Mechanisms Underlying Sinus Node Dysfunction in a Rat Model of Genetic Atrial Cardiomyopathy
<i>Myl4-p.E11K</i><sup><i>+/+</i></sup> mutation causes progressive SND with aging, as a result of extensive abnormalities in the underlying determinants of SAN function, including ion-channel properties, Ca<sup>2+</sup>-homeostasis, and SAN structure. These observations provide new insights into the mechanisms of SAN abnormality in atrial cardiomyopathy.
Authors
- Thomas Alexander Quinn (ORCID: https://orcid.org/0000-0002-2437-5785)
- Martin Mackasey
- Patrice Naud (ORCID: https://orcid.org/0009-0005-3733-1393)
- Jean‐Claude Tardif (ORCID: https://orcid.org/0000-0002-8200-8983)
- Deanna K. Sosnowski (ORCID: https://orcid.org/0000-0001-6557-6690)
- Stanley Nattel (ORCID: https://orcid.org/0000-0002-5565-3311)
- Martin G. Sirois (ORCID: https://orcid.org/0000-0002-6395-4587)
- Louis Villeneuve
- Édouard Marcoux (ORCID: https://orcid.org/0009-0005-1107-0033)
Institutions
- United States Nuclear Regulatory Commission (US)
- Dalhousie University (CA)
- Montreal Heart Institute (CA)
- McGill-Queen's University Press (CA)
- West German Heart and Vascular Center Essen (DE)
- McGill University (CA)
- Université de Montréal (CA)
Publication Details
- Journal
- Circulation Arrhythmia and Electrophysiology
- Published
- 2025-05-27
- DOI
- https://doi.org/10.1161/circep.124.013180
- Primary Topic
- Cardiomyopathy and Myosin Studies
- Type
- article
- Field-Weighted Citation Impact
- 0.00