Does metabolic syndrome influence bioprosthetic mitral valve degeneration and reoperation rate?

Steven R. Meyer, Rakesh M. Suri, R. Scott Wright, Joseph A. Dearani, Thomas A. Orszulak, Richard C. Daly, Harold M. Burkhart, Soon J. Park, Hartzell V Schaff

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background: Evidence suggests that metabolic syndrome (MbS) is associated with early senescence of bioprosthetic aortic valve prostheses. The purpose of this study was to determine whether MbS is also associated with accelerated failure of bioprosthetic valves prostheses in the mitral position. Methods: Records of all patients undergoing bioprosthetic mitral valve replacement (MVR) from 1993 to 2000 were reviewed. Results: Of 114 patients undergoing bioprosthetic MVR, 48 (42%) had MbS. Mean age was 73 years (vs. 74 years for no MbS). Patients underwent MVR for regurgitation (n = 97; 85%), stenosis (n = 12; 11%), or mixed lesions (n = 4; 4%). Etiology was degenerative (n = 35; 32%), rheumatic (n = 26; 24%), ischemic (n = 30; 28%), calcific (n = 9; 8%), and endocarditis (n = 8; 8%). Mean follow-up was 4.5 years. Overall survival at 5 and 10 years was 56% and 26%, respectively. Survival was similar between groups (p = 0.15). Five patients (2 MbS; 4% vs. 3 no MbS; 5%) required mitral reoperation at a mean of 3.8 years after initial MVR. The risk of prosthetic valve failure was not different between groups (p = 0.66). Despite no initial difference in transmitral gradients, gradients beyond five-year follow-up were greater for those with MbS (6.8 mmHg MbS vs. 4.7 mmHg no MbS, p = 0.007). Independent predictors of gradient progression beyond two years were MbS (p = 0.027) and female gender (p = 0.012). There were no significant differences in valve area, regurgitation, or ejection fraction. Conclusions: Although overall survival following bioprosthetic MVR is challenging, MbS did not predict diminished survival or excess reoperative risk compared to non-MbS patients. The trend toward more rapid progression of transprosthetic gradients in MbS patients warrants further investigation.

Original languageEnglish (US)
Pages (from-to)146-151
Number of pages6
JournalJournal of Cardiac Surgery
Volume27
Issue number2
DOIs
StatePublished - Mar 2012

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Mitral Valve
Reoperation
Survival
Prostheses and Implants
Mitral Valve Insufficiency
Endocarditis
Aortic Valve
Pathologic Constriction

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Does metabolic syndrome influence bioprosthetic mitral valve degeneration and reoperation rate? / Meyer, Steven R.; Suri, Rakesh M.; Wright, R. Scott; Dearani, Joseph A.; Orszulak, Thomas A.; Daly, Richard C.; Burkhart, Harold M.; Park, Soon J.; Schaff, Hartzell V.

In: Journal of Cardiac Surgery, Vol. 27, No. 2, 03.2012, p. 146-151.

Research output: Contribution to journalArticle

Meyer, Steven R. ; Suri, Rakesh M. ; Wright, R. Scott ; Dearani, Joseph A. ; Orszulak, Thomas A. ; Daly, Richard C. ; Burkhart, Harold M. ; Park, Soon J. ; Schaff, Hartzell V. / Does metabolic syndrome influence bioprosthetic mitral valve degeneration and reoperation rate?. In: Journal of Cardiac Surgery. 2012 ; Vol. 27, No. 2. pp. 146-151.
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title = "Does metabolic syndrome influence bioprosthetic mitral valve degeneration and reoperation rate?",
abstract = "Background: Evidence suggests that metabolic syndrome (MbS) is associated with early senescence of bioprosthetic aortic valve prostheses. The purpose of this study was to determine whether MbS is also associated with accelerated failure of bioprosthetic valves prostheses in the mitral position. Methods: Records of all patients undergoing bioprosthetic mitral valve replacement (MVR) from 1993 to 2000 were reviewed. Results: Of 114 patients undergoing bioprosthetic MVR, 48 (42{\%}) had MbS. Mean age was 73 years (vs. 74 years for no MbS). Patients underwent MVR for regurgitation (n = 97; 85{\%}), stenosis (n = 12; 11{\%}), or mixed lesions (n = 4; 4{\%}). Etiology was degenerative (n = 35; 32{\%}), rheumatic (n = 26; 24{\%}), ischemic (n = 30; 28{\%}), calcific (n = 9; 8{\%}), and endocarditis (n = 8; 8{\%}). Mean follow-up was 4.5 years. Overall survival at 5 and 10 years was 56{\%} and 26{\%}, respectively. Survival was similar between groups (p = 0.15). Five patients (2 MbS; 4{\%} vs. 3 no MbS; 5{\%}) required mitral reoperation at a mean of 3.8 years after initial MVR. The risk of prosthetic valve failure was not different between groups (p = 0.66). Despite no initial difference in transmitral gradients, gradients beyond five-year follow-up were greater for those with MbS (6.8 mmHg MbS vs. 4.7 mmHg no MbS, p = 0.007). Independent predictors of gradient progression beyond two years were MbS (p = 0.027) and female gender (p = 0.012). There were no significant differences in valve area, regurgitation, or ejection fraction. Conclusions: Although overall survival following bioprosthetic MVR is challenging, MbS did not predict diminished survival or excess reoperative risk compared to non-MbS patients. The trend toward more rapid progression of transprosthetic gradients in MbS patients warrants further investigation.",
author = "Meyer, {Steven R.} and Suri, {Rakesh M.} and Wright, {R. Scott} and Dearani, {Joseph A.} and Orszulak, {Thomas A.} and Daly, {Richard C.} and Burkhart, {Harold M.} and Park, {Soon J.} and Schaff, {Hartzell V}",
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T1 - Does metabolic syndrome influence bioprosthetic mitral valve degeneration and reoperation rate?

AU - Meyer, Steven R.

AU - Suri, Rakesh M.

AU - Wright, R. Scott

AU - Dearani, Joseph A.

AU - Orszulak, Thomas A.

AU - Daly, Richard C.

AU - Burkhart, Harold M.

AU - Park, Soon J.

AU - Schaff, Hartzell V

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Y1 - 2012/3

N2 - Background: Evidence suggests that metabolic syndrome (MbS) is associated with early senescence of bioprosthetic aortic valve prostheses. The purpose of this study was to determine whether MbS is also associated with accelerated failure of bioprosthetic valves prostheses in the mitral position. Methods: Records of all patients undergoing bioprosthetic mitral valve replacement (MVR) from 1993 to 2000 were reviewed. Results: Of 114 patients undergoing bioprosthetic MVR, 48 (42%) had MbS. Mean age was 73 years (vs. 74 years for no MbS). Patients underwent MVR for regurgitation (n = 97; 85%), stenosis (n = 12; 11%), or mixed lesions (n = 4; 4%). Etiology was degenerative (n = 35; 32%), rheumatic (n = 26; 24%), ischemic (n = 30; 28%), calcific (n = 9; 8%), and endocarditis (n = 8; 8%). Mean follow-up was 4.5 years. Overall survival at 5 and 10 years was 56% and 26%, respectively. Survival was similar between groups (p = 0.15). Five patients (2 MbS; 4% vs. 3 no MbS; 5%) required mitral reoperation at a mean of 3.8 years after initial MVR. The risk of prosthetic valve failure was not different between groups (p = 0.66). Despite no initial difference in transmitral gradients, gradients beyond five-year follow-up were greater for those with MbS (6.8 mmHg MbS vs. 4.7 mmHg no MbS, p = 0.007). Independent predictors of gradient progression beyond two years were MbS (p = 0.027) and female gender (p = 0.012). There were no significant differences in valve area, regurgitation, or ejection fraction. Conclusions: Although overall survival following bioprosthetic MVR is challenging, MbS did not predict diminished survival or excess reoperative risk compared to non-MbS patients. The trend toward more rapid progression of transprosthetic gradients in MbS patients warrants further investigation.

AB - Background: Evidence suggests that metabolic syndrome (MbS) is associated with early senescence of bioprosthetic aortic valve prostheses. The purpose of this study was to determine whether MbS is also associated with accelerated failure of bioprosthetic valves prostheses in the mitral position. Methods: Records of all patients undergoing bioprosthetic mitral valve replacement (MVR) from 1993 to 2000 were reviewed. Results: Of 114 patients undergoing bioprosthetic MVR, 48 (42%) had MbS. Mean age was 73 years (vs. 74 years for no MbS). Patients underwent MVR for regurgitation (n = 97; 85%), stenosis (n = 12; 11%), or mixed lesions (n = 4; 4%). Etiology was degenerative (n = 35; 32%), rheumatic (n = 26; 24%), ischemic (n = 30; 28%), calcific (n = 9; 8%), and endocarditis (n = 8; 8%). Mean follow-up was 4.5 years. Overall survival at 5 and 10 years was 56% and 26%, respectively. Survival was similar between groups (p = 0.15). Five patients (2 MbS; 4% vs. 3 no MbS; 5%) required mitral reoperation at a mean of 3.8 years after initial MVR. The risk of prosthetic valve failure was not different between groups (p = 0.66). Despite no initial difference in transmitral gradients, gradients beyond five-year follow-up were greater for those with MbS (6.8 mmHg MbS vs. 4.7 mmHg no MbS, p = 0.007). Independent predictors of gradient progression beyond two years were MbS (p = 0.027) and female gender (p = 0.012). There were no significant differences in valve area, regurgitation, or ejection fraction. Conclusions: Although overall survival following bioprosthetic MVR is challenging, MbS did not predict diminished survival or excess reoperative risk compared to non-MbS patients. The trend toward more rapid progression of transprosthetic gradients in MbS patients warrants further investigation.

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