Schöder H, Silverman D H, Campisi R, Karpman H, Phelps M E, Schelbert H R, Czernin J
Department of Molecular and Medical Pharmacology, School of Medicine, University of California, Los Angeles 90095-6942, USA.
J Nucl Med. 2000 Jan;41(1):11-6.
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.
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.
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.
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.
在冠心病（CAD）患者中，精神压力可能会引发缺血性心电图改变以及局部和整体左心室功能异常。然而，对于这些患者潜在的心肌血流反应（MBF）却知之甚少。
我们调查了17例CAD患者和17名年龄相仿的健康志愿者对精神压力的血流动力学、神经体液和心肌血流反应。通过要求个体以逐渐增加难度的顺序进行数学减法运算来诱发精神压力；使用13N氨PET在静息状态和精神压力期间对MBF进行定量。
精神压力使患者（从7826±2006增加到10586±2800）和健康志愿者（从8227±1272增加到10618±2468）以每分钟心跳次数×毫米汞柱测量的心率 - 血压乘积显著（P < 0.01）且相当程度地增加。血清肾上腺素（患者增加58%，健康志愿者增加52%）和去甲肾上腺素（患者增加22%，健康志愿者增加27%）也有相当程度的增加。虽然患者（从0.67±0.15增加到0.77±0.18 mL/min/g，P < 0.05）和健康志愿者（从0.73±0.13增加到0.95±0.22 mL/min/g，P < 0.001）的MBF均增加，但患者血流增加幅度（14%±17%）小于健康志愿者（29%±14%）（P = 0.01）。精神压力期间MBF的增加与健康志愿者的心脏作功变化显著相关（r = 0.77；P < 0.001），但在患者中无此相关性。
尽管CAD患者和健康志愿者的心脏作功增加相似且交感神经刺激相当，但CAD患者对精神压力的血流反应减弱，这可能导致日常生活中精神压力诱发的缺血发作。
