Influence of Gender on the Relationships between Metabolic Syndrome and Left Ventricular Mass in Essential Hypertensive Subjects

Abstract

Although the definition and clinical importance of the metabolic syndrome (MetS) are still under debate [1], there is clear evidence that MetS considerably increases the risk of cardiovascular (CV) and renal events, in general population and also in subjects with high blood pressure (BP), even in absence of diabetes [2-5]. In some studies the CV morbidity and mortality risk associated with MetS was found to be higher in the female sex [3]. Several lines of evidence suggest that this enhanced CV risk may partially be mediated by the increased prevalence of preclinical CV and renal damage observed in individuals with the MetS [6-14]. Recently, the results of the Framingham Offspring study highlighted the importance of subclinical cardiovascular changes in mediating the CV risks associated with MetS, showing that subjects with MetS who had preclinical disease had a 2.7-fold increased CV risk, compared with individuals without preclinical disease, MetS, or diabetes (who served as referent). In contrast, participants with the presence of MetS or diabetes but without any preclinical CV disease were not at a statistically significant increased risk compared with the referent group [14]. Among the various markers of preclinical cardiovascular damage, LV hypertrophy (LVH) is one of the most investigated [5-7,9-14]. It is well known that LVH, detected either by electrocardiography or echocardiography, is a strong predictor of cardiovascular morbidity and mortality [15]. Several studies have demonstrated that the MetS is associated with a high prevalence of LVH in hypertensive patients and in general population. The effect of the metabolic syndrome on left ventricular structure has been reported to be partly independent of the effect of hemodynamic and non-hemodynamic determinants of left ventricular mass [5-7,9-14], including BP values over 24 hours [5,7,10,12] and intra- arterial BP levels [13]. More recently, it has been also documented, in a longitudinal study conducted in general population, that the MetS markedly increases the odds of developing LVH. The adjusted risk to develop new onset LVH was 2.6 times greater in individuals with than in those without the MetS [16]. Only in a few studies was the influence of MetS on LVM analyzed separately in men and women [5,10-12,17]. Recently, we evaluated cross-sectionally in both sexes the relationships of MetS with LV mass and LV hypertrophy in 475 patients with essential hypertension, of whom 40% had MetS [17]. The definition based on Adult Treatment Panel III guidelines, recently slightly revised by an American Heart Association /National Heart, Lung, and Blood Institute scientific statement [2], was used to identify subjects with MetS. Measurements were obtained with patients off antihypertensive medications and included 24-hour BP monitoring and an echocardiogram. LV mass was indexed both by height elevated by a power of 2.7 (LVMH2.7) and by body surface area (LVMI). A cut-off point of 51 g/m2.7 in either gender was set to separate normal from LVH. Left ventricular hypertrophy was defined also as LVMI ≥ 125 g/m2 for men and ≥ 110 g/m2 for women, as suggested by the 2007 guidelines of the European Society of Hypertension [18]. In the group of female subjects, participants with MetS showed significantly higher values of LV mass, either normalized for height2.7 (Figure 1) or for body surface area (Figure 2) [17]. In male gender slightly less pronounced differences, but equally significant, were observed in the two subgroups of hypertensive patients with and without MetS, regarding left ventricular mass, independently of the method used for indexation (Figures 1-2) [17]. Also in the subset of hypertensive patients never pharmacologically treated for high BP, LVMH2.7 and LVMI were higher in both females and males with MetS compared with their counterparts without i