1461-P: Cardiac Troponin T and Troponin I and Incident Diabetes in the General Population: Generation Scotland Scottish Family Health Study

Abstract

Background: Recent data demonstrate that cardiac troponin T (cTnT) and I (cTnI) have different associations with cardiovascular risk factors and outcomes. Although limited data have reported associations of troponins with incident type 2 diabetes, no large study has directly compared cTnT and cTnI. Methods: High-sensitivity cTnT and cTnI were measured in serum from 18,775 individuals without baseline diabetes in the Generation Scotland Scottish Family Health Study. Median follow-up was 6.6 years (IQR 5.8-8.0). Each troponin was split into three groups (low; cTnT ≤3ng/L (n=8932) cTnI ≤1.8ng/L (n=9172), intermediate; cTnT 3-5.8ng/L (n=5024) cTnI 1.9-3.0ng/L (n=4879), high; cTnT ≥5.9ng/L (n=4819) cTnI ≥3.1ng/L (n=4724)), so that the proportion within each grouping was similar for each troponin. Associations of troponin with incident diabetes (490 cases from national electronic health records) was determined using Cox models, including adjustment for age, sex, BMI, lipids, systolic blood pressure, smoking, socioeconomic deprivation, rheumatoid arthritis, glucose, baseline CVD and medication use. Results: After adjustment for age and sex only, cTnI was strongly associated with risk of diabetes (HR 1.73 for high compared to low; 95% CI 1.36-2.21) whereas for cTnT the association was slightly weaker (HR 1.35 for high compared to low; 95% CI 1.05-1.73). On further adjustment for additional risk factors, the association for cTnI attenuated to the null (HR 1.31; 95% CI 1.01-1.71), whereas the association for cTnT became slightly stronger (HR 1.44; 95% CI 1.11-1.88). High levels of both cTnT and cTnI increased risk further (HR 1.63; 95% CI 1.17-2.28). Exclusion of 740 participants with baseline CVD did not materially affect the results. Conclusions: These results demonstrate a consistent association of subclinical myocardial injury, as measured by both cTnI and cTnT, with risk of future diabetes independent of common risk factors. Disclosure P. Welsh: Research Support; Self; AstraZeneca, Boehringer Ingelheim International GmbH. D. Preiss: Other Relationship; Self; Boehringer Ingelheim International GmbH. A. Campbell: None. D.J. Porteous: None. N.L. Mills: Speaker's Bureau; Self; Abbott Laboratories, Siemens Corporation. N. Sattar: Advisory Panel; Self; Amgen Inc., AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Novo Nordisk A/S. Consultant; Self; NAPP Pharmaceuticals Limited. Research Support; Self; Boehringer Ingelheim Pharmaceuticals, Inc. Speaker's Bureau; Self; Amgen Inc., Eli Lilly and Company, Mitsubishi Tanabe Pharma Corporation, Novo Nordisk A/S, Roche Diagnostics France, Sanofi. Funding Chief Scientist Office of the Scottish Government Health Directorates (ASM/14/1, CZD/16/6); Scottish Funding Council (HR03006); Medical Research Council UK; Butler British Heart Foundation (FS/16/14/32023 to N.L.M.)