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.

Treatment of ruptured or elongated anterior mitral valve chordae by partial transposition of the posterior leaflet: experience with 29 patients.

We report a series of 29 patients, 5 to 75 years of age (mean age, 31.8 +/- 21.4 [SD] years), with pure mitral regurgitation caused by ruptured or elongated chordae of the anterior mitral leaflet. These patients underwent mitral valve repair by segmental transposition of the posterior leaflet with its attached chordae sutured to the free edge of the flail anterior leaflet. There were 2 hospital deaths. Follow-up ranged from 1 to 35 months (mean follow-up, 14.9 +/- 8.5 months). One patient is lost to follow-up. Two patients are in New York Heart Association Functional Class II; all others are in Class I. In 17 patients there is no detectable murmur; in 5 patients a mild to moderate systolic murmur can be detected, while 4 have a marked systolic murmur. The adequacy of the repair could be confirmed by Doppler echocardiography, which has shown no evidence of prolapse in 22 patients. A mild regurgitation jet is present in 4 patients, and a marked jet, in 3. Postoperative cardiac catheterization performed in 5 patients has confirmed the Doppler echocardiographic findings. Although longer follow-up is necessary, this technique appears adequate for repairing a major prolapse of the anterior leaflet caused by multiple ruptured or elongated chordae, therefore obviating the need for a prosthetic valve substitute.

[Treatment of anterior mitral valve prolapse by partial transposition of the posterior leaflet. Apropos of 7 cases]. / Traitement des prolapsus de la valve antérieure de la mitrale par transposition partielle de la valve postérieure. A propos de 7 cas.

Seven patients aged 8 to 62 years with massive mitral regurgitation due to anterior leaflet prolapse related to rupture or elongation of the chordae tendinae underwent reconstructive mitral valvuloplasty between June 1984 and September 1985, consisting in transposition of a bandlet of the posterior leaflet and its chordae to the free edge of the anterior leaflet. Medium term results with 2 to 16 months follow-up (average 8 months) showed all patients to have returned to Class I of the NYHA Classification; 5 patients had no systolic murmur, a mild systolic murmur 1 and 2/6 was present in 2 cases. The quality of the repair was confirmed by pulsed Doppler examination in all patients and by catheterisation and angiography in 3 cases. This surgical technique offers a good solution to the problem of mitral regurgitation due to severe prolapse of the anterior leaflet caused by rupture or elongation of the chordae tendinae.

Transposition of posterior leaflet for treatment of ruptured main chordae of the anterior mitral leaflet.

A 13-year-old girl with mitral regurgitation resulting from rupture of multiple chordae of the anterior leaflet had repair by transposition of a part of the posterior leaflet to the free edge of the anterior mitral cusp. Postoperative clinical hemodynamic, and angiographic studies showed perfect function of the mitral valve. This technique seems to be a good solution for mitral repair in the presence of ruptured anterior mitral chordae.

Limitations of fluorocarbons in reducing myocardial infarct size.

The effects of the oxygen-carrier fluorocarbons on myocardial infarct size were assessed in non-exchange-transfused dogs subjected either to a 3-hour occlusion of the left anterior descending coronary artery (LAD) followed by 2 hours of reperfusion (protocol I) or to a 5-hour permanent LAD occlusion (protocol II). Fluorocarbon administration was begun 30 minutes after LAD occlusion and was continued over the entire period of ischemia. After 5 hours, the hearts were excised and areas of necrosis were visualized by triphenyl tetrazolium chloride staining while risk regions were assessed by radiolabeled microspheres injected after coronary occlusion just before the onset of therapy, and further, in protocol I, by thallium-201 perfusion imaging performed at the end of fluorocarbon administration. In protocol I experiments, the ratio of necrotic area to area at risk was 81 +/- 35% (mean +/- standard deviation) in control saline-treated dogs (n = 6) and 67 +/- 27% in fluorocarbon-treated dogs (n = 6) (difference not significant). There was no significant difference between risk regions measured after and before fluorocarbon treatment. In protocol II, the ratio of necrotic area to area at risk was 47 +/- 30% in control dogs (n = 5) and 63 +/- 29% in fluorocarbon-treated dogs (n = 5) (difference not significant). However, in control dogs, the ratio of necrotic area to area at risk increased from 47 +/- 30% in the dogs that underwent permanent occlusion to 81 +/- 35% in the group that underwent reperfusion (p less than 0.001) while this ratio was similar in the corresponding subsets of fluorocarbon-treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)