Inflammation and ventricular-vascular coupling in hypertensive patients with metabolic syndrome

Abstract

Background and aims: Metabolic syndrome (MetS) is currently considered to raise the risk for type 2 diabetes and cardiovascular events. It has been suggested that part of this risk excess may be due to a cluster of additional factors associated with MetS. We aimed to investigate the role of inflammation on the ventricular-vascular coupling in patients with MetS. Methods and results: We enrolled a total of 227 hypertensive patients (106 with MetS and 121 without MetS) matched for age and gender. Aortic pulse wave velocity (aPWV), intima-media thickness (IMT) and high sensitivity C-reactive protein (CRP) increased according to the number of MetS components. Patients with MetS showed increased aPWV (11.5 AE 3.7 vs. 10.3 AE 2.5 m/s, P Z 0.03) compared with controls. In a model adjusted for age, sex, heart rate and mean blood pressure, aPWV resulted increased in patients with CKD (beta 1.29 m/s, 95%CI 0.61e1.96 m/s, P < 0.001) and MetS (beta 0.89 m/s, 95%CI 0.28e1.51 m/s, P Z 0.005). After additional adjustment for CRP and IMT, the slope of aPWV was respectively reduced by 16% and 62%, suggesting that inflammation and intima-media thickening could contribute to aortic stiffening in patients with MetS. In these patients, aPWV was also associated with left-ventricular mass index (beta 0.79 g/m 2.7 , 95%CI 0.05e1.52 g/m 2.7 , P Z 0.05). Conclusion: MetS is characterized by an inflammation-dependent acceleration in cardiovascular ageing. This pattern of pathophysiological abnormalities may contribute to amplify the burden of cardiovascular risk in patients with MetS.

Associations between circulating resistin concentrations and left ventricular mass are not accounted for by effects on aortic stiffness or renal dysfunction

“…Furthermore, although circulating concentrations of TNF-α, and IL-6 independently associate with concentric LV remodeling, there is no relationship between these molecules and LVM [30]. Although C-reactive protein may in-part explain ventricularvascular coupling [22], the relationships between resistin and LVM in the present study were independent of Creactive protein. Hence, it is unlikely that the resistin-LVM relationships can be explained by general inflammatory effects.…”

“…As it is uncertain whether associations between circulating resistin concentrations and adverse cardiac effects may be accounted for by indirect (renal dysfunction or ventricular-vascular coupling) or direct effects, in the present study we assessed the extent to which independent relationships between circulating resistin concentrations and LVM in a large community-based sample are explained by an impact of resistin on renal or aortic function. Furthermore, as general inflammation (as indexed by circulating C-reactive protein [CRP]) may inpart explain the relationship between aortic stiffness and LVM (ventricular-vascular coupling) in hypertensive patients with metabolic syndrome [22], we assessed whether relationships between circulating resistin concentrations and LVM in a large community-based sample are independent of CRP.…”

Weight Loss and Hypertension in Obese Subjects

“…Furthermore, a strong association has been reported between visceral adipose tissue and greater serum levels of cytokine, such as leptin, interleukin-6, plasminogen activator inhibitor-1, all of which are related both to endothelial dysfunction and hypertension [21,22,23]. The inflammation pattern promoted by cytokines release is involved in an inflammation-dependent aortic stiffening [24] and it can also lead to left ventricular stiffness and mass increase [24]. This hypothesis is well described in the clinical model of metabolic syndrome [24].…”

“…The inflammation pattern promoted by cytokines release is involved in an inflammation-dependent aortic stiffening [24] and it can also lead to left ventricular stiffness and mass increase [24]. This hypothesis is well described in the clinical model of metabolic syndrome [24]. Moreover, all the components of metabolic syndrome are shown to be related to augmented carotid-femoral pulse wave velocity [25,26], whereas the same relation cannot be described with the cardio-ankle vascular index [25].…”

The Pathogenic Role of Very Low Density Lipoprotein on Atrial Remodeling in the Metabolic Syndrome

“…Watanabe et al reported that even in the absence of diabetes and hypertension, MetS is an independent risk factor for AF [38]. Zanoli et al reported significant correlation between high-sensitive C-reactive protein (hsCRP) to atherosclerosis and arterial stiffness reflected by intima-medial thickness and aortic pulse wave velocity, respectively [39]. They suggested that MetS is characterized by an inflammation-dependent acceleration in cardiovascular ageing, which can lead to vascular dysfunction, and would contribute to make patients with MetS more susceptible to atrial remodeling [39].…”