Related Experiment Video
Updated: Mar 16, 2026
Primary Outcome Assessment in a Pig Model of Acute Myocardial Infarction
Published on: October 14, 2016
Effect of Smoking on Infarct Size and Major Adverse Cardiac Events in Patients With Large Anterior ST-Elevation
Giustino Gennaro1, Sorin J Brener2, Björn Redfors3
1Department of Medicine, Interventional Cardiovascular Research and Clinical Trials, Icahn School of Medicine at Mount Sinai, New York, New York; Clinical Trials Center, Cardiovascular Research Foundation, New York, New York.
Insights
Smoking did not significantly impact infarct size in ST-elevation myocardial infarction patients. While smokers showed lower crude major adverse cardiac events, adjusted analyses revealed no significant difference, suggesting baseline risk factors explain the
Area of Science:
- Cardiology
- Interventional Cardiology
- Cardiovascular Research
Background:
- Smoking is a major risk factor for cardiovascular disease.
- The
- smoker's paradox
- describes lower mortality rates in smokers compared to non-smokers for certain conditions.
- Its impact on infarct size and major adverse cardiac events (MACE) after primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) requires further investigation.
Purpose of the Study:
- To investigate the effect of smoking status on infarct size (IS) and MACE in patients with large anterior STEMI undergoing primary PCI.
- To determine if the
- smoker's paradox
- is related to infarct size or clinical outcomes in this patient population.
Main Methods:
- Analysis of data from the Intracoronary Abciximab and Aspiration Thrombectomy in Patients with Large Anterior Myocardial Infarction (ATLAST) study.
- Patients were categorized by smoking status (current/previous smokers vs. non-smokers).
- Primary outcomes included cardiac MRI-assessed IS at 30 days and MACE at 30 days and 1 year, with multivariable regression analyses.
Main Results:
- Smokers were younger and had fewer comorbidities than non-smokers.
- No significant difference in IS at 30 days between smokers and non-smokers (16.8% vs. 17.4%, p=0.67).
- Crude 1-year MACE rates were lower in smokers (7.6% vs. 15%, p=0.01), but this difference was not significant after multivariable adjustment (aHR 0.73, p=0.30).
Conclusions:
- Smoking history did not significantly affect infarct size at 30 days post-primary PCI in STEMI patients.
- The observed lower crude MACE rates in smokers were attributable to differences in baseline demographic and clinical risk factors, not infarct size.
- These findings suggest the
- smoker's paradox
- in this context is largely explained by confounding factors rather than a protective effect of smoking on infarct healing or short-term outcomes.
Abstract:
We sought to investigate the effect of smoking on infarct size (IS) and major adverse cardiac events (MACE) in patients with large anterior ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention. Participants from the Intracoronary Abciximab and Aspiration Thrombectomy in Patients with Large Anterior Myocardial Infarction study were categorized according to smoking status (current or previous smoking vs no history of smoking). The primary imaging outcome was cardiac magnetic resonance imaging-assessed IS of left ventricular mass (%) at 30 days. The primary clinical outcome was the rate of MACE at 30 days and 1 year, defined as the composite of death, reinfarction, new-onset heart failure, or rehospitalization. Of 447 patients enrolled in Intracoronary Abciximab and Aspiration Thrombectomy in Patients with Large Anterior Myocardial Infarction, 271 (60.6%) were current or past smokers. Compared with nonsmokers, smokers were almost 10 years younger and had a lower prevalence of clinical co-morbidities. Smokers had better procedural success and angiographic reperfusion compared with nonsmokers. At 30 days, there were no differences between smokers and nonsmokers in median IS (16.8% vs 17.4%, p = 0.67) or metrics of left ventricular function. By multivariable linear regression analysis, smoking was not significantly associated with IS at 30 days (beta coefficient: 0.83, p = 0.42). At 1 year, smokers had lower crude rates of MACE (7.6% vs 15%, p = 0.01). After multivariable adjustment, there were no significant differences in 1-year MACE between smokers and nonsmokers (adjusted hazard ratio 0.73, 95% CI 0.40 to 1.33, p = 0.30). In conclusion, smoking history had no significant effect on IS at 30 days. Although current or previous smokers had lower rates of 1-year MACE than those with no history of smoking, adjustment for baseline characteristics rendered this association nonsignificant. These findings support the hypothesis that the smoker's paradox is largely attributable to differences in demographic and clinical baseline risk, rather than differences in IS after primary percutaneous coronary intervention.
Related Concept Videos
01:30Acute Coronary Syndrome I: Introduction
01:26Angina IV: Management
01:28Acute Coronary Syndrome IV: Interprofessional Care
01:19Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
01:17Ischemic Heart Disease: Overview
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...
01:30Acute Coronary Syndrome III: Diagnostic Studies