<i>In vivo</i> temporal and spatial distribution of depolarization and repolarization and the illusive murine T wave

Liu, Gang; B., Iden, Jason,; Kovithavongs, Kay; Gulamhusein, Rashida; Duff, Henry J.; Kavanagh, Katherine M.

doi:10.1113/jphysiol.2003.054064

Cited by 77 publications

(86 citation statements)

References 52 publications

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“…In humans, multichannel MCG systems provide simultaneous multipoint cardiac mapping, with spatial and temporal resolution adequate to reveal electrophysiological markers for risk of life-threatening arrhythmias (43,44,74). In experimental animal studies, only a few of the 12 ECG leads are usually recorded (9,18,24,47), although high-quality multichannel BSPM in rats has been reported (3,8,49,66,67). MCG mapping has advantages over BSPM: 1) it is contactless, and 2) its sensor configuration is fixed and reproducible.…”

Section: Discussionmentioning

confidence: 99%

“…This limits the possibility of quantitative analysis of transient events, such as unsustained arrhythmias or rate-dependent changes of VR. However, after 300 s of continuous recording were averaged, MCG resolution was sufficient to reveal reproducible age-and sex-related differences in VR intervals, with sensitivity adequate to study the major repolarization wave, usually described as the b wave (24) or J wave (47). The terminal part of VR [i.e., the "c wave" sometimes observed in the rat ECG (24)] cannot be detected with an unshielded instrument but could probably be investigated with high-resolution recordings in magnetically shielded rooms with high-end multichannel systems (42,65).…”

Section: Study Limitationsmentioning

confidence: 99%

“…However, to the best of our knowledge, this is impossible, because instrumentations for "in vivo" optical mapping, specifically designed to avoid magnetic artifacts during MCG recordings, do not exist. Alternatively, simultaneous recording of MCG and monophasic action potential (MAP), similar to the method used to interpret the murine ECG (24,47), can be attempted (32,40). In a preliminary case, an MCG estimate of QT end corresponded to ϳ75-80% of the duration of a single epicardial ventricular MAP recorded with a percutaneous amagnetic catheter (Fig.…”

Section: Ajp-heart Circ Physiolmentioning

confidence: 99%

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Contactless magnetocardiographic mapping in anesthetized Wistar rats: evidence of age-related changes of cardiac electrical activity

Brisinda¹,

Caristo²,

Fenici³

2006

American Journal of Physiology-Heart and Circulatory Physiology

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Brisinda, Donatella, Maria Emiliana Caristo, and Riccardo Fenici. Contactless magnetocardiographic mapping in anesthetized Wistar rats: evidence of age-related changes of cardiac electrical activity. Am J Physiol Heart Circ Physiol 291: H368 -H378, 2006. First published December 22, 2005 doi:10.1152/ajpheart.01048.2005 is the recording of the magnetic field (MF) generated by cardiac electrophysiological activity. Because it is a contactless method, MCG is ideal for noninvasive cardiac mapping of small experimental animals. The aim of this study was to assess age-related changes of cardiac intervals and ventricular repolarization (VR) maps in intact rats by means of MCG mapping. Twenty-four adult Wistar rats (12 male and 12 female) were studied, under anesthesia, with the same unshielded 36-channel MCG instrumentation used for clinical recordings. Two sets of measurements were obtained from each animal: 1) at 5 mo of age (297.5 Ϯ 21 g body wt) and 2) at 14 mo of age (516.8 Ϯ 180 g body wt). RR and PR intervals, QRS segment, and QTpeak, QTend, JTpeak, JTend, and Tpeak-end were measured from MCG waveforms. MCG imaging was automatically obtained as MF maps and as inverse localization of cardiac sources with equivalent current dipole and effective magnetic dipole models. After 300 s of continuous recording were averaged, the signal-to-noise ratio was adequate for study of atrial and ventricular MF maps and for three-dimensional localization of the underlying cardiac sources. Clear-cut age-related differences in VR duration were demonstrated by significantly longer QT end, JTend, and Tpeak-end in older Wistar rats. Reproducible multisite noninvasive cardiac mapping of anesthetized rats is simpler with MCG methodology than with ECG recording. In addition, MCG mapping provides new information based on quantitative analysis of MF and equivalent sources. In this study, statistically significant age-dependent variations in VR intervals were found. magnetocardiography; cardiac mapping; ventricular repolarization; aging; sex ACCORDING TO RECENT GUIDELINES (7,21,26,27,35,39,48,60,63,65), several ECG indexes, such as QT duration and its dispersion, are used to identify risk of sudden death and assess potential cardiotoxicity of new drugs. The latter requires a large number of animal studies in the preclinical phase of new drug development. For noninvasive assessment of ventricular repolarization (VR) in small experimental animals, the most frequently used method is the 12-lead ECG (24). Extensive body surface potential mapping (BSPM), although more sensitive than the standard ECG for evaluation of repolarization inhomogeneity (2,19,38,57,70), is difficult in small animals, and its use is limited (8, 49).Magnetocardiography (MCG), an easier method for simplification of noninvasive cardiac electrophysiological mapping, can be an appealing alternative to BSPM. Multichannel MCG mapping measures the magnetic fields (MF) generated by cardiac activation currents, with minimal distortion due to the shape and conductivity of the lungs...

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Section: Discussionmentioning

confidence: 99%

Section: Study Limitationsmentioning

confidence: 99%

Section: Ajp-heart Circ Physiolmentioning

confidence: 99%

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Contactless magnetocardiographic mapping in anesthetized Wistar rats: evidence of age-related changes of cardiac electrical activity

Brisinda¹,

Caristo²,

Fenici³

2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…Needle electrodes were inserted through the skin following a three-lead scheme (left foreleg, right foreleg, and left rear leg), and ECG signals were amplified with a fourchannel amplifier (1700, A-M Systems). Data were collected using a Digidata 1200 analog/digital converter with Axoscope 8 software (Axon Instrument) and analyzed using Clampfit (version 8.0, Molecular Devices) (39,40).…”

Section: Mice and Isolated Working Heart Preparation-c57bl6 Wt And Cd36mentioning

confidence: 99%

CD36 Protein Influences Myocardial Ca2+ Homeostasis and Phospholipid Metabolism

Pietka¹,

Sulkin²,

Kuda³

et al. 2012

Journal of Biological Chemistry

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“…Analysis of ECG recordings revealed significantly (PϽ0.05) longer QT and corrected QT (QT c ) intervals in TAC, compared with sham, mice ( Figure 3B and 3C and supplemental Table IV). In addition, the J wave, corresponding to the early repolarization phase of murine ventricular action potentials, 20 was significantly (PϽ0.05) flattened or inverted ( Figure 3B and 3D and supplemental Table IV), suggesting that the dispersion of ventricular repolarization is altered in TAC LV.…”

Section: Marionneau Et Almentioning

confidence: 99%

Left Ventricular Hypertrophy

Ebert¹

2005

Easy ECG

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Abstract-Left ventricular hypertrophy (LVH) is associated with electric remodeling and increased arrhythmia risk, although the underlying mechanisms are poorly understood. In the experiments here, functional voltage-gated (Kv) and inwardly rectifying (Kir) K ϩ channel remodeling was examined in a mouse model of pressure overload-induced LVH, produced by transverse aortic constriction (TAC). Action potential durations (APDs) at 90% repolarization in TAC LV myocytes and QT c intervals in TAC mice were prolonged. Mean whole-cell membrane capacitance (C m ) was higher, and Key Words: hypertrophy Ⅲ arrhythmia Ⅲ heart failure L eft ventricular hypertrophy (LVH) is an adaptive response of the myocardium to an increase in load. 1 LVH is seen in various disease states including hypertension and myocardial infarction, as well as in valvular and congenital heart diseases. 1 LVH is also observed in physiological states following rigorous, prolonged exercise. 2 Although physiological LVH does not confer increased morbidity and mortality, pathological LVH is consistently associated with prolongation of ventricular action potentials and alterations in the dispersion of repolarization, both of which result in electric instability and increase the propensity to develop lifethreatening arrhythmias. 3 Several lines of evidence suggest that these electric changes reflect, at least in part, alterations in the functioning of the K ϩ channels that underlie ventricular action potential repolarization. 3,4 Various experimental models of LVH, 5-7 including pressure overload-induced LVH, 8,9 have been developed to explore the mechanisms underlying K ϩ current remodeling.Although several studies have examined regional differences in remodeling, 8 -11 few have probed the underlying molecular and cellular mechanisms. In the studies here, a mouse model of pressure overload-induced LVH, produced by transverse aortic constriction (TAC), was exploited to quantify the effects of LVH on repolarizing K ϩ currents in LV myocytes and to delineate the mechanisms underlying K ϩ current remodeling. These experiments revealed that APDs were prolonged in TAC LV myocytes and that QT c intervals were increased in TAC mice. Mean whole-cell membrane capacitance (C m ) was increased significantly, and the densities of voltage-gated K ϩ (Kv) and inwardly rectifying K ϩ (Kir) currents were reduced in TAC LV myocytes. Further electrophysiological, molecular, and biochemical analyses revealed marked regional differences in the effects of LVH and that distinct cellular and molecular mechanisms contribute to the functional remodeling of repolarizing Kv and Kir currents.

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In vivo temporal and spatial distribution of depolarization and repolarization and the illusive murine T wave

Cited by 77 publications

References 52 publications

Contactless magnetocardiographic mapping in anesthetized Wistar rats: evidence of age-related changes of cardiac electrical activity

Contactless magnetocardiographic mapping in anesthetized Wistar rats: evidence of age-related changes of cardiac electrical activity

CD36 Protein Influences Myocardial Ca2+ Homeostasis and Phospholipid Metabolism

Left Ventricular Hypertrophy

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