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

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.

Pain modulation efficiency delays seeking medical help in patients with acute myocardial infarction.

Rapid reperfusion is crucial to reduce mortality in patients with ST elevation myocardial infarction. Prehospital patient delay, defined as time from symptoms onset to the decision to seek medical attention, accounts for a large proportion of cases with delayed reperfusion. However, whether pain modulation processes are involved in this phenomenon is not known. We hypothesized that prehospital patient delay may be affected by a reduction of perceived pain perception and pain modulation pattern. Pain threshold, magnitude estimation of suprathreshold stimulation, mechanical temporal summation and conditioned pain modulation (CPM), and recalls of pain magnitude at the onset of chest pain were obtained in 67 patients with first ST elevation myocardial infarction. The study's primary outcome was prehospital patient delay. The median patient delay was 24 (interquartile range, 0.5-72) hours. Of all psychophysical pain measures including pain threshold, magnitude estimation of suprathreshold stimulation, mechanical temporal summation, as well as CPM, only warm sensation threshold was independently associated with lower clinical chest pain intensity (P = 0.01). Multivariable regression analysis (R = 0.449; P < 0.0001) revealed an inverse independent association between chest pain intensity (P < 0.001) and patient delay, whereas efficient CPM was positively associated with prolonged patient delay (P = 0.034). The electrocardiography-derived myocardial ischemic area was not associated with chest pain intensity or patient delay, indicating that the affected ischemic tissue is not a dominant component that determines pain response. In conclusion, beyond the perceived chest pain intensity, the activation pattern of descending inhibition pathways during coronary occlusion affects pain interpretation and behavior during acute coronary occlusion.

The role of stimulation parameters on the conditioned pain modulation response.

Background and purpose Conditioned pain modulation (CPM) is a testing paradigm representing features of diffuse noxious inhibitory control. There is large diversity in the paradigms applied to induce CPM, and the consistency in CPM responses assessed by different paradigms is largely unknown. We aimed to characterize and explore the associations between the CPM responses assessed by different paradigms in the same cohort. Methods Thirty-three healthy middle-aged subjects underwent six CPM paradigms. The 'test-stimuli', consisted of thermal and mechanical modalities, using pain thresholds, suprathreshold pain and temporal summation types of measurements. The 'conditioning-stimulus' consisted of a contact heat stimulus applied to the thener of the left hand for 60s at an intensity of 46.5°C. Results Large variability was observed among the responses to the different CPM paradigms. Surprisingly, no correlations were found between the various CPM responses. Conclusions The variability in the CPM responses may suggest that the capacity of pain modulation is a multifaceted trait, whose expression varies with the application of different CPM paradigms. Implications Considering that CPM responses may represent different processes when assessed by different paradigms, we encourage the use of more than one CPM paradigm.