CMR evidence of improved infarct healing after STEMI: a call to intensify smoking cessation efforts

This editorial refers to ‘Smoking cessation after first STEMI enhances infarct healing: a cardiac MRI study’, by F. Troger et al., https://doi.org/10.1093/ehjci/jeag087. Smoking remains a major modifiable determinant of cardiovascular risk and is strongly associated with the development and progression of atherosclerotic disease.1 Through mechanisms including endothelial dysfunction, oxidative stress, inflammation, and enhanced thrombogenicity, tobacco use contributes to plaque instability and acute coronary events.2 Beyond its biological effects, smoking is closely linked to socioeconomic status and lower levels of education, emphasizing the importance of targeted information and structured support to improve both primary and secondary prevention.3,4 In the setting of ST-segment elevation myocardial infarction (STEMI), smoking is not only a trigger of the acute event but also a key determinant of subsequent outcomes.5 While the harmful effects of continued smoking after myocardial infarction are well established, its impact on myocardial remodelling has been less extensively explored, and even less is known about the potential benefits of smoking cessation on infarct healing. Myocardial remodelling after STEMI, characterized by changes in left ventricular (LV) structure and function, is a central determinant of long-term prognosis, influencing the development of heart failure (HF) and survival. In this context, cardiac magnetic resonance imaging (CMR) offers a unique opportunity to quantify infarct size and monitor myocardial recovery over time. In the present issue of European Heart Journal: Cardiovascular Imaging, Troger et al.6 report a prospective study providing important mechanistic and clinical insights into the effect of smoking cessation on cardiac remodelling and outcomes after STEMI (Figure 1). The investigators enrolled 672 patients with a first-time STEMI who underwent successful revascularization. CMR was performed at baseline and repeated at 4 and 12 months, allowing detailed assessment of infarct evolution. Patients were followed for a median of 3.4 years to evaluate major adverse cardiovascular events (MACE). Out of 382 active smokers, only 183 patients (48%) successfully discontinued smoking, highlighting the persistent challenge of smoking cessation in clinical practice. The study demonstrates that smoking cessation is associated with significantly improved infarct healing. At 12 months, infarct size reduction was greater in patients who quit smoking compared with those who continued (62% vs. 47%, P < 0.001). This finding suggests that smoking cessation favourably modulates myocardial repair, potentially through reductions in oxidative stress, inflammation, and microvascular dysfunction. Importantly, these imaging findings translated into clinical benefit. MACE occurred less frequently among patients who quit smoking (4% vs. 12%, P = 0.005), and continued smoking remained independently associated with both impaired infarct healing and increased risk of MACE after multivariable adjustment. These findings are highly relevant from both mechanistic and clinical perspectives (Figure 1). Smoking cessation is here directly linked to improved myocardial healing assessed by serial CMR, providing objective evidence that quitting smoking has a measurable impact on cardiac recovery after STEMI. This shifts smoking cessation from a general preventive recommendation to a determinant of post-infarction remodelling. When contextualized with established therapies, the magnitude of benefit is noteworthy. Pharmacological strategies such as angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and mineralocorticoid receptor antagonists are well known to attenuate adverse remodelling and improve outcomes after myocardial infarction.7 Angiotensin-converting enzyme inhibitors reduce mortality and MACE in patients with reduced LV ejection fraction, while mineralocorticoid receptor antagonists further improve outcomes in selected high-risk populations.7,8 In contrast, recent evidence suggests that beta-blockers do not confer a prognostic benefit in patients with preserved LV ejection fraction after myocardial infarction, questioning their routine use in this subgroup.9 Against this background, the reduction in MACE observed with smoking cessation, from 12% to 4%,6 is clinically meaningful and comparable to or greater than that observed with several pharmacological interventions. The associated improvement in infarct healing supports a direct biological effect. Smoking cessation can therefore be considered a non-pharmacological intervention with therapeutic relevance for myocardial recovery and prevention of HF. Residual cardiovascular risk remains a major challenge despite optimal medical therapy and control of traditional risk factors. While considerable effort has been devoted to the development of new pharmacological strategies targeting inflammation and lipid metabolism, lifestyle factors such as smoking continue to play a substantial role and are often under-addressed.10 The present study highlights that continued smoking contributes meaningfully to this residual risk and that addressing it can yield significant benefits. Smoking cessation should therefore receive the same level of attention as pharmacological optimization in post-STEMI care. Routine assessment of smoking status, structured counselling, and access to cessation programmes should be integral components of management. Smoking cessation effects on myocardial healing after STEMI. CMR, cardiac magnetic resonance; ECV, extracellular volume; HF, heart failure; LV, left ventricle; MACE, major adverse cardiovascular events; STEMI, ST-segment elevation myocardial infarction. Future research should further explore the impact of different forms of smoking on myocardial remodelling. In addition to traditional combustible cigarettes, alternative nicotine delivery systems such as electronic cigarettes and heated tobacco products are increasingly used.11 Their cardiovascular effects are not fully understood, although current evidence suggests adverse effects on endothelial function, arterial stiffness, and hemodynamic, particularly with nicotine-containing products.11 Understanding their impact on infarct healing and outcomes after STEMI is essential to guide clinical practice. Moreover, future studies should investigate the effect of smoking cessation not only on infarct size but also on the remote myocardium. The peripheral zone beyond the infarcted area has emerged as an important determinant of prognosis.12,13 Advanced CMR parameters such as extracellular volume (ECV) have been shown to capture diffuse myocardial changes in the remote myocardium and to provide prognostic information in STEMI patients.12,13 Assessing whether smoking cessation favourably influences these markers would provide additional mechanistic insight into its role in post-infarction remodelling. It is also important to acknowledge some limitations of the present study. Although infarct size was carefully assessed, no data were provided on advanced CMR tissue characterization parameters such as ECV, native T1 and T2 mapping, or feature tracking derived strain imaging. These techniques allow a more comprehensive evaluation of myocardial injury, oedema, fibrosis, and deformation, and could have further elucidated the mechanisms linking smoking cessation to improved myocardial recovery. Another important area for future investigation is the role of structured smoking cessation strategies in this patient population. Behavioural interventions, patient education, and pharmacological therapies including nicotine replacement therapy, varenicline, and bupropion have demonstrated efficacy in increasing smoking cessation rates.14 Varenicline, in particular, has been shown to significantly improve abstinence rates without increasing cardiovascular risk.14 Whether these interventions can also translate into improved myocardial remodelling and reduced MACE after STEMI remains to be determined in dedicated studies. From an economic perspective, smoking cessation after STEMI has important implications. Adverse remodelling can lead to HF, a condition associated with high healthcare costs, recurrent hospitalizations, and reduced quality of life. By improving infarct healing and reducing MACE, smoking cessation may decrease the burden of HF and associated healthcare expenditures.15 In addition, improved cardiovascular health contributes to increased productivity and fewer lost working days. The mechanistic insights provided by this study support ongoing clinical and public health efforts to reduce smoking prevalence. At the policy level, measures such as tobacco taxation, advertising restrictions, and smoke-free legislation remain essential. At the clinical level, cardiologists should systematically assess smoking status, provide counselling, and initiate evidence-based cessation therapies when appropriate. Importantly, these findings offer a strong motivational message for patients. Demonstrating that smoking cessation can directly improve myocardial healing and reduce the risk of future events provides a tangible and immediate benefit. This can enhance patient engagement and adherence. Combining behavioural support with pharmacological therapy is likely to maximize success rates and should be encouraged. In conclusion, the study by Troger et al.6 provides compelling evidence that smoking cessation after STEMI is associated with improved infarct healing as assessed by CMR and with a lower risk of MACE, independent of traditional risk factors. These findings support the concept that smoking cessation should be considered a key therapeutic target in post-STEMI care. Addressing smoking as a contributor to residual risk and integrating cessation strategies into routine clinical practice are essential steps to improve myocardial recovery and long-term outcomes. Federico Fortuni (Conceptualization, Investigation, Methodology, Project administration, Resources, Software, Validation, Visualization, Writing—original draft [lead]), and Erberto Carluccio (Conceptualization, Investigation, Methodology, Project administration, Resources, Validation, Visualization, Writing—original draft [supporting], Supervision, Writing—review & editing [lead]) No new data were generated or analyzed in support of this research.