(Circulation. 1996;94:2641-2648.)
© 1996 American Heart Association, Inc.
Articles |
In Vivo Cardiac Electrophysiology Studies in the Mouse
the Divisions of Pediatric Cardiology (C.I.B.) and Cardiology (M.J.A., P.J.W., M.E.M.) and the Molecular Cardiology Research Center (C.I.B., M.E.M.), New England Medical Center and Tufts University School of Medicine, Boston, Mass.
Correspondence to Charles I. Berul, MD, or Michael E. Mendelsohn, MD, Molecular Cardiology Research Center, Tufts–New England Medical Center, Box 80, 750 Washington St, Boston, MA 02111.
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Abstract |
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Background This report describes a novel in vivo mouse epicardial cardiac electrophysiology study based on clinical protocols used to evaluate cardiac conduction in human patients. The technique allows extensive electrophysiological evaluation, including the response to pacing, programmed stimulation, and pharmacological agents.
Methods and Results Surface six-lead ECG data from 18 C57BL/6J mice are presented. Normal cardiac conduction properties for 14 of 18 mice that underwent the procedure are summarized, including determination of sinus node recovery times, AV conduction properties, and atrial, AV, and ventricular effective refractory periods. A subset of six mice was studied after the administration of either procainamide (n=3) or quinidine (n=3). All animals in the procainamide group developed either second-degree or complete AV block spontaneously. The sinus cycle length and refractory periods prolonged on procainamide or quinidine, but no tachyarrhythmias could be induced with atrial or ventricular programmed stimulation.
Conclusions This mouse electrophysiology method allows rapid assessment of the conduction properties of the murine heart. The ability to analyze cardiac conduction in normal and transgenic mice provides a powerful tool for examining molecular electrophysiological mechanisms in normal physiology and disease states.
Key Words: electrophysiology • mice • genes • arrhythmia
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Introduction |
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Transgenic mice have become increasingly important as models for cardiovascular diseases because of advances in molecular biology and the ease of creation and increase in availability of transgenic strains.1 2 Recent examples of transgenic models relevant to cardiovascular physiology and disease include mice overexpressing the ß2-adrenergic receptor3 or a constitutively active
1ß-adrenergic receptor,4 a mouse model of familial hypertrophic cardiomyopathy,5 the MLC-2v-ras mouse,6 as well as ACE-deficient mice7 and mice in which the angiotensin II type 1 or type 2 receptor genes have been disrupted.8 9 10 These mouse models provide powerful new tools for evaluating the effects of specific genes or mutations on cardiovascular phenotypes and diseases. Although a mouse model of vascular injury has been developed and applied,11 12 no such model exists for the electrophysiological evaluation of cardiac conduction. Electrophysiological studies in humans are routinely performed to evaluate arrhythmias and disorders of cardiac conduction. In larger animals, such as the dog or sheep, ex vivo models and whole-animal methods have been used to investigate their electrophysiological properties.13 14 Because mice have become the principal mammalian species for transgenic studies, we developed an in vivo method for electrophysiological testing in mice. This report describes a mouse cardiac electrophysiological study and characterizes both the ECG and standard electrophysiological parameters for normal control C57BL/6J mice, a strain commonly used in transgenic studies.
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Methods |
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Animals
Male and female 6- to 8-week-old C57BL/6J mice (Taconic Laboratories, Germantown, NY) weighing 22 to 28 g each were maintained on regular rodent chow (PROLAB) and allowed free access to food and water. Mice were housed five per cage at 24°C in a facility with 12-hour light/dark cycles, monitored by the Medical Center Laboratory Animal Medicine staff in full compliance with the Public Health Service animal welfare policy and the American Association for the Accreditation of Laboratory Animal Care. An animal research protocol was approved by the Institutional Animal Care and Use Committee.
Preoperative Preparation
For each study, an animal was anesthetized with a mixture of pentobarbital and ketamine (0.033 mg/g each IP). Intubation was achieved via direct laryngoscopy, visualizing the vocal cords with transillumination of the ventral neck, and placement of a ¾-in Teflon outer sheath from a 24-gauge intravenous catheter (Terumo, Inc) into the distal trachea. The mice were mechanically ventilated with a rodent respirator (model 683, Harvard Apparatus) at 130 breaths per minute with a tidal volume of 1.0 mL. A surface six-lead ECG was then obtained by placement of subcutaneous 27-gauge needles in each limb, secured with tape. The ECG channels were amplified (0.1 mV/cm) and filtered between 10 and 100 Hz, and a stable signal was reliably obtained before we proceeded. Respiratory rate, body temperature, cardiac rhythm, and heart rate were continuously monitored during the procedure. A warming light was used to maintain body temperature within a range of 34°C to 37°C for prevention of hypothermia.
Epicardial and Endocardial Access
Under sterile conditions, a midline sternotomy approach was used to gain access to the cardiac structures. Under an operating microscope (Zeiss) at x24 magnification, the pericardial sac was incised and four epicardial temporary pacing/recording wires were attached to the exposed right ventricle, left ventricle, and two on the right atrial surface with 7-0 silk and a Micropoint cutting needle (Ethicon, Inc). A representative example of the procedure as viewed through the operating microscope is shown in Fig 1
. Pacing electrodes were stainless steel Teflon-coated wires (A-M Systems, Inc) of 0.003-in diameter, with the ends stripped of insulating material. In some cases, wires were externalized through the skin at the posterior neck, the lungs were reexpanded with positive end-expiratory pressure, and the sternotomy incision was sutured closed in two layers.
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Electrophysiology Study Protocol
Unipolar and bipolar electrogram recordings were obtained from the right atrium and right and left ventricles via the epicardial route. Signals were amplified and filtered (EVR recorder, E for M Corp) for oscilloscopic display and thermal paper printout at 50 to 200-mm/s speed. Pacing thresholds (in milliamperes) were determined for each lead, and stimulation was performed for 1.0-ms pulse widths at twice the diastolic capture threshold.
Bipolar pacing was performed by use of a paired unipolar electrode configuration for stimulation (Bloom stimulator, Fischer Imaging Corp). The electrophysiological stimulator was modified by the manufacturer to pace at coupling intervals as short as 17 ms to allow for the rapid stimulation rates necessary in mice. Cardiac rhythm was continuously monitored and recorded (at 100 mm/s), and all ECG frontal axes (P and QRS) and time intervals (PR, QRS, QT, JT, QTc, JTc, RR) were calculated for each animal in standard fashion.15 16 The PR interval is marked from the beginning of the surface P wave to the beginning of the QRS complex. The JT interval is marked from the end of the QRS complex (J-point) to the end of the T wave, defined as the point at which it returns to the isoelectric baseline. The QT intervals were rate-corrected with Bazett's formula, and JT intervals also were rate-corrected by analogy using the formula JT/RR1/2, as previously described,17 18 although these formulas may not be directly applicable at rapid cycle lengths (see below). Standard clinical electrophysiological pacing protocols were used to determine all basic electrophysiological parameters (reviewed in References 19 and 20). The sinus node function was evaluated by indirect measurement of SNRT by pacing for 30 seconds at cycle lengths of 200, 150, and 100 ms and measuring the duration of the return cycle. The maximum return cycle length from all three pacing drives was used in calculations of SNRT, analogous to human studies.21 The CSNRT (SNRT minus the steady-state SCL) and SNRT/SCL percentages were determined by adjustment of the maximum absolute SNRT and correction for sinus cycle length. The AV-His-Purkinje conduction properties were assessed through the use of rapid atrial pacing at rates up to 1200 bpm. The minimum cycle length required to maintain 1:1 AV conduction, the Wenckebach paced cycle length, and the maximum paced cycle length causing 2:1 AV block were determined for each animal.22 23 Programmed right atrial stimulation was performed at two paced drive rates to determine AVERP and atrial ERP. Single- and double-extrastimulation techniques (down to a minimum coupling interval of 40 ms) were performed in an attempt to induce potential atrial arrhythmias.20
Next, right and left ventricular burst pacing was performed at rates of 250 to 1200 bpm to assess retrograde VA conduction, including measurements of VA Wenckebach block rates, and ventricular pacing exit block.24 Right and left ventricular ERPs also were determined by use of programmed stimulation at two paced drive rates with single extrastimuli. Double and triple extrastimulation techniques were then performed to attempt induction of ventricular arrhythmias, similar to the atrial pacing protocol.19 25 Dispersion of refractoriness between the epicardial right and left ventricle sites also was calculated to evaluate any heterogeneity of regional repolarization times.26 27
Pharmacological Effects on Basal ECG and Electrophysiological Parameters
To determine whether pharmacological manipulations are feasible with these techniques, a preliminary assessment of two Vaughan-Williams class 1A agents (procainamide and quinidine) was made to attempt to alter the ECG and electrophysiological parameters pharmacologically. In three mice each, after completion of the baseline EP study, intraperitoneal procainamide (procainamide hydrochloride injectable 100 mg/mL, Elkins-Sinn, Inc) or quinidine (quinidine gluconate 80 mg/mL, Eli Lilly & Co) was administered. The animals were given 300 mg/kg IP (equivalent to 3 to 10 times the therapeutic human oral dose) and first observed for 20 minutes, followed by repeat study with the full EP protocol described above. A six-lead ECG was recorded at 5-minute intervals after drug administration to assess for arrhythmias or conduction abnormalities.
Statistical Analysis
Data are presented as the mean±SD. Statistical analysis included a two-tailed Student's t test and multivariate ANOVA, with Scheffe subgroup testing when appropriate. A value of P<.05 was considered statistically significant.
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Baseline Surface ECG and Intracardiac Electrogram Recordings
Electrophysiological data were obtained from 14 of 18 mice (13 male, 5 female) that underwent the operative procedure; 4 mice died during the procedure (ie, 78% survival). Mortality was higher in the early phases of the experiments, with survival through the full procedure of only 4 of the initial 7 mice (57%), compared with 10 of the last 11 mice (91%) (P<.01, Student's t test). The most common cause of operative death was atrial perforation with resultant hemorrhage and AV block (3 of 4 nonsurvivors). One mouse developed an atrial tachycardia (with AV block and a regular ventricular response) secondary to atrial trauma. Six-lead ECGs were recorded with reliable signal stability from all 18 animals, with a representative example shown in Fig 2
, top. An example of a representative intracardiac electrogram demonstrating normal and abnormal conduction is shown in Fig 2, middle and bottom, recorded simultaneously from the right atrium and ventricle along with the surface ECG. ECG measurements and calculations for all animals studied are summarized in Table 1. The mean±SD cycle length was 189.4±50.5 ms (equivalent to an average heart rate of 317 bpm). The P and QRS axes ranged between -20° and +120°.
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Findings of Programmed Electrical Stimulation
The electrophysiological parameters obtained are displayed in Table 2. The rate-adjusted SNRTs included a mean CSNRT of 53±20 ms and mean SNRT/SCL of 129% (Fig 3, top). AV conduction remained intact with atrial pacing down to an average paced cycle length of 128±19 ms (469 bpm), after which more rapid pacing caused AV-His-Purkinje system block (Fig 3, middle). With programmed atrial stimulation with single and double atrial premature extrastimuli at two pacing drive rates, the mean AVERP was 120±19 ms with pacing at 200-ms cycles and 57.5±13 ms with pacing at 100-ms cycles (Fig 3, bottom). The mean AERPs were 100±12 ms at 200-ms drive rates and 51±11 ms pacing at 100-ms cycles (Table 2). Faster pacing led to exit block at pacing rates faster than tissue conduction. Neither burst atrial pacing nor programmed atrial stimulation could provoke any atrial arrhythmias.
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Ventricular pacing demonstrated retrograde VA conduction in 80% of the animals. In those animals showing intact retrograde VA conduction, the conduction remained intact to a minimum paced ventricular cycle length of 129±63 ms (Fig 4, middle), similar to the antegrade block rates (antegrade versus retrograde conduction, P=NS). There were no significant differences between right and left ventricular conduction properties, refractoriness, or arrhythmia inducibility (Table 2
). The right ventricular ERP was found to be 89±21 ms during programmed ventricular stimulation at cycle lengths of 200 ms and 61±20 ms at paced cycle lengths of 100 ms. The left ventricular ERPs were 97±24 ms at paced cycle lengths of 200 ms and 62.5±20 ms at 100-ms paced cycle lengths, as shown in Fig 4, top. Single, double, and triple premature extrastimuli did not provoke any arrhythmias in any of the control mice under basal conditions (Fig 4, bottom).
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Pharmacological Experiments
A total of 6 of the 18 mice received either procainamide hydrochloride (300 mg/kg IP) or quinidine gluconate (300 mg/kg IP). All animals in the procainamide group (n=3) developed either second-degree or complete (third-degree) AV block after high-dose procainamide administration. Before the onset of AV block, the ECG conduction durations all prolonged, including SCL, PR, QRS, JT, and QT intervals. The mean rate-corrected QT (and JT) intervals also both prolonged, from a mean QTc of 251±44 ms to a QTc of 307±73 ms after intraperitoneal procainamide administration. The SCL prolonged to 248±65 ms (242 bpm), with 1 mouse (mouse 6) demonstrating a markedly prolonged SNRT (baseline CSNRT, 85 ms; procainamide CSNRT, 380 ms). The refractory periods were also altered by procainamide, with the AERP at 200-ms drive rate prolonged to 185±15 ms (baseline, 100±12 ms; P<.05), right and left ventricular ERPs at 200-ms pacing cycles prolonged to 155±25 ms (compared with baseline, 89 to 97±24 ms; P<.05). No tachyarrhythmias could be induced on procainamide with atrial or ventricular programmed stimulation.
With administration of intraperitoneal quinidine (n=3), the effects on cardiac conduction were similar, although only 1 mouse in this group developed AV block. Another mouse developed sinus node dysfunction with a junctional escape rhythm after the atrial stimulation protocols. The mean spontaneous cycle length slowed to 265±63 ms, with prolongation of surface ECG PR, QRS, and QT intervals (but not JT interval) in each of the 3 animals examined (see Table 3). The maximum atrial burst pacing cycle length that caused AV Wenckebach was 200±0 ms (compared with 106±62 ms without drug, P<.01), and the AERP at 200-ms paced cycle length was 103±6 ms (versus 100±12 ms, P=NS). Ventricular pacing revealed intact VA conduction down to a paced cycle length of 195±60 ms, with VA block first evident at an average paced cycle length of 173±53 ms. The ventricular ERP at 200-ms pacing cycles prolonged to 147±65 ms (compared with baseline, 89 to 97±24 ms; P=.05). No tachyarrhythmias could be induced with quinidine by programmed stimulation.
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Discussion |
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This report describes the development of an in vivo mouse cardiac EP study and application of these techniques to the study of normal C57BL/6J mice. ECG and electrophysiological values and variations were determined for these control mice, and the feasibility of studying effects of pharmacological agents on cardiac conduction was also examined in a small subpopulation of the animals.
The mouse EP techniques described are straightforward and use commercially available materials to measure ECG and electrophysiological data similar to those collected routinely in human clinical studies. EP parameters obtained in some human protocols cannot be reproduced with epicardial recording techniques. For example, His-bundle electrogram signals cannot be obtained directly from the epicardial surface. However, most of the information obtained in human EP studies was also determined in these mouse studies. The rate-correction of repolarization times with Bazett's formula did not appear to correlate with the SCL at the rapid heart rates seen in the mice, perhaps because the square-root determinant in the formula does not hold for the rapid rates characteristic of murine cardiac conduction. The normal values determined in this report for C57BL/6J mice provide standards and a starting point for future studies of transgenic mice in this strain. Earlier reports of ECG recordings in normal mice of a different strain28 demonstrate cycle lengths and intervals similar to those of the present study, with the exception of the QT interval. In those studies, murine ECG intervals were affected by temperature, oxygenation state, and potassium concentrations as well.28 The electrophysiological data obtained from C57BL/6J mice also are comparable to those of previous studies evaluating mouse cardiac conduction, although the basal heart rates and timing intervals are somewhat slower than in some studies.29 30 31 32 This disparity may be due to differences in the methods used in previous mouse preparations and our own, to differences in anesthetic agents and other medications administered, or to differences in measuring and recording techniques. For example, older recording techniques may have been unable to obtain high-fidelity electrogram tracings for precise determination of intervals, particularly at slower paper speeds. However, the likely interstrain variation in EP parameters suggests that it will be necessary in future studies to develop baseline control values for other mouse strains in a manner similar to that reported here. As an example, in preliminary studies of normal 129/SV mice in our laboratory, we find that the basal heart rate is significantly faster than that of the C57BL/6J mice in the present study (cycle length, 164±32 ms; heart rate, 378±79 bpm; n=5) (C.I.B., M.J.A., and M.E.M., unpublished observations).
Electrophysiological properties have been evaluated in many species by a variety of methods from single-cell to whole-animal recordings. However, this study, to the best of our knowledge, is the first describing in detail the measurement of surface ECG and simultaneous electrophysiological parameters obtained by pacing and recording directly from the myocardium of an intact mouse. The development of a mouse model analogous to a human clinical cardiac EP study now allows several types of electrophysiological investigation of transgenic animals. First, specific disease models can be studied to understand better the relationship between single gene defects and their electrophysiological phenotypes in whole animals. For example, the aforementioned mouse model of hypertrophic cardiomyopathy5 and recent isolation of mutations responsible for congenital long-QT syndrome33 34 35 will allow mouse models of these disorders to be directly examined with the EP method described here. The recently described atrial natriuretic factor–SV40 T antigen transgenic mouse line demonstrates atrial arrhythmias on a single-lead ECG recording, which are progressive as the mice age.36 These mice similarly would be of interest to study with simultaneous intracardiac electrogram and ECG recordings at baseline and during programmed stimulation. In addition, transgenic animals harboring mutations in genes encoding proteins that are highly expressed in myocytes or that lead to cardiovascular abnormalities may prove to have interesting and informative electrophysiological phenotypes.1 2 35 37 Finally, mutations in or disruption of individual ion channel genes in transgenic mice will allow the role of specific ion channels in in vivo cardiac conduction to be studied in the near future by methods such as those reported here. Future studies also will address the development of a transvenous endocardial system with ambulatory recording capabilities.
Study Limitations
Whole-animal electrophysiology may be subject to species variability, and the human clinical EP protocols may not be as informative in a rodent model. In addition, the high basal heart rates of mice might make accurate delineation of timing intervals more difficult. Because no data on mouse EP parameters have been published, we are not aware of any information on hemodynamic derangements at rapid paced rates, although this remains a theoretical possibility. Nonetheless, the majority of the animals tolerated the procedure, and there were no obvious hemodynamic deaths. The heart rates and ECG intervals might also have been affected by the open-chest surgical procedure and/or the actions of anesthetic agents used for premedication. The action potential durations in mouse myocardial tissue preparations have been shown to be short (<30 ms),38 which differs somewhat from our mean JT interval (repolarization time) of 79 ms. Intact in vivo preparations may be difficult to compare directly with in vitro cellular and tissue preparations for the assessment of cardiac conduction times. Finally, all studies were performed with the mice under warming lights to prevent hypothermia, and the operative procedures and anesthetic medications were identical in all animals. Therefore, although the heart rate and intervals may be slower in this in vivo preparation than in the unsedated, active mouse, the uniformity of the procedure will likely allow a fair comparison among different subgroups and between different transgenic strains in future studies.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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We gratefully acknowledge N.A. Mark Estes, MD, and Richard H. Karas, MD, PhD, for useful discussions and critical review of the manuscript, and David R. Fulton, MD, for his constant help and support. We thank Patricia Nayak for her expert assistance with manuscript preparation. Dr Mendelsohn is an Established Investigator of the American Heart Association.
Received February 22, 1996; revision received August 19, 1996; accepted August 19, 1996.
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X. H.T. Wehrens, S. Kirchhoff, and P. A. Doevendans Mouse electrocardiography: An interval of thirty years Cardiovasc Res, January 1, 2000; 45(1): 231 - 237. [Abstract] [Full Text] [PDF]
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A. Hagendorff, B. Schumacher, S. Kirchhoff, B. Luderitz, and K. Willecke Conduction Disturbances and Increased Atrial Vulnerability in Connexin40-Deficient Mice Analyzed by Transesophageal Stimulation Circulation, March 23, 1999; 99(11): 1508 - 1515. [Abstract] [Full Text] [PDF]
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