Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice

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Standard

Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice. / Soltysinska, Ewa; Speerschneider, Tobias; Winther, Sine V; Thomsen, Morten Bækgaard.

I: Cardiovascular Diabetology, Bind 13, Nr. 1, 122, 12.08.2014, s. 1-11.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Soltysinska, E, Speerschneider, T, Winther, SV & Thomsen, MB 2014, 'Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice', Cardiovascular Diabetology, bind 13, nr. 1, 122, s. 1-11. https://doi.org/10.1186/s12933-014-0122-y

APA

Soltysinska, E., Speerschneider, T., Winther, S. V., & Thomsen, M. B. (2014). Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice. Cardiovascular Diabetology, 13(1), 1-11. [122]. https://doi.org/10.1186/s12933-014-0122-y

Vancouver

Soltysinska E, Speerschneider T, Winther SV, Thomsen MB. Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice. Cardiovascular Diabetology. 2014 aug. 12;13(1):1-11. 122. https://doi.org/10.1186/s12933-014-0122-y

Author

Soltysinska, Ewa ; Speerschneider, Tobias ; Winther, Sine V ; Thomsen, Morten Bækgaard. / Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice. I: Cardiovascular Diabetology. 2014 ; Bind 13, Nr. 1. s. 1-11.

Bibtex

@article{3e408d7267a7460cb4b17de668036cb1,
title = "Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice",
abstract = "Background: The aim of this study was to probe cardiac complications, including heart-rate control, in a mouse model of type-2 diabetes. Heart-rate development in diabetic patients is not straight forward: In general, patients with diabetes have faster heart rates compared to non-diabetic individuals, yet diabetic patients are frequently found among patients treated for slow heart rates. Hence, we hypothesized that sinoatrial node (SAN) dysfunction could contribute to our understanding the mechanism behind this conundrum and the consequences thereof.MethodsCardiac hemodynamic and electrophysiological characteristics were investigated in diabetic db/db and control db/+mice.ResultsWe found improved contractile function and impaired filling dynamics of the heart in db/db mice, relative to db/+controls. Electrophysiologically, we observed comparable heart rates in the two mouse groups, but SAN recovery time was prolonged in diabetic mice. Adrenoreceptor stimulation increased heart rate in all mice and elicited cardiac arrhythmias in db/db mice only. The arrhythmias emanated from the SAN and were characterized by large RR fluctuations. Moreover, nerve density was reduced in the SAN region.ConclusionsEnhanced systolic function and reduced diastolic function indicates early ventricular remodeling in obese and diabetic mice. They have SAN dysfunction, and adrenoreceptor stimulation triggers cardiac arrhythmia originating in the SAN. Thus, dysfunction of the intrinsic cardiac pacemaker and remodeling of the autonomic nervous system may conspire to increase cardiac mortality in diabetic patients.",
author = "Ewa Soltysinska and Tobias Speerschneider and Winther, {Sine V} and Thomsen, {Morten B{\ae}kgaard}",
year = "2014",
month = aug,
day = "12",
doi = "10.1186/s12933-014-0122-y",
language = "English",
volume = "13",
pages = "1--11",
journal = "Cardiovascular Diabetology",
issn = "1475-2840",
publisher = "BioMed Central Ltd.",
number = "1",

}

RIS

TY - JOUR

T1 - Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice

AU - Soltysinska, Ewa

AU - Speerschneider, Tobias

AU - Winther, Sine V

AU - Thomsen, Morten Bækgaard

PY - 2014/8/12

Y1 - 2014/8/12

N2 - Background: The aim of this study was to probe cardiac complications, including heart-rate control, in a mouse model of type-2 diabetes. Heart-rate development in diabetic patients is not straight forward: In general, patients with diabetes have faster heart rates compared to non-diabetic individuals, yet diabetic patients are frequently found among patients treated for slow heart rates. Hence, we hypothesized that sinoatrial node (SAN) dysfunction could contribute to our understanding the mechanism behind this conundrum and the consequences thereof.MethodsCardiac hemodynamic and electrophysiological characteristics were investigated in diabetic db/db and control db/+mice.ResultsWe found improved contractile function and impaired filling dynamics of the heart in db/db mice, relative to db/+controls. Electrophysiologically, we observed comparable heart rates in the two mouse groups, but SAN recovery time was prolonged in diabetic mice. Adrenoreceptor stimulation increased heart rate in all mice and elicited cardiac arrhythmias in db/db mice only. The arrhythmias emanated from the SAN and were characterized by large RR fluctuations. Moreover, nerve density was reduced in the SAN region.ConclusionsEnhanced systolic function and reduced diastolic function indicates early ventricular remodeling in obese and diabetic mice. They have SAN dysfunction, and adrenoreceptor stimulation triggers cardiac arrhythmia originating in the SAN. Thus, dysfunction of the intrinsic cardiac pacemaker and remodeling of the autonomic nervous system may conspire to increase cardiac mortality in diabetic patients.

AB - Background: The aim of this study was to probe cardiac complications, including heart-rate control, in a mouse model of type-2 diabetes. Heart-rate development in diabetic patients is not straight forward: In general, patients with diabetes have faster heart rates compared to non-diabetic individuals, yet diabetic patients are frequently found among patients treated for slow heart rates. Hence, we hypothesized that sinoatrial node (SAN) dysfunction could contribute to our understanding the mechanism behind this conundrum and the consequences thereof.MethodsCardiac hemodynamic and electrophysiological characteristics were investigated in diabetic db/db and control db/+mice.ResultsWe found improved contractile function and impaired filling dynamics of the heart in db/db mice, relative to db/+controls. Electrophysiologically, we observed comparable heart rates in the two mouse groups, but SAN recovery time was prolonged in diabetic mice. Adrenoreceptor stimulation increased heart rate in all mice and elicited cardiac arrhythmias in db/db mice only. The arrhythmias emanated from the SAN and were characterized by large RR fluctuations. Moreover, nerve density was reduced in the SAN region.ConclusionsEnhanced systolic function and reduced diastolic function indicates early ventricular remodeling in obese and diabetic mice. They have SAN dysfunction, and adrenoreceptor stimulation triggers cardiac arrhythmia originating in the SAN. Thus, dysfunction of the intrinsic cardiac pacemaker and remodeling of the autonomic nervous system may conspire to increase cardiac mortality in diabetic patients.

U2 - 10.1186/s12933-014-0122-y

DO - 10.1186/s12933-014-0122-y

M3 - Journal article

C2 - 25113792

VL - 13

SP - 1

EP - 11

JO - Cardiovascular Diabetology

JF - Cardiovascular Diabetology

SN - 1475-2840

IS - 1

M1 - 122

ER -

ID: 124321361