Smoke signals of risk in the young: rethinking sudden cardiac arrest in the era of preventive inertia

This editorial refers to ‘Smoking and the risk of sudden cardiac arrest in young-aged adults: a Korean nationwide population-based study’, by Y.G. Kim et al. https://doi.org/10.1093/eurjpc/zwaf327 Despite decades of public health campaigns and tobacco control policies, cigarette smoking remains a global health burden, particularly among young adults.1 Although the association between smoking and long-term cardiovascular disease is well established, its role in precipitating sudden cardiac events at a young age is less clearly defined and often underestimated. Sudden cardiac arrest (SCA), while rare in younger populations, carries devastating consequences due to its abrupt onset and high mortality.2 Addressing preventable risk factors in this demographic is a pressing need, especially as shifting patterns in lifestyle, substance use, and risk perception complicate the prevention landscape. The recent Korean nationwide population-based study by Kim et al.3 published in this issue of the European Journal of Preventive Cardiology, provides a timely and compelling challenge to conventional paradigms.3 Their findings show that current smoking significantly increases the risk of SCA in individuals aged 20 to 39 years. The study's strengths lie in its vast sample size, long follow-up period, and robust statistical methodology, making it one of the largest and most rigorous investigations of lifestyle-related SCA risk in this age group to date. Kim et al.3 analyzed nearly 6.3 million individuals, all free from prior cardiovascular disease, stroke, or malignancy at baseline, and demonstrated a clear, graded association between smoking status and incident SCA. After adjusting for covariates, current smokers had a 69% higher risk of SCA compared to never-smokers (adjusted HR 1.69, 95% CI: 1.57–1.81), while no significant increase was observed in former smokers. These findings were robust across multiple sensitivity analyses and consistent in key subgroups, including those defined by sex, alcohol use, and physical activity. Importantly, the association was even more pronounced among individuals without chronic kidney disease and those who did not exercise regularly. Although the absolute incidence of SCA in this young population was low, the relative risks were clinically significant. The study also demonstrated a clear dose–response relationship: compared with non-smokers, light, moderate, and heavy smokers had a 34%, 74%, and 115% increased risk of SCA, respectively. Notably, the hazard ratio for SCA among current smokers (HR 1.72) exceeded that for myocardial infarction (HR 1.42) and stroke (HR 1.18), underscoring the unique and acute vulnerability of young smokers to fatal arrhythmic events. This study fills a significant gap in the evidence base. Current European and international prevention strategies, including the 2021 European Society of Cardiology (ESC) Guidelines on Cardiovascular Disease Prevention, focus primarily on 10-year risk predictions calibrated for middle-aged and older adults.4 The SCORE2 and SCORE2-OP models, for example, target individuals aged 40 and above.5,6 Consequently, clinicians are left without validated tools to assess cardiovascular risk in those under 40. This shortfall contributes to a reactive approach to smoking cessation in youth, typically motivated by concerns about respiratory symptoms or social consequences, rather than cardiovascular outcomes. The perception that young adults are inherently protected from cardiovascular events often leads to what might be described as ‘preventive inertia’.7 Both patients and providers may be drawn into false sense of security. However, SCA remains a leading cause of death in this age group and often represents the first manifestation of an underlying cardiovascular disorder.8 Kim et al.'s3 findings reinforce the notion that modifiable lifestyle factors, particularly smoking, exert significant cardiovascular risk even in the absence of clinically overt heart disease.3 These conclusions are supported by a growing body of evidence pointing to the long-term effects of early exposure to cardiovascular risk factors. The CARDIA (Coronary Artery Risk Development in Young Adults) study, among others, has shown that early-life risk factors predict coronary calcification, atherosclerosis, and structural cardiac changes later in life.9 Smoking accelerate vascular inflammation, increases sympathetic tone, and contributes to the development of arrhythmogenic myocardial substrates.10 In susceptible individuals, these effects can culminate in sudden electrical instability.10 Importantly, Kim et al.'s3 study underscores the urgency of shifting how we communicate cardiovascular risk to younger populations. Rather than focusing solely on long-term threats such as myocardial infarction or stroke, public health campaigns should emphasize the more immediate and dramatic risks such as SCA. This reframing may enhance message salience and drive behavioural changes, particularly among adolescents and young adults. The findings also challenge existing risk classification frameworks. According to the ESC guidelines, high-risk individuals are typically identified using numerical calculators like SCORE2, which exclude those under 40.4 There is growing consensus that a broader approach, incorporating lifetime risk, family history, polygenic risk scores, and risk-enhancing biomarkers, is needed for effective prevention in younger adults.4 Until such tools become standardized and widely available, lifestyle factors such as smoking remain the most accessible and impactful intervention targets. From a systems perspective, current healthcare infrastructures may not be designed to deliver preventive cardiology effectively to young people. Many in this age group have irregular contact with primary care and are not the typical focus of preventive efforts. Alternative strategies, including school- and workplace-based interventions, mobile health technologies, and peer-led initiatives, may offer more effective engagement. In addition, smoking cessation programs tailored to younger demographics must be recalibrated to reflect the acute cardiovascular dangers illuminated by this study. At the research level, the study by Kim et al.3 offers a model for future investigations. High-resolution population-based registries can uncover patterns and interactions not visible in smaller cohorts. Future studies could examine whether genetic predispositions, early autonomic dysfunction, or subtle structural abnormalities contribute to SCA risk in young smokers. It would also be valuable to assess interactions between smoking and emerging lifestyle factors like recreational drug use, digital screen exposure, and sleep deprivation. Geographical variability may further complicate the interpretation and application of these findings. SCA incidence and smoking prevalence show marked regional differences, influenced by healthcare access, public health infrastructure, and cultural norms.1,8,11 In some Western countries, youth smoking rates have declined due to aggressive prevention campaigns, while in others, including parts of Asia and Eastern Europe, rates remain troublingly high.1 Moreover, environmental exposures, dietary patterns, and genetic predispositions vary across populations, potentially modifying the impact of smoking on cardiac electrophysiology and vascular inflammation. Ethnic and geographical heterogeneity in SCA incidence among young adults has been observed in previous epidemiological analyses, suggesting that risk may not be uniformly distributed globally. These nuances highlight the need for regional validation of risk models and locally tailored prevention strategies. Lastly, it is crucial to contextualize these findings within a broader societal lens. While the absolute number of SCA events in young adults is relatively small, each incident represents a tragic, often preventable loss with profound familial and community impact. Even modest reductions in relative risk, when applied to large populations, can translate into significant public health gains. This reframes cardiovascular prevention in youth not merely as a clinical responsibility, but as a moral and societal imperative. In conclusion, Kim et al.'s3 study delivers a powerful message: smoking is not a deferred cardiovascular hazard but an immediate and dangerous trigger for life-threatening events, even in young adults without known heart disease. Much has been achieved in reducing global smoking rates, yet there is still a long way to go, particularly among young adults in Asia and low- and middle-income countries.12 As cardiovascular prevention moves toward precision and personalisation, it must also become more anticipatory. Young adults should be recognized not only as future patients but as current high-priority targets for intervention. This work was supported by the Swedish Heart-Lung Foundation [grant agreement no: 20240797] and the Swedish Society of Cardiology. No new data were generated or analysed in support of this research.