Granot Michal, Dagul Pnina, Aronson Doron
The Laboratory of Clinical Neurophysiology, The Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Faculty of Social Welfare and Health Studies, University of Haifa, Haifa, Israel.
Pain Rep. 2019 Apr 10;4(3):e714. doi: 10.1097/PR9.0000000000000714. eCollection 2019 May-Jun.
Animal models and human studies show that resting blood pressure (BP) is inversely associated with pain sensitivity. The phenomenon of "hypertension-associated hypoalgesia" was proposed as a possible explanation for the intervariability in pain perception. Given that a portion of patients with acute myocardial infarction (AMI) do not experience significant pain, we used the model of severe cardiac ischemia to explore whether BP affects the intensity of chest pain.
Patients with AMI admitted to the cardiac intensive care unit with coronary catheterization-proven completely occluded coronary artery were included (n = 67). Resting BP at admission and 5 days after AMI was obtained. Participants reported chest pain intensity and underwent psychophysical evaluation including pain ratings for pressure, heat, and pinprick stimuli as well as temporal summation and conditioned pain modulation paradigms.
Patients with lower systolic BP (≤120 mm Hg) vs higher (≥140 mm Hg) reported higher chest pain scores at symptom onset (82.3 vs 61.7, = 0.048) and during peak AMI (82.8 vs 57.5, = 0.019). Higher pain ratings in response to pinprick stimulus were associated with lower BP at admission (analysis of variance = 0.036). Patients with hypertension demonstrated lower pain sensitivity in response to pressure stimulation (531.7 ± 158.9 kPa/s vs 429.1 ± 197.4). No significant associations were observed between BP and the other assessed psychophysical measures.
Study findings reinforce the phenomenon of hypertension-associated hypoalgesia through characterization of the association between BP and clinical pain experiences at onset and during AMI in a model of acute clinical pain.
动物模型和人体研究表明，静息血压（BP）与疼痛敏感性呈负相关。“高血压相关性痛觉减退”现象被提出作为疼痛感知个体差异的一种可能解释。鉴于部分急性心肌梗死（AMI）患者未经历显著疼痛，我们使用严重心脏缺血模型来探究血压是否影响胸痛强度。
纳入入住心脏重症监护病房且经冠状动脉导管检查证实冠状动脉完全闭塞的AMI患者（n = 67）。获取入院时及AMI后5天的静息血压。参与者报告胸痛强度，并接受心理物理学评估，包括对压力、热和针刺刺激的疼痛评分以及时间总和和条件性疼痛调制范式。
收缩压较低（≤120 mmHg）的患者与较高（≥140 mmHg）的患者相比，在症状发作时（82.3对61.7，P = 0.048）和AMI高峰期（82.8对57.5，P = 0.019）报告的胸痛评分更高。对针刺刺激的疼痛评分较高与入院时较低的血压相关（方差分析P = 0.036）。高血压患者对压力刺激的疼痛敏感性较低（531.7±158.9 kPa/s对429.1±197.4）。未观察到血压与其他评估的心理物理学指标之间存在显著关联。
研究结果通过在急性临床疼痛模型中表征血压与AMI发作时及期间临床疼痛体验之间的关联，强化了高血压相关性痛觉减退现象。
