First-degree relatives of type 2 diabetics exhibited significantly higher sympathovagal imbalance compared to controls (LF-HF ratio 1.41 vs 0.67, p<0.0001), which independently predicted increased cardiovascular risk.
Cross-Sectional (n=176)
Single-blind
No
Does sympathovagal imbalance contribute to cardiovascular risks and prehypertension in first-degree relatives of type 2 diabetics?
Sympathovagal imbalance, characterized by sympathetic activation and vagal withdrawal, independently contributes to prehypertension and cardiovascular risk in first-degree relatives of type 2 diabetics.
Absolute Event Rate: 1.41% vs 0.67%
p-value: p=<0.0001
BACKGROUND: Though cardiovascular (CV) risks are reported in first-degree relatives (FDR) of type 2 diabetics, the pathophysiological mechanisms contributing to these risks are not known. We investigated the association of sympathovagal imbalance (SVI) with CV risks in these subjects. SUBJECTS AND METHODS: Body mass index (BMI), basal heart rate (BHR), blood pressure (BP), rate-pressure product (RPP), spectral indices of heart rate variability (HRV), autonomic function tests, insulin resistance (HOMA-IR), lipid profile, inflammatory markers, oxidative stress (OS) marker, rennin, thyroid profile and serum electrolytes were measured and analyzed in subjects of study group (FDR of type 2 diabetics, n = 72) and control group (subjects with no family history of diabetes, n = 104). RESULTS: BMI, BP, BHR, HOMA-IR, lipid profile, inflammatory and OS markers, renin, LF-HF (ratio of low-frequency to high-frequency power of HRV, a sensitive marker of SVI) were significantly increased (p<0.0001) in study group compared to the control group. SVI in study group was due to concomitant sympathetic activation and vagal inhibition. There was significant correlation and independent contribution of markers of insulin resistance, dyslipidemia, inflammation and OS to LF-HF ratio. Multiple-regression analysis demonstrated an independent contribution of LF-HF ratio to prehypertension status (standardized beta 0.415, p<0.001) and bivariate logistic-regression showed significant prediction (OR 2.40, CI 1.128-5.326, p = 0.002) of LF-HF ratio of HRV to increased RPP, the marker of CV risk, in study group. CONCLUSION: SVI in FDR of type 2 diabetics occurs due to sympathetic activation and vagal withdrawal. The SVI contributes to prehypertension status and CV risks caused by insulin resistance, dyslipidemia, inflammation and oxidative stress in FDR of type 2 diabetics.
Pal et al. (2013) conducted a cross-sectional in First-degree relatives of type 2 diabetics (n=176). First-degree relative of type 2 diabetic vs. No family history of diabetes was evaluated on LF-HF ratio (marker of sympathovagal imbalance) (p=<0.0001). First-degree relatives of type 2 diabetics exhibited significantly higher sympathovagal imbalance compared to controls (LF-HF ratio 1.41 vs 0.67, p<0.0001), which independently predicted increased cardiovascular risk.