Opposite effects of myocardial stretch and verapamil on the complexity of the ventricular fibrillatory pattern: an experimental study.
An experimental model is used to analyze the effects of ventricular stretching and verapamil on the activation patterns during VF. Ten Langendorff-perfused rabbit hearts were used to record VF activity with an epicardial multiple electrode before, during, and after stretching with an intraventricular balloon, under both control conditions and during verapamil (Vp) infusion (0.4-0.8 mumol). The analyzed parameters were dominant frequency (FrD) spectral analysis, the median (MN) of the VF intervals, and the type of activation maps during VF (I = one wavelet without block lines, II = two simultaneous wavelets with block lines, III = three or more wavelets with block lines). Stretch accelerates VF (FrD: 22.8 +/- 6.4 vs 15.2 +/- 1.0 Hz, P < 0.01; MN: 48 +/- 13 vs 68 +/- 6 ms, P < 0.01). On fitting the FrD time changes to an exponential model after applying and suppressing stretch, the time constants (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 = 36.5%, 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 < 0.001 vs control) and diminishes activation maps complexity (I = 25.5%, II = 60.5%, III = 14%, P < 0.001 vs control). On applying stretch during Vp perfusion, the fibrillatory process is not accelerated to any greater degree. However, type I and II map decrements and type III increments are recorded, though reaching percentages similar to control (I = 16.5%, II = 53%, III = 30.5%, NS vs control). The following conclusions were found: (1) myocardial stretching accelerates VF and increases the complexity of the VF activation pattern; (2) time changes in the FrD of VF during and upon suppressing stretch fit an exponential model with similar time constants; and (3) although stretching and verapamil accelerate the VF process, they exert opposite effects upon the complexity of the fibrillatory pattern.
Chorro
F J
FJ
Servicio de Cardiología, Hospital Clínico Universitario, Avda. Blasco Ibañez 17, 46010, Valencia, Spain.
Canoves
J
J
Guerrero
J
J
Mainar
L
L
Sanchis
J
J
Soria
E
E
Such
L M
LM
Rosado
A
A
Such
L
L
López-Merino
V
V
D000818:Animals; D004108:Dilatation, Pathologic / Q000473:pathology / Q000503:physiopathology*; D004566:Electrodes; D006352:Heart Ventricles / Q000187:drug effects / Q000503:physiopathology; D066298:In Vitro Techniques; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000473:pathology*; D011817:Rabbits; D013314:Stress, Mechanical; D014693:Ventricular Fibrillation / Q000188:drug therapy* / Q000503:physiopathology*; D014700:Verapamil / Q000494:pharmacology*
D014700:Verapamil