Chronic pain-related changes in cardiovascular regulation and impact on comorbid hypertension in a general population: the Tromsø study

• Published in: Pain
• Main Authors: Bruehl, Stephen, Olsen, Roy Bjørkholt, Tronstad, Christian, Sevre, Knut, Burns, John W., Schirmer, Henrik, Nielsen, Christopher Sivert, Stubhaug, Audun, Rosseland, Leiv Arne
• Format: Article in Journal/Newspaper
• Language: English
• Published: Ovid Technologies (Wolters Kluwer Health) 2017
• Subjects: Tromsø
• Online Access: http://dx.doi.org/10.1097/j.pain.0000000000001070; https://journals.lww.com/00006396-201801000-00016

Abstract 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.