Saturday, March 03, 2007

American Heart Association on pain control*

Cardiologists have launched a save-the-heart-and-bear-the-pain campaign. Their cardiocentric viewpoint may leave those of us at risk for heart disease sidelined with aging, aching joints.

The AHA just issued new guidelines discouraging the use of COX-2 inhibitors such as Celebrex in heart patients or even those at risk for heart disease. Noting that these drugs increase sodium retention, decrease blood flow to the kidneys, and increase blood pressure, they encouraged non-drug treatments such as weight loss and physical therapy as the first-line defense against musculoskeletal pain.

If these measures are 'too little too late,' they recommended reaching for tylenol, tramodol, or narcotics before considering the so-called NSAIDs (non-steroidal anti-inflammatory drugs). Of all these various drugs (ibuprofen, piroxicam, etodolac and others), they endorsed naproxen (OTC Aleve) as cardiac neutral.

In the real world of aching joints holding up aging hearts, these guidelines create as many problems as they seek to avoid. There's obviously no losing weight without exercise, and there's no exercising while the arthritic knees are screaming. Naproxen may be cardiac neutral, but I just sent a middle-aged lady to the ER yesterday when she began passing blood clots instead of stool after five days on this drug. And another sixty-something patient in the midst of training for a triatholon is hobbling instead of running now that she's off NSAIDs and on blood thinners for intermittent atrial fibrillation.

Cardiologist Dr Scott Solomon of Brigham and Women's Hospital summed up the broader picture:

Physicians need to weigh any potential cardiovascular risks of nonselective NSAIDs together with the clear increased risk of GI bleeding against risk of abuse with narcotics.

*Information from AHA updates NSAID advice

1 comment:

Unknown said...

Aspirin versus acetaminophen for pain control in patients with cardiovascular risk

In his article published in the August 29, 2006 issue of the Canadian Medical Association Journal, Dr. Jacob Karsh(1) claimed that both coxibs and traditional NSAIDs should not be prescribed in patients at higher cardiovascular (CV) risk.

He also noted that in many painful conditions treatment with NSAIDs is not necessary or can be substituted for acetaminophen. In my opinion the rational choice for patients with CV and gastrointestinal(GI) risk factors is the use of aspirin combined with a proton-pump inhibitor.

There is good evidence that analgesic doses of aspirin (up to 1500mg) are associated with protection from CV events.(2,3) Furthermore, aspirin dose or its higher lifetime use is not significantly associated with hypertension(4) or renal toxicity.(5,6) Importantly, a recent meta- analysis of 24 randomised controlled trials found no evidence of dose- responsiveness for bleeds over a wide range of doses (50 to 1500 mg/day).(7) Indeed, aspirin in doses commonly used in practice, has an excellent safety profile.(8)

On the contrary, recent evidence suggest that both NSAIDs and acetaminophen can raise cardiovascular risk. (9) High acetaminophen use may also increase the risk of hypertension(4) and a decrease of renal function.(5) Interestingly, increased acetaminophen use has now been linked to increased prevalence of asthma and chronic obstructive pulmonary disease, and with lowered lung function.(10)

Surprisingly, a recent case-control study showed that paracetamol (>2 g per day) was associated with a greater risk of GI perforation or bleed(11) and one cohort study reported a dose-response relationship between paracetamol and dyspepsia.(12) It appears that regular use of acetaminophen is also associated with symptoms of severe diverticular disease, particularly bleeding.(13)

Lastly, compelling evidence suggests that aspirin and other NSAIDs are superior to acetaminophen for improving moderate-to-severe pain in patients with osteoarthritis(14,15,16) and rheumatoid arthritis.(17) Likewise, in acute pain states aspirin provides significant and more rapid analgesia than paracetamol.(18)

References

1. Karsh J. Anti-inflammatory drugs: what is safe? CMAJ 2006;175:449.

2. Antithrombotic Trialists' Collaboration. Collaborative meta- analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002;324:71-86.

3. Johnson ES, Lanes SF, Wentworth CE 3rd, Satterfield MH, Abebe BL, Dicker LW.A metaregression analysis of the dose-response effect of aspirin on stroke. Arch Intern Med 1999;159:1248-53.

4. Forman JP, Stampfer MJ, Curhan GC. Non-narcotic analgesic dose and risk of incident hypertension in US women. Hypertension 2005;46:500-7.

5. Curhan GC, Knight EL, Rosner B, Hankinson SE, Stampfer MJ. Lifetime nonnarcotic analgesic use and decline in renal function in women. Arch Intern Med 2004;164:1519-24.

6. Dubach UC, Rosner B, Sturmer T. An epidemiologic study of abuse of analgesic drugs. Effects of phenacetin and salicylate on mortality and cardiovascular morbidity (1968 to 1987) N Engl J Med 1991;324:155-60.

7. Derry S, Loke YK. Risk of gastrointestinal haemorrhage with long term use of aspirin: meta-analysis. BMJ 2000;321:1183-7.

8. Fries JF, Ramey DR, Singh G, Morfeld D, Bloch DA, Raynauld JP. A reevaluation of aspirin therapy in rheumatoid arthritis. Arch Intern Med 1993;153:2465-71.

9. Chan AT, Manson JE, Albert CM, Chae CU, Rexrode KM, Curhan GC, et al. Nonsteroidal antiinflammatory drugs, acetaminophen, and the risk of cardiovascular events. Circulation 2006;113:1578-87.

10. McKeever TM, Lewis SA, Smit HA, Burney P, Britton JR, Cassano PA. The association of acetaminophen, aspirin, and ibuprofen with respiratory disease and lung function. Am J Respir Crit Care Med 2005;171:966-71.

11. Garcia Rodriguez LA, Hernandez-Diaz S. Relative risk of upper gastrointestinal complications among users of acetaminophen and nonsteroidal anti-inflammatory drugs. Epidemiology 2001;12:570-6.

12. Rahme E, Pettitt D, LeLorier J. Determinants and sequelae associated with utilization of acetaminophen versus traditional nonsteroidal antiinflammatory drugs in an elderly population. Arthritis Rheum 2002;46:3046-54.

13. Aldoori WH, Giovannucci EL, Rimm EB, Wing AL, Willett WC. Use of acetaminophen and nonsteroidal anti-inflammatory drugs: a prospective study and the risk of symptomatic diverticular disease in men. Arch Fam Med 1998;7:255-60.

14. Lee C, Straus WL, Balshaw R, Barlas S, Vogel S, Schnitzer TJ. A comparison of the efficacy and safety of nonsteroidal antiinflammatory agents versus acetaminophen in the treatment of osteoarthritis: a meta- analysis. Arthritis Rheum 2004;51:746-54.

15. Towheed TE, Maxwell L, Judd MG, Catton M, Hochberg MC, Wells G. Acetaminophen for osteoarthritis. Cochrane Database Syst Rev 2006;(1):CD004257.

16. Zhang W, Jones A, Doherty M. Does paracetamol (acetaminophen) reduce the pain of osteoarthritis? A meta-analysis of randomised controlled trials. Ann Rheum Dis 2004;63:901-7.

17. Wienecke T, Gotzsche PC. Paracetamol versus nonsteroidal anti- inflammatory drugs for rheumatoid arthritis. Cochrane Database Syst Rev 2004;(1):CD003789.

18. Seymour RA, Hawkesford JE, Sykes J, Stillings M, Hill CM. An investigation into the comparative efficacy of soluble aspirin and solid paracetamol in postoperative pain after third molar surgery. Br Dent J 2003;194:153-7.

Michal R. Pijak, Assistant Professor and Consultant in Internal Medicine, Rheumatology and Clinical Immunology, Department of Internal Medicine, Slovak Medical University, Bratislava, Slovakia