Cardiac arrhythmias are a major cause of morbidity and mortality worldwide. Although recent advances in cell-based models, including human-induced pluripotent stem cell-derived cardiomyocytes (iPSC-CM), are contributing to our understanding of electrophysiology and arrhythmia mechanisms, preclinical animal studies of cardiovascular disease remain a mainstay. Over the past several decades, animal models of cardiovascular disease have advanced our understanding of pathological remodeling, arrhythmia mechanisms, and drug effects and have led to major improvements in pacing and defibrillation therapies. There exist a variety of methodological approaches for the assessment of cardiac electrophysiology and a plethora of parameters may be assessed with each approach. This guidelines article will provide an overview of the strengths and limitations of several common techniques used to assess electrophysiology and arrhythmia mechanisms at the whole animal, whole heart, and tissue level with a focus on small animal models. We also define key electrophysiological parameters that should be assessed, along with their physiological underpinnings, and the best methods with which to assess these parameters.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Dec 2022|
Bibliographical noteFunding Information:
This work was supported by MAESTRIA Grant 965286 and British Heart Foundation Accelerator Award AA/18/2/34218, DZHK (to L.F.); National Institutes of Health (NIH) Grants R01HL136389, R01HL163277, and R01HL147108 (to N.L); NIH Grants R01HL139472 and R01HD108839 (to N.G.P.); NIH Grants R01HL153042 and R01HL141343 (to B.P.D.); Canadian Institutes of Health Research (CIHR) Grant MOP 342562, Natural Sciences and Engineering Research Council of Canada Grant RGPIN-2022-03150, Government of Canada’s New Frontiers in Research Fund NFRFE-2021-00219, and Heart and Stroke Foundation of Canada Grant G-22-0032127 (to T.A.Q.); CIHR Grants PJT166105 and PJT180474 and Heart and Stroke Foundation of Canada Grant G-22-0032033 (to R.A.R.); NIH Grants R01HL141214, R01HL139738, and R01HL146652 (to A.V.G.); NIH Grants R01HL156652 and R01HL135096 (to T.J.H.); NIH Grants R01HL146169, R01HL147279, and R01HL144157 (to M.W.K.); NIH Grant R01HL133127 and American Heart Association Basic Project Grant 18SFRN34230125 (to K.M.); Netherlands Cardio Vascular Research Initiative CVON (Dutch Heart Foundation, Dutch Federation of University Medical Centres, ZonMw, and Royal Netherlands Academy of Sciences) Grants CVON2018-30 PREDICT2 and CVON2015-12 eDETECT (to C.A.R.); NIH Grant R35HL144980 (to B.C.K.); NIH Grants R01HL138003, R01HL141855, and R01HL102298 (to S.P.); NIH Grants R01HL085727, R01HL085844, and R01HL137228 and VA Merit Review Grants I01 BX000576 and I01 CX001490 (to N.C.); NIH Grants R01HL130212 and R01HL163274 and Burroughs Wellcome Fund CAMS (1009884) (to S.L.R.); and NIH Grants R01HL111600 and OT2OD026580 (to C.M.R.).
L.F. has received institutional research grants and nonfinancial support from European Union, DFG, British Heart Foundation, Medical Research Council (UK), NIHR, and several biomedical companies. L.F. is listed as an inventor of two patents (Atrial Fibrillation Therapy WO 2015140571, Markers for Atrial Fibrillation WO 2016012783). None of the other authors has any conflicts of interest, financial or otherwise, to disclose.
Copyright © 2022 The Authors.
- cardiac electrophysiology
- small animals
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)