Extensive calcification of the mitral valve anulus is a pathologic entity frequently associated with degenerative valvular disease. The calcification process remains localized to the anulus in 77% of the cases. It may extend, however, to the underlying myocardium. Whenever an operation is necessary for an associated valve insufficiency, the question arises whether it is preferable to repair or to replace the valve and how to manage the calcification. In the first part of this paper the pathology of this disease is studied, and in the discussion a mechanism is proposed to explain the development of the process of calcification. In the second part, a new operation is described, which comprises the temporary detachment of the leaflets, en bloc resection of the calcium deposit, annular reconstruction, and valve repair. For patients in whom the calcification extends to the myocardium a "sliding atrioplasty" of the left atrium is described, which allows the area of exposed muscular fibers to be covered. Between 1986 and 1994, among 68 patients with extensive calcification of the anulus and severe mitral valve insufficiency, 67 benefited from these repair techniques. Ages ranged from 18 to 82 years (mean 62 years). Thirty-two patients had a billowing mitral valve (Barlow), 27 a fibroelastic deficiency, and two Marfan's disease. The calcification involved more than one third of the anulus in 88% of the patients, the posterior anulus in 10.5%, and the whole anulus in 1.5%. The calcification process extended to the myocardial wall in 12% of the patients and to the papillary muscles in 4.5%. In the group of 67 valve repairs, there were two hospital deaths (2.9%), no instances of anulus dehiscence, and no early reoperations. The follow-up period extended from 4 months to 8 years (mean 3 years 8 months). There were two late deaths, 2 and 17 months after the operations, for an actuarial survival of 93% at 7 years. Late reoperation (6 to 62 months) was necessary in four patients (6.4%) for residual mitral valve incompetence (n=2), hemolysis (n=1), or endocarditis (n=1). In one of these patients a new repair was possible, whereas the three other patients required a valve replacement. All patients but one survived the reoperation. Actuarial freedom from reoperation was 87% at 7 years. All 60 patients with valve repair were reviewed for this study by clinical examination and echocardiography. All but one were in functional class I or II. There was no incompetence or trivial residual mitral valve incompetence in 55 patients and moderate incompetence in five. Two thromboembolic events have been recorded for a linearized rate of 1%/pt-yr. This study shows that complete anulus decalcification and valve repair can be done safely in patients with mitral valve insufficiency and extensive calcification of the anulus, even when the calcification process deeply involves the myocardium. It also demonstrates that an initially good result remained stable up to 7 years.
Background-Results of conservative surgery are well established in degenerative mitral valve (MV) insufficiency.However, there are controversies in rheumatic disease. This study is the evaluation of one center for rheumatic MV insufficiency based on a functional approach. Methods and Results-From 1970 to 1994, 951 patients with rheumatic MV insufficiency were operated on with the reconstructive techniques elaborated by Alain Carpentier. Aortic valve diseases were excluded. Mean age was 25.8 years (4 to 75), and sinus rhythm was present in 63%. The functional classification used was type I, normal leaflet motion, 71 patients (7%); type II, prolapsed leaflet, 311 patients (33%); and type III, restricted leaflet motion, 345 patients (36%). The combined lesion of prolapse of the anterior leaflet and restriction of the posterior was present in 224 patients (24%). Surgical techniques used were implantation of a prosthetic ring in 95%, shortening of the chords and leaflet enlargement with autologous pericardium, and commissurotomy. Hospital mortality rate was 2%. The mean follow-up was 12 years (maximum, 29 years): 8618 patients per year. Actuarial survival was 89Ϯ19% at 10 years and 82Ϯ18% at 20 years. The rate of thromboembolic events was 0.4% patients per year (33 events), with 3 deaths. Freedom from reoperation was 82Ϯ19% at 10 years and 55Ϯ25% at 20 years. The main cause (83%) of reoperation was progressive fibrosis of the MV. The actuarial rate of reoperation was 2% patients per year and was correlated to the degree of preoperative fibrosis. Conclusions-Conservative
et al.. Percutaneous repair or medical treatment for secondary mitral regurgitation: outcomes at 2 years Methods and results. AimsThe MITRA-FR trial showed that among symptomatic patients with severe secondary mitral regurgitation, percutaneous repair did not reduce the risk of death or hospitalization for heart failure at 12 months compared with guideline-directed medical treatment alone.At 37 centres, we randomly assigned 304 symptomatic heart failure patients with severe secondary mitral regurgitation (effective regurgitant orifice area >20 mm 2 or regurgitant volume >30 mL), and left ventricular ejection fraction between 15% and 40% to undergo percutaneous valve repair plus medical treatment (intervention group, n = 152) or medical treatment alone (control group, n = 152). The primary efficacy outcome was the composite of all-cause death and unplanned hospitalization for heart failure at 12 months. At 24 months, all-cause death and unplanned hospitalization for heart failure occurred in 63.8% of patients (97/152) in the intervention group and 67.1% (102/152) in the control group [hazard ratio (HR) 1.01, 95% confidence interval (CI) 0.77-1.34]. All-cause *Corresponding author. Hôpital Cardiovasculaire Louis Pradel, Chirurgie Cardio-Vasculaire et Transplantation Cardiaque, mortality occurred in 34.9% of patients (53/152) in the intervention group and 34.2% (52/152) in the control group (HR 1.02, 95% CI 0.70-1.50). Unplanned hospitalization for heart failure occurred in 55.9% of patients (85/152) in the intervention group and 61.8% (94/152) in the control group (HR 0.97, 95% CI 0.72-1.
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