A comprehensive protocol combining in vivo and ex vivo electrophysiological experiments in an arrhythmogenic animal model

Figures

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  Figure 1.. Representative surface ECGs from the in vivo pacing protocol. A: determination of the atrial pacing threshold. Each stimulus (^) at a CL of 120 ms results in successful atrial capture. B: determination of the ventricular pacing threshold. Each stimulus (*) at a CL of 120 ms results in successful ventricular capture. C: ventricular PES (S1–S3) showing successful capture on S1 and S2, but loss of capture on S3. D: initial SR followed by ventricular PES (S1–S2) that triggers a short nonsustained VT lasting four beats before returning to SR. E: ventricular PES (S1–S2) that induces a nonsustained VT (total duration ∼5.5 s) with spontaneous conversion to SR. F: initial SR (with a CL of ∼145 ms) followed by ventricular PES (S1–S3) that induces a sustained VT (with a CL of ∼70 ms) accompanied by a changed axis deviation. G: continuation of the arrhythmia shown in E, where the monomorphic VT has degenerated into polymorphic VT. A first unsuccessful attempt at external defibrillation with 5 J (red arrow) is followed by a second attempt with 5 J (yellow arrow), which successfully converts the VT back to SR (with a CL of ∼155 ms). Note that the external shock briefly causes deviation of the…

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  Figure 2.. Representative epicardial ECGs from the ex vivo pacing protocol. A: example of ventricular PES, S1–S2 in a healthy heart without any arrhythmic behavior. B: example ventricular PES, S1–S5 in a healthy heart without arrhythmic behavior. C: example of ventricular PES, S1–S3 in a MI heart that triggers a short nonsustained VT, lasting ∼2 s before returning to SR spontaneously. D: example of ventricular PES, S1–S4 in a MI heart that induces a sustained VT. ECG, electrocardiogram; MI, myocardial infarction; PES, programmed electrical stimulation; SR, sinus rhythm; VT, ventricular tachycardia.

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  Figure 3.. Comparison of VT susceptibility during an S1–S2 protocol in sedentary animals with sham surgery and MI surgery, observed both in vivo and ex vivo. The Mann–Whitney U two-tailed test was used to test for group differences. MI sed, sedentary rats with myocardial infarction; VT, ventricular tachycardia.

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  Figure 4.. Ex vivo setup and optical mapping. A: illustration (I) and a labeled experimental picture (II) of a Langendorff-perfused heart placed horizontally in a temperature-controlled chamber with Tyrode’s solution. ECG electrodes are positioned near the base and apex of the heart, with the pacing electrode on the RA. B: simultaneous recordings of ECG and AP from the RA with a 224-ms CL. C: the upper panel illustrates the imaging site on the heart (I) with a brightfield image with the pacing electrode, and an isochronal map of AP activation (II). The lower panel shows the fastest conduction axis indicated by red asterisks and slowest conduction axis indicated by black asterisks (III), along with the relationship between time and distance in the fastest axis (IV) and slowest axis (V). D: example illustrating regional differences in AP duration (APD90 and APD50) in a healthy heart (I) compared with a MI heart (II). E: pixel frequency distribution of each 2-ms APD90 category obtained from mapping of a healthy heart (I) compared with a MI heart (II). AP, action potential; APD; action potential duration; CL, cycle length; ECG, electrocardiogram; LA, left atrium; LV, left ventricle; MI,…

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  Figure 5.. Example of optical mapping during S1–S2 protocol in healthy and MI hearts. A: ECG (upper panel) and spatially averaged AP (lower panel) from a healthy heart during ventricular S1–S2. B: the upper panels illustrate site of imaging (I) with a brightfield image of the epicardial surface and isochronal maps of APD50 comparing S1 (II) and S2 (III). The lower panels show APs from different regions with little variation between S1 (arrows on the far left) and S2 (arrows on the far right) in a healthy heart. C: ECG (upper panel) and spatially averaged AP (lower panel) from a MI heart during the ventricular S1–S2 protocol. D: the upper panels illustrate site of imaging (I) with a brightfield image of the epicardial surface where the white parts correspond to connective tissue/infarction. II is an isochronal map of APD50 during S1, and III shows the corresponding isochronal map of S2. The lower panels show that APs from different regions during S1 deviate somewhat (arrows on the far left), but with the addition of S2, the AP from the border zone of the MI (arrows on the far right) exhibits substantial alterations compared with the AP from S1. AP, action potential; APD; action potential…