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J Am Coll Cardiol, 2001; 37:1359-1366
© 2001 by the American College of Cardiology Foundation
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CLINICAL STUDY

Effects of mental stress on coronary epicardial vasomotion and flow velocity in coronary artery disease: relationship with hemodynamic stress responses1

Willem J. Kop, PhD* {dagger}, David S. Krantz, PhD* {dagger}, Robert H. Howell, PhD*, Michael A. Ferguson, MD*, Vasilios Papademetriou, MD, FACC{ddagger}, David Lu, MD{ddagger}, Jeffrey J. Popma, MD, FACC§, John F. Quigley, MA*, Marina Vernalis, DO, FACC* and John S. Gottdiener, MD, FACC||

* Department of Medical and Clinical Psychology, Uniformed Services, University of the Health Sciences, Bethesda, Maryland, USA
{dagger} Division of Cardiology, Department of Medicine, Georgetown University Medical Center, Washington, D.C., USA
{ddagger} Department of Cardiology, Veterans Affairs Medical Center, Washington, D.C., USA
§ Department of Cardiology, Brigham and Women’s Hospital, Boston, Massachusetts, USA
|| Department of Cardiology?1, St. Francis Hospital, Roslyn, New York, USA

Manuscript received April 7, 2000; revised manuscript received October 25, 2000, accepted December 18, 2000.

Reprint requests and correspondence: Dr. Willem J. Kop, Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda Maryland 20814
wjkop{at}mxb.usuhs.mil

OBJECTIVES

This study examines the prevalence and hemodynamic determinants of mental stress-induced coronary vasoconstriction in patients undergoing diagnostic coronary angiography.

BACKGROUND

Decreased myocardial supply is involved in myocardial ischemia triggered by mental stress, but the determinants of stress-induced coronary constriction and flow velocity responses are not well understood.

METHODS

Coronary vasomotion was assessed in 76 patients (average age 59.9 ± 10.4 years; eight women). Coronary flow velocity responses were assessed in 20 of the 76 patients using intracoronary Doppler flow. Repeated angiograms were obtained after a baseline control period, a 3-min mental arithmetic task and administration of 200 µg intracoronary nitroglycerin. Arterial blood pressure (BP) and heart rate assessments were made throughout the procedure.

RESULTS

Mental stress resulted in significant BP and heart rate increases (p < 0.001). Coronary constriction (>0.15 mm) was observed in 11 of 59 patients with coronary artery disease (CAD) (18.6%). Higher mental stress pressor responses were associated with more constriction in diseased segments (r{Delta}SBP = –0.26, r{Delta}DBP = –0.30, r{Delta}MAP = –0.29; p’s < 0.05) but not with responses in nonstenotic segments. The overall constriction of diseased segments was not significant (p > 0.10), whereas a small but significant constriction occurred in nonstenotic segments (p = 0.04). Coronary flow velocity increased in patients without CAD (32.2%; p = 0.008), but not in patients with CAD (6.4%; p = ns). Cardiovascular risk factors were not predictive of stress-induced vasomotion in patients with CAD.

CONCLUSIONS

Coronary vasoconstriction in angiographically diseased arteries varies with hemodynamic responses to mental arousal. Coronary flow responses are attenuated in CAD patients. Thus, combined increases in cardiac demand and concomitant reduced myocardial blood supply may contribute to myocardial ischemia with mental stress.

Abbreviations and Acronyms
  APV = average peak velocity
  CAD = coronary artery disease
  DBP = diastolic blood pressure
  DSVR = diastolic systolic velocity ratio
  HR = heart rate
  LDL = low density lipoprotein
  QCA = quantitative coronary angiography
  SBP = systolic blood pressure




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