Kojo Amoakwa1, Oluwaseun E Fashanu2, Martin Tibuakuu3, Di Zhao4, Eliseo Guallar4, Seamus P Whelton2, Wesley T O'Neal5, Wendy S Post4, Matthew J Budoff6, Erin D Michos7. 1. Saint Agnes Healthcare, Baltimore, MD, USA. 2. Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins School of Medicine, Baltimore, MD, USA. 3. Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins School of Medicine, Baltimore, MD, USA; Department of Medicine, St. Luke's Hospital, Chesterfield, MO, USA. 4. Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins School of Medicine, Baltimore, MD, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. 5. Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA. 6. Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Los Angeles, CA, USA. 7. Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins School of Medicine, Baltimore, MD, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. Electronic address: edonnell@jhmi.edu.
Abstract
BACKGROUND AND AIMS: Left-sided valvular calcification is associated with cardiovascular disease (CVD) morbidity and mortality. Resting heart rate (RHR) may influence valvular calcium progression through shear stress. Whether RHR, an established CVD risk factor, is associated with valvular calcium progression is unknown. We assessed whether RHR predicts incidence and progression of mitral annular calcium (MAC) and aortic valve calcium (AVC) in a community-based cohort free of CVD at baseline. METHODS: RHR was obtained from baseline electrocardiograms of 5498 MESA participants. MAC and AVC were quantified using Agatston scoring from cardiac computed tomography scans obtained at baseline and at a second examination during follow-up. We examined associations of RHR with incident MAC/AVC and annual change in MAC/AVC scores, after adjusting for demographics, CVD risk factors, physical activity, and atrioventricular nodal blocker use. RESULTS: At baseline, participants had mean age of 62 ± 10 years and mean RHR of 63 ± 10 bpm; 12.3% and 8.9% had prevalent AVC and MAC, respectively. Over a median of 2.3 years, 4.1% and 4.5% developed incident AVC and MAC, respectively. Each 10 bpm higher RHR was significantly associated with incident MAC [Risk Ratio 1.17 (95% CI 1.03-1.34)], but not incident AVC. However, RHR was associated with AVC progression [β = 1.62 (0.45-2.80) Agatston units/year for every 10 bpm increment], but not MAC progression. CONCLUSIONS: Higher RHR was associated with MAC incidence and AVC progression, independent of traditional CVD risk factors. Future studies are needed to determine whether modification of RHR through lifestyle or pharmacologic interventions can reduce valvular calcium incidence or progression.
BACKGROUND AND AIMS: Left-sided valvular calcification is associated with cardiovascular disease (CVD) morbidity and mortality. Resting heart rate (RHR) may influence valvular calcium progression through shear stress. Whether RHR, an established CVD risk factor, is associated with valvular calcium progression is unknown. We assessed whether RHR predicts incidence and progression of mitral annularcalcium (MAC) and aortic valve calcium (AVC) in a community-based cohort free of CVD at baseline. METHODS: RHR was obtained from baseline electrocardiograms of 5498 MESAparticipants. MAC and AVC were quantified using Agatston scoring from cardiac computed tomography scans obtained at baseline and at a second examination during follow-up. We examined associations of RHR with incident MAC/AVC and annual change in MAC/AVC scores, after adjusting for demographics, CVD risk factors, physical activity, and atrioventricular nodal blocker use. RESULTS: At baseline, participants had mean age of 62 ± 10 years and mean RHR of 63 ± 10 bpm; 12.3% and 8.9% had prevalent AVC and MAC, respectively. Over a median of 2.3 years, 4.1% and 4.5% developed incident AVC and MAC, respectively. Each 10 bpm higher RHR was significantly associated with incident MAC [Risk Ratio 1.17 (95% CI 1.03-1.34)], but not incident AVC. However, RHR was associated with AVC progression [β = 1.62 (0.45-2.80) Agatston units/year for every 10 bpm increment], but not MAC progression. CONCLUSIONS: Higher RHR was associated with MAC incidence and AVC progression, independent of traditional CVD risk factors. Future studies are needed to determine whether modification of RHR through lifestyle or pharmacologic interventions can reduce valvular calcium incidence or progression.
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