Effects of mental stress on coronary epicardial vasomotion and flow velocity in coronary artery disease: relationship with hemodynamic stress responses11The opinions and assertions expressed herein are those of the authors and should not be construed as reflecting those of the USUHS or the US Department of Defense

• Published in: Journal of the American College of Cardiology Vol. 37; no. 5; pp. 1359 - 1366
• Main Authors: Kop, Willem J, Krantz, David S, Howell, Robert H, Ferguson, Michael A, Papademetriou, Vasilios, Lu, David, Popma, Jeffrey J, Quigley, John F, Vernalis, Marina, Gottdiener, John S
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 01.04.2001
• Subjects: SBP; DBP; LDL; APV; CAD; HR; DSVR; QCA
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/S0735-1097(01)01136-6

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 (rΔSBP = −0.26, rΔDBP = −0.30, rΔMAP = −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.