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High-sensitivity troponin I is associated with cardiovascular outcomes but not with breast arterial calcification among postmenopausal women

BACKGROUND: Prior studies support the utility of high sensitivity troponin I (hsTnI) for cardiovascular disease (CVD) risk stratification among asymptomatic populations; however, only two prior studies examined women separately. The association between hsTnI and breast arterial calcification is unkn...

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Detalles Bibliográficos
Autores principales: Iribarren, Carlos, Chandra, Malini, Lee, Catherine, Sanchez, Gabriela, Sam, Danny L., Azamian, Farima Faith, Cho, Hyo-Min, Ding, Huanjun, Wong, Nathan D., Molloi, Sabee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9789357/
https://www.ncbi.nlm.nih.gov/pubmed/36573194
http://dx.doi.org/10.1016/j.ijcrp.2022.200157
Descripción
Sumario:BACKGROUND: Prior studies support the utility of high sensitivity troponin I (hsTnI) for cardiovascular disease (CVD) risk stratification among asymptomatic populations; however, only two prior studies examined women separately. The association between hsTnI and breast arterial calcification is unknown. METHODS: Cohort study of 2896 women aged 60–79 years recruited after attending mammography screening between 10/2012 and 2/2015. BAC status (presence versus absence) and quantity (calcium mass mg) was determined using digital mammograms. Pre-specified endpoints were incident coronary heart disease (CHD), ischemic stroke, heart failure and its subtypes and all CVD. RESULTS: After 7.4 (SD = 1.7) years of follow-up, 51 CHD, 30 ischemic stroke and 46 heart failure events were ascertained. At a limit of detection of 1.6 ng/L, 98.3 of the cohort had measurable hsTnI concentration. HsTnI in the 4–10 ng/L range were independently associated of CHD (adjusted hazard ratio[aHR] = 2.78; 95% CI, 1.48–5.22; p = 0.002) and all CVD (aHR = 2.06; 95% CI, 1.37–3.09; p = 0.0005) and hsTnI over 10 ng/L was independently associated with CHD (aHR = 4.75; 95% CI, 1.83–12.3; p = 0.001), ischemic stroke (aHR = 3.81; 95% CI, 1.22–11.9; p = 0.02), heart failure (aHR = 3.29; 95% CI, 1.33–8.13; p = 0.01) and all CVD (aHR = 4.78; 95% CI, 2.66–8.59; p < 0.0001). No significant association was found between hsTnI and BAC. Adding hsTnI to a model containing the Pooled Cohorts Equation resulted in significant and clinical important improved calibration, discrimination (Δ C(index) = 6.5; p = 0.02) and reclassification (bias-corrected clinical NRI = 0.18; 95% CI, −0.13-0.49 after adding hsTnI categories). CONCLUSIONS: Our results support the consideration of hsTnI as a risk enhancing factor for CVD in asymptomatic women that could drive preventive or therapeutic decisions.