scholarly journals Myxomatous degeneration of the mitral valve

2018 ◽  
Vol 8 (4) ◽  
Author(s):  
Felippe Lazar ◽  
Laís Costa Marques ◽  
Vera Demarchi Aiello
1970 ◽  
Vol 25 (1) ◽  
pp. 127 ◽  
Author(s):  
Benjamin Schuster ◽  
Robert H. Davis ◽  
John H. Kohler ◽  
Suzanne B. Knoebel

2018 ◽  
Vol 59 (6) ◽  
pp. 1288-1295
Author(s):  
Ying Guo ◽  
Changpeng Song ◽  
Xi Wu ◽  
Xinxin Zheng ◽  
Jie Lu ◽  
...  

1989 ◽  
Vol 98 (5) ◽  
pp. 987-993 ◽  
Author(s):  
Lawrence H. Cohn ◽  
Verdi J. DiSesa ◽  
Gregory S. Couper ◽  
Pamela S. Peigh ◽  
Wendy Kowalker ◽  
...  

2017 ◽  
Vol 156 (4) ◽  
pp. 371-383 ◽  
Author(s):  
G. Markby ◽  
K.M. Summers ◽  
V.E. MacRae ◽  
J. Del-Pozo ◽  
B.M. Corcoran

2020 ◽  
Vol 31 (1) ◽  
pp. 28-34 ◽  
Author(s):  
Igor Belluschi ◽  
Elisabetta Lapenna ◽  
Andrea Blasio ◽  
Benedetto Del Forno ◽  
Andrea Giacomini ◽  
...  

Abstract OBJECTIVES Previous series of minimally invasive mitral valve repairs showed excellent results at up to 10 years of follow-up. The goal of this study was to assess the long-term durability beyond 10 years of the edge-to-edge repair for myxomatous degeneration performed through a minimally invasive approach. METHODS Ninety-seven consecutive patients (mean age 35 ± 9 years; left ventricular ejection fraction 63 ± 6%) with severe myxomatous mitral regurgitation (MR) underwent mitral valve repair through a right minithoracotomy between 1999 and 2006. MR was due to lesions involving the posterior leaflet (7.2% of patients), anterior leaflet (12.4%) and both leaflets (80.4%). RESULTS No hospital deaths occurred. At hospital discharge all patients had no or trivial MR. Follow-up was 100% complete (median 15.5 years; interquartile range 13.6–17.0, max 19.3 years). The 16-year overall survival rate was 95.9 ± 2.02% [95% confidence interval (CI) 89.39–98.43]. At 16 years, the cumulative incidence function of cardiac death, with non-cardiac death as a competing risk, was 3.1 ± 1.75 (95% CI 0.83–8.02). Only 3 patients (4.1%) had redo operations for recurrent severe MR. At 16 years, the cumulative incidence functions of reoperation for and recurrence of MR ≥3+, with death as a competing risk, were 3.1 ± 1.76% (95% CI 0.83–8.02) and 5.6 ± 2.47% (95% CI 2.06–11.83), respectively. No predictors of recurrence of MR ≥3+ were identified. At the last follow-up, moderate MR (2+/4+) was detected in 17 patients (17.5%); most of the patients were in New York Heart Association functional class I–II (97%) and in sinus rhythm (90%). CONCLUSIONS Minimally invasive mitral valve edge-to-edge repair through a right minithoracotomy for myxomatous degeneration appears to be an effective and durable approach even in the long-term follow-up (up to 19 years).


2014 ◽  
Vol 31 (6) ◽  
pp. E195-E196
Author(s):  
Lutfi Ocal ◽  
Macit Kalcik ◽  
Cuneyt Toprak ◽  
Alev Kılıcgedik ◽  
Atilla Koyuncu ◽  
...  

2015 ◽  
Vol 42 (1) ◽  
pp. 30-34 ◽  
Author(s):  
Xiaoyan Gu ◽  
Yihua He ◽  
Zhian Li ◽  
Jiancheng Han ◽  
Jian Chen ◽  
...  

This retrospective study attempted to establish the prevalence of multiple-valve involvement in Marfan syndrome and to compare echocardiographic with histopathologic findings in Marfan patients undergoing valvular or aortic surgery. We reviewed echocardiograms of 73 Marfan patients who underwent cardiovascular surgery from January 2004 through October 2009. Tissue histology was available for comparison in 29 patients. Among the 73 patients, 66 underwent aortic valve replacement or the Bentall procedure. Histologic findings were available in 29 patients, all of whom had myxomatous degeneration. Of 63 patients with moderate or severe aortic regurgitation as determined by echocardiography, 4 had thickened aortic valves. The echocardiographic findings in 18 patients with mitral involvement included mitral prolapse in 15. Of 11 patients with moderate or severe mitral regurgitation as determined by echocardiography, 4 underwent mitral valve repair and 7 mitral valve replacement. Histologic findings among mitral valve replacement patients showed thickened valve tissue and myxomatous degeneration. Tricuspid involvement was seen echocardiographically in 8 patients, all of whom had tricuspid prolapse. Two patients had severe tricuspid regurgitation, and both underwent repair. Both mitral and tricuspid involvement were seen echocardiographically in 7 patients. Among the 73 patients undergoing cardiac surgery for Marfan syndrome, 66 had moderate or severe aortic regurgitation, although their valves manifested few histologic changes. Eighteen patients had mitral involvement (moderate or severe mitral regurgitation, prolapse, or both), and 8 had tricuspid involvement. Mitral valves were most frequently found to have histologic changes, but the tricuspid valve was invariably involved.


2004 ◽  
Vol 65 (2) ◽  
pp. 198-206 ◽  
Author(s):  
Brendan M. Corcoran ◽  
Alexander Black ◽  
Heather Anderson ◽  
Joanna Dukes McEwan ◽  
Anne French ◽  
...  

2020 ◽  
Vol 21 (15) ◽  
pp. 5372
Author(s):  
Jaime Ibarrola ◽  
Mattie Garaikoetxea ◽  
Amaia Garcia-Peña ◽  
Lara Matilla ◽  
Eva Jover ◽  
...  

Mitral valve prolapse (MVP) patients develop myocardial fibrosis that is not solely explained by volume overload, but the pathophysiology has not been defined. Mineralocorticoid receptor antagonists (MRAs) improve cardiac function by decreasing cardiac fibrosis in other heart diseases. We examined the role of MRA in myocardial fibrosis associated with myxomatous degeneration of the mitral valve. Myocardial fibrosis has been analyzed in a mouse model of mitral valve myxomatous degeneration generated by pharmacological treatment with Nordexfenfluramine (NDF) in the presence of the MRA spironolactone. In vitro, adult human cardiac fibroblasts were treated with NDF and spironolactone. In an experimental mouse, MRA treatment reduced interstitial/perivascular fibrosis and collagen type I deposition. MRA administration blunted NDF-induced cardiac expression of vimentin and the profibrotic molecules galectin-3/cardiotrophin-1. In parallel, MRA blocked the increase in cardiac non-fibrillar proteins such as fibronectin, aggrecan, decorin, lumican and syndecan-4. The following effects are blocked by MRA: in vitro, in adult human cardiac fibroblasts, NDF-treatment-induced myofibroblast activation, collagen type I and proteoglycans secretion. Our findings demonstrate, for the first time, the contribution of the mineralocorticoid receptor (MR) to the development of myocardial fibrosis associated with mitral valve myxomatous degeneration. MRA could be a therapeutic approach to reduce myocardial fibrosis associated with MVP.


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