Coronary artery disease and opioid use

Marmor, Michael; Penn, Arthur; Widmer, Kyle; Levin, Richard I.; Maslansky, Robert

doi:10.1016/j.amjcard.2004.01.072

Cited by 61 publications

(43 citation statements)

References 13 publications

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“…Other responses, including PC and postconditioning, are well conserved across species, and opioid-mediated protection is documented in species from mouse to human (Gross, 2003). Indirect epidemiological evidence (Marmor et al, 2004) indicates that long-term opiate exposure in drug users attenuates coronary artery disease severity/mortality, implicating cardioprotection from prolonged opioid exposure in humans. A key future goal will be to test for occurrence of SLP in other species and ultimately humans.…”

Section: Discussionmentioning

confidence: 99%

Sustained Ligand-Activated Preconditioning via δ-Opioid Receptors

Peart¹,

Hoe²,

Gross³

et al. 2010

J Pharmacol Exp Ther

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We have previously described novel cardioprotection in response to sustained morphine exposure, efficacious in young to aged myocardium and mechanistically distinct from conventional opioid or preconditioning (PC) responses. We further investigate opioid-dependent sustained ligand-activated preconditioning (SLP), assessing duration of protection, opioid receptor involvement, additivity with conventional responses, and signaling underlying preischemic induction of the phenotype. Male C57BL/6 mice were treated with morphine (75-mg subcutaneous pellet) for 5 days followed by morphine-free periods (0, 3, 5, or 7 days) before ex vivo assessment of myocardial tolerance to 25-min ischemia/45-min reperfusion. SLP substantially reduced infarction (by ϳ50%) and postischemic contractile dysfunction (eliminating contracture, doubling force development). Cardioprotection persisted for 5 to 7 days after treatment. SLP was induced specifically by ␦-receptor and not -or -opioid receptor agonism, was eliminated by ␦-receptor and nonselective antagonism, and was additive with adenosinergic but not acute morphine-or PC-triggered protection. Cotreatment during preischemic morphine exposure with the phosphoinositide-3 kinase (PI3K) inhibitor wortmannin, but not the protein kinase A (PKA) inhibitor myristoylated PKI-(14-22)-amide, prevented induction of SLP. This was consistent with shifts in total and phospho-Akt during the induction period. In summary, data reveal that SLP triggers sustained protection from ischemia for up to 7 days after stimulus, is ␦-opioid receptor mediated, is induced in a PI3K-dependent/PKA-independent manner, and augments adenosinergic protection. Mechanisms underlying SLP may be useful targets for manipulation of ischemic tolerance in young or aged myocardium.

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Section: Discussionmentioning

confidence: 99%

Sustained Ligand-Activated Preconditioning via δ-Opioid Receptors

Peart¹,

Hoe²,

Gross³

et al. 2010

J Pharmacol Exp Ther

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“…A postmortem analysis of the incidence of coronary artery disease (CAD) in 98 methadone or opiod users vs 97 frequency-matched non-users revealed that chronic opioid use may reduce the severity of CAD [104]. Multiple logistic regression analysis yielded an odds ratio of 0.43 (0.20 to 0.94 confidence interval) for opioid use after adjustment for potentially confounding factors.…”

Section: Opioid-induced Cardioprotection In Humansmentioning

confidence: 99%

Opioid-induced Cardioprotection

Tanaka¹,

Kersten²,

Riess³

2014

CPD

102

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Ischemic heart disease and myocardial infarction continue to be leading causes of cardiovascular morbidity and mortality. Activation of opioid, adenosine, bradykinin, adrenergic and other G-protein coupled receptors have been found to be cardioprotective. κ- and/or δ-opioid receptor activation is involved in direct myocardial protection, while the role of μ-opioid receptors seems less clear. In addition, differential affinities to the three opioid-receptor subtypes by various agonists and cross-talk among different G-protein coupled receptors render conclusions regarding opioid-mediated cardioprotection challenging. The present review will focus on the protective effects of endogenously released opioid peptides as well as exogenously administered opioids such as morphine, fentanyl, remifentanil, butorphanol, and methadone against myocardial ischemia/reperfusion injury. Receptor heterodimerization and cross-talk as well as interactions with other cardioprotective techniques will be discussed. Implications for opioid-induced cardioprotection in humans and for future drug development to improve myocardial salvage will be provided.

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“…Asadi Karam et al (2004) reported that opium addicted patients with non-insulin dependent diabetic mellitus (NIDDM) had lower plasma level of HDL compared to their none-addicted control. On the other hand, some studies show that some opioids including morphine have cardio protective functions (Peart et al, 2005) or long-term exposure to opiates reduce severity of coronary artery disease and incidence of fatal myocardial infarction (Marmor et al, 2000). Human studies are along with many confounding factors, for example: differences in opium constituents, dose, frequency and route of consumption and association with other substances (tobacco and cigarette smoking, alcohol and narcotic or tranquilizer drugs).…”

Section: Introductionmentioning

confidence: 98%