Impact of prehospital opioid dose on angiographic and clinical outcomes in acute coronary syndromes.

BACKGROUND: An adverse interaction whereby opioids impair and delay the gastrointestinal absorption of oral P2Y12 inhibitors has been established, however the clinical significance of this in acute coronary syndrome (ACS) is uncertain. We sought to characterise the relationship between prehospital opioid dose and clinical outcomes in patients with ACS. METHODS: Patients given opioid treatment by emergency medical services (EMS) with ACS who underwent percutaneous coronary intervention (PCI) between 1 January 2014 and 31 December 2018 were included in this retrospective cohort analysis using data linkage between the Ambulance Victoria, Victorian Cardiac Outcomes Registry and Melbourne Interventional Group databases. Patients with cardiogenic shock, out-of-hospital cardiac arrest and fibrinolysis were excluded. The primary end point was the risk-adjusted odds of 30-day major adverse cardiac events (MACE) between patients who received opioids and those that did not. RESULTS: 10 531 patients were included in the primary analysis. There was no significant difference in 30-day MACE between patients receiving opioids and those who did not after adjusting for key patient and clinical factors. Among patients with ST-elevation myocardial infarction (STEMI), there were significantly more patients with thrombolysis in myocardial infarction (TIMI) 0 or 1 flow pre-PCI in a subset of patients with high opioid dose versus no opioids (56% vs 25%, p<0.001). This remained significant after adjusting for known confounders with a higher predicted probability of TIMI 0/1 flow in the high versus no opioid groups (33% vs 11%, p<0.001). CONCLUSIONS: Opioid use was not associated with 30-day MACE. There were higher rates of TIMI 0/1 flow pre-PCI in patients with STEMI prescribed opioids. Future prospective research is required to verify these findings and investigate alternative analgesia for ischaemic chest pain.

Long-term predictors of mortality after percutaneous coronary intervention in the era of drug-eluting stents.

The aim was to examine timing, causes, and predictors of death during long-term follow-up after contemporary percutaneous coronary intervention (PCI) using a large multicenter Australian registry. The cohort consisted of 10,682 consecutive patients from the Melbourne Interventional Group registry undergoing PCI (February 2004 through November 2009). For the first time in Australia, long-term mortality rates of a PCI cohort were defined by linkage to the National Death Index database. The cohort (mean age 64 ± 12 years) comprised 75% men, 24% diabetics, 59% with multivessel disease, 4.4% with renal failure, 25% with ST-elevation myocardial infarction (STEMI), 2.5% with cardiogenic shock, and 5.1% with heart failure. Drug-eluting stents (DES) were used in 43% of cases. Mean follow-up was 3.2 ± 0.5 years. In-hospital, 30-day, 12-month, and long-term (3.2 ± 0.5 years) mortalities were 1.6% (80% cardiac), 2.1% (79%), 3.9% (61%), and 8.2% (50%), respectively. Independent predictors of long-term mortality included age (hazard ratio 1.05, 95% confidence interval 1.04 to 1.06), cardiogenic shock (4.58, 3.60 to 5.83), renal failure (3.14, 2.58 to 3.82), previous heart failure (1.97, 1.60 to 2.41), STEMI (1.79, 1.47 to 2.18), peripheral vascular disease (1.72, 1.4 to 2.11), non-STEMI (1.58, 1.32 to 1.90), multivessel disease (1.47, 1.24 to 1.74), current smoking (1.39, 1.12 to 1.71), diabetes (1.36, 1.16 to 1.59), and cerebrovascular disease (1.33, 1.06 to 1.60, p <0.01 for all comparisons). DES deployment appeared protective against late mortality (hazard ratio 0.85, 0.73 to 0.99, p = 0.04); however, after 30 days, there was no difference in mortality rates between those who received a bare metal stent and those who received a DES. In conclusion, different clinical variables such as renal and heart failure predicted long-term mortality after PCI, whereas DES use in this large registry was not associated with late mortality risk.