title: Effects of therapy with nifedipine GITS or atenolol on mental stress-induced ischemic left ventricular dysfunction.
abstract: OBJECTIVE
  We sought to determine the effect of nifedipine gastrointestinal therapeutic system (GITS) or atenolol on ischemic left ventricular dysfunction induced by mental stress.
  
  
  BACKGROUND
  The efficacy of conventional antianginal therapy in preventing myocardial ischemia induced by mental stress is unknown.
  
  
  METHODS
  Nifedipine GITS, atenolol and placebo were administered to 15 subjects with stable angina in a double-blind crossover trial. Subjects underwent a series of mental stressors at the end of each treatment. Radionuclide ventriculography was performed at baseline and at peak mental stress. Other measured variables included time to ischemia on exercise treadmill testing, ischemia on 48-h ambulatory electrocardiogram (ECG) monitoring, and resting and mental stress-induced levels of plasma catecholamines, tissue plasminogen activator antigen, plasminogen activator inhibitor-1 and platelet aggregability.
  
  
  RESULTS
  Mental stress resulted in a significant increase in plasma epinephrine and norepinephrine levels during each treatment phase. Atenolol therapy was associated with lower baseline and postmental stress rate-pressure product compared with nifedipine or placebo. Therapy with either nifedipine GITS or atenolol prevented the development of wall-motion abnormalities and the decline in regional ejection fraction (EF) in the segment with the largest deterioration in wall motion during placebo therapy. Both medications prevented the decrease in global EF in subjects who demonstrated at least a 5% fall in global EF on placebo therapy. No therapy exerted a statistically significant benefit on exercise performance or frequency of ischemia during ambulatory ECG monitoring.
  
  
  CONCLUSIONS
  Both nifedipine GITS and atenolol are effective at preventing mental stress-induced wall-motion abnormalities, although the mechanisms may be different.
authors.affiliation: Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, USA.
authors.forename: T C
authors.initials: TC
authors.lastname: Andrews
authors.forename: J D
authors.initials: JD
authors.lastname: Parker
authors.forename: S
authors.initials: S
authors.lastname: Jacobs
authors.forename: R
authors.initials: R
authors.lastname: Friedman
authors.forename: N
authors.initials: N
authors.lastname: Cummings
authors.forename: G
authors.initials: G
authors.lastname: MacCallum
authors.forename: F
authors.initials: F
authors.lastname: Mannting
authors.forename: G H
authors.initials: GH
authors.lastname: Tofler
authors.forename: W
authors.initials: W
authors.lastname: Carlson
authors.forename: J E
authors.initials: JE
authors.lastname: Muller
authors.forename: P H
authors.initials: PH
authors.lastname: Stone
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000328:Adult; D000368:Aged; D001262:Atenolol / Q000627:therapeutic use*; D018592:Cross-Over Studies; D003971:Diastole; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000209:etiology*; D009543:Nifedipine / Q000008:administration & dosage* / Q000627:therapeutic use; D013315:Stress, Psychological / Q000150:complications*; D013599:Systole; D014665:Vasodilator Agents / Q000008:administration & dosage* / Q000627:therapeutic use; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy* / Q000209:etiology* / Q000503:physiopathology
chemical_list: D000319:Adrenergic beta-Antagonists; D014665:Vasodilator Agents; D001262:Atenolol; D009543:Nifedipine