ArticlePain reports
Resting blood pressure modulates chest pain intensity in patients with acute myocardial infarction.
Article in Pain reports. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Is Physical Activity an Effective Factor for Modulating Pressure Pain Threshold and Pain Tolerance after Cardiovascular Incidents?International journal of environmental research and public health · 2022Article
- Associated risk factors of postoperative pain after glaucoma surgery: a prospective study.International ophthalmology · 2022Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
INTRODUCTION AND
objectivesAnimal 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.
methodsPatients 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.
resultsPatients 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,
conclusionStudy 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.
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