RESUMEN
OBJECTIVES: In healthy individuals, elevated blood pressure is associated with diminished acute pain sensitivity. These cardiovascular/pain regulatory system interactions appear altered in patients with chronic pain; elevated blood pressure is associated with increased acute and chronic pain responsiveness. If these alterations reflect failure of overlapping systems modulating pain and blood pressure, it was expected that prevalence of clinical hypertension would be increased in the chronic pain population. METHODS: A retrospective review was conducted on randomly selected records of 300 patients with chronic pain (Pain) evaluated at a tertiary care pain center and 300 nonpain internal medicine (Medicine) patients seen at the same institution. RESULTS: Results revealed that 39% of the Pain group was diagnosed with clinical hypertension, compared with 21% of the Medicine group (P < 0.001). Analyses by sex revealed similar group differences in males (P < 0.05) and females (P < 0.001), although the difference in females was double in magnitude compared with males. In contrast to more frequent male hypertension in the general population and the Medicine sample, females were more often diagnosed with hypertension (41.2%) than males (35.6%) in the Pain group. Similar group differences were obtained for antihypertensive use (P < 0.001). Stepwise logistic regression in the Pain group revealed that chronic pain intensity was a significant predictor of hypertensive status independent of the effects of age, race/ethnicity, and parental hypertension (P < 0.05). DISCUSSION: These results suggest that chronic pain may be associated with increased risk of hypertension. Factors that may underlie this association are discussed.
Asunto(s)
Antihipertensivos/uso terapéutico , Hipertensión/tratamiento farmacológico , Hipertensión/epidemiología , Dolor/epidemiología , Medición de Riesgo/métodos , Adulto , Distribución por Edad , Estudios de Casos y Controles , Enfermedad Crónica , Comorbilidad , Estudios Transversales , Femenino , Humanos , Hipertensión/diagnóstico , Masculino , Persona de Mediana Edad , Dolor/diagnóstico , Prevalencia , Grupos Raciales , Estudios Retrospectivos , Factores de Riesgo , Estados Unidos/epidemiologíaRESUMEN
Recent work suggests that an expressive anger management style (anger-out) is associated with elevated acute pain sensitivity due to endogenous opioid antinociceptive dysfunction. We tested the hypothesis that this opioid dysfunction mediates the previously reported positive association between anger-out and chronic pain intensity. To assess endogenous opioid antinociception in the laboratory, 71 subjects with chronic low back pain received opioid blockade (8 mg naloxone i.v.) or placebo in counterbalanced order in separate sessions. During each, subjects participated in a 1-min finger pressure pain task followed by an ischemic forearm pain task, providing acute pain ratings on the McGill Pain Questionnaire-Short Form (MPQ) immediately following each task. Subjects also completed a 7-day chronic pain diary based on the MPQ between laboratory sessions. To index opioid antinociceptive function, blockade effects were derived, subtracting placebo from blockade condition pain ratings. Greater anger-out was associated with both smaller blockade effects (suggesting impaired opioid antinociception) and greater chronic pain intensity, and blockade effects were inversely associated with chronic pain intensity. Sequential hierarchical regressions suggested that opioid dysfunction partially mediates the positive association between anger-out and total MPQ chronic pain intensity. Inclusion of blockade effects in the first step of the regression resulted in a decrease from 7 to 3% in chronic pain variance accounted for by anger-out. Opioid dysfunction did not mediate the positive association between anger-in and chronic pain. These results provide preliminary support for the hypothesis that the positive association between anger expression and chronic pain intensity is mediated by opioid antinociceptive system dysfunction.