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1.  Association of hypertension status and cardiovascular risks with sympathovagal imbalance in first degree relatives of type 2 diabetics 
Abstract
Aims/Introduction
As reports show cardiovascular (CV) risks in first‐degree relatives (FDR) of type 2 diabetics, and autonomic imbalance predisposing to CV risks, in the present study we have assessed the contribution of sympathovagal imbalance (SVI) to CV risks in these subjects.
Materials and Methods
Body mass index (BMI), waist‐to‐hip ratio (WHR), basal heart rate (BHR), blood pressure (BP), rate pressure product (RPP), and spectral indices of heart rate variability (HRV) were reordered and analyzed in FDR of type 2 diabetics (study group, n = 293) and in subjects with no family history of diabetes (control group, n = 405).
Results
The ratio of low‐frequency (LF) to high‐frequency (HF) power of HRV (LF–HF), a sensitive marker of SVI, was significantly increased (P < 0.001) in the study group compared with the control group. The SVI in the study group was due to concomitant sympathetic activation (increased LF) and vagal inhibition (decreased HF). In the study group, the LF–HF ratio was significantly correlated with BMI, WHR, BHR, BP and RPP. Multiple regression analysis showed an independent contribution of LF–HF to hypertension status (P = 0.000), and bivariate logistic regression showed significant prediction (odds ratio 2.16, confidence interval 1.130–5.115) of LF–HF to increased RPP, the marker of CV risk, in the study group.
Conclusions
Sympathovagal imbalance in the form of increased sympathetic and decreased parasympathetic activity is present in FDR of type 2 diabetics. Increased resting heart rate, elevated hypertension status, decreased HRV and increased RPP in these subjects make them vulnerable to CV risks. SVI in these subjects contributes to CV risks independent of the degree of adiposity.
doi:10.1111/jdi.12166
PMCID: PMC4210069  PMID: 25411606
Autonomic imbalance; Cardiovascular risk; First‐degree relatives of type 2 diabetics
2.  Slow Yogic Breathing Through Right and Left Nostril Influences Sympathovagal Balance, Heart Rate Variability, and Cardiovascular Risks in Young Adults 
Background:
Specific nostril breathing is known to influence autonomic functions.
Aim:
The study was to assess the effects of right nostril breathing (RNB) and left nostril breathing (LNB) on heart rate variability (HRV) and cardiovascular functions.
Material and Methods:
Eighty-five student volunteers were divided into three groups: RNB group (n = 30), LNB group (n = 30), and control group (n = 25). RNB and LNB group subjects practiced right and left nostril breathing, respectively, every day 1 h for 6 weeks. The control group did not practice nostril breathing. Cardiovascular parameters and spectral indices of HRV were recorded before and after 6-week practice of nostril breathing. In RNB and LNB groups, prediction of rate-pressure product (RPP) by low-frequency to high-frequency ratio (LF-HF) of HRV was assessed by bivariate logistic regression.
Results:
HRV indices representing sympathetic activity were increased in the RNB group and indices representing parasympathetic activity were increased in LNB group following 6-week nostril breathing. Prediction of LF-HF to RPP, the marker of cardiovascular risks, was more significant (OR 2.65, P = 0.005) in the LNB group compared to the RNB group (OR 1.452, P = 0.016).
Conclusions:
Short-term practice of LNB improves vagal tone, increases HRV, and promotes cardiovascular health of medical students. Practice of RNB increases sympathetic tone and could jeopardize cardiovascular health.
doi:10.4103/1947-2714.128477
PMCID: PMC3978938  PMID: 24741554
Autonomic functions; Cardiovascular risk; Heart rate variability; Nostril breathing; Sympathovagal balance
3.  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 
PLoS ONE  2013;8(11):e78072.
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.
doi:10.1371/journal.pone.0078072
PMCID: PMC3827034  PMID: 24265679
4.  Association of Sympathovagal Imbalance with Cardiovascular Risks in Overt Hypothyroidism 
Background:
Cardiovascular morbidities have been reported in hypothyroidism.
Aims:
The objective of this study is to investigate the link of sympathovagal imbalance (SVI) to cardiovascular risks (CVRs) and the plausible mechanisms of CVR in hypothyroidism.
Materials and Methods:
Age-matched 104 females (50 controls, 54 hypothyroids) were recruited and their body mass index (BMI), cardiovascular parameters, autonomic function tests by spectral analysis of heart rate variability (HRV), heart rate response to standing, deep breathing and blood pressure response to isometric handgrip were studied. Thyroid profile, lipid profile, immunological and inflammatory markers were estimated and their association with low-frequency to the high-frequency ratio (LF-HF) of HRV, the marker of SVI was assessed by multivariate regression.
Results:
Increased diastolic pressure, decreased HRV, increased LF-HF, dyslipidemia and increased high-sensitive C-reactive protein (hsCRP) were observed in hypothyroid patients and all these parameters had significant correlation with LF-HF. BMI had no significant association with LF-HF. Atherogenic index (β 1.144, P = 0.001) and hsCRP (b 0.578, P = 0.009) had independent contribution to LF-HF. LF-HF could significantly predict hypertension status (odds ratio 2.05, confidence interval 1.110-5.352, P = 0.008) in hypothyroid subjects.
Conclusions:
SVI due to sympathetic activation and vagal withdrawal occurs in hypothyroidism. Dyslipidemia and low-grade inflammation, but not obesity contribute to SVI and SVI contributes to cardiovascular risks.
doi:10.4103/1947-2714.118921
PMCID: PMC3818829  PMID: 24251274
Autonomic imbalance; Body mass index; Cardiovascular risks; Dyslipidemia; High-sensitive C-reactive protein; Hypothyroidism; Sympathovagal imbalance
5.  Body mass index contributes to sympathovagal imbalance in prehypertensives 
Background
The present study was conducted to assess the nature of sympathovagal imbalance (SVI) in prehypertensives by short-term analysis of heart rate variability (HRV) to understand the alteration in autonomic modulation and the contribution of BMI to SVI in the genesis of prehypertension.
Methods
Body mass index (BMI), basal heart rate (BHR), blood pressure (BP), rate pressure product (RPP) and HRV indices such as total power (TP), low-frequency power (LF), normalized LF (LFnu), high-frequency power (HF), normalized HF (HFnu), LF-HF ratio, mean heart rate (mean RR), square root of the mean squared differences of successive normal to normal intervals (RMSSD), standard deviation of normal to normal RR interval (SDNN), the number of interval differences of successive NN intervals greater than 50 ms (NN50) and the proportion derived by dividing NN50 by the total number of NN intervals (pNN50) were assessed in three groups of subjects: normotensives having normal BMI (Group 1), prehypertensives having normal BMI (Group 2) and prehypertensives having higher BMI (Group 3). SVI was assessed from LF-HF ratio and correlated with BMI, BHR, BP and RPP in all the groups by Pearson correlation. The contribution of BMI to SVI was assessed by multiple regression analysis.
Results
LF and LFnu were significantly increased and HF and HFnu were significantly decreased in prehypertensive subjects in comparison to normotensive subjects and the magnitude of these changes was more prominent in subjects with higher BMI compared to that of normal BMI. LF-HF ratio, the sensitive indicator of sympathovagal balance had significant correlation with BMI (P = 0.000) and diastolic blood pressure (DBP) (P = 0.002) in prehypertensives. BMI was found to be an independent contributing factor to SVI (P = 0.001) in prehypertensives.
Conclusions
It was concluded that autonomic imbalance in prehypertensives manifested in the form of increased sympathetic activity and vagal inhibition. In prehypertensives with higher BMI, vagal withdrawal was predominant than sympathetic overactivity. Magnitude of SVI (alteration in LF-HF ratio) was linked to changes in BMI and DBP. BMI had an independent influence on LF-HF ratio. It was advised that life-style modifications such as yoga and exercise would enable achieve the sympathovagal balance and blood pressure homeostasis in prehypertensives.
doi:10.1186/1471-2261-12-54
PMCID: PMC3441642  PMID: 22812583
Prehypertension; Heart rate variability; Body mass index; Sympathovagal imbalance; LF-HF ratio
6.  Sympathovagal Imbalance in Prehypertensive Offspring of Two Parents versus One Parent Hypertensive 
Objective. Though prehypertension has strong familial predisposition, difference in pathophysiological mechanisms in its genesis in offspring of both parents and single parent hypertensive have not been elucidated. Methods. Body mass index (BMI), waist-hip ratio (WHR), basal heart rate (BHR), blood pressure (BP), HR and BP response to standing, deep breathing difference, BP response to handgrip and spectral indices of heart rate variability (HRV) were analyzed in normotensive offspring of two parents hypertensive (Group I), normotensive offspring of one parent hypertensive (Group II), prehypertensive offspring of two parents hypertensive (Group III) and prehypertensive offspring of one parent hypertensive (Group IV). Results. Sympathovagal imbalance (SVI) in prehypertensive offspring was observed due to increased sympathetic and decreased vagal activity. In group III, SVI was more prominent with greater contribution by vagal withdrawal. LF-HF ratio, the marker of SVI was correlated more with diastolic pressure, 30 : 15 ratio and E : I ratio in prehypertensives and the degree of correlation was more in group III prehypertensives. Conclusion. Vagal withdrawal plays a critical role in development of SVI in prehypertensive offspring of hypertensive parents. The intensity of SVI was more in offspring of two parents hypertensive compared to single parent hypertensive.
doi:10.4061/2011/263170
PMCID: PMC3202093  PMID: 22121472
7.  Vagal Withdrawal and Sympathetic Overactivity Contribute to the Genesis of Early-Onset Pregnancy-Induced Hypertension 
Objective. In this study, we have assessed sympathovagal imbalance (SVI) by spectral analysis of heart rate variability (HRV) that contributes to the genesis of early-onset PIH. Methods. Body mass index (BMI), basal heart rate (BHR), blood pressure (BP) and HRV indices such as LFnu, HFnu, LF-HF ratio, mean RR, SDNN and RMSSD were assessed in normal pregnant women (Control group) and pregnant women having risk factors for PIH (Study group) at all the trimesters pregnancy. Retrospectively, those who did not develop PIH (Study group I) were separated from those who developed PIH (Study group II). Study group II was subdivided into early-onset and late-onset PIH. Sympathovagal balance (LF-HF ratio) was correlated with BMI, BHR and BP. Results. LF-HF ratio was significantly high in study group II compared to study group I and control group, and in early-onset PIH group compared to the late-onset category at all the trimesters of pregnancy, which was significantly correlated with BHR and BP. Alteration in HFnu in early-onset category was more prominent than the alteration in LFnu. Conclusion. Though the SVI in PIH is contributed by both sympathetic overactivity and vagal withdrawal, especially in early-onset type, SVI is mainly due to vagal inhibition.
doi:10.4061/2011/361417
PMCID: PMC3095942  PMID: 21629868

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