Arterial function in cardio-metabolic diseases: from the microcirculation to the large conduits.

The metabolic syndrome (MetS) is characterized as a constellation of metabolic risk factors such as obesity, hypertension, dyslipidemia, and hyperglycemia that co-occur within a given individual. This consultation of risk factors exposes MetS to a 3-fold increased risk of cardiovascular disease and an even higher risk of developing type 2 diabetes compared to healthy individuals. The pathophysiological mechanisms underlying this increased cardiovascular risk are incompletely understood but likely include alterations to macro- and micro-vasculature. The vasculature plays an important role not only in delivery and adjusting the quantity of blood delivered to the tissues, but the dynamic changes in structure and compliance significantly alter the hemodynamic stress imposed on the heart and end-organs. This review will give an overview of the pathophysiological changes to the vasculature that accompany MetS in both human and animal models, as well as the possible mechanistic pathways.