Coronary artery disease and opioid use

doi:10.1016/j.amjcard.2004.01.072

The American Journal of Cardiology

Volume 93, Issue 10, 15 May 2004, Pages 1295-1297

https://doi.org/10.1016/j.amjcard.2004.01.072 Get rights and content

Abstract

Over the past 20 years, we have observed a paucity of morbidity and mortality due to cardiovascular disease among drug users in a methadone maintenance clinic. The present study investigated whether long-term exposure to opiates or opioids is associated with decreased severity of coronary artery disease (CAD) by comparing 98 decedents with methadone or opiates (M/O) in their blood at autopsy with 97 frequency-matched decedents without M/O. Severe CAD was found significantly less often in M/O-positive decedents (5 of 98) than in M/O-negative decedents (16 of 97). Multiple logistic regression analysis contrasting those with moderate or severe CAD to those with no or mild CAD yielded an odds ratio of 0.43 (95% confidence interval 0.20 to 0.94) for M/O positivity after adjustment for potential confounding. Long-term opiate exposure thus may mitigate CAD severity and its often fatal consequences.

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Acknowledgements

We thank Barbara Sampson, MD, PhD, Office of the Chief Medical Examiner of the City of New York, for providing the data analyzed in this report.

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^☆: This work was supported in part by grant 1 R01 DA 15303 from the National Institute on Drug Abuse, Bethesda, Maryland, and a Grant-in-Aid from the American Heart Association (Southeast Affiliate), Marietta, Georgia.

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Coronary artery disease and opioid use☆

Abstract

Section snippets

Acknowledgements

Jpn J Pharmacol

J Biol Chem

Eur J Pharmacol

J Am Coll Cardiol

Morphine enhances pharmacological preconditioning by isofluranerole of mitochondrial K(ATP) channels and opioid receptors

Anesthesiology

Adenosine and opioid receptor-mediated cardioprotection in the ratevidence for cross-talk between receptors

Am J Physiol Heart Circ Physiol

Opiate drugs and delta-receptor-mediated myocardial protection

Circulation

Protection of cardiac myocytes via delta-1 opioid receptors, protein kinase C and mitochondrial K+ATP channels

Am J Physiol

Opioid Analgesics and Antagonists