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[A case of thrombosed St. Jude Medical valve 16 years after initial mitral valve replacement].

We report successful surgery for a thrombosed St. Jude Medical (SJM) valve 16 years after the initial mitral valve replacement even under conditions of satisfactory anticoagulation therapy. A 61-year-old-female had intermittent claudication and was admitted to our hospital for examination. The prosthetic valve sounds were normal to auscultation and the left ankle-pressure index was decreased to 0.6. Transthoracic echocardiography revealed no mitral regurgitation and a mean mitral valve gradient of 6-7 mmHg. Furthermore, transesophageal echocardiography revealed that one of the leaflets of the prosthetic valve was entirely immobilized at the closing position and a mobile soft tissue mass, 5 mm in diameter, was detected at the atrial side of the obstructed leaflet. Although 96,0000 IU of urokinase was administered intravenously for a week, we could not confirm any change in leaflet mobility. At the time of surgery, the posterior leaflet of the SJM valve, which was implanted at an anatomical orientation, was obstructed at the closing position with old and fresh thrombi. We decided upon replacement with a CarboMedics 29 M prosthetic valve. Postoperative medication consisted of warfarin plus low-dose aspirin. Generally, valve thrombosis occurs within 5 years after valve replacement. However, valve thrombosis is possible even in a reliable SJM valve and as long as 16 years after replacement. Therefore, the implantation of an SJM valve at an anti-anatomical orientation might lower the incidence of valve thrombosis in addition to life-long anticoagulation therapy.

Female↗

Experiences with the Björk-Shiley tilting disc valve in aortic and mitral valve surgery.

During a four-year period, aortic or mitral valve replacements with the Björk-Shiley tilting disc valve were performed in 114 cases. The series comprises 75 aortic, 34 mitral and 5 double valve replacements. In the aortic valve group (AVR) concomitant resection of the ascending aorta (cystic medial necrosis aneurysm)) was carried out in 5 cases, aortocoronary bypass in 2 cases and closure of a VSD in one case. Antibiotic prophylaxis and postoperative anticoagulant treatment were used routinely. The hospital mortality rates were6 8.0% in the AVR-group (single aortic valve mortality 7.1 %), 8.8% in the MVR-group and 60% in the double valve group. Late mortality in the AVR-group was 2.8%. There were no late thromboembolic complications in this group. Aortography showed grade II--III regurgitation (paravalvular leaks) in 15 % of the cases. In the MVR-group the late mortality was 9.7%. One patient died because of malfunction (thrombosis) of the prosthesis. The thrombotic complication was obviously caused by discontinuation of anticoagulant therapy. The clinically estimated functional capacity NYHA classification) improved considerably, especially in the MVR-group.

Adolescent↗

Left ventricular-coronary sinus fistula following repeated mitral valve replacements.

After mitral valve replacement, symptomatic deterioration and new murmurs characterstistic of atrioventricular valvular regurgitation are usually the result of periprosthetic leaks or prosthetic dysfunction with or without endocarditis. In the case which we are reporting, an iatrogenic fistula between the left ventricle and coronary sinus was responsible for the murmur and symptoms. This type of shunt has not been previously reported. Thorough debridement of the anulus is necessary during mitral valve replacement; additionally, previously implanted prostheses are occasionally embedded in the endocardial wall and must be excised. Hematoma in the atrioventricular groove and perforations of the posterior left ventricular wall are widely recognized complications of mitral valve replacement. Similar mechanisms of injury can cause other problems such as left ventricular-right atrial communications and the unique anatomic shunt described in this report.

Adult↗

Mitral valve area calculations immediately after percutaneous balloon mitral valvuloplasty: effect of the atrial septal defect.

OBJECTIVES: The aim of this study was to assess the effect of the atrial septal defect on mitral valve area calculations after balloon mitral valvuloplasty. BACKGROUND: There is poor correlation between the hemodynamic-derived and Doppler mitral valve area immediately after mitral valvuloplasty. The reasons for this are unclear. METHODS: Twenty-five patients with severe mitral stenosis were studied. After balloon mitral valvuloplasty, serial mitral valve area calculations were performed with 1) the mitral dilating catheter across the atrial septum, 2) the 7F catheter across the atrial septum, and 3) with the atrial puncture site occluded with the balloon catheter. RESULTS: The mitral valve area determined by the Gorlin formula with balloon occlusion of the atrial septum was smaller than the mitral valve area determined without balloon occlusion (mean +/- SD 1.8 +/- 0.43 vs. 2.24 +/- 0.67 cm2, p < 0.005 for the mitral dilating catheter across the atrial septum and 1.8 +/- 0.43 vs. 2.19 +/- 0.52, p < 0.05 for the 7F catheter across the atrial septum). The mean of the differences between the mitral valve area derived by the Gorlin formula and by the Doppler pressure half-time method was smaller with the atrial septum occluded than when the dilating catheter or the 7F catheter was across the atrial septum (0.12 +/- 0.26 vs. 0.56 +/- 0.48 cm2 [p < 0.005] and 0.12 +/- 0.26 vs. 0.48 +/- 0.55 cm2 [p < 0.05]). Left to right shunting was detected less frequently by oximetry (60%), than by shunt ratios calculated by using the cardiac output measurements with and without balloon occlusion of the atrial septum (84%). CONCLUSIONS: The presence of left to right shunts after mitral valvuloplasty may account for some of the discrepancies between mitral valve area found at cardiac catheterization and that by the Doppler pressure half-time method; thus, the latter method may be reliably used to follow up patients in the long term.

Adult↗

Repair of the mitral valve because of pure rheumatic mitral valvar incompetence in the young.

Between January 1985 and April 1994, 42 children aged between 7 and 14 years (mean 11.3 years) underwent repair of severely incompetent rheumatic mitral valves with no accompanying mitral stenosis. In 19 patients the tricuspid valve was severely incompetent, while 8 patients had severe aortic incompetence. Overall, the repair incorporated shortening of elongated tendinous cords and insertion of a Duran or Carpentier prosthetic ring. The repair was the sole procedure in 15 patients, whilst 19 patients also had a De Vega tricuspid valvar annuloplasty and 8 had repair or replacement of the aortic valve. There were no hospital deaths. Postoperative transthoracic echocardiographic studies revealed trivial residual mitral valvar regurgitation in 6 patients, mild regurgitation in 18, moderate in 15, and regurgitation severe enough to warrant replacement of the mitral valve in 3 patients. The mean follow-up period was 37 months (maximum 120 months, minimum 1 month). Of 39 patients followed-up, 28 attended for more than 5 years. Of these, 7 underwent replacement of the mitral valve for severe regurgitation within 4 years of the repair. Severe mitral regurgitation in 3 patients was controlled by medical therapy. One was eventually lost to follow-up, and one patient died of causes unrelated to surgery. The remaining 16 patients had absent to moderate mitral valvar regurgitation. These results contrast with 10 repairs of congenital mitral incompetence, where no patients required re-operation in the immediate 5 years period of follow-up. Every effort should be made in children with rheumatic mitral incompetence to preserve the natural valve by conservative repair, despite the fact that repair of the incompetent rheumatic mitral valve is not so durable as repair of congenitally incompetent valves.

Adolescent↗

Cardiopulmonary exercise testing before and one year after mitral valve repair for severe mitral regurgitation.

For the evaluation of efficacy of cardiopulmonary exercise testing, we compared New York Heart Association functional class with peak oxygen consumption rate (VO(2)peak) in 31 patients with severe mitral regurgitation who underwent mitral valve repair surgery. One year later, the VO(2)peak values did not show significant improvement; however, the patients who had more than a mild degree of residual mitral regurgitation (n = 14) after 1 year of surgery had a VO(2)peak value that was significantly decreased (from 22.7 +/- 6.4 to 21.0 +/- 6.3 ml/kg/min, p = 0.04). Patients with a higher preoperative VO(2)peak value (>/=18.5 ml/kg/min) had a significantly better New York Heart Association functional class 1 year after surgery than patients with a lower VO(2)peak value (<18.5 ml/kg/min, p = 0.03).

Adult↗

[Use of echocardiography in mitral regurgitation for the assessment of its mechanism and etiology for the morphological analysis of the mitral valve].

Echocardiographic assessment of mitral regurgitation allows the diagnosis of its mechanism and cause which are major determinants in the feasibility of mitral valve repair. This assessment is based on a systematic analysis of the different structures of the mitral valve apparatus: mitral annulus (enlargement, calcification), mitral valve morphology (thickening, calcification, floppy valve, vegetations, perforation), mitral valve motion (restriction, identification of the prolapsed leaflets and scallops in patients with mitral valve prolapse or flail leaflets), subvalvular apparatus (ruptured chordae, thickening), papillary muscles, and left ventricular wall. This analysis can diagnose the mechanism of mitral regurgitation according to the Carpentier classification, and can clarify its cause: degenerative lesions (prolapse or flail leaflet with or without ruptured chordae), rheumatic lesions (thickened valves with restricted motion), endocarditis (vegetations, perforation, ruptured chordae), ischemic mitral regurgitation (restricted valve motion with inferior or posterior left ventricular wall asynergy), or functional mitral regurgitation (annular dilatation, displacement of papillary muscles with restricted leaflet motion). Transthoracic echocardiography with harmonic imaging usually allows a comprehensive assessment of functional anatomy of mitral regurgitation. Transesophageal echocardiography is indicated if transthoracic echocardiography is inadequate. It is also indicated just before surgery and as an intraoperative procedure. Real time 3D echocardiography should probably complete the evaluation of mitral regurgitation in the near future.

Echocardiography↗

Pulsed Doppler evaluation of regurgitation in mitral valve prostheses.

Prosthetic mitral valve regurgitation was evaluated by both pulsed Doppler ultrasound and left ventriculography. Pulsed Doppler ultrasound was found to have only a 20% sensitivity in detecting prosthetic mitral valve regurgitation documented by left ventriculography. Possible reasons for this poor sensitivity include 1) an eccentric jet not identified by the small pulsed Doppler sample volume; 2) prosthesis interference with the Doppler signal in the apical four chamber view; and 3) the large angle of incidence between the pulsed Doppler signal and the regurgitant jet. Mitral insufficiency, especially when not severe, may be missed by this technique. Care must be taken in interpreting negative results from a pulsed Doppler ultrasound evaluation of a prosthetic mitral valve.

Echocardiography↗

Trans-ventricular septal defect approach for resection of accessory mitral valve tissue.

Accessory mitral valve tissue is a rare cause of left ventricular outflow tract obstruction, which can be difficult to recognize. Surgical resection by the conventional transaortic approach with or without left atriotomy is extremely difficult in infants with a small aorta. When a ventricular septal defect is present, it may be the best way to approach the accessory mitral valve tissue, because the ventricular septal defect is located just in front of it. Five infants underwent resection of accessory mitral valve tissue together with repair of other intracardiac malformations. In 3 infants, resection of accessory mitral valve tissue was easily performed through the ventricular septal defect, which required enlargement in 2 patients.

Female↗

Emergency redo mitral valve replacement in a 27-year-old pregnant female with a clotted prosthetic mitral valve, preoperative fetal demise and postoperative ventricular assist device: a case report.

A 27-year-old Laotian woman with a St Jude mechanical mitral valve became pregnant, requiring a change in her anticoagulant after the first trimester when her warfarin sodium (coumadin) was replaced with enoxaparin sodium (lovenox). Her prosthetic valve clotted and became dysfunctional. She was 16 weeks pregnant and was taken to the operating room for emergency surgery for replacement of the valve. The fetus had not been viable for 1-2 weeks, but still remained in utero. The clotted valve was replaced with another St Jude valve of a slightly smaller diameter (27 mm). The patient could not be weaned from bypass so a right ventricular assist device (RVAD) was inserted. The patient was weaned from the RVAD after 2 days of support. Two days following removal of the RVAD the fetus spontaneously aborted. The patient had a long, complicated hospital course and was discharged 3 months later. She subsequently died 4 months after discharge of a cerebral hemorrhage from excessive anticoagulation.

Adult↗