Abstract 14244: Gender-Specific Association Between Serum Markers of Systemic Inflammation and Interstitial Cardiac Fibrosis: The Multi-Ethnic Study of Atherosclerosis (MESA)
Introduction: Inflammation contributes to pathogenic ventricular remodeling. Recently, T1 mapping has been used to non-invasively measure interstitial myocardial fibrosis. We examined the association between baseline markers of systemic inflammation and interstitial fibrosis measured using T1 mapping at 10 years follow-up in MESA. Methods and Results: 1,156 participants underwent cardiac magnetic resonance imaging with T1 mapping. All analyses were stratified by gender. Three hierarchical multivariable linear regression models were constructed to assess the risk-adjusted association of baseline C-reactive protein (CRP), interleukin 6 (IL-6) and fibrinogen with 25 minutes post-contrast myocardial T1 time (T1Myo25). Shorter T1Myo25 reflect increasing levels of interstitial fibrosis. We found a non-linear relationship between IL-6 and T1Myo25 in males (Figure 1A). A significant negative association between T1Myo25 and increasing levels of IL-6 was found in males that reversed at IL-6 levels ≥2.7pg/ml. Moreover in males, increasing levels of fibrinogen were significantly negatively associated with T1Myo25, while a similar but non-significant trend was found for CRP (Figure 1B). In women, there was a similar inverse association between T1Myo25 and increasing levels of all three markers of systemic inflammation prior to adjusting for body mass index that became statistically non-significant following adjustment (Figure 1B). Similar associations with markers of inflammation were found using extracellular volume fraction and T1Myo12 as measures of interstitial fibrosis. Conclusions: Markers of systemic inflammation in males, particularly IL-6 and fibrinogen, are independently associated with increased interstitial fibrosis. In females, this association may be mediated by the obesity-induced inflammatory-state. These findings highlight the early role of inflammation in the pathogenesis of heart failure.