[Surgical treatment for mitral regurgitation: mid-term outcome following mitral valve repair].

Mid-term results of mitral valve repair for mitral regurgitation were evaluated in 173 consecutive patients (mean age 53 years, 107 males, 66 females) treated from July 1991 to March 1998. Pathological causes of the mitral valve disease were degenerative in 118 patients, infective endocarditis in 25, rheumatic in 13, and ischemic in 8 (ischemic cardiomyopathy in 7). The principal technique was chordal replacement with expanded polytetrafluoroethylene sutures for prolapse of the anterior leaflet, and Carpentier's sliding leaflet technique for prolapse of the posterior leaflet. Most patients received ring annuloplasty with a rigid ring and flexible band (physiological remodeling annuloplasty). Intraoperative transesophageal echocardiography was used after 1993. There were 7 operative deaths (4%) and 7 mitral valve replacements (4%) during the same operation. Successful repair was achieved in 96% of patients with mitral regurgitation. Mean follow-up was 35 months (range 2 to 78 months). Survival at 6 years was 85 +/- 10% of all patients, 98 +/- 2% in degenerative cases. Six patients required reoperation (1.2%/patient-year) and mean time interval between initial operation and reoperation was 33.1 months. Four patients with atrial fibrillation had thromboembolic events (0.8%/patient-year). There were no anticoagulant-related complications. Freedom from reoperation and all valve-related event at 6 years was 88 +/- 6% and 84 +/- 6%. Late postoperative Doppler echocardiography revealed satisfactory results in 93% of the patients. Mitral valve repair using chordal replacement, sliding plasty and ring annuloplasty provides excellent mid-term results.

Intraoperative TEE during mitral valve repair: does it predict early and late postoperative mitral valve dysfunction?

BACKGROUND: Intraoperative transesophageal echocardiography (TEE) using color Doppler flow mapping can accurately measure residual mitral regurgitation (MR), but it is unknown to what extent such measurements correlate with those obtained with postoperative transthoracic echocardiography (TTE). METHODS: We used intraoperative TEE (based on direct planimetry of the maximal regurgitant jet area) to measure residual MR in 42 patients who underwent mitral valve reconstruction for MR and compared these measurements with those obtained with early and late postoperative TTE. RESULTS: Residual MR as measured by intraoperative TEE correlated significantly with values obtained with both early (r = 0.66; p < 0.0001) and late (r = 0.71; p < 0.0001) postoperative TTE. Forty patients with no or trivial MR (< or =2 cm2) as measured by intraoperative TEE also had no or trivial MR as measured by early (probability of 87.5%) and late (probability of 80.0%) postoperative TEE. Of the 40 patients, 6 had clinically insignificant mild MR (< or =4 cm2) when measured by late postoperative TTE. Two other patients in whom intraoperative TEE showed mild MR developed moderate regurgitation about 3 months later. CONCLUSIONS: Intraoperative TEE correlates with early and late postoperative TTE in measurement of residual MR, suggesting it can reliably predict early and late postoperative mitral valve dysfunction.

[Entrapment of broken guidewire in the right coronary artery during percutaneous transluminal coronary angioplasty].

The distal 2 cm end of guidewire was broken and retained in the right coronary artery (RCA), during percutaneous transluminal coronary angioplasty for 99% narrowing of the middle RCA in a 53-year-old male patient with effort angina. Because of the stable condition of the patient, elective A-C bypass surgery was performed successfully 2 weeks after this event. However, the broken end of guidewire was not found out in the opened RCA lumen. One and a half year postoperatively, the patient is doing well while the guidewire remains in the same position.

[Effect of regional phase delay on left ventricular performance studied by radionuclide angiography].

When cardiac hypokinesis in myocardial infarction is analyzed by means of phase analysis of radionuclide (RI) angiography, there are some cases in which the amount of regional wall movement of the left ventricle does not so decline, but the phase delay of regional wall movement is great. Hence, a simulation experiment was performed with a computer to evaluate the influences of regional phase delay on cardiac work. It was assumed that the radius of the model of the left ventricle varies from 3 cm in the late diastolic phase to 2 cm in the late systolic phase, and that in the initial 1/3 time of diastole, the radius alters by 90% of the change. One cardiac cycle (360 degrees) was divided into 60 fractions (1 fraction = 6 degrees), 0 degree being the end of diastole and 180 degrees the end of systole. An ischemic area was supposed to cover S% of the whole volume of the left ventricle, its amount of regional wall movement being P% of the normal area, and the phase delay being R degrees. By varying S, P and R, and taking weighted means of volume curves and normal ones, their assumed volume curves of the left ventricle were computed. Stroke volume (SV) and ejection fraction (EF) obtained from these curves were compared to those obtained from the normal curves, and were expressed in percentage (%SV, %EF). The influences of the changes of S, P and R on the volume curve and on the cardiac work were examined. Then the count curves of the left ventricle (LV) were obtained by gated RI angiography in 22 cases of myocardial infarction and 8 healthy controls, and LV regional wall movements were examined by means of the Fourier analysis. The circular volume was partitioned from the center into eight sections on the LV image of LAO 45 degrees, and the amount of wall movement and the phase delay of each section were evaluated from the count curves of each section. The following results were obtained. %SV and %EF declined with sole occurrence of regional phase delay. Occurrence of the regional phase delay flattened the slope of the volume curve of the initial diastolic phase and formed shoulders on this curve. This was observed also on the count curves actually determined from cases with myocardial infarction. When regional wall movement was markedly decreased, the influence of the regional phase delay on the pattern of the volume curve was slight even if the phase delay was extensive.(ABSTRACT TRUNCATED AT 400 WORDS)

[Characteristic findings of mitral valve and mechanism of mitral valve prolapse in Marfan syndrome].

To elucidate the mechanism of generation of mitral valve prolapse (MVP) in Marfan syndrome, we studied the relations of the length of the anterior mitral leaflet to the diameter of the mitral ring. In 13 cases of Marfan syndrome associated with MVP (Group I), 21 of isolated MVP (Group II), and 24 controls free from valvular disease (Group C), the maximal length of the anterior mitral leaflet (L) and the end-diastolic and end-systolic diameters of the mitral ring (Rd and Rs) were measured in the long-axis views on two-dimensional echocardiograms. In addition, the measurements were corrected with the body surface area; designated as L(c), Rd(c) and Rs(c), respectively. Furthermore, L/Rd and L/Rs, and the percentage of shortening of the mitral ring in systole, (Rd-Rs)/Rd X 100, were obtained. The body surface area in Group I was greater than that in Group II (p less than 0.05), but there was no significant difference between Groups II and C. The L was obviously different between Groups I and II or C (p less than 0.001, respectively). Similarly, there was a significant difference in L(c) between Groups I and II (p less than 0.02) or C (p less than 0.001), indicating the remarkably long anterior mitral leaflet in Group I. The Rd in Group I and II was greater than that in Group C (p less than 0.01 and p less than 0.02, respectively), while there was no significant difference in the Rd(c) among the 3 groups. There was also no statistical difference in either Rs or Rs(c) among the 3 groups. Both L/Rd and L/Rs in Group I were remarkably higher than those in Groups II and C (p less than 0.001, respectively), whereas these parameter did not differentiate Group II from Group C. (Rd-Rs)/Rd X 100 was higher in Group I than that in Groups II and C (p less than 0.05 and p less than 0.01, respectively), but it was not significantly different between Groups II and C. These results suggested that one of the probable mechanisms of generation of MVP in Marfan's syndrome is the redundant mitral valve resulting from a remarkably long leaflet and increased systolic shortening of the enlarged mitral ring.