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Query: UMLS:C0033377 (prolapse)
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Coronary artery steal resulting from a large unligated intercostal or pericardial side branch of the internal mammary artery graft causing postoperative angina has been previously described. Transcatheter coil occlusion of internal mammary artery side branch has successfully been performed to treat coronary steal syndrome. Unsuccessful deployment of the microcoils can be due to inadequate guiding support in the LIMA or prolapse of the delivery catheter in the side branch. We report a new approach for the precise deployment of coils in the side branch of a LIMA graft, when inadequate guiding support is present.
Cathet Cardiovasc Diagn 1997 Oct
PMID:Novel technique for coil embolization of intercostal branch of internal mammary artery graft. 932 17

We observed cardiac prolapse following right pneumonectomy in which the patient experienced a 90 degree rotation of the heart and compression of right ventricular outflow tract from behind by the aorta, which led to an increase in right atrial pressure and a decrease of pulmonary artery pressure and cardiac output. Compression of the right ventricular outflow tract by the base of the aorta was observed as an additional shock inducing factor in right cardiac prolapse.
Jpn J Thorac Cardiovasc Surg 1998 Feb
PMID:Obstruction of the right ventricle outflow tract during right cardiac prolapse. 955 54

Repair of prolapsed anterior mitral leaflet has remained technically difficult. The purpose of this study was to assess the clinical results after using the flip-over technique for patients with anterior mitral leaflet prolapse due to dhordal rupture or elongation. Between January 1993 and September 1997, fifteen adult patients with pure mitral valve regurgitation (MR) due to prolapse of the anterior mitral leaflet underwent repair using the flip-over technique. The indication for this procedure were; 1) all mitral structures except the prolapsed area must appear to be intact, and 2) the corresponding chordae attached to the posterior leaflet should be sufficiently strong to be transferred to the anterior leaflet. The prognoses following this technique were retrospectively studied to assess the early and mid-term clinical outcome of this procedure. Follow up was complete in all patients and ranged from 2 to 56 months (with a mean of 25 +/- 17.9 months). There was no hospital death, None required reoperation. One patient died because of acute recurrent MR during follow-up. No other complication was experienced. Doppler echocardiographic studies at the final follow-up showed less than mild regurgitation in 11 (78.6%) of the 14 surviving patients. We believe that this procedure was effective for that the obtained repair of a prolapsed anterior mitral valve and early and mid-term clinical outcome from this procedure has been satisfactory.
Jpn J Thorac Cardiovasc Surg 1998 Aug
PMID:[Mitral valve regurgitation with anterior mitral leaflet chordal rupture or elongation--repair using the flip-over technique]. 978 65

Mitral regurgitation caused by prolapse of the anterior mitral leafleft has been considered to be difficult for reconstruction. In Japan, these cases have been repaired mainly by replacement of chordae with artificial sutures. We have repaired them by Carpentier's technique. We report a series of 9 patients with pure mitral regurgitation caused by ruptured or elongated chordae of the anterior mitral leaflet. Two of them had lesions at both anterior and posterior leaflet. All patients underwent mitral valve repair by segmental transposition of the posterior leaflet. As for associated procedures, there were ring annuloplasty with Carpenter rings (9 cases), sliding technique (8 cases) reported by Carpentier, reinforcement by transposition of secondary chordae of the posterior leaflet (6 cases), commissuroplasty (1 case), and closure of leaflet perforation. All patients survived operations and all patients except one underwent left ventriculography postoperatively. In only 2 patients, residual mitral regurgitation classed as I/IV was observed. All patients returned home in New York Heart Association class I. Follow-up ranged from 7 to 45 months (mean follow-up 20 months). All patients were free from reoperation or thromboembolism. Although longer follow-up is necessary, this technique appears to be adequate for the repair of patients with anterior leaflet prolapse.
Jpn J Thorac Cardiovasc Surg 1998 Sep
PMID:[Repair of mitral regurgitation caused by prolapse of the anterior mitral leaflet]. 979 88

We report here a case of active infective endocarditis caused by Methicilin-Resistant Staphylococcus aureus (MRSA). A 24-year-old woman was admitted to the Osaka Medical Collage Hospital with continuous fever. After admission, MRSA was detected by blood culture and chemotherapy with Vancomycin was started. However, after 1 week, her condition had not improved. Moreover, a pedicled vegetation on the posterior wall of the left atrium and mitral regurgitation due to prolapse of the anterior leaflet were revealed by transesophageal echocardiography. The vegetation grew to about 2 cm in diameter and prolapsed into the left ventricle during diastole. We performed an early operation although the infection was still active due to its rapid growth and the risk of embolism. There was a large pedicled vegetation on the posterior wall of the left atrium as shown by preoperative echocardiography, but the mitral valve appeared to be intact. Therefore, the vegetation was completely removed and the mitral annulus was plicated by Kay's method to treat the associated mitral regurgitation. Postoperatively, we administered VCM 2 g/day for 24 days. The course was uneventful. The patient was discharged from the hospital on the 31st postoperative day.
Jpn J Thorac Cardiovasc Surg 1998 Sep
PMID:[A case report of infective endocarditis caused by MRSA and characterized by pedicled vegetation on the posterior wall of left atrium]. 979 97

A seventy-year-old man was admitted at our hospital because of dyspnea. Echocardiogram and left ventriculogram showed an aneurysm formation of the membranous ventricular septum and small left-to-right shunt through ventricular septum defect and also severe mitral and tricuspid insufficiency. Operation was performed after medical therapy for congestive heart failure. During operation, mitral leaflets showed no organic lesions nor prolapse, but the annulus was dilated. The cause of mitral insufficiency, we thought, might be congenital, and the annulus dilatation was caused of mitral insufficiency, we thought, might be congenital, and the annulus dilatation was caused to produce tricuspid insufficiency secondary. The ventricular septal communication became small (diameter; 5 mm) and was associated with aneurysm formation of the remaining portion of the membranous septum. And the aneurysm, protruding to the septal leaflet of tricuspid valves, enhanced tricuspid insufficiency. It was reported by many authors that the aneurysm formation was related to spontaneous closure of ventricular septal defect. Patients with small ventricular septal defect, without any symptoms, must be followed intensively, or they might get cardiac complications, such as arrhythmia, right ventricular outflow obstruction, tricuspid insufficiency, and so on.
Jpn J Thorac Cardiovasc Surg 1998 Oct
PMID:[Aneurysm of the membranous ventricular septum with ventricular septal defect, mitral and tricuspid insufficiency]. 984 79

We reviewed 25 patients who underwent a mitral valvuloplasty, from 1984 to 1996, for mitral regurgitation (MR) associated with atrial septal defect (ASD). Mean grade of MR was 2.3 +/- 0.7. The locations of mitral valve lesion were as follows; Postero-medial side of the anterior leaflet (AML) (11 patients: 44%), posteromedial side to center of the AML (7 patients: 28%), whole of the AML (5 patients: 20%), center of the AML (1 patient: 4%), posteromedial side of the posterior leaflet (PML) (1 patient: 4%). In summary, the mitral valve lesion was located in the AML in 96% patients and were seen in the postero-medial side of 96% patients. Mitral valve repair was performed as follows; chordae shortening only (3 patients: 12%), chordae shortening + Kay's annuloplasty (9 patients: 36%), Kay's anuloplasty (10 patients: 40%), using artificial chordae only (1 patient: 4%), using artificial chordae + Kay's annuloplasty (1 patient: 4%), using artificial chordae + ring annuloplasty (1 patient: 4%). In 24 patients, the grade of MR was less than 2/4 in the early postoperative period. In one patient, the grade of 3/4 MR was still remained. Reoperation were required in 2 patients, because of gradual increase of MR, 9 years and 10 years after the initial operation, respectively. In another patient, the grade 3/4 MR recurrently occurred at 6 months after the operation. He has been well maintained medically. In all 4 patients who had more than the grade 3/4 MR postoperatively, the annuloplasty was performed with Kay's method and the cause of MR was poor coaptation around the center of the AML. The mitral valve lesion associated with ASD seemed to be the dislocation of the AML which cause the discrepancy of the coaptation zone between both leaflets, without any prominent prolapse and chordae elongation. We put a particular emphasis on that the mitral valve repair should be performed with the recognition of the etiology of the mitral valve lesion. Especially, if the lesion extends around the center of the AML, sufficient coaptation area of both leaflets at the center of the AML should be obtained by anuloplasty.
Jpn J Thorac Cardiovasc Surg 1998 Dec
PMID:[Surgical treatment for mitral regurgitation associated with secundum atrial septal defect]. 1003 43

The direct relationship between minor plaque prolapsed within stents and late in-stent restenosis is unknown. Therefore, we evaluated the impact of minor plaque prolapse on late angiographic in-stent restenosis. Intravascular ultrasonography (IVUS)-guided single-coronary stenting was successfully performed on 384 consecutive patients with 407 native coronary lesions. Six-month follow-up angiographic evaluation was performed on 315 patients (82. 0%) with 334 lesions (82.1%). Minor plaque prolapsed within the stent was found in 75 of 334 lesions (22.5%). Results were evaluated using angiographic and IVUS methods. The development of minor plaque prolapse was significantly associated with infarct-related artery (P = 0.000) and small pre-intervention minimal lumen diameter (P = 0. 001). The overall angiographic restenosis rate was 23.1% (77/334)-21.3% (16/75) in the lesions with plaque prolapse vs. 23.6% (61/259) in the lesions without plaque prolapse (P = 0.806). In conclusion, minor plaque prolapsed within stents might not be associated with late angiographic in-stent restenosis.
Catheter Cardiovasc Interv 2000 Sep
PMID:Long-term outcomes of minor plaque prolapsed within stents documented with intravascular ultrasound. 1097 13

Ventricular septal defects (VSDs) are the most common congenital heart malformations seen in children. Because spontaneous closure occurs frequently, patients with small VSDs should be followed clinically with no limitations except endocarditis prophylaxis. Surgical closure is recommended for only small defects with significant associated lesions such as aortic regurgitation, aortic valve prolapse, right or left ventricular outflow obstruction, tricuspid regurgitation, left ventricle to right atrial shunt, or recurrent endocarditis. Enlarging left ventricular size or deteriorating left ventricular function would also be an indication for surgical repair. Moderate and large VSDs in infancy often require treatment of congestive heart failure with diuretics, digitalis, and afterload reduction. Surgical closure before 9 months of age is indicated for large VSDs and by 2 years of age for moderate shunts to prevent pulmonary vascular obstructive disease and the consequences of long-standing volume overload. Device closure of VSD is still in the investigational stage but holds promise for treatment of apical or multiple muscular VSDs.
Curr Treat Options Cardiovasc Med 1999 Dec
PMID:Ventricular Septal Defect. 1109 97

It is well recognized that the floppy mitral valve (FMV) complex is the central issue in the FMV, mitral valve prolapse (MVP), and mitral valvular regurgitation (MVR) story. MVP associated with the FMV results from the systolic movement of portions or segments of the FMV complex into the left atrium (LA). Prolapse of the FMV results in unique forms of mitral valvular dysfunction and MVR. When the FMV is recognized as the basic point of reference, diagnostic and nosologic characterizations are simplified. Each of the consequences of FMV dysfunction--MVP, MVR, and FMV surface phenomena--are dynamic entities and contribute to the symptoms and clinical course in this patient population. Although MVP may occur in the absence of a FMV in individuals with small left ventricular (LV) volume, hyperdynamic, or hypercontractile LV, we do not consider this phenomenon as part of FMV/MVP/MVR. The natural history of the FMV/MVP/MVR is long, and understanding the life history requires long-term follow-up with serial evaluations. Identification of those individuals with FMV/MVP whose symptoms are related to, or associated with, autonomic nervous system dysfunction (ie, the FMV/MVP syndrome) is important, as this distinction has diagnostic and therapeutic implications. In general, patients with FMV/MVP should receive antibiotic prophylaxis for infective endocarditis. Data suggest that therapy with angiotensin-converting enzyme inhibitors for FMV/MVP and significant MVR may slow the natural regression of the disease. Surgical therapy should be considered in patients with significant MVR and symptoms related to MVR. Explanation for the nature of these symptoms, reassurance, avoidance of volume depletion, catecholamines or other cycle-AMP stimulants and a regular exercise program constitute the basic principles of management for patients with FMV/MVP syndrome.
Curr Treat Options Cardiovasc Med 2001 Feb
PMID:Floppy Mitral Valve, Mitral Valve Prolapse, and Mitral Valvular Regurgitation. 1113 86


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