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• W1973719005 abstract "Objective To assess the relationship between insulin resistance and baroreflex gain (BRS) in the context of the metabolic syndrome. Design Observational population study. Patients We studied the healthy population of a small Mediterranean island (Linosa, about 0.5 square miles, 450 inhabitants) where genetic, psychosocial and behavioral bias is likely to be minimal for historical and social reasons. Measures Baroreflex gain (BRS, by the frequency domain α index) and indices of autonomic regulation of the sino-atrial (SA) node derived from spectral analysis of RR interval variability were obtained, together with metabolic and behavioral indicators in the 144 participating subjects (age range 20–82 years). Carotid artery thickness (CCA) was also obtained with computer-aided ultrasound techniques. Insulin resistance was estimated by the homeostasis model assessment (HOMA), and subjects divided in tertiles accordingly. Results BRS appeared to be reduced progressively with increasing levels of HOMA (respectively, 21.0 ± 2.6, 17.7 ± 1.7, 15.7 ± 1.9 ms/mmHg, P < 0.03), while spectral indices of autonomic SA regulation appeared to be only insignificantly affected. Conversely, CCA was significantly increased with increasing HOMA (P < 0.024). Furthermore, BRS appeared to be significantly correlated with various elements of the metabolic syndrome, with CCA and abdominal obesity showing the strongest link. Conclusions In an otherwise healthy population, BRS, but not spectrally derived indices of SA node autonomic regulation, are progressively reduced with increasing severity of insulin resistance, possibly as a consequence of attendant carotid artery thickening." @default.
• W1973719005 created "2016-06-24" @default.
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• W1973719005 date "2006-02-01" @default.
• W1973719005 modified "2023-10-18" @default.
• W1973719005 title "Is reduced baroreflex gain a component of the metabolic syndrome? Insights from the LINOSA study" @default.
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• W1973719005 doi "https://doi.org/10.1097/01.hjh.0000202817.02836.9c" @default.
• W1973719005 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16508585" @default.
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