Circadian rhythm in QT interval is preserved in mice deficient of potassium channel interacting protein 2

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Standard

Circadian rhythm in QT interval is preserved in mice deficient of potassium channel interacting protein 2. / Gottlieb, Lisa A; Lubberding, Anniek; Larsen, Anders Peter; Thomsen, Morten B.

I: Chronobiology International, Bind 34, Nr. 1, 01.2017, s. 45-56.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Gottlieb, LA, Lubberding, A, Larsen, AP & Thomsen, MB 2017, 'Circadian rhythm in QT interval is preserved in mice deficient of potassium channel interacting protein 2', Chronobiology International, bind 34, nr. 1, s. 45-56. https://doi.org/10.1080/07420528.2016.1225074

APA

Gottlieb, L. A., Lubberding, A., Larsen, A. P., & Thomsen, M. B. (2017). Circadian rhythm in QT interval is preserved in mice deficient of potassium channel interacting protein 2. Chronobiology International, 34(1), 45-56. https://doi.org/10.1080/07420528.2016.1225074

Vancouver

Gottlieb LA, Lubberding A, Larsen AP, Thomsen MB. Circadian rhythm in QT interval is preserved in mice deficient of potassium channel interacting protein 2. Chronobiology International. 2017 jan.;34(1):45-56. https://doi.org/10.1080/07420528.2016.1225074

Author

Gottlieb, Lisa A ; Lubberding, Anniek ; Larsen, Anders Peter ; Thomsen, Morten B. / Circadian rhythm in QT interval is preserved in mice deficient of potassium channel interacting protein 2. I: Chronobiology International. 2017 ; Bind 34, Nr. 1. s. 45-56.

Bibtex

@article{a4efc78df5fc48ff855d0e3747ae0ee9,
title = "Circadian rhythm in QT interval is preserved in mice deficient of potassium channel interacting protein 2",
abstract = "Potassium Channel Interacting Protein 2 (KChIP2) is suggested to be responsible for the circadian rhythm in repolarization duration, ventricular arrhythmias, and sudden cardiac death. We investigated the hypothesis that there is no circadian rhythm in QT interval in the absence of KChIP2. Implanted telemetric devices recorded electrocardiogram continuously for 5 days in conscious wild-type mice (WT, n = 9) and KChIP2(-/-) mice (n = 9) in light:dark periods and in complete darkness. QT intervals were determined from all RR intervals and corrected for heart rate (QT100 = QT/(RR/100)(1/2)). Moreover, QT intervals were determined from complexes within the RR range of mean-RR ± 1% in the individual mouse (QTmean-RR). We find that RR intervals are 125 ± 5 ms in WT and 123 ± 4 ms in KChIP2(-/-) (p = 0.81), and QT intervals are 52 ± 1 and 52 ± 1 ms, respectively(p = 0.89). No ventricular arrhythmias or sudden cardiac deaths were observed. We find similar diurnal (light:dark) and circadian (darkness) rhythms of RR intervals in WT and KChIP2(-/-) mice. Circadian rhythms in QT100 intervals are present in both groups, but at physiological small amplitudes: 1.6 ± 0.2 and 1.0 ± 0.3 ms in WT and KChIP2(-/-), respectively (p = 0.15). A diurnal rhythm in QT100 intervals was only found in WT mice. QTmean-RR intervals display clear diurnal and circadian rhythms in both WT and KChIP2(-/-). The amplitude of the circadian rhythm in QTmean-RR is 4.0 ± 0.3 and 3.1 ± 0.5 ms in WT and KChIP2(-/-), respectively (p = 0.16). In conclusion, KChIP2 expression does not appear to underlie the circadian rhythm in repolarization duration.",
author = "Gottlieb, {Lisa A} and Anniek Lubberding and Larsen, {Anders Peter} and Thomsen, {Morten B}",
year = "2017",
month = jan,
doi = "10.1080/07420528.2016.1225074",
language = "English",
volume = "34",
pages = "45--56",
journal = "Chronobiology International",
issn = "0742-0528",
publisher = "Taylor & Francis",
number = "1",

}

RIS

TY - JOUR

T1 - Circadian rhythm in QT interval is preserved in mice deficient of potassium channel interacting protein 2

AU - Gottlieb, Lisa A

AU - Lubberding, Anniek

AU - Larsen, Anders Peter

AU - Thomsen, Morten B

PY - 2017/1

Y1 - 2017/1

N2 - Potassium Channel Interacting Protein 2 (KChIP2) is suggested to be responsible for the circadian rhythm in repolarization duration, ventricular arrhythmias, and sudden cardiac death. We investigated the hypothesis that there is no circadian rhythm in QT interval in the absence of KChIP2. Implanted telemetric devices recorded electrocardiogram continuously for 5 days in conscious wild-type mice (WT, n = 9) and KChIP2(-/-) mice (n = 9) in light:dark periods and in complete darkness. QT intervals were determined from all RR intervals and corrected for heart rate (QT100 = QT/(RR/100)(1/2)). Moreover, QT intervals were determined from complexes within the RR range of mean-RR ± 1% in the individual mouse (QTmean-RR). We find that RR intervals are 125 ± 5 ms in WT and 123 ± 4 ms in KChIP2(-/-) (p = 0.81), and QT intervals are 52 ± 1 and 52 ± 1 ms, respectively(p = 0.89). No ventricular arrhythmias or sudden cardiac deaths were observed. We find similar diurnal (light:dark) and circadian (darkness) rhythms of RR intervals in WT and KChIP2(-/-) mice. Circadian rhythms in QT100 intervals are present in both groups, but at physiological small amplitudes: 1.6 ± 0.2 and 1.0 ± 0.3 ms in WT and KChIP2(-/-), respectively (p = 0.15). A diurnal rhythm in QT100 intervals was only found in WT mice. QTmean-RR intervals display clear diurnal and circadian rhythms in both WT and KChIP2(-/-). The amplitude of the circadian rhythm in QTmean-RR is 4.0 ± 0.3 and 3.1 ± 0.5 ms in WT and KChIP2(-/-), respectively (p = 0.16). In conclusion, KChIP2 expression does not appear to underlie the circadian rhythm in repolarization duration.

AB - Potassium Channel Interacting Protein 2 (KChIP2) is suggested to be responsible for the circadian rhythm in repolarization duration, ventricular arrhythmias, and sudden cardiac death. We investigated the hypothesis that there is no circadian rhythm in QT interval in the absence of KChIP2. Implanted telemetric devices recorded electrocardiogram continuously for 5 days in conscious wild-type mice (WT, n = 9) and KChIP2(-/-) mice (n = 9) in light:dark periods and in complete darkness. QT intervals were determined from all RR intervals and corrected for heart rate (QT100 = QT/(RR/100)(1/2)). Moreover, QT intervals were determined from complexes within the RR range of mean-RR ± 1% in the individual mouse (QTmean-RR). We find that RR intervals are 125 ± 5 ms in WT and 123 ± 4 ms in KChIP2(-/-) (p = 0.81), and QT intervals are 52 ± 1 and 52 ± 1 ms, respectively(p = 0.89). No ventricular arrhythmias or sudden cardiac deaths were observed. We find similar diurnal (light:dark) and circadian (darkness) rhythms of RR intervals in WT and KChIP2(-/-) mice. Circadian rhythms in QT100 intervals are present in both groups, but at physiological small amplitudes: 1.6 ± 0.2 and 1.0 ± 0.3 ms in WT and KChIP2(-/-), respectively (p = 0.15). A diurnal rhythm in QT100 intervals was only found in WT mice. QTmean-RR intervals display clear diurnal and circadian rhythms in both WT and KChIP2(-/-). The amplitude of the circadian rhythm in QTmean-RR is 4.0 ± 0.3 and 3.1 ± 0.5 ms in WT and KChIP2(-/-), respectively (p = 0.16). In conclusion, KChIP2 expression does not appear to underlie the circadian rhythm in repolarization duration.

U2 - 10.1080/07420528.2016.1225074

DO - 10.1080/07420528.2016.1225074

M3 - Journal article

C2 - 27736193

VL - 34

SP - 45

EP - 56

JO - Chronobiology International

JF - Chronobiology International

SN - 0742-0528

IS - 1

ER -

ID: 167473778