What to consider for ECG in mice—with special emphasis on telemetry

Abstract

Genetically or surgically altered mice are commonly used as models of human cardiovascular diseases. Electrocardiography (ECG) is the gold standard to assess cardiac electrophysiology as well as to identify cardiac phenotypes and responses to pharmacological and surgical interventions. A variety of methods are used for mouse ECG acquisition under diverse conditions, making it difficult to compare different results. Non-invasive techniques allow only short-term data acquisition and are prone to stress or anesthesia related changes in cardiac activity. Telemetry offers continuous long-term acquisition of ECG data in conscious freely moving mice in their home cage environment. Additionally, it allows acquiring data 24/7 during different activities, can be combined with different challenges and most telemetry systems collect additional physiological parameters simultaneously. However, telemetry transmitters require surgical implantation, the equipment for data acquisition is relatively expensive and analysis of the vast number of ECG data is challenging and time-consuming. This review highlights the limits of non-invasive methods with respect to telemetry. In particular, primary screening using non-invasive methods can give a first hint; however, subtle cardiac phenotypes might be masked or compensated due to anesthesia and stress during these procedures. In addition, we detail the key differences between the mouse and human ECG. It is crucial to consider these differences when analyzing ECG data in order to properly translate the insights gained from murine models to human conditions.

Co and N2 Are No Humane Alternatives to Co2 Euthanasia in Rats.

“…Additionally, animals might experience discomfort due to bradycardia which occurred with CO 2 and iso urane before LOM. Animals in all groups presented arrhythmias before LOC 43 , which was faster with CO 2 . Chest pain has been reported in humans experiencing certain types of arrhythmias 44 .…”

Multi-level transcriptomic analysis ofLMNA-related dilated cardiomyopathy identifies disease-driving processes

“…First, unlike complete lamin A/C deletion, the reduction in lamin A/C protein levels mimics the reduced lamin levels frequently seen in clinical cases of LMNA-DCM 14,29,58,59 . Furthermore, the Lmna-cKO model closely recapitulates LMNA-DCM disease pathology, including ventricular wall thinning, impaired contractile function, and sudden cardiac death, although a definitive determination of the cause of death is difficult due to the lack of reliable ways to study arrhythmias in mice [86][87][88] . In addition, inducing lamin A/C depletion in adulthood allows for separating the effects of lamins on cardiac development from those on cardiac function.…”

Loss of protein phosphatase 2A regulatory subunit PPP2R5A is associated with increased incidence of stress-induced proarrhythmia

“…No standardized definition has yet been established for determining the duration of excitation recovery. In mice, the QRS complex is immediately followed by a positive J-wave, which is then followed by an often negative T-wave, particularly in anesthetized mice ( 22 , 23 ). Therefore, the so-called QT long time was determined ( 24 ).…”