In an add-on study of the WHO Solidarity trial, Norwegian investigators examined the effect of remdesivir and hydroxychloroquine on the degree of clinical respiratory failure, on SARS-CoV-2 viral load in the oropharynx, and on levels of inflammatory variables in plasma or serum.
Resting blood pressure (BP) is inversely related to pain sensitivity in individuals free of chronic pain, reflecting homeostatic interactions between cardiovascular and pain modulatory systems. Several laboratory studies indicate that BP-related hypoalgesia is diminished in chronic pain patients, suggesting dysfunction in these interacting systems. Separate epidemiological findings reveal elevated hypertension prevalence in the chronic pain population. This study for the first time simultaneously evaluated both hypertension prevalence and BP-related hypoalgesia as they relate to chronic pain in the same sample. Resting BP and pain sensitivity were evaluated in a large general population sample (n=10,135, aged 30-87years). Subjects participated in a standardized 106s cold pressor test, providing pain ratings at 9s intervals. Self-reported presence of chronic pain and history of hypertension and use of antihypertensive medication were assessed. Significant interactions between chronic pain status and resting systolic (P<.001) and diastolic BP (P<.001) on mean pain ratings were observed. These interactions were due to significant (P<.001) BP-related hypoalgesia in individuals free of chronic pain that was twice the magnitude of the hypoalgesia observed in the group reporting chronic pain. Presence of chronic pain was associated with significantly increased odds of comorbid hypertension (P<.001). Within the chronic pain group, higher chronic pain intensity was a significant predictor of positive hypertension status beyond the effects of traditional demographic risk factors (P<.05). Results are consistent with the hypothesis that increased hypertension risk in the chronic pain population might be linked in part to chronic pain-related dysfunction in interacting cardiovascular-pain modulatory systems.
Heart rate variability (HRV) and baroreflex sensitivity (BRS) are indexes reflecting the ability to maintain cardiovascular homeostasis amidst changing conditions. Evidence primarily from small studies suggests that both HRV and BRS may be reduced in individuals with chronic pain (CP), with potential implications for cardiovascular risk. We compared HRV and BRS between individuals with CP (broadly defined) and pain-free controls in a large unselected population sample. Participants were 1143 individuals reporting clinically meaningful CP and 5640 pain-free controls who completed a 106-second cold pressor test (CPT). Participants self-reported hypertension status. Resting HRV and BRS were derived from continuous beat-to-beat blood pressure recordings obtained before and after the CPT. Hierarchical regressions for the pre-CPT period indicated that beyond effects of age, sex, and body mass index, the CP group displayed significantly lower HRV in both the time domain (SDNN and rMSSD) and frequency domain (high-frequency HRV power), as well as lower BRS. Results were somewhat weaker for the post-CPT period. Mediation analyses indicated that for 6 of 7 HRV and BRS measures tested, there were significant indirect (mediated) effects of CP status on the presence of comorbid hypertension via reduced HRV or BRS. Results confirm in the largest and broadest sample tested to date that the presence of CP is linked to impaired cardiovascular regulation and for the first time provide support for the hypothesis that links between CP and comorbid hypertension reported in previous population studies may be due in part to CP-related decrements in cardiovascular regulation.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.