It is well known that carbon monoxide (CO) produced by the combustion of cigarettes reduces the oxygen-carrying capacity of the blood, but do elevated CO levels affect the prognosis of smokers presenting with acute cardiac events?
As part of a fascinating Late-Breaking Science session yesterday, Professor Patrick Henry (AP-HP - Hospital Lariboisière, Université de Paris Cité - Paris, France) described results of the prospective ADDICT-ICCU study, which was designed to evaluate this important question. CO levels were assessed with an expiratory CO testing device in all 1,379 patients admitted to ICCU in 39 centres across France over a 2-week period in April 2021. Patients were excluded if they were hospitalised for a planned interventional procedure or hospitalised for more than 24 hours at any hospital facility before ICCU admission. The primary outcome was in-hospital major adverse cardiac events (MACE), defined as death, resuscitated cardiac arrest or cardiogenic shock.
With a mean age of 64 years, most patients were male (70%), around half had hypertension (53%), 38% had dyslipidaemia and 21% had diabetes mellitus. Almost half of the overall population had known coronary artery disease (46%). The main final diagnosis was acute coronary syndrome in 52% of patients (57% had NSTEMI and 43% had STEMI) and acute heart failure in 13% of patients. One-third of the study population were non-smokers (33%), 40% were former smokers and 27% were active smokers.
Mean (± SD) CO levels were similar between non-smokers and former smokers (3.6 ± 3.6 and 3.3 ± 2.8 ppm, respectively; p=0.12); however, they were significantly increased in active smokers (9.9 ± 6.4 ppm; p<0.001). There were 58 (4.2%) in-hospital MACE and CO levels were found to be significantly associated with MACE in active smokers (odds ratio [OR] 1.14; 95% CI 1.08 to 1.20 per unit ppm). In three different models, CO levels >13 ppm were significantly associated with MACE (model 1 based on comorbidities: OR 23.0; 95% CI 8.1 to 78.3; model 2 based on in-hospital severity: OR 19.7; 95% CI 6.9 to 65.1; and model 3 based on respiratory parameters: OR 37.8; 95% CI 11.4 to 167). Interestingly, in smokers with CO level ≤13 ppm, the rate of MACE was not significantly different to non-smokers or former smokers (p=0.65). The authors found similar results when CO levels and total mortality were analysed, with a significant association between CO levels >13 ppm and death in smokers admitted to the ICCU.
Prof. Henry ended the presentation by highlighting that further studies are needed to understand whether oxygen therapy, similar to that performed in CO poisoning, could significantly decrease MACE in patients with elevated CO levels.
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