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Rosiglitazone influences adipose tissue distribution without deleterious impact on heart rate variability in coronary heart disease patients with type 2 diabetes

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Abstract

Introduction

Obesity is associated with decreased heart rate variability (HRV). Rosiglitazone, a PPARγ agonist, is generally associated with increases in body mass.

Purpose

To assess whether the gain in body mass and adiposity expected from rosiglitazone treatment has an influence on HRV in patients with type 2 diabetes and coronary artery disease.

Methods

One hundred and twenty-five patients with type 2 diabetes and coronary artery disease aged between 40 and 75 years were studied. Anthropometric measurements: (1) body mass index (BMI), (2) waist circumference (WC), (3) abdominal computed tomography (CT) scan, and HRV (using a 24 h Holter) were measured at baseline and after 12 months of treatment. Patients were randomized to rosiglitazone or placebo regimen.

Results

In the rosiglitazone vs. placebo group, there were significant increases in body mass [3.5 (2.6;4.4); mean (95 % CI) vs. 0.2 (−0.4;0.8)] kg), BMI [1.3 (1.0;1.6) vs. 0.1 (−0.1;0.3) kg/m2], WC [2.1 (0.9;3.3) vs. 0.4 (−0.4;1.2) cm, all p ≤ 0.001] and subcutaneous adipose tissue [253 (187;319) vs. 6 (−24;36) cm3, p ≤ 0.001] without statistically significant changes in visceral adipose tissue [−22 (−91;47) vs. 57 (43;71) cm3, p = 0.546], respectively. There was no change in HRV in either group after 12 months. There were no correlations between changes in HRV variables and fat distribution.

Conclusion

Our results suggest that changes in adiposity indices observed after 12 months of rosiglitazone therapy have no deleterious influence on HRV in patients with type 2 diabetes and coronary artery disease.

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Abbreviations

HRV:

Heart rate variability

PPARγ:

Peroxisome proliferator-activated receptor gamma

BMI:

Body mass index

WC:

Waist circumference

CT:

Computed tomography

CVD:

Cardiovascular disease

VAT:

Visceral adipose tissue

SAT:

Subcutaneous adipose tissue

SNS:

Sympathetic nervous system

PNS:

Parasympathetic nervous system

T2D:

Type 2 diabetes

TZD:

Sthiazolidinediones

VICTORY:

VeIn Coronary aTherOsclerosis and Rosiglitazone after bypass surgerY

CABG:

Coronary artery bypass graft surgery

HbAlc :

Glycated hemoglobin

NYHA:

New York Heart Association

DEXA:

Dual-energy X-ray absorptiometry

LDL-C:

Low-density lipoprotein cholesterol

HDL-C:

High-density lipoprotein cholesterol

CRP:

C-reactive protein

FFA:

Free fatty acids

TNF-α:

Tumor necrosis factor α

Il-6:

Interleukine 6

SDNN:

Standard deviation of all normal-to-normal (NN) interval

SDANN:

Standard deviation of the averages of NN intervals in all 5 min segments of the entire recording

rMSSD:

Square root of the mean of the squared differences between adjacent NN intervals

NN50:

Number of pairs of adjacent NN intervals differing by more than 50 ms in the entire recording

pNN50:

NN50 divided by the total number or all NN intervals

VLF:

Very low frequencies

LF:

Low frequencies

HF:

High frequencies

CI:

Confidence interval of 95 %

TG:

Triglycerides

HOMA-IR:

Homeostasis model assessment of insulin resistance

ACE:

Angiotensin-converting enzyme

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Acknowledgments

VICTORY was designed and executed as an investigator-initiated trial and supported by an unrestricted grant from GlaxoSmithKline. This clinical study have been approved by the ethics committee of Institut universitaire de cardiologie et de pneumologie de Québec. The authors thank the staff and the patients from VICTORY trial for their important contribution. Dr. JP Després is the scientific director of the International Chair on Cardiometabolic Risk. Dr. P Poirier is a clinician-research scholar from the Fonds de la Recherche du Québec-Santé (FRQS). Dr. P Brassard is a Junior 1 research scholar from the FRQS.

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Grenier, A., Brassard, P., Bertrand, O.F. et al. Rosiglitazone influences adipose tissue distribution without deleterious impact on heart rate variability in coronary heart disease patients with type 2 diabetes. Clin Auton Res 26, 407–414 (2016). https://doi.org/10.1007/s10286-016-0373-7

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  • DOI: https://doi.org/10.1007/s10286-016-0373-7

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