Wednesday, January 30, 2013

Does Chronic Pain Raise Hypertension Risks?

Blood PressureExperienced pain practitioners have noted that unrelieved pain often may be objectively assessed by clinical signs in patients with chronic pain conditions. Results of a recently reported, large-scale research study suggest that these patients may exhibit a greater risk of hypertension and increased sensitivity to acute pain.

According to background information provided in the study report, published in the February 2013 edition of the journal PAIN, systems modulating blood pressure (BP) and influencing pain overlap physiologically and interact functionally, such that blood pressure is usually stabilized in the presence of acute pain [Olsen et al. 2013]. At the same time, relatively higher resting BP levels are generally associated with hypoalgesia, or reduced sensitivity to acute pain.

However, this BP-related hypoalgesia may be diminished or absent in persons with chronic pain conditions. And, although exact mechanisms for the effect are undetermined, changes in the cardiovascular-pain-modulating system also appear to increase hypertension risk in persons with chronic pain. For example, one large epidemiological study indicated that chronic low back pain was associated with a 50% increased risk for hypertension.

To further examine these relationships, a research team in Norway conducted a first of its kind study to evaluate hypertension prevalence and measure the effect of blood pressure (BP) on acute pain sensitivity in a large general population of persons with chronic pain compared with pain-free controls. Subjects — N=10,135; mean age 56 years, range 30–87 years — were part of a large epidemiological and prospective study of health problems, symptoms, and chronic diseases initiated in 1974 — the Norwegian Tromsø Study — and most recently updated during 2007-2008 from which subjects were recruited for the present investigation.

Data on the self-reported presence of chronic pain in any part of the body, history of hypertension, and use of antihypertensive medications were gathered for all subjects:

  • Nearly a third (32%) of subjects (61% female) reported chronic pain of any sort, while the remainder (47% female) were free of chronic pain.

  • Among those with chronic pain the typical intensity was 5.0±1.8 on a 0-to-10 scale and mean duration of pain was 10 years.

  • Persons with chronic pain reported significantly more hypertension. Among subjects with chronic pain, 31% had been diagnosed with hypertension and 23% were taking antihypertensive medications, compared with 26% of pain-free subjects with hypertension and 20% taking antihypertensive meds (P<0.001 for differences between groups).

All subjects participated in a standardized cold pressor test, requiring them to immerse their hands in a container of freezing cold water and provide pain ratings at regular intervals. Significant interactions were observed between (a) chronic pain status, (b) resting BP — both systolic and diastolic — and (c) acute-pain tolerance. In pain-free subjects, having higher resting blood pressure allowed significantly greater tolerance of the painful stimulus (cold pressor test); whereas, no such effects were observed overall in those with chronic pain.

In conclusion, the researchers note that there was significant BP-related hypoalgesia (reduced acute pain sensitivity) in persons free of chronic pain (P<0.001), and the magnitude of this effect was twice the hypoalgesia observed in the group with chronic pain. At the same time — even after adjusting for age, sex, and body mass index — the presence of chronic pain was associated with a significant 23% increased odds of having comorbid hypertension (adjusted Odds Ratio=1.23; 95% Confidence Interval, 1.11-1.35; P<0.001). Additionally, higher intensity of chronic pain was a significant predictor of reported hypertension, beyond the effects of traditional demographic risk factors for elevated blood pressure (P<0.05).

COMMENTARY: This present investigation by Olsen and colleagues, and prior epidemiological studies noted by the authors, suggest that chronic pain may be a significant contributor to the onset and persistence of hypertension. Along with that, the ability of cardiovascular mechanisms to modulate acute pain sensitivity were dysfunctional in persons with chronic pain.

It should be noted, however, that data in this observational study are associative in nature and, thereby, do not prove cause-effect relationships or which came first, chronic pain or hypertension. Additionally, subjects in the chronic pain group reported overall typical pain of moderate intensity (5.0 on a 10 point scale), which may suggest that their pain was under some degree of control; although, the researchers do note that higher pain intensity among select subjects was correlated with an increasing likelihood of hypertension.

It also might be suspected that subjects’ use of antihypertensive medications and/or analgesics might have skewed outcomes. However, the researchers conducted a sensitivity analysis controlling for these variables and did not find any significant alterations of results.

A strength of this study was its large and diverse population of patients, albeit from a single Nordic region, and a broad definition of chronic pain; ie, pain of >3 months duration in any part of the body. But a limitation is that chronic pain status, as well as hypertension status and antihypertensive use, were determined solely by self-reports of participants. While inaccuracies of such reports may not have been sufficient to strongly affect outcomes, this is unknown.

While there was a 23% increased likelihood of hypertension associated with chronic pain, in absolute terms there was a 5.5% greater prevalence of hypertension in subjects with chronic pain than in their pain-free counterparts. This is less than reported in other studies of chronic pain and may not seem large, but on a population level it could be of considerable consequence.

For example, in the United States, with an estimated 100+ million persons suffering chronic pain, this could amount to 5.5-million cases of health-threatening hypertension requiring attention in pain-care settings. The prevalence rate of hypertension might expectedly be much greater specifically among patients with severe and/or unrelieved chronic pain.

Decreased tolerance to acute pain stimuli by persons with chronic pain, as evidenced in this study by Olsen et al., also could be of some importance. Such patients may be more sensitive to breakthrough pain during continuous analgesia and/or pain associated with injury or medical procedures than previously imagined. Further research, using prospective, randomized, and controlled designs might better elucidate the interrelationships of blood pressure, chronic pain, and response to acute pain in this population of patients.

Concern about hypertension, or at least elevated blood pressure, prevalence in patients with chronic pain is not a new concept. In a previous paper for Pain Treatment Topics — “Using Objective Signs of Severe Pain to Guide Opioid Prescribing” [PDF available here] — Forest Tennant, MD, DrPH, notes that uncontrolled chronic pain may be objectively assessed clinically by elevated blood pressure, as well as by increased pulse rate and pupil size, and the many ways in which these patients seek positional or postural relief and sensory avoidance. These signs can be helpful for determining appropriate treatments and measuring patient responses to therapy.

Furthermore, a prior large-scale research investigation observed a profound link between severe chronic pain and a 70% increased risk of all-cause mortality [see UPDATE here]. Hypertension, as a contributor to cardiovascular-related death, could be of special concern in elderly patients with chronic pain and whenever prescribing analgesic therapies that may carry risks of cardiovascular adverse effects in patients of any age.

REFERENCE: Olsen RB, Bruehl S, Nielsen CS, et al. Hypertension prevalence and diminished blood pressure–related hypoalgesia in individuals reporting chronic pain in a general population: The Tromsø Study. 2013(Feb);154(2):257-262 [abstract].

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