RESUMEN
Metabolic syndrome (MetS) involves multi-factorial conditions linked to an elevated risk of type 2 diabetes mellitus and cardiovascular disease. Pre-metabolic syndrome (pre-MetS) possesses two MetS components but does not meet the MetS diagnostic criteria. Although cardiac autonomic derangements are evident in MetS, there is little information on their status in pre-MetS subjects. In this study, we sought to examine cardiac autonomic functions in pre-MetS and to determine which MetS component is more responsible for impaired cardiac autonomic functions. A total of 182 subjects were recruited and divided into healthy controls (n=89) and pre-MetS subjects (n=93) based on inclusion and exclusion criteria. We performed biochemical profiles on fasting blood samples to detect pre-MetS. Using standardized protocols, we evaluated anthropometric data, body composition, baroreflex sensitivity (BRS), heart rate variability (HRV), and autonomic function tests (AFTs). We further examined these parameters in pre-MetS subjects for each MetS component. Compared to healthy controls, we observed a significant cardiac autonomic dysfunction (CAD) through reduced BRS, lower overall HRV, and altered AFT parameters in pre-MetS subjects, accompanied by markedly varied anthropometric, clinical and biochemical parameters. Furthermore, all examined BRS, HRV, and AFT parameters exhibited an abnormal trend and significant correlation toward hyperglycemia. This study demonstrates CAD in pre-MetS subjects with reduced BRS, lower overall HRV, and altered AFT parameters. Hyperglycemia was considered an independent determinant of alterations in all the examined BRS, HRV, and AFT parameters. Thus, hyperglycemia may contribute to CAD in pre-MetS subjects before progressing to MetS.
RESUMEN
CONTEXT: Abdominal obesity (AO) is a definitive link between cardiometabolic complications and metabolic syndrome (MetS). Many traditional and novel anthropometric indices have been identified to determine AO, and their relationship to MetS has been investigated. However, whether these indices are useful in a clinical setting is unknown. Moreover, the cut-off points for these indices to determine MetS have yet to be defined among Southern-Indian adults. AIMS: We aimed to evaluate the cut-off values and clinical efficacy of novel anthropometric indices in identifying MetS and its components. MATERIALS AND METHODS: Subjects (n = 202) were recruited and then grouped into cases (MetS = 106) and controls (healthy = 96). We measured anthropometric data and assayed glycemic and lipid profiles. Using these, we computed a-body shape index (ABSI), abdominal volume index (AVI), body adiposity index (BAI), body roundness index (BRI), conicity index (CI), lipid-accumulation product (LAP), visceral adiposity index (VAI) and waist-triglyceride index (WTI) from published equations. RESULTS: Compared to the control group, all the novel anthropometric indices were noticeably higher in both male and female subjects of the MetS group. The area under the curve values (AUCs) demonstrated that BRI, CI, AVI, and WTI had superior detection power in identifying MetS, and the AUCs varied upon stratification by gender. BRI was strongly associated with the highest odds of having MetS (OR 66.03). CONCLUSIONS: The optimal cut-off and AUC values attained for BRI, CI, AVI, and WTI have a clinical approach in identifying MetS and its components. The efficacy of these indices to identify MetS differed by gender.
RESUMEN
BACKGROUND: Hypertension has been reported to cause impaired cardiovagal modulation and a wide variety of cognitive loss. However, the link cardiovagal modulation to neurocognitive impairment has not been studied yet. The present study has compared the link cardiovagal modulation to neurocognitive impairment between prehypertension and newly diagnosed hypertension in young adults. METHODS: One hundred forty-seven subjects (42 normotensives, 54 prehypertensives and 51 newly diagnosed hypertensives) aged between 18-44 years were included in this case-control study. The demographic, anthropometric, basal parameters, heart rate variability (HRV), cardiovascular autonomic function tests (CAFTs), event-related potential P300 and biochemical parameters were recorded in all the groups. Association of various parameters with neurocognitive deficit was studied by Pearson correlation analysis and independent contribution of various factors to cognitive deficit was assessed by multiple regression analysis in the study groups. RESULTS: Total power (TP) of HRV, the marker of cardiovagal modulation was reduced in both prehypertensives and hypertensives compared to controls. Among CAFTs, the ΔDBPIHG was increased, and 30:15 ratio and E:I ratio were decreased in both study groups. The latency of P300 (the marker of neurocognition) was significantly prolonged in prehypertensives and hypertensives and P300 latency was significantly associated with reduction in TP in both the groups. HOMA-IR was increased, and total oxidant capacity was decreased in prehypertensives and hypertensives, and both these parameters had independent contribution to P300. CONCLUSION: Prehypertensives had considerable autonomic imbalance, reduced cardiovagal modulation and neurocognitive deficit that were comparable to newly diagnosed hypertensives. Though the causal relationship between cardiovagal modulation and neurocognitive impairment can't be established from the findings of the present study, it appears that neurocognitive deficit might have some possible link to the decreased cardiovagal modulation and metabolic derangements in young prehypertensives and hypertensives.