Abstract
Background: Longitudinal increases in metabolic syndrome (MS) components are associated with increased heart failure (HF) risk, but the association of MS change over time with subclinical myocardial injury is unknown. Hypothesis: Greater progression and duration of MS is associated with subclinical myocardial injury, as reflected by high-sensitivity cardiac troponin T (hs-cTnT). Methods: We studied 8,170 participants (mean age 63, 59% female) without coronary heart disease, HF or diabetes at ARIC Visit 4 (1996-1998) with available data on MS components from the first four ARIC visits and hs-cTnT data at Visit 4. We defined MS using AHA/NHLBI criteria for high waist circumference (WC), hyperglycemia, elevated blood pressure (BP), low HDL-C and hypertriglyceridemia, with a diagnosis of MS made by ≥ 3 components. Using data on MS components from Visit 1 (1987-89) through 4, we used logistic regression models adjusted for demographics and cardiovascular risk factors to evaluate associations of changes in MS components over time and duration of MS with elevated hs-cTnT (≥ 14 ng/L) at Visit 4. Results: 3,644 (45%) of Visit 4 participants had MS. Greater number of MS components at Visit 4 was associated with a higher likelihood of elevated hs-cTnT, with the highest odds seen for those with 5 MS components (OR 2.32; 95%CI: 1.39-3.87) compared to those with none. Among MS components, the strongest associations were seen for elevated BP and high WC. Among participants without MS at V1, those with no MS components at both Visits 1 and 4 had the lowest odds of elevated hs-cTnT (reference), with progressively higher likelihood of elevated hs-cTnT for those increasing to 1-2 (OR 1.12; 95%CI 0.61-2.06), 3 (OR 1.90; 95%CI 1.04-3.45) and 4-5 (OR 2.64; 95%CI 1.41-4.92) MS components by Visit 4. MS duration was also significantly associated with elevated hs-cTnT, with an OR of 1.08 (95%CI: 1.06-1.11) per year of MS duration. Conclusions: Greater MS severity and progression, and longer duration of MS, are associated with a higher likelihood of subclinical myocardial injury. This may have mechanistic implications for the association between MS and HF, and underscores the need to refine strategies to prevent MS onset and progression.
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