Post-STEMI ‘smoker’s paradox’ debunked by meta-analysis
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A meta-analysis of 10 randomized trials demonstrated that the so-called “smoker’s paradox” of favorable short-term outcomes after primary PCI in STEMI may not exist after adjustment for other risk factors.
After adjustment, smoking was not associated with infarct size or microvascular obstruction and conferred greater risk for death or HF hospitalization.
The perceived protective effects of smoking were associated with younger age and fewer CV risk factors among the smoking group, according to the researchers.
According to findings published in the Journal of the American College of Cardiology, among 2,564 patients with STEMI (43% smokers), infarct size was similar between smokers and nonsmokers (adjusted difference, 0%; 95% CI, –3.3 to 3.3).
In addition, there was no significant difference between the groups in microvascular obstruction (adjusted difference, –0.3%; 95% CI, –1.4 to 0.9).
Smokers experienced lower crude 1-year rates for all-cause mortality (1% vs. 2.9%; P < .001) and death or HF hospitalization (3.3% vs. 5.1%; P = .009) and similar reinfarction rates. However, after adjusting for age and other risk factors, researchers found that smokers had similar 1-year risk for all-cause mortality (aHR = 0.92; 95% CI, 0.46-1.84) and greater risk for death or HF hospitalization (aHR = 1.49; 95% CI, 1.09-2.02) and reinfarction (aHR = 1.97; 95% CI, 1.17-3.33) compared with nonsmokers.
According to the study, patients in the smoking group were on average 10 years younger than the nonsmokers and had fewer comorbidities.
Age makes difference
“The observed lower 1-year crude rates of adverse events among smokers compared with nonsmokers was explained predominantly by their younger age. After accounting for this factor and other baseline differences, smokers were at substantially higher risk for reinfarction and the composite of death or HF hospitalization,” Björn Redfors, MD, PhD, medical director of the Data Coordinating Center at the Cardiovascular Research Foundation, assistant professor of clinical medicine in the division of cardiology at NewYork-Presbyterian Hospital/Columbia University Medical Center and associate professor of cardiology at Sahlgrenska University Hospital in Gothenburg, Sweden, and colleagues wrote. “This fact, compounded by the occurrence of STEMI 10 years earlier in smokers compared with nonsmokers, should lay to rest any residual belief that smoking is beneficial to atherosclerosis development, progression or treatment.”
For this pooled analysis of randomized trials, patients with infarct size assessed by either cardiac MRI or technetium-99m sestamibi single-photon emission CT within 1 month of reperfusion were included. All patients were followed up for at least 6 months.
Unintended consequences
“The term ‘smoker’s paradox’ is often used to describe a counterintuitive result, and the aim of deconstruction is to expose biases, flaws or inconsistencies. This paper does this very well. However, can a paradox be completely deconstructed with observational data?” Harvey D. White, DSC, of Green Lane Cardiovascular Services, Auckland City Hospital and University of Auckland, New Zealand, wrote in a related editorial. “The improvement in epicardial TIMI flow grade 3 in smokers compared with nonsmokers surprisingly did not translate into improved microcirculatory perfusion, reduced infarct size, reduced microvascular obstruction or improved prognosis; this remains a paradox opposite to the previous smoker’s paradox.
“We are now faced with the possibility that the unintended consequences of using vaping to quit may result in new vapers taking up smoking and a new generation of smokers having MIs 10 years earlier,” he wrote. – by Scott Buzby
Disclosures: Redfors reports no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures. White reports he received grant support from American Regent, CSL Behring, DalCor, Eisai, Esperion Therapeutics, Omthera, Pfizer, Regeneron, Sanofi and Sanofi Australia; served on the advisory board for Genentech; and received lecture fees from AstraZeneca.
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Redfors B, et al. J Am Coll Cardiol. 2020;doi:10.1016/j.jacc.2020.02.045.
White HD. J Am Coll Cardiol. 2020;doi:10.1016/j.jacc.2020.02.044.
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