Abstract Atrial fibrillation (AF) is a globally prevalent cardiac arrhythmia with significant genetic underpinnings, as highlighted by recent large-scale genetic studies. A prominent clinical and genetic overlap exists between AF, heritable ventricular cardiomyopathies, and arrhythmia syndromes, underlining the potential of AF as an early indicator of severe ventricular disease in younger individuals. Indeed, several recent studies have demonstrated meaningful yields of rare pathogenic variants among early-onset AF patients (∼4%–11%), most notably for cardiomyopathy genes in which rare variants are considered clinically actionable. Genetic testing thus presents a promising opportunity to identify monogenetic defects linked to AF and inherited cardiac conditions, such as cardiomyopathy, and may contribute to prognosis and management in early-onset AF patients. A first step towards recognizing this monogenic contribution was taken with the Class IIb recommendation for genetic testing in AF patients aged 45 years or younger by the 2023 American College of Cardiology/American Heart Association guidelines for AF. By identifying pathogenic genetic variants known to underlie inherited cardiomyopathies and arrhythmia syndromes, a personalized care pathway can be developed, encompassing more tailored screening, cascade testing, and potentially genotype-informed prognosis and preventive measures. However, this can only be ensured by frameworks that are developed and supported by all stakeholders. Ambiguity in test results such as variants of uncertain significance remain a major challenge and as many as ∼60% of people with early-onset AF might carry such variants. Patient education (including pretest counselling), training of genetic teams, selection of high-confidence genes, and careful reporting are strategies to mitigate this. Further challenges to implementation include financial barriers, insurability issues, workforce limitations, and the need for standardized definitions in a fast-moving field. Moreover, the prevailing genetic evidence largely rests on European descent populations, underscoring the need for diverse research cohorts and international collaboration. Embracing these challenges and the potential of genetic testing may improve AF care. However, further research—mechanistic, translational, and clinical—is urgently needed. 

Genetic testing in early-onset atrial fibrillation

Prevalence of disease-associated cardiomyopathy gene variants in ethnic minorities with atrial fibrillation

Clinical characteristics including family history between early-onset and late-onset lone atrial flutter across race-ethnicity

Association between smoking history and response to anti-arrhythmic therapy in atrial fibrillation patients across race-ethnicity


 BACKGROUND:
 Smoking is associated with increased risk of developing atrial fibrillation (AF) and stroke. Yet, it remains unclear if it also predicts response to rhythm control therapy across race-ethnicity. We sought to determine if response to rhythm control therapy for AF is modulated by smoking across race-ethnicity.
 
 
 Methods:
 529 patients treated with a rhythm control strategy were prospectively enrolled in the Chicagoland area. Patients were classified into White, Black or Hispanic\Latino based on race\ethnicity and ancestry markers. Rhythm control included antiarrhythmic drugs (AADs) and/or catheter ablation. Successful response was defined as continuation of the same AAD for at least 6 months and/or successful catheter ablation without recurrence of AF for 12 months.
 
 
 Results:
 235 (44%) were Black, 192 (36%) were White, and 102 (19%) were Hispanic. 299 (57%) were treated with AADs and 230 (44%) with catheter ablation. One-hundred sixty-eight (35%) patients had a history of smoking. Baseline co-morbidities were similar across responders and non-responders. In multivariate regression analysis (Table 1), patients with a smoking history were more likely to have a recurrence of AF when treated with a rhythm control strategy (odds ratio [OR] 1.51, 95% confidence interval [CI] 1.03-2.21,
 P
 =0.03). Stratified multivariate regression analysis showed that smokers were more likely to have a recurrence of AF after ablation therapy as compared to AADs (OR 1.49, 95% CI 1.03-2.17,
 P
 = 0.03). Multivariate logistic regression showed that patients that smoked for >20 years were twice as likely to have a recurrence of AF with a rhythm control therapy than those who smoked for <20 years (OR 1.88, 95% CI 1.20- 2.93,
 P
 = 0.01).
 
 
 Conclusions:
 A smoking history modulates response to rhythm control therapy for AF across race-ethnicity. Our study highlights the importance of smoking cessation before initiation of rhythm control agents in patients with AF.
 
 
 


Abstract 11171: Smoking Modulates Response to Anti-Arrhythmic Therapy for Atrial Fibrillation Patients Across Race-Ethnicity

Association of bmp10 with disease progression in atrial fibrillation

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