Robinson T G, James M, Youde J, Panerai R, Potter J
University Division of Medicine for the Elderly, Glenfield Hospital, Leicester Royal Infirmary, UK.
Stroke. 1997 Sep;28(9):1671-6. doi: 10.1161/01.str.28.9.1671.
The blood pressure (BP) fall and increased BP variability after acute stroke have been previously described. The underlying pathophysiological mechanisms producing these findings are unclear but may include abnormalities of cardiac baroreceptor reflex arc and/or changes in sympathetic nervous system activity. To date, evidence of impaired cardiac baroreceptor sensitivity (BRS) after stroke is limited to patients with chronic disease as determined by invasive methodology. Therefore, it was proposed to assess cardiac BRS and sympathovagal balance with the use of novel noninvasive techniques after acute stroke.
Thirty-seven acute stroke patients underwent simultaneous surface electrocardiographic and noninvasive beat-to-beat BP recording. Cardiac BRS was assessed by power spectral analysis techniques, and sympathovagal balance was determined from the ratio of the low- to high-frequency powers for pulse interval variability. The responses were compared with a control group matched for age, sex, and BP.
Median cardiac BRS was significantly lower in stroke patients than in control subjects (high-frequency alpha-index, 4.89 versus 6.50 ms/mm Hg; P = .007; combined alpha-index, 4.65 versus 5.46 ms/mm Hg; P = .02). Median normalized high- but not low-frequency power of systolic BP variability was significantly greater in stroke patients (11.0 versus 6.7 normalized units; P < .001), probably reflecting differences in the mechanical effects of respiration on BP in stroke patients. No significant differences were observed in the power spectrum of pulse interval variability between stroke patients and control subjects. Patients with tight hemisphere strokes, however, had a significant reduction in median high-frequency pulse interval power compared with patients with left hemisphere strokes (8 versus 20 normalized units; P = .03), which may reflect a change in sympathovagal balance in favor of increased sympathetic tone in this group.
The impairment of cardiac BRS may be important in explaining the increased BP variability after stroke. There was no significant difference in surrogate measures of sympathovagal activity between acute stroke patients and control subjects, but right hemisphere stroke patients had a significant alteration in the sympathovagal balance of pulse interval variability compared with left hemisphere stroke patients. This sympathetic predominance in right hemisphere strokes may be important in the development of cardiac arrhythmias after stroke. The prognostic implications of these findings need to be further explored.
急性卒中后血压（BP）下降及血压变异性增加此前已有描述。产生这些结果的潜在病理生理机制尚不清楚，但可能包括心脏压力感受器反射弧异常和/或交感神经系统活动变化。迄今为止，卒中后心脏压力感受器敏感性（BRS）受损的证据仅限于采用侵入性方法确定的慢性病患者。因此，有人提议在急性卒中后使用新型非侵入性技术评估心脏BRS和交感迷走神经平衡。
37例急性卒中患者同时进行表面心电图和无创逐搏血压记录。通过功率谱分析技术评估心脏BRS，并根据脉搏间期变异性的低频与高频功率之比确定交感迷走神经平衡。将这些反应与年龄、性别和血压匹配的对照组进行比较。
卒中患者的心脏BRS中位数显著低于对照组（高频α指数，4.89对6.50 ms/mm Hg；P = 0.007；综合α指数，4.65对5.46 ms/mm Hg；P = 0.02）。卒中患者收缩压变异性的归一化高频功率中位数显著高于低频功率中位数（11.0对6.7归一化单位；P < 0.001），这可能反映了卒中患者呼吸对血压的机械作用差异。卒中患者与对照组之间在脉搏间期变异性的功率谱上未观察到显著差异。然而，与左侧半球卒中患者相比，右侧半球卒中患者的高频脉搏间期功率中位数显著降低（8对20归一化单位；P = 0.03），这可能反映了该组交感迷走神经平衡的变化，有利于交感神经张力增加。
心脏BRS受损可能在解释卒中后血压变异性增加方面具有重要意义。急性卒中患者与对照组之间在交感迷走神经活动的替代指标上无显著差异，但与左侧半球卒中患者相比，右侧半球卒中患者在脉搏间期变异性的交感迷走神经平衡方面有显著改变。右侧半球卒中的这种交感神经优势可能在卒中后心律失常的发生中起重要作用。这些发现的预后意义需要进一步探讨。
