Abstract
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.
Original language | English |
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Pages (from-to) | 205-223 |
Number of pages | 19 |
Journal | Journal of the American College of Cardiology |
Volume | 77 |
Issue number | 2 |
DOIs | |
State | Published - 19 Jan 2021 |
Externally published | Yes |
Keywords
- QT-prolongation
- arrhythmia
- dextromethorphan
- endocarditis
- hERG channel
- levacetylmethadol
- loperamide
- methadone
- mortality
- opioid mortality
- opioid overdose
- opioid withdrawal
- opioids
- propoxyphene
- torsade de pointes