Abstract MP29: High-Sensitivity Troponin-T is Associated With Incident Diabetic Foot Infections in the Atherosclerosis Risk in Communities Study

Abstract

Background: Diabetic foot infections (DFI) are associated with substantial morbidity and mortality. Glycemic control and prevalent cardiovascular disease have been associated with DFI risk, but the association of subclinical cardiovascular disease with incident DFI has not been explored. Hypothesis: We hypothesized that high-sensitivity troponin-T (hs-cTnT, a marker of microvascular disease) and N-terminal-pro hormone BNP (NT-proBNP, a marker of cardiac wall stress) would be associated with incident DFI in adults without prevalent cardiovascular disease. Methods: We conducted a prospective cohort analysis of 1733 Black and White participants in the Atherosclerosis Risk in Communities (ARIC) study who had diabetes without prevalent cardiovascular disease at visit 2 (1990-1992, mean age 57.7 yrs). We estimated the cumulative incidence of incident DFI through 2019 using hospitalization discharge codes. We used Cox models to assess the associations of categories of cardiac biomarkers (using clinical cut-points) with DFI after adjusting for traditional risk factors. Results: During a median follow-up of 25 years, there were 417 incident DFI events. The 25-year cumulative incidence of DFI was higher among participants with elevated hs-cTnT (≥14 ng/L) vs not elevated (35% vs. 21%; P<0.001), but not among participants with elevated NT-proBNP (≥125 pg/mL) (23% vs. 23%; P=0.73). In adjusted models, elevated hs-cTnT was associated with incident DFI (HR 1.98, 95%CI 1.46, 2.68). Elevated NT-proBNP was not significantly associated with incident DFI (HR 1.04, 95%CI 0.78, 1.41). Our results were similar when the biomarkers were modeled more flexibly using splines: we observed a robust association of hs-cTnT, but not NT-proBNP, with incident DFI ( Figure ). Conclusions: Elevated hs-cTnT was associated with incident DFI among middle-aged adults without prevalent cardiovascular disease. This suggests subclinical cardiovascular disease, possibly in the form of microvascular ischemia, may play a role in the etiology of DFI.