The influence of inflammation outweighing the metabolic syndrome on cardiovascular risk and mortality

Abstract

☆ The authors declare no conflict of interests and no financial support from any institute. ⁎ Corresponding author. Department of Internal Medicine, Hualien Armed Forces General Hospital. No.163, Jiali Rd., Xincheng Township, Hualien County 97144, Hualien, Taiwan. Tel.: +886 3 826 0601. E-mail address: farmer507@yahoo.com.tw (G.-M. Lin). In a systemic review andmeta-analysis, the metabolic syndrome is associated with a 2-fold increase in cardiovascular outcomes and a 1.5-fold increase in all-cause mortality [1]. Most participants came from general populations and were free of cardiovascular disease. However, we have observed that the influence of metabolic syndrome on cardiovascular risk was blunted in the cohorts of the placebo arm in the JUPITER trial [2]. In the subgroup analysis, the cardiovascular hazard ratio for menwithmetabolic syndrome to thosewithout it was estimated at 0.92, for women: 1.02, for the elderlyN70 years old: 0.80 and for the total placebo cohorts: 0.92 [3,4]. Since the populations enrolled in JUPITER are unique for their baseline characteristics without diabetes, with normal lipid profiles and high C-reactive protein levels (N2 mg/L), those with metabolic syndrome should mainly include central obesity and systemic hypertension in addition to one or more of the other metabolic abnormalities such as an increase of triglyceride, reduction of the HDL-cholesterol and impaired fasting glucose. Obviously obesity, which demonstrates the phenomenon of reverse epidemiology regardless of age and gender, is the only variable in the components of metabolic syndrome (except the cardiovascular incidence rate of fasting glucose was not shown in JUPITER) that could reduce the cardiovascular risk [3,4]. Previously, Aizawa et al. suggested that the five metabolic components do cluster and obesity and insulin resistance were likely to be linked with metabolic syndrome more than hypertension or high triglyceride [5]. As we know, those with obesity and insulin resistance have an increase of inflammatory status and cardiovascular risk compared to general populations. It is surprising that to replace the risk factor of obesity or insulin resistance by inflammation would not alter the cardiovascular incidence for those who have not fulfilled the criteria of themetabolic syndrome. This reflects that inflammation may play a central role in the genesis of metabolic syndrome related cardiovascular risk [6]. Accordingly, the influence of inflammation outweighing metabolic syndrome on cardiovascular risk and mortality is clinically proven. Further, we reason that the finding of Aizawa et al. why obesity and insulin resistance prefer to be clustered in the metabolic syndrome than in other components, is possibly due to these two factors just representing a status of inflammation. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [7].