title: The potential mechanisms of reduced incidence of ventricular fibrillation as the presenting rhythm in sudden cardiac arrest.
abstract: OBJECTIVE
  In the last two decades, the incidence of ventricular fibrillation has significantly decreased as the presenting rhythm in sudden cardiac arrest. We hypothesized that beta-adrenergic receptor blocker (beta-blocker) and angiotensin converting enzyme inhibitor, which were commonly used in the primary and secondary prevention strategies recommended by the American Heart Association during the same decades, decrease the duration of ventricular fibrillation after onset of cardiac arrest.
  
  
  METHODS
  Randomized prospective animal study.
  
  
  METHODS
  University affiliated research laboratory.
  
  
  METHODS
  Male Sprague-Dawley rats.
  
  
  RESULTS
  Male Sprague-Dawley rats, weighing 450-550 g were administered either beta-blocker, propranolol, angiotensin converting enzyme inhibitor, captopril, or placebo for 2 wks. In the phase 1 study, ventricular fibrillation was induced by ligation of the proximal left coronary artery. In the phase 2 study, the experiments were repeated with the measurements of duration of monophasic action potential and threshold of ventricular fibrillation. Both propranolol and captopril significantly decreased the duration of ventricular fibrillation in comparison with controls (p < 0.05). In the phase 2 study, both propranolol and captopril significantly increased the threshold of ventricular fibrillation (p < 0.05) and monophasic action potential (p < 0.05).
  
  
  CONCLUSIONS
  Ventricular fibrillation remains as the leading causal rhythm of sudden cardiac arrest. However, the drugs widely used in primary and secondary coronary artery disease prevention strategies shortened the duration of ventricular fibrillation. This may result in the reduced incidence of ventricular fibrillation as the presenting rhythm in sudden cardiac arrest. Increased threshold of ventricular fibrillation and monophasic action potential after administration of those agents may be the potential mechanisms of reduced duration of ventricular fibrillation.
authors.affiliation: Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA.
authors.forename: Hao
authors.initials: H
authors.lastname: Wang
authors.forename: Wanchun
authors.initials: W
authors.lastname: Tang
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Ristagno
authors.forename: Yongqin
authors.initials: Y
authors.lastname: Li
authors.forename: Shijie
authors.initials: S
authors.lastname: Sun
authors.forename: Tong
authors.initials: T
authors.lastname: Wang
authors.forename: Max Harry
authors.initials: MH
authors.lastname: Weil
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D002216:Captopril / Q000627:therapeutic use*; D016757:Death, Sudden, Cardiac; D015994:Incidence; D011433:Propranolol / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000453:epidemiology* / Q000209:etiology / Q000517:prevention & control*
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002216:Captopril; D011433:Propranolol