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对精神和运动应激的缺血、血流动力学及神经激素反应。心肌缺血心理生理学研究(PIMI)的经验。

Ischemic, hemodynamic, and neurohormonal responses to mental and exercise stress. Experience from the Psychophysiological Investigations of Myocardial Ischemia Study (PIMI).

作者信息

Goldberg A D, Becker L C, Bonsall R, Cohen J D, Ketterer M W, Kaufman P G, Krantz D S, Light K C, McMahon R P, Noreuil T, Pepine C J, Raczynski J, Stone P H, Strother D, Taylor H, Sheps D S

机构信息

Henry Ford Heart and Vascular Institute, Detroit, MI 48202, USA.

出版信息

Circulation. 1996 Nov 15;94(10):2402-9. doi: 10.1161/01.cir.94.10.2402.

Abstract

BACKGROUND

The pathophysiology of mental stress-induced myocardial ischemia, which occurs at lower heart rates than during physical stress, is not well understood.

METHODS AND RESULTS

The Psychophysiological Investigations of Myocardial Ischemia Study (PIMI) evaluated the physiological and neuroendocrine functioning in unmedicated patients with stable coronary artery disease and exercise-induced ischemia. Hemodynamic and neurohormonal responses to bicycle exercise, public speaking, and the Stroop test were measured by radionuclide ventriculography, ECG, and blood pressure and catecholamine monitoring. With mental stress, there were increases in heart rate, systolic blood pressure, cardiac output, and systemic vascular resistance that were correlated with increases in plasma epinephrine. During exercise, systemic vascular resistance fell, and there was no relationship between the hemodynamic changes and epinephrine levels. The fall in ejection fraction was greater with mental stress than exercise. During mental stress, the changes in ejection fraction were inversely correlated with the changes in systemic vascular resistance. Evidence for myocardial ischemia was present in 92% of patients during bicycle exercise and in 58% of patients during mental stress. Greater increases in plasma epinephrine and norepinephrine occurred with ischemia during exercise, and greater increases in systemic vascular resistance occurred with ischemia during mental stress.

CONCLUSIONS

Mental stress-induced myocardial ischemia is associated with a significant increase in systemic vascular resistance and a relatively minor increase in heart rate and rate-pressure product compared with ischemia induced by exercise. These hemodynamic responses to mental stress can be mediated by the adrenal secretion of epinephrine. The pathophysiological mechanism involved are important in the understanding of the etiology of myocardial ischemia and perhaps in the selection of appropriate anti-ischemic therapy.

摘要

背景

精神应激诱发的心肌缺血发生时的心率低于身体应激时,其病理生理学机制尚未完全明确。

方法与结果

心肌缺血的心理生理学研究(PIMI)评估了未接受药物治疗的稳定型冠心病和运动诱发缺血患者的生理和神经内分泌功能。通过放射性核素心室造影、心电图、血压和儿茶酚胺监测来测量对自行车运动、公开演讲和Stroop测试的血流动力学和神经激素反应。在精神应激时,心率、收缩压、心输出量和全身血管阻力增加,且与血浆肾上腺素增加相关。运动时,全身血管阻力下降,血流动力学变化与肾上腺素水平之间无关联。精神应激时射血分数的下降幅度大于运动时。在精神应激期间,射血分数的变化与全身血管阻力的变化呈负相关。92%的患者在自行车运动期间出现心肌缺血证据,58%的患者在精神应激期间出现。运动期间缺血时血浆肾上腺素和去甲肾上腺素升高幅度更大,精神应激期间缺血时全身血管阻力升高幅度更大。

结论

与运动诱发的缺血相比,精神应激诱发的心肌缺血与全身血管阻力显著增加以及心率和心率-血压乘积相对较小的增加有关。这些对精神应激的血流动力学反应可由肾上腺分泌的肾上腺素介导。所涉及的病理生理机制对于理解心肌缺血的病因以及可能在选择合适的抗缺血治疗方面具有重要意义。

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