Resting blood pressure modulates chest pain intensity in patients with acute myocardial infarction

• Main Authors: Michal Granot, Pnina Dagul, Doron Aronson
• Format: Article
• Language: English
• Published: Wolters Kluwer 2019-06-01
• Series: PAIN Reports
• Online Access: http://journals.lww.com/painrpts/fulltext/10.1097/PR9.0000000000000714

Abstract. Introduction and Objectives:. 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. Methods:. 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. Results:. 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, P = 0.048) and during peak AMI (82.8 vs 57.5, P = 0.019). Higher pain ratings in response to pinprick stimulus were associated with lower BP at admission (analysis of variance P = 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. Conclusion:. 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.