Valve Replacement For Mitral Stenosis Research Articles

A Case of Mitral Valve Replacement for Mitral Stenosis with Narrow Annulus after TAVI and PTMC

A Case of Mitral Valve Replacement for Mitral Stenosis with Narrow Annulus after TAVI and PTMC

Hazards of Mitral Valve Replacement for Mitral Stenosis Caused by Massive Mitral Annular Calcium With or Without Aortic Valve Replacement for Aortic Stenosis

Mitral annular calcium (MAC) is common in older adults in the Western World and if extensive may cause mitral stenosis . The purpose of this report is to describe outcomes of 12 patients having mitral valve replacement for mitral stenosis secondary to massive MAC. Operatively excised deposits of calcium removed from the mitral annular area and the accompanying stenotic mitral valves were examined and then the patients' medical records were examined to confirm the diagnosis and the degree of valvular dysfunction. A total of 12 patients with massive MAC causing mitral stenosis and receiving mitral valve replacement with or without aortic valve replacement for aortic stenosis were observed in 2013 to 2015. Of the 12 patients, 7 died from 5 to 44 days (mean 19) after the valve operation and all had "stormy" postoperative courses; one survived 150 days and another, 600 days; the remaining 3 were improved by the operation and are alive 22, 27, and 59 months postoperatively. In conclusion, the high mortality in these patients suggests that mitral valve replacement in the setting of massive MAC be considered with caution.

5. Mitral valve replacement for mitral stenosis: 15 years single center experience

Mitral valve replacement (MVR) with either a bioprosthetic or a mechanical valve is the treatment of choice for severe mitral stenosis. This study aimed to evaluate and compare the early and late outcome of mitral valve replacement (mechanical versus bioprosthetic) for severe mitral stenosis. A retrospective cohort study was performed on prospectively collected data involving mitral stenosis patients who have undergone MVR with either bioprosthetic (BMV) ( n =50) or mechanical (MMV) ( n =145) valves in our institute from 1999 to 2012. Data were analyzed for early and late mortality, NYHA functional classes, stroke, early and late valve-related complications, and survival. Chi Square test, logistic regression, Kaplan Meier curve, and dependent proportions tests were performed. A total of 195 patients were included in the study with a follow-up of 190 patients (97.5%). One patient died early post-operatively; twelve patients died late in the post-operative period, BMV group (6) and the MMV (6). The Late mortality had significantly associated with post-op stroke ( p p =0.002). Post-op NYHA class was significantly associated with age ( p =0.003), pulmonary disease ( p =0.02), mitral valve implant type ( p =0.01), and post-op stroke ( p =0.02); 14 patients had strokes in the MMV (9) and in the BMV (5) groups. NYHA classes were significantly better after the replacement surgeries ( p p =0.03), worse NYHA post-op ( p =0.01), and more re-operations ( p =0.006). Survival was significantly better with mechanical valves ( p =0.03). When the two groups were matched for age and mitral regurgitation, the analysis revealed that bioprosthetic valves were significantly associated with re-operations ( p =0.02) but not significantly associated with worse survival ( p =0.4) or worse NYHA ( p =0.4). Mechanical mitral valve replacement in mitral stenosis patients is associated with lower re-operation rate, but no difference in survival as compared to bioprosthetic mitral valve replacement. Furthermore, post-operative stroke occurrence (14%) is associated with late mortality and worse NYHA classes.

Mitral valve replacement for mitral stenosis: A 15-year single center experience

ObjectivesMitral valve replacement with either a bioprosthetic or a mechanical valve is the treatment of choice for severe mitral stenosis. However, choosing a valve implant type is still a subject of debate. This study aimed to evaluate and compare the early and late outcomes of mitral valve replacement [mechanical (MMV) vs. bioprosthetic (BMV)] for severe mitral stenosis. MethodsA retrospective cohort study was performed on data involving mitral stenosis patients who have undergone mitral valve replacement with either BMV (n=50) or MMV (n=145) valves from 1999 to 2012. Data were collected from the patients’ records and follow-up through telephone calls. Data were analyzed for early and late mortality, New York Heart Association (NYHA) functional classes, stroke, pre- and postoperative echocardiographic findings, early and late valve-related complications, and survival. Chi-square test, logistic regression, Kaplan–Meier curve, and dependent proportions tests were some of the tests employed in the analysis. ResultsA total of 195 patients were included in the study with a 30-day follow-up echocardiogram available for 190 patients (97.5%), while 103 (53%) were available for follow-up over the telephone. One patient died early postoperatively; twelve patients died late in the postoperative period, six in the bioprosthesis group and six in the mechanical group. The late mortality had a significant association with postoperative stroke (p<0.001) and postoperative NYHA Classes III and IV (p=0.002). Postoperative NYHA class was significantly associated with age (p=0.003), pulmonary disease (p=0.02), mitral valve implant type (p=0.01), and postoperative stroke (p=0.02); 14 patients had strokes in the mechanical (9) and in the bioprosthetic (5) groups. NYHA classes were significantly better after the replacement surgeries (p<0.001). BMV were significantly associated with worse survival (p=0.03), worse NYHA postoperatively (p=0.01), and more reoperations (p=0.006). Survival was significantly better with MMV (p=0.03). When the two groups were matched for age and mitral regurgitation, the analysis revealed that BMV were significantly associated with reoperations (p=0.02) but not significantly associated with worse survival (p=0.4) or worse NYHA (p=0.4). ConclusionMMV replacement in mitral stenosis patients is associated with a lower reoperation rate, but there was no difference in survival compared with BMV replacement.

Thiazolidinediones may contribute to the intramyocardial lipid accumulation in diabetic myocardium: effects on cardiac function

To the editor: Treatment with thiazolidinedione (TZD), an agonist of peroxisome proliferator-activated receptor-γ (PPARγ), has been associated with a significant increase in heart failure in type 2 diabetic patients.1 These...

Surgical Treatment for Mitral Stenosis in Scheie’s Syndrome: Mucopolysaccharidosis Type I-S

Scheie's syndrome is a subtype of mucopolysaccharidosis, which is a rare hereditary disorder of proteoglycan degrading enzymes. Deposition of mucopolysaccharide often causes cardiac disease, especially valvular lesion, but reports of its surgical treatment have been rare. We report a case of 41-year-old woman with Scheie's syndrome who successfully underwent mitral valve replacement for mitral stenosis.

Reconstruction of a friable posterior mitral annulus after removing a calcified artificial ring using flipover technique of the anterior mitral leaflet

We report a new technique for reinforcement of a friable posterior mitral annulus using the anterior leaflet after removing a calcified artificial ring. A 72-year-old woman underwent mitral valve replacement for mitral stenosis and recurrence of regurgitation after mitral valve repair at 53 years of age. She had been on chronic hemodialysis for 20 years. The posterior mitral annulus became highly friable after débridement of the calcified artificial ring. The anterior mitral leaflet was detached from its annulus and transferred to the posterior annulus to cover the defect. The anterior leaflet was anchored to the posterior annulus by valve sutures, and mitral valve replacement was performed successfully. Postoperative ultrasonic cardiography revealed preservation of left ventricular function with no perivalvular leakage.

Mitral commissurotomy and valve replacement for mitral stenosis: observations on selection of surgical procedures.

Mitral commissurotomy and valve replacement for mitral stenosis: observations on selection of surgical procedures.

Effect of inotropic stimulation on motion and thickening of the ventricular septum following either coronary artery bypass grafting or mitral valve replacement for mitral stenosis

Effect of inotropic stimulation on motion and thickening of the ventricular septum following either coronary artery bypass grafting or mitral valve replacement for mitral stenosis

Comparison of balloon valvuloplasty with operative treatment for mitral stenosis

To determine the optimal role for percutaneous balloon mitral valvuloplasty or open mitral commissurotomy, the outcome of 164 consecutive patients undergoing either percutaneous balloon mitral valvuloplasty, open mitral commissurtomy, or mitral valve replacement for mitral stenosis was reviewed. No preoperative differences existed between percutaneous balloon mitral valvuloplasty and open mitral commissurotomy in age, symptoms, or mitral valve characteristics. Symptoms improved similarly in all groups, and median hospital stays after procedures were 2, 9, and 10 days for percutaneous balloon mitral vaivuloplasty, open mitral commissurotomy, and mitrai valve replacement ( p < 0.005). Actuarial survivals at 36 months did not differ significantly (83% ± 6%, 94% ± 4%, and 90% ± 4%). Actuarial freedoms from subsequent mitral valve procedures at 36 months were 66% ± 7%, 87% ± 6%, and 100% ± 13% ( p < 0.005), with the linearized rate of subsequent mitral valve procedures being 12% ± 3%, 4% ± 2%, and 1.2% ± 0.8%/patient-year for percutaneous balloon mitral valvuloplasty, open mitral commissurotomy, and mitral valve replacement ( p < 0.01). Prior mitral commissurotomy increased the likelihood of subsequent mitral procedures after percutaneous balloon mitral valvuloplasty from 10% ± 3% to 20% ± 7%/patient-year.

Inhaled nitric oxide after mitral valve replacement in patients with chronic pulmonary artery hypertension.

Patients with mitral valve disease can develop pulmonary artery hypertension that persists after mitral valve replacement. In 1987, nitric oxide (NO) was reported to be an important factor accounting for the biologic activity of endothelium-derived relaxing factor. Inhaled NO was subsequently reported to be a selective pulmonary vasodilator in animals and patients. Therefore we investigated the vasodilating effect of inhaled NO in patients with mild pulmonary artery hypertension after mitral valve replacement. Six patients who underwent mitral valve replacement for mitral stenosis presented with a mean pulmonary artery pressure greater than 25 mmHg within 24 h after surgery. During mechanical ventilation at FIO2 0.5, NO (36.8-38.4 ppm) was breathed for 10 min. Hemodynamic data were recorded before NO, after 10 min of NO inhalation, and 30 min after the end of NO inhalation. Statistically significant (P < 0.05) hemodynamic response to inhaled NO included a transient decrease in systolic (-10%), diastolic (-8%), and mean (-10%) pulmonary artery pressures; a decrease in pulmonary vascular resistance (-22%); an increase in mixed venous hemoglobin O2 saturation (+6%); and a decrease in arteriovenous O2 content difference (-7%). During NO inhalation, there was no change in systemic arterial or pulmonary wedge pressures. Methemoglobin levels remained < 1%. Inhalation of this concentration of NO for 10 min causes transient pulmonary artery vasodilation and hemodynamic improvement in patients with mild chronic pulmonary artery hypertension after mitral valve replacement.

Modified preservation of all annular-papillary continuity in replacement of the calcified mitral valve.

The technique described here is a modification of the mitral valve replacement with preservation of chordae tendineae for calcified mitral stenosis. After commissurotomy, the middle portion of the anterior leaflet is excised to get two parts with accessible chordal insertion. Each thickened and calcified segment is debrided by means of an ultrasonic tool and then attached to the mural leaflet. Finally mitral valve replacement is carried out. This procedure will extend surgical indication of chordae-sparing methods in mitral valve replacement for mitral stenosis.

Clinical and anatomic observations in patients having mitral valve replacement for mitral stenosis and simultaneous tricuspid valve replacement

Certain clinical and morphologic findings are described in 67 patients (aged 23 to 76 years [mean 52]; 55 women [82%]) who had mitral valve replacement for mitral stenosis (with or without associated regurgitation), and simultaneous tricuspid valve replacement for pure tricuspid regurgitation (58 patients) or tricuspid stenosis (all with associated regurgitation; 9 patients). Of the 58 patients with pure tricuspid regurgitation, 21 had anatomically normal and 37 had anatomically abnormal (diffusely fibrotic leaflets) tricuspid valves. Among these 58 patients, no clinical or hemodynamic variable was useful before surgery in distinguishing the group without from that with anatomically abnormal tricuspid valves. All 9 patients with stenotic tricuspid valves had anatomically abnormal tricuspid valves. The latter group had a lower average right ventricular systolic pressure (tricuspid valve closing pressure) than those with pure tricuspid regurgitation, and none had severe pulmonary arterial hypertension (present in 20 [30%] of the 58 patients with pure tricuspid regurgitation).

Left ventricular dimension changes after chordal preservation in mitral valve replacement

Clinical and experimental evidence regarding the benefits of preserving the subvalvular apparatus during mitral valve replacement has been debated. Reductions in the left ventricular end-diastolic dimensions have been shown, by echocardiography, to correlate well with the levels of clinical improvement following successful valve surgery. Seventynine patients underwent mitral valve replacement for mitral stenosis, regurgitation or both. In 42 patients, a conventional valve replacement was performed, excising both leaflets along with their chordae. In the remaining 37, a modified technique was used preserving the posterior leaflet and chordae. The two groups did not differ significantly in their demographic profiles, clinical classes and pathology. Echocardiographic assessment of left atrial and left ventricular dimensions was done preoperatively and prior to discharge. Median left atrial dimensions decreased in both groups. Postoperatively, the left ventricular end-diastolic and end-systolic parameters remained either the same or showed an increase in the conventional group. Patients in the modified group, however registered a decrease in left ventricular dimensions. Such changes further supported the clinical evidence suggesting benefits of preserving the chordae tendinae in mitral valve replacement.

Rupture of the left ventricular free wall following mitral valve replacement for mitral stenosis: A cause of complete (fatal) or contained (false aneurysm) cardiac rupture

Complete or incomplete left ventricular free wall rupture is a known complication of mitral valve replacement. Complete free wall rupture may result in fatal bleeding, whereas incomplete rupture may result in the formation of a pseudoaneurysm with survival possible. Two necropsy patients are described illustrating both of these complications. Proposed mechanisms for injury to the left ventricular free wall are reviewed.

Time course of human atrial natriuretic factor release during cardiopulmonary bypass in mitral valve and coronary artery diseased patients

We determined the time-course of the release of atrial natriuretic factor (ANF) during cardiopulmonary bypass (CPB) in six patients undergoing coronary artery bypass (CAD) and eight patients undergoing valve replacement for mitral stenosis (MS). Before CPB, the arterial ANF was significantly higher in MS patients than in CAD patients (243 +/- 38 and 29 +/- 5.8 pg/ml respectively, P less than 0.01). With the onset of CPB, the acute pressure unloading of the atria induced a significant, rapid decrease of ANF only in MS patients (-64% of pre-CPB value at 5 min) and no major changes in CAD patients. Clamping of the aorta induced a further progressive reduction of ANF release to almost zero in both groups. Readmission of coronary flow to the empty atria with declamping resulted in an increase in the plasma level of ANF in both groups to reach the concentration present in MS patients before CPB. After CPB, the ANF levels decreased in CAD patients while remaining elevated in MS patients. These data suggest that ANF release from human atria depends on atrial filling pressure and other unknown factors.

Pulmonary vascular disease and hypertension after valve surgery for mitral stenosis

The reduction of pulmonary hypertension that occurs within 24 hours of valve replacement for mitral stenosis is well documented, but patients who die after surgery have not been adequately studied. Clinical and autopsy data for 16 patients who died following mitral valve replacement were reviewed. The emphasis was on preoperative and postoperative pulmonary arterial pressure and pulmonary vascular disease, including arterial, venous, and capillary changes. Morphologic features were graded and summed to obtain an additive histologic assessment (AHA). Patients were divided into three groups: 1) those who had uneventful operations and early postoperative periods but died prior to discharge; 2) those who had postoperative difficulty, with identifiable acute anatomic causes of death; and 3) those who had postoperative difficulty, with no apparent acute anatomic cause of death. In group 1 (n = 4) the preoperative pulmonary arterial pressure was 43 +/- 17 mm Hg, and AHA ranged from 0 to 4; in group 2 (n = 5) the preoperative pulmonary arterial pressure was 60 +/- 15 mm Hg, but AHA ranged only from 2 to 5. In group 3 (n = 7) the preoperative pulmonary arterial pressure was 59 +/- 12 mm Hg; AHA ranged from 6 to 9, significantly higher than that of the other groups (P less than 0.005). Three patients from group 3 had elevated pulmonary arterial pressure (60, 52, and 50 mm Hg three, six, and 15 days after surgery, respectively). Two additional patients had right heart failure with normally contracting left ventricles terminally. It is concluded that some patients with mitral stenosis who die after surgery with persistently elevated pulmonary arterial pressure have sufficiently severe pulmonary vascular disease to account for their persistent pulmonary hypertension and death.

Re-evaluation of the indications for cardiac valve replacement.

We re-evaluated the indications for mitral valve replacement and reconstruction, and attempted to determine the optimal time for aortic valve replacement. (1) The actuarial event-free survival rate in patients undergoing open mitral commissurotomy for mitral stenosis with far-advanced subvalvular deformities was 78 per cent at 11 years after surgery and similar in patients undergoing mitral valve replacement for mitral stenosis. Postoperative clinical improvements compared favorably with those in patients undergoing mitral valve replacement. If quality of postoperative life in patients not requiring anticoagulants is borne in mind, open mitral commissurotomy should be given strong consideration as the procedure of choice for the majority of patients with mitral stenosis. (2) The long-term results of reconstructive procedures for mitral regurgitation largely depend upon the pathological anatomies contributing to the development of mitral regurgitation. The results were less satisfactory in patients with fibrotic changes of valvular and subvalvular tissue than in patients undergoing mitral valve replacement for mitral regurgitation. (3) In aortic valve replacement, the postoperative prognosis was poor in patients with a preoperative left ventricular end-systolic volume index exceeding 200 ml/m2 and left ventricular ejection fraction less than 0.35. Operative management of patients with aortic valve disease should be considered, before severe left ventricular systolic dysfunction is evident.

Relationship between left ventricular morphology and postoperative cardiac function following valve replacement for mitral stenosis

The left ventricular myocardium excised from 14 patients who had mitral stenosis and who underwent mitral valve replacement was examined, and myocardial fibrosis was quantitated in relation to cardiac function. Conventional mitral valve replacement was performed with cold potassium-induced cardioplegia associated with systemic hypothermia (28 degrees C rectal temperature) and topical cooling. All 14 patients had perivascular fibrosis; the amounts ranged from 16% to 54% of the whole tissue excised. The mean left ventricular end-diastolic volume index (LVEDVI) determined by M-mode echocardiography increased significantly (p less than 0.001) from 66.9 +/- 4.6 ml/m2 preoperatively to 79.0 +/- 2.9 ml/m2 postoperatively. The difference between preoperative and postoperative LVEDVIs was significantly correlated (p less than 0.01) to the percentage of myocardial fibrosis (r = 0.72), in that the index increased postoperatively when myocardial fibrosis was more than 35% and decreased when fibrosis was less than 35%. After mitral valve replacement, the mean ejection fraction increased when fibrosis was less than 35% of whole tissue (+0.12 +/- 0.04) and decreased when fibrosis was greater than 35% (-0.02 +/- 0.02, p less than 0.01). No measured preoperative hemodynamic parameters were predictive of prognosis. These data suggest that the degree of myocardial fibrosis is related to left ventricular performance after mitral valve replacement.

Immediate Hemodynamic Response to Correction of Cardiac Valvular Lesions

The immediate hemodynamic response to prosthetic replacement of the aortic and mitral valves was evaluated in 50 patients by intraoperative measurement of cardiac output, intracardiac pressures, and other hemodynamic variables. Hemodynamics returned to near-normal immediately after correction of aortic stenosis, aortic regurgitation, and mitral regurgitation. In contrast, little immediate hemodynamic improvement occurred after mitral valve replacement for mitral stenosis. This difference could not be explained by blood volume deficits, the presence of the prosthesis, or residual valvular lesions. The most likely explanation appears to be that pulmonary vascular resistance does not immediately decrease, while an increased mechanical load is placed on the chronically diseased right ventricle. Impairment of left ventricular function may also play a role in the altered hemodynamic state observed early after correction of long-standing mitral stenosis.