J Scott Rankin1, Maria Grau-Sepulveda2, David M Shahian3, A Marc Gillinov4, Rakesh Suri4, James S Gammie5, Steven F Bolling6, Patrick M McCarthy7, Vinod H Thourani8, Niv Ad9, Sean M O'Brien2, Jeffrey P Jacobs10, Vinay Badhwar9. 1. Department of Cardiovascular and Thoracic Surgery, West Virginia University, Morgantown, West Virginia. Electronic address: jsrankinmd@cs.com. 2. Duke Clinical Research Institute, Durham, North Carolina. 3. Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. 4. Department of Thoracic and Cardiovascular Surgery, Cleveland Clinic Foundation, Cleveland, Ohio. 5. Division of Cardiac Surgery, Department of Cardiothoracic Surgery, University of Maryland School of Medicine, Baltimore, Maryland. 6. Department of Cardiac Surgery, University of Michigan, Ann Arbor, Michigan. 7. Department of Cardiac Surgery, Northwestern University, Chicago, Illinois. 8. Department of Cardiac Surgery, MedStar Washington Hospital Center, Georgetown University, Washington, DC. 9. Department of Cardiovascular and Thoracic Surgery, West Virginia University, Morgantown, West Virginia. 10. Division of Cardiovascular Surgery, Johns Hopkins University, St. Petersburg, Florida.
Abstract
BACKGROUND: The pathoetiology of mitral regurgitation (MR) has been suggested as a mediator of outcomes after mitral valve (MV) operations, particularly in ischemic functional mitral regurgitation (IMR). This study examined the independent association of MV etiology with mortality. METHODS: The Society of Thoracic Surgeons Database was utilized to assess all patients undergoing MV replacement or repair from 2011 to 2014. Patients who underwent concomitant surgical ablation, septal defect closure, tricuspid valve repair, or coronary artery bypass grafting were included. All other concomitant operations were excluded, producing a final cohort of 89,085 patients. A hierarchical etiology decision tree was developed to categorize the population into eight etiology groups: endocarditis, reoperation, acute IMR, rheumatic, uncommon etiologies (hypertrophic obstructive cardiomyopathy, trauma, tumor, or congenital), degenerative primary MR, chronic IMR, and pure annular dilatation. The statistical association of etiology with unadjusted and risk-adjusted operative mortality was evaluated by logistic regression and supplemented by sensitivity analyses using established risk models. RESULTS: The decision tree showed that etiology categories appeared clinically aligned with published population distributions, baseline characteristics, and unadjusted outcomes. Unadjusted operative mortality ranged from 1.2% for degenerative MV repair to 15.1% for MV replacement in acute IMR. After risk adjustment, MV etiologies per se exhibited insignificant independent associations with risk-adjusted operative mortality. CONCLUSIONS: Mortality after mitral operations is determined primarily by standard clinical risk factors. Mitral etiology does not appear to add independent predictive value.
BACKGROUND: The pathoetiology of mitral regurgitation (MR) has been suggested as a mediator of outcomes after mitral valve (MV) operations, particularly in ischemic functional mitral regurgitation (IMR). This study examined the independent association of MV etiology with mortality. METHODS: The Society of Thoracic Surgeons Database was utilized to assess all patients undergoing MV replacement or repair from 2011 to 2014. Patients who underwent concomitant surgical ablation, septal defect closure, tricuspid valve repair, or coronary artery bypass grafting were included. All other concomitant operations were excluded, producing a final cohort of 89,085 patients. A hierarchical etiology decision tree was developed to categorize the population into eight etiology groups: endocarditis, reoperation, acute IMR, rheumatic, uncommon etiologies (hypertrophic obstructive cardiomyopathy, trauma, tumor, or congenital), degenerative primary MR, chronic IMR, and pure annular dilatation. The statistical association of etiology with unadjusted and risk-adjusted operative mortality was evaluated by logistic regression and supplemented by sensitivity analyses using established risk models. RESULTS: The decision tree showed that etiology categories appeared clinically aligned with published population distributions, baseline characteristics, and unadjusted outcomes. Unadjusted operative mortality ranged from 1.2% for degenerative MV repair to 15.1% for MV replacement in acute IMR. After risk adjustment, MV etiologies per se exhibited insignificant independent associations with risk-adjusted operative mortality. CONCLUSIONS: Mortality after mitral operations is determined primarily by standard clinical risk factors. Mitral etiology does not appear to add independent predictive value.
Authors: David Messika-Zeitoun; Pascal Candolfi; Maurice Enriquez-Sarano; Ian G Burwash; Vincent Chan; Jean-Francois Philippon; Jean-Manuel Toussaint; Partrick Verta; Ted E Feldman; Bernard Iung; David Glineur; Jean-Francois Obadia; Alec Vahanian; Thierry Mesana Journal: Open Heart Date: 2020-08