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Y Z Ge

Publications and source records attributed to Y Z Ge.

3 recordsLinked to original sources

Spatial and temporal linking of epicardial activation directions during ventricular fibrillation in dogs. Evidence for underlying organization.

BACKGROUND: It remains controversial as to whether electrical activation during ventricular fibrillation (VF) is organized. To detect the presence of organization in VF, the direction of epicardial activation (EA) at multiple sites was examined by using vector mapping. If VF is not a random process, EA direction at a given site should be related to adjacent sites and prior beats. METHODS AND RESULTS: Thirteen dogs with healing myocardial infarction (MI) and four dogs without MI had VF induced by programmed stimulation. Using a plaque electrode array with a 2.5-mm interelectrode distance, 91 vector loops were created for each "beat" of VF. Direction of maximum EA was determined at each site for the first 10 consecutive beats of VF and for 10 consecutive beats recorded 5 seconds after VF was established. Spatial and temporal linking of EA directions was evaluated by the ability of activation direction at a given site to be predicted by activation directions at eight adjacent sites for the index beat and at eight adjacent sites and the site of interest for the preceding beat using stepwise linear regression. The strength of the model as reflected by the correlation coefficient (r) indicated the degree of linking. We determined 1) changes in the degree of linking over time during a given episode of VF (using a paired-difference t test), 2) differences in the degree of linking between the anterior and posterolateral walls in animals with (n = 4) and without (n = 4) MI (using two-way ANOVA), and 3) the effect of repeated inductions (n = 10) on the degree of linking (using one-way ANOVA with repeated measures). During 57 episodes of VF, r for each model ranged from 0.64 to 0.88 during the transition to VF to 0.39-0.78 during established VF (p < 0.0001 for the difference). The presence of MI, the site of recording, and repeated inductions did not affect the degree of linking. For each episode, spatial linking was more prominent than temporal linking. CONCLUSIONS: Electrical activation during VF is organized. The degree of linking of EA directions during VF is not affected by the presence of MI, the site of recording, or repeated inductions of VF. During the first 5 seconds of VF, the degree of linking decreases.

Animals

Monophasic action potential duration during programmed electrical stimulation.

UNLABELLED: To examine changes in monophasic action potential duration (APD) with a pacing protocol similar to that used during electrophysiological testing, action potentials were recorded in vivo from the left ventricular apical endocardium of 12 normal mongrel dogs. The atrioventricular node was ablated and the dogs paced from the anterior right ventricle at a baseline cycle length of 1000 ms between interventions. Mean steady-state APD (APDss) was 266 +/- 7 ms at a pacing cycle length (PCL) of 1000 ms. Two pacing protocols were used. The first consisted of a sudden acceleration in pacing from a cycle length of 1000 ms to one between 300 and 600 ms. The second consisted of an 8-beat train at a cycle length of 400 ms followed by a premature beat at a coupling interval of 280 ms followed by a pause. The inter-train pause varied between 1 second and 32 seconds. With a sudden acceleration in pacing rate, steady-state values for APD at the faster PCLs were significantly smaller than APDss at 1000 ms with a change to cycle lengths of 600 ms (247 +/- 29 ms), 500 ms (229 +/- 21 ms), 400 ms (220 +/- 17 ms), and 300 ms (203 +/- 31 ms; P less than 0.01 for all comparisons). The time constant of the change in APD was shorter at a PCL of 300 ms (14.9 +/- 0.8 s) than 600 ms (20.3 +/- 4.7 s; P less than 0.05). With drive train pacing and incorporating an inter-train pause, the percent drop in steady-state APD compared to APD for the first train ranged from 10.1% with a 1-second inter-train pause to 2.1% with a 32-second pause. The difference in APD between the first drive train and drive trains after at least 3 minutes of pacing when APD had stabilized was not significant for an inter-train pause exceeding 8 seconds. IN CONCLUSION: (1) with a sudden acceleration in pacing rate, endocardial APD in vivo decreases exponentially. The faster the new rate, the shorter the new steady-state APD and the shorter the time constant. (2) When pacing using an 8-beat drive train and an inter-train pause, there is a decremental shortening in APD for pause lengths shorter than 16 seconds. Thus, while performing programmed stimulation using a pause, a conditioning period of at least 2 minutes should be used prior to diastole scanning to allow APD to achieve a steady state.

Action Potentials