Abstract
The clustering of cardio-metabolic risk factors, either when called metabolic syndrome (MetS) or not, substantially increases the risk of cardiovascular disease (CVD) and causes mortality. One of the possible mechanisms for this clustering's adverse effect is an increase in arterial stiffness (AS), and in high central aortic blood pressure (CABP), which are significant and independent CVD risk factors. Arterial hypertension was connected to AS long ago; however, other MetS components (obesity, dyslipidaemia, dysglycaemia) or MetS associated abnormalities not included in MetS diagnostic criteria (renal dysfunction, hyperuricaemia, hypercoaglutability, menopause, non alcoholic fatty liver disease, and obstructive sleep apnea) have been implicated too. We discuss the evidence connecting these cardio-metabolic risk factors, which negatively affect AS and finally increase CVD risk. Furthermore, we discuss the impact of possible lifestyle and pharmacological interventions on all these cardio-metabolic risk factors, in an effort to reduce CVD risk and identify features that should be taken into consideration when treating MetS patients with or without arterial hypertension.
Highlights
Arterial compliance plays a key role in the function of the cardiovascular system, given the intermittent contraction of left ventricle (LV) and the endless need of organs and tissues for oxygen and nutrients [1]
Decreases in aortic pulse wave velocity (PWV) with exercise intervention are related to the corresponding changes in baPWV [12]. These results suggest that baPWV may provide qualitatively similar information to those derived from aortic PWV, a well-established index of central arterial stiffness
The renin-angiotensin-aldosterone system (RAAS) is activated in the diseased vascular beds, with up regulation of the angiotensin II type 1 receptor (AT1R). This results in arterial hypertension, which is a component of metabolic syndrome (MetS), while the increased AT1R mediated activity in the vasculature is central to the development of increased Arterial stiffness (AS), which is further deteriorates insulin resistance (IR) within a vicious cycle [22]
Summary
Athyros *, Andromachi Reklou, Antonis Lazarides, Eudoxia Mitsiou and Asterios Karagiannis. Received: 20 June 2013; in revised form: 9 November 2013 / Accepted: 14 November 2013 /
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