low surgical and late mortality, and an acceptable rate of reoperation.

[Even distribution of myocardial protection in surgery of the coronary arteries: successive cardioplegia at the origin of the aorta and at the coronary sinus]. / Pour une répartition uniforme de la protection myocardique dans la chirurgie des coronaires: cardioplégie successive dans la racine de l'aorte et dans le sinus coronaire.

In coronary bypass surgery myocardial protection by injection of a cardioplegic fluid is made uneven by the presence of stenotic segments. In order to make it even, the authors suggest that the fluid should be injected first into the aortic origin, then into the coronary sinus. This method should provide greater safety when multiples bypasses are performed and in cases of impaired left ventricular function.