Jonathan D Kochav1, Jiwon Kim2, Robert Judd3, Han W Kim3, Igor Klem3, John Heitner4, Dipan Shah5, Chetan Shenoy6, Afshin Farzaneh-Far7, Venkateshwar Polsani8, Ramsey Kalil2, Pablo Villar-Calle9, Lakshmi Nambiar2, Razia Sultana2, Michele Parker3, Preston Cargile10, Omar K Khalique11, Martin B Leon11, Dimitrios Karmpaliotis11, Mark Ratcliffe12, Robert Levine13, William A Zoghbi5, Richard B Devereux2, Chaya S Moskowitz14, Raymond Kim3, Jonathan W Weinsaft15. 1. Division of Cardiology, Weill Cornell Medicine, New York, New York, USA; Division of Cardiology, Columbia University Irving Medical Center, New York, New York, USA. 2. Division of Cardiology, Weill Cornell Medicine, New York, New York, USA. 3. Duke Cardiovascular Magnetic Resonance Center, Duke University Medical Center, Durham, North Carolina, USA. 4. Division of Cardiology, NewYork-Presbyterian Brooklyn Methodist Hospital, New York, New York, USA. 5. Division of Cardiology, Houston Methodist DeBakey Heart and Vascular Center, Houston, Texas, USA. 6. Division of Cardiology, University of Minnesota Medical Center, Minneapolis, Minnesota, USA. 7. Division of Cardiology, University of Illinois at Chicago, Chicago, Illinois, USA. 8. Peidmont Heart Institute, Peidmont Atlanta Hospital, Atlanta Georgia, USA. 9. Department of Cardiology, Sant Pau Hospital, Barcelona, Spain. 10. Heart Imaging Technologies, Durham, North Carolina, USA. 11. Division of Cardiology, Columbia University Irving Medical Center, New York, New York, USA. 12. Division of Cardiac Surgery, University of California, San Francisco, California, USA. 13. Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts, USA. 14. Department of Epidemiology and Biostatics, Memorial Sloan Kettering Cancer Center, New York, New York, USA. 15. Division of Cardiology, Weill Cornell Medicine, New York, New York, USA. Electronic address: jww2001@med.cornell.edu.
Abstract
OBJECTIVES: The goal of this study was to test whether ischemia-mediated contractile dysfunction underlying the mitral valve affects functional mitral regurgitation (FMR) and the prognostic impact of FMR. BACKGROUND: FMR results from left ventricular (LV) remodeling, which can stem from myocardial tissue alterations. Stress cardiac magnetic resonance can assess ischemia and infarction in the left ventricle and papillary muscles; relative impact on FMR is uncertain. METHODS: Vasodilator stress cardiac magnetic resonance was performed in patients with known or suspected coronary artery disease at 7 sites. Images were centrally analyzed for MR etiology/severity, mitral apparatus remodeling, and papillary ischemia. RESULTS: A total of 8,631 patients (mean age 60.0 ± 14.1 years; 55% male) were studied. FMR was present in 27%, among whom 16% (n = 372) had advanced (moderate or severe) FMR. Patients with ischemia localized to subpapillary regions were more likely to have advanced FMR (p = 0.003); those with ischemia localized to other areas were not (p = 0.17). Ischemic/dysfunctional subpapillary myocardium (odds ratio: 1.24/10% subpapillary myocardium; confidence interval: 1.17 to 1.31; p < 0.001) was associated with advanced FMR controlling for infarction. Among a subgroup with (n = 372) and without (n = 744) advanced FMR matched (1:2) on infarct size/distribution, patients with advanced FMR had increased adverse mitral apparatus remodeling, paralleled by greater ischemic/dysfunctional subpapillary myocardium (p < 0.001). Although posteromedial papillary ischemia was more common with advanced FMR (p = 0.006), subpapillary ischemia with dysfunction remained associated (p < 0.001), adjusting for posteromedial papillary ischemia (p = 0.074). During follow-up (median 5.1 years), 1,473 deaths occurred in the overall cohort; advanced FMR conferred increased mortality risk (hazard ratio: 1.52; 95% confidence interval: 1.25 to 1.86; p < 0.001) controlling for left ventricular ejection fraction, infarction, and ischemia. CONCLUSIONS: Ischemic and dysfunctional subpapillary myocardium provides a substrate for FMR, which predicts mortality independent of key mechanistic substrates.
OBJECTIVES: The goal of this study was to test whether ischemia-mediated contractile dysfunction underlying the mitral valve affects functional mitral regurgitation (FMR) and the prognostic impact of FMR. BACKGROUND: FMR results from left ventricular (LV) remodeling, which can stem from myocardial tissue alterations. Stress cardiac magnetic resonance can assess ischemia and infarction in the left ventricle and papillary muscles; relative impact on FMR is uncertain. METHODS: Vasodilator stress cardiac magnetic resonance was performed in patients with known or suspected coronary artery disease at 7 sites. Images were centrally analyzed for MR etiology/severity, mitral apparatus remodeling, and papillary ischemia. RESULTS: A total of 8,631 patients (mean age 60.0 ± 14.1 years; 55% male) were studied. FMR was present in 27%, among whom 16% (n = 372) had advanced (moderate or severe) FMR. Patients with ischemia localized to subpapillary regions were more likely to have advanced FMR (p = 0.003); those with ischemia localized to other areas were not (p = 0.17). Ischemic/dysfunctional subpapillary myocardium (odds ratio: 1.24/10% subpapillary myocardium; confidence interval: 1.17 to 1.31; p < 0.001) was associated with advanced FMR controlling for infarction. Among a subgroup with (n = 372) and without (n = 744) advanced FMR matched (1:2) on infarct size/distribution, patients with advanced FMR had increased adverse mitral apparatus remodeling, paralleled by greater ischemic/dysfunctional subpapillary myocardium (p < 0.001). Although posteromedial papillary ischemia was more common with advanced FMR (p = 0.006), subpapillary ischemia with dysfunction remained associated (p < 0.001), adjusting for posteromedial papillary ischemia (p = 0.074). During follow-up (median 5.1 years), 1,473 deaths occurred in the overall cohort; advanced FMR conferred increased mortality risk (hazard ratio: 1.52; 95% confidence interval: 1.25 to 1.86; p < 0.001) controlling for left ventricular ejection fraction, infarction, and ischemia. CONCLUSIONS: Ischemic and dysfunctional subpapillary myocardium provides a substrate for FMR, which predicts mortality independent of key mechanistic substrates.
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