title: Enhancement of myocardial vulnerability by atrial fibrillation.
abstract: Certain groups are known to have an increased risk for sudden cardiac death. Epidemiologic studies have suggested that patients with atrial fibrillation may be at higher risk. The authors hypothesize that atrial fibrillation may increase myocardial vulnerability. To test this hypothesis, 37 dogs were studied using programmed electrical stimulation techniques to determine myocardial vulnerability as assessed by the ability to provoke ventricular tachycardia. Prior to atrial fibrillation, programmed electrical stimulation did not induce ventricular tachycardia. Aconitine was then topically applied to the right atrial appendage with care taken not to make contact with the ventricle. Application of aconitine caused atrial fibrillation with an increase in ventricular rate, but did not affect arterial blood pressure. Ventricular tachycardia was induced by programmed electrical stimulation studies in 25 of 26 dogs in atrial fibrillation. The enhanced vulnerability was noted following atrial fibrillation, not after aconitine application to the great veins, which did not cause atrial fibrillation. To further exclude the possibility that aconitine application may cause changes in ventricular threshold, atrial fibrillation was induced by pacing techniques in five dogs. Prior to atrial fibrillation induction, programmed electrical stimulation did not induce ventricular tachycardia. Following atrial fibrillation, ventricular tachycardia could be repeatedly induced. Mean heart rate following atrial fibrillation increased, while pacing animals at this increment in rate did not change the noninducibility of dogs in sinus rhythm. Six patients with a history of atrial fibrillation and ventricular tachycardia were studied to determine if AF lowered myocardial threshold to VT induction. Ventricular tachycardia could only be induced by PES techniques in four of five patients when the patients' rhythm was AF (P < 0.05). This study suggests that atrial fibrillation lowers myocardial threshold for ventricular tachycardia induction and thus enhances myocardial vulnerability. The association of AF with a higher incidence of sudden death may be due to an enhanced electrical instability.
authors.affiliation: Department of Medicine & Pharmacology, Rush University and American Institute of Therapeutics, 21 N. Skokie Valley Highway, Suite G-3, Lake Bluff, IL 60044, USA.
authors.forename: John C
authors.initials: JC
authors.lastname: Somberg
authors.forename: Vilma
authors.initials: V
authors.lastname: Torres
authors.forename: Gad
authors.initials: G
authors.lastname: Keren
authors.forename: Brenda
authors.initials: B
authors.lastname: Butler
authors.forename: David
authors.initials: D
authors.lastname: Tepper
authors.forename: Herman
authors.initials: H
authors.lastname: Kleinbaum
authors.forename: Janos
authors.initials: J
authors.lastname: Molnar
mesh_terms: D000157:Aconitine; D000818:Animals; D001281:Atrial Fibrillation / Q000150:complications*; D003645:Death, Sudden / Q000517:prevention & control; D004195:Disease Models, Animal; D004198:Disease Susceptibility; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D006339:Heart Rate; D006352:Heart Ventricles; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D017180:Tachycardia, Ventricular / Q000209:etiology* / Q000503:physiopathology
chemical_list: D000157:Aconitine