title: Effect of mental stress on myocardial blood flow and vasomotion in patients with coronary artery disease.
abstract: In patients with coronary artery disease (CAD), mental stress may provoke ischemic electrocardiograph changes and abnormalities in regional and global left ventricular function. However, little is known about the underlying myocardial blood flow response (MBF) in these patients.
  
  
  METHODS
  We investigated the hemodynamic, neurohumoral, and myocardial blood flow responses to mental stress in 17 patients with CAD and 17 healthy volunteers of similar age. Mental stress was induced by asking individuals to solve mathematic subtractions in a progressively challenging sequence; MBF was quantified at rest and during mental stress using 13N ammonia PET.
  
  
  RESULTS
  Mental stress induced significant (P < 0.01) and comparable increases in rate-pressure product, measured in beats per minute x mm Hg, in both patients (from 7826 +/- 2006 to 10586 +/- 2800) and healthy volunteers (from 8227 +/- 1272 to 10618 +/- 2468). Comparable increases also occurred in serum epinephrine (58% in patients versus 52% in healthy volunteers) and norepinephrine (22% in patients versus 27% in healthy volunteers). Although MBF increased in patients (from 0.67 +/- 0.15 to 0.77 +/- 0.18 mL/min/g, P < 0.05) and healthy volunteers (from 0.73 +/- 0.13 to 0.95 +/- 0.22 mL/min/g, P < 0.001), the magnitude of flow increase was smaller in patients (14% +/- 17%) than in healthy volunteers (29% +/- 14%) (P = 0.01). The increase in MBF during mental stress correlated significantly with changes in cardiac work in healthy volunteers (r = 0.77; P < 0.001) but not in patients.
  
  
  CONCLUSIONS
  Despite similar increases in cardiac work and comparable sympathetic stimulation in CAD patients and healthy volunteers, CAD patients exhibit an attenuated blood flow response to mental stress that may contribute to mental stress-induced ischemic episodes in daily life.
authors.affiliation: Department of Molecular and Medical Pharmacology, School of Medicine, University of California, Los Angeles 90095-6942, USA.
authors.forename: H
authors.initials: H
authors.lastname: Schöder
authors.forename: D H
authors.initials: DH
authors.lastname: Silverman
authors.forename: R
authors.initials: R
authors.lastname: Campisi
authors.forename: H
authors.initials: H
authors.lastname: Karpman
authors.forename: M E
authors.initials: ME
authors.lastname: Phelps
authors.forename: H R
authors.initials: HR
authors.lastname: Schelbert
authors.forename: J
authors.initials: J
authors.lastname: Czernin
mesh_terms: D000641:Ammonia; D016022:Case-Control Studies; D003326:Coronary Circulation / Q000502:physiology*; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000503:physiopathology*; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000209:etiology; D009590:Nitrogen Radioisotopes; D013315:Stress, Psychological / Q000503:physiopathology*; D014055:Tomography, Emission-Computed; D014655:Vascular Resistance / Q000502:physiology; D014666:Vasomotor System / Q000503:physiopathology*
chemical_list: D009590:Nitrogen Radioisotopes; D000641:Ammonia