Opposite effects of myocardial stretch and verapamil on the complexity of the ventricular fibrillatory pattern: An experimental study

Citation
Fj. Chorro et al., Opposite effects of myocardial stretch and verapamil on the complexity of the ventricular fibrillatory pattern: An experimental study, PACE, 23(11), 2000, pp. 1594-1603
Citations number
59
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY
ISSN journal
0147-8389 → ACNP
Volume
23
Issue
11
Year of publication
2000
Part
1
Pages
1594 - 1603
Database
ISI
SICI code
0147-8389(200011)23:11<1594:OEOMSA>2.0.ZU;2-#
Abstract
An experimental model is used to analyze the effects of ventricular stretch ing and verapamil on the activation patterns during VF. Ten Longendorff-per fused rabbit hearts were used to record VF activity with an epicardial mult iple electrode before, during, and offer stretching with an intraventricula r balloon, under both control conditions and during verapamil (Vp) infusion (0.4-0.8 mu mol). The analyzed parameters were dominant frequency (FrD) sp ectral analysis, the median (MN) of the VF intervals, and the type of activ ation maps during VF (I = one wavelet without block lines, II = two simulta neous wavelets with block lines, III = three or more wavelets with block li nes). Stretch accelerates VF (FrD: 22.8 +/- 6.4 vs 25.2 +/- 1.0 Hz, P < 0.0 1; MN: 48 +/- 13 vs 68 +/- 6 ms, P < 0.02). On fitting the Fro time changes to an exponential model after applying and suppressing stretch, the time c onstants (stretch: 101.2 +/- 19.6 s; stretch suppression: 97.8 +/- 33.2 s) do not differ significantly. Stretching induces a significant variation in the complexity of the VF activation maps with type III increments and type I and II decrements (control: I = 17.5%, II = 50.5%, III = 32%; stretch: I = 7% II = 6.5%, III = 56.5%, P < 0.001). Vp accelerates VF (FrD: 20.9 +/- 1 .9 Hz, P ( 0.001 vs control; MN: 50 +/- 5 ms, P < 0.002 vs control) and dim inishes activation maps complexity (I = 25.5%, II = 60.5 %, III = 14%, P < 0.002 vs control). On applying stretch during Vp perfusion, the fibrillator y process is not accelerated to any greater degree. However, type I and II map decrements and type III increments are recorded, though reaching percen tages similar to control (I = 16.5%, II = 53%, III = 30.5%, NS vs control). The following conclusions were found: (1) myocardial stretching accelerate s VF and increases the complexity of the VF activation pattern; (2) time ch anges in the Fro of VF during and upon suppressing stretch fit an exponenti al model with similar time constants; and (3) although stretching and verap amil accelerate the VF process, they exert opposite effects upon the comple xity of the fibrillatory pattern.