No abstract

Each intervention (dietary counseling or n-3 PUFA supplements) reduced sTM and sICAM-1 concentrations, indicating decreased endothelial activation. The tPAag increase in the groups not receiving dietary counseling (pooled), which indicates progression of atherosclerosis, was significantly counteracted by dietary counseling.

We observed a tendency toward reduction in all-cause mortality in the n-3 PUFA groups that, despite a low number of participants, reached borderline statistical significance. The magnitude of risk-reduction suggests that a larger trial should be considered in similar populations.

OBJECTIVE -The aim of this study was to investigate the role of inflammatory markers as potential predictors of cardiovascular events in subjects with and without the metabolic syndrome.RESEARCH DESIGN AND METHODS -This was a post hoc analysis from the Diet and Omega-3 Intervention Trial (DOIT), comprising 563 elderly men with (n ϭ 221) and without (n ϭ 342) metabolic syndrome. Circulating inflammatory markers were measured.RESULTS -During 3 years, 68 cardiovascular events were recorded. In the total population, C-reactive protein (CRP) (P Ͻ 0.001), interleukin-18 (IL-18) (P ϭ 0.008), and IL-6 (P ϭ 0.003) were elevated in subjects with events. In subjects with metabolic syndrome, IL-18 was the strongest predictor (adjusted odds ratio 2.9 [95% CI 1.1-7.8]). In subjects without metabolic syndrome, only CRP seemed to be an independent predictor (3.3 [1.5-7.3]). There was a significant interaction between fasting glucose and IL-18 (P ϭ 0.008) and IL-6 (P ϭ 0.024) but not CRP. Elevated fasting glucose (Ͼ6.2 mmol/l) markedly increased the predictive power of inflammatory markers (IL-18: 5.5 [1.4 -21.1], IL-6: 3.5 [1.0 -11.8], and CRP: 3.5 [1.0 -11.9]). For IL-18, there was a stepwise increase in event rate by quartiles of fasting glucose.CONCLUSIONS -IL-18 was an independent predictor of cardiovascular events in subjects with metabolic syndrome and even more so in the presence of elevated fasting glucose. Our findings suggest a mutually potentiating effect of hyperglycemia and inflammation in cardiovascular risk prediction. Diabetes Care 32:486-492, 2009