Insulin Resistance Impairs Arterial Stiffness and Peripheral Vascular Resistance in Metabolic Syndrome Patients

Abstract

Besides autonomic alterations, metabolic syndrome (MetS) causes changes in the vascular system directly related to cardiovascular events and death. Since insulin resistance is strongly associated with sympathetic hiperactivation, we tested the hypothesis that the presence of impaired fasting glucose (IFG) is the main cause of structural and functional worsening on large and small vessels. Never treated, newly diagnosed MetS (ATP‐III) patients were divided into: fasting glucose >100mg/dL (MetS+IFG, n=28, 49.1±1.3 yrs) and fasting glucose <100mg/dL (MetS‐IFG, n=22, 46.1±1.4 yrs). A healthy control group was also involved (C, n=17, 49.6±1.4 yrs). We measured the arterial stiffness (PWV, pulse wave velocity), muscle sympathetic nerve activity (MSNA, microneurography), forearm blood flow (plethysmography), mean blood pressure (MBP, oscillometric), and peripheral vascular resistance (VR=MBP/forearm blood flow). MetS+IFG had similar PWV vs. MetS‐IFG, but had higher PWV than C (9.6±0.3, 9.1±0.2, and 8.7±0.2, P=0.02). Similarly, MetS+IFG had no different VR vs. MetS‐IFG, albeit had higher VR vs. C group (72.1±3.9, 57.5±5.4 and 47.4±9.2, P=0.01). Further analysis showed that PWV was correlated with MSNA (R=0.47; P<0.01). In conclusion, sympathetic hyperactivation may be, at least partially, the base mechanism that increase arterial stiffness. Impaired fasting glucose appears to be the main factor to aggravate the cardiovascular risk in metabolic syndrome patients.