Wunan Zhou1, Navkranbir Bajaj1, Ankur Gupta1, Yee-Ping Sun1,2, Sanjay Divakaran1, Courtney Bibbo1, Jon Hainer1, Viviany Taqueti1,2, Sharmila Dorbala1,2, Ron Blankstein1,2, Pinak Shah2, Tsuyoshi Kaneko3, Dale Adler2, Patrick O'Gara2, Marcelo Di Carli4,5. 1. Cardiovascular Imaging Program, Departments of Medicine and Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. 2. Brigham and Women's Hospital Heart and Vascular Center, Harvard Medical School, 75 Francis St, ASB-L1 037C, Boston, MA, USA. 3. Division of Cardiac Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. 4. Cardiovascular Imaging Program, Departments of Medicine and Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. mdicarli@bwh.harvard.edu. 5. Brigham and Women's Hospital Heart and Vascular Center, Harvard Medical School, 75 Francis St, ASB-L1 037C, Boston, MA, USA. mdicarli@bwh.harvard.edu.
Abstract
BACKGROUND: We investigated role of coronary microvascular disease (CMD) in maladaptive LV remodeling and prognosis in patients with aortic sclerosis or stenosis and no overt CAD. METHODS: This was a retrospective cohort study of patients with aortic sclerosis or stenosis, normal myocardial perfusion and LV ejection fraction (EF) > 50% (n = 43) and matched controls without AS (n = 43). PET and echocardiograms were performed within 1 year of each other. Myocardial perfusion and myocardial flow reserve (MFR) were quantified using PET imaging. LV structure and function, including global longitudinal strain (GLS), were quantified by transthoracic echocardiography. RESULTS: Global MFR declined with increasing AS severity (P = 0.04). Probability of impaired MFR increased with severity of adverse LV remodeling (OR 1.88, CI 1.03 to 3.41, P =0.04). Reduced MFR associated with impaired GLS (r = - 0.29, P = 0.002) and associated with reduced MACE-free survival at 7.27 years median follow-up. Adjusted annualized rate of MACE was highest in those with impaired GLS and MFR and lowest in those with normal GLS and MFR (30.99% vs 1.86%, P =0.002). CONCLUSION AND RELEVANCE: In patients with AS and no overt CAD, impaired MFR associates with adverse LV remodeling and subclinical LV mechanical dysfunction, and is a marker increased clinical risk.
BACKGROUND: We investigated role of coronary microvascular disease (CMD) in maladaptive LV remodeling and prognosis in patients with aortic sclerosis or stenosis and no overt CAD. METHODS: This was a retrospective cohort study of patients with aortic sclerosis or stenosis, normal myocardial perfusion and LV ejection fraction (EF) > 50% (n = 43) and matched controls without AS (n = 43). PET and echocardiograms were performed within 1 year of each other. Myocardial perfusion and myocardial flow reserve (MFR) were quantified using PET imaging. LV structure and function, including global longitudinal strain (GLS), were quantified by transthoracic echocardiography. RESULTS: Global MFR declined with increasing AS severity (P = 0.04). Probability of impaired MFR increased with severity of adverse LV remodeling (OR 1.88, CI 1.03 to 3.41, P =0.04). Reduced MFR associated with impaired GLS (r = - 0.29, P = 0.002) and associated with reduced MACE-free survival at 7.27 years median follow-up. Adjusted annualized rate of MACE was highest in those with impaired GLS and MFR and lowest in those with normal GLS and MFR (30.99% vs 1.86%, P =0.002). CONCLUSION AND RELEVANCE: In patients with AS and no overt CAD, impaired MFR associates with adverse LV remodeling and subclinical LV mechanical dysfunction, and is a marker increased clinical risk.
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