Why the study?
Widespread opioid prescribing and misuse have led to surges in unintentional deaths, drug-associated acute coronary syndrome, and endocarditis, prompting a call to action from the American College of Cardiology.
This perspective highlights the significant cardiovascular risks associated with opioid use, overdose, and withdrawal, emphasizing the need for cardiovascular care teams to be aware of these complications.
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Alerts clinicians to opioid-related MACE risks; leaves open prospective studies on prevention and mechanisms.
Opioids are the most potent of all analgesics. Although traditionally used solely for acute self-limited conditions and palliation of severe cancer-associated pain, a movement to promote subjective pain (scale, 0 to 10) to the status of a "fifth vital sign" bolstered widespread prescribing for chronic, noncancer pain. This, coupled with rising misuse, initiated a surge in unintentional deaths, increased drug-associated acute coronary syndrome, and endocarditis. In response, the American College of Cardiology issued a call to action for cardiovascular care teams. Opioid toxicity is primarily mediated via potent μ-receptor agonism resulting in ventilatory depression. However, both overdose and opioid withdrawal can trigger major adverse cardiovascular events resulting from hemodynamic, vascular, and proarrhythmic/electrophysiological consequences. Although natural opioid analogues are devoid of repolarization effects, synthetic agents may be proarrhythmic. This perspective explores cardiovascular consequences of opioids, the contributions of off-target electrophysiologic properties to mortality, and provides practical safety recommendations.
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Krantz et al. (2021) studied this question.
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