What is the clinical evidence from this study?

Study design: Cross-Sectional. Population: First-degree relatives of type 2 diabetics (n=176). Intervention: First-degree relative of type 2 diabetic vs. No family history of diabetes. Primary outcome: LF-HF ratio (marker of sympathovagal imbalance) (p=<0.0001).

November 12, 2013PLoS ONE65 citationsOpen Access

Sympathovagal Imbalance Contributes to Prehypertension Status and Cardiovascular Risks Attributed by Insulin Resistance, Inflammation, Dyslipidemia and Oxidative Stress in First Degree Relatives of Type 2 Diabetics

Q: What are the key findings of this study?

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.

GPGopal Krushna Pal CAChandrasekaran Adithan PAPalghat Hariharan Ananthanarayanan

Key Result

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.

Study Design

Type

Cross-Sectional (n=176)

Blinding

Single-blind

Multicenter

Structured PICO

Does sympathovagal imbalance contribute to cardiovascular risks and prehypertension in first-degree relatives of type 2 diabetics?

Population

176 healthy young adults, including 72 first-degree relatives of type 2 diabetics and 104 controls without a family history, evaluated for sympathovagal imbalance and cardiovascular risks.

Comparator

Subjects with no family history of diabetes (n=104)

Outcome

Association of sympathovagal imbalance (LF-HF ratio) with prehypertension status and rate-pressure productsurrogate

Sympathovagal imbalance, characterized by sympathetic activation and vagal withdrawal, independently contributes to prehypertension and cardiovascular risk in first-degree relatives of type 2 diabetics.

Main Result

Absolute Event Rate: 1.41% vs 0.67%

p-value: p=<0.0001

Limitations

Did not assess cardiovascular functions by continuous blood pressure variability analysis to determine cardiovascular reactivity and dysfunction
Did not estimate plasma norepinephrine or its metabolites in urine to support sympathovagal imbalance
Did not perform analysis of body fat composition to assess the influence of visceral fat on sympathovagal imbalance

Abstract

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.

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