Journal of Arrhythmia最新文献

The association between alcohol intake and the development of atrial fibrillation (AF) has been well documented across various populations. Nevertheless, the potential influence of sex differences on this relationship has remained unresolved. The present study provides important insights by showing that higher alcohol intake was consistently associated with an incremental risk of AF in both sexes, while even lower levels of alcohol intake conferred an elevated risk only in men, but not in women [1]. These findings are intriguing and merit careful interpretation.

The underlying pathophysiological mechanisms responsible for the observed sex-specific differences are still uncertain. The authors suggested that different beverage preferences between sexes may play a role [1]. Women may consume wine more frequently than men, and wine contains potentially protective compounds such as polyphenols. However, this explanation remains insufficient because prior epidemiological studies have also demonstrated that heavy wine consumption in women is associated with a higher incidence of AF.

The interaction between alcohol consumption and dietary patterns should not be overlooked. Alcohol is commonly consumed alongside meals, and certain dietary components may influence the risk of AF. For example, the Mediterranean diet, which is generally considered cardioprotective, includes abundant marine omega-3 fatty acids, yet recent evidence paradoxically suggests that high omega-3 intake may increase the risk of AF [2]. Such factors could act as hidden confounders when interpreting the relationship between alcohol and AF prevalence.

Lifestyle-related factors that differ by sex may have contributed to the findings. Recent studies have linked low-carbohydrate diets, sometimes preferred by Japanese women, with an increased incidence of AF [3]. Moreover, differences in body composition, hormonal milieu, alcohol metabolism, and the prevalence of comorbidities such as hypertension or obesity may all interact with alcohol exposure to influence AF risk differently in men and women [4]. These factors highlight the complexity of disentangling the causal pathway linking alcohol to AF across sexes.

While the cross-sectional nature of the present study provides valuable epidemiological evidence, it cannot establish causality. Well-designed prospective cohort studies, and ideally randomized controlled trials stratified by sex, will be required to confirm whether alcohol restriction can effectively reduce the incidence of AF.

The authors have nothing to report.

The authors have nothing to report.

The authors declare no conflicts of interest.

Aortomitral continuity calcification (AMCC) may contribute to conduction disturbances after TAVI. This Letter highlights key methodological limitations including short-term endpoints, omission of pre-existing RBBB, and lack of spatial AMCC assessment that must be addressed to enhance the accuracy and clinical relevance of AMCC as a risk stratification tool.

An 11-year-old boy presented with dilated cardiomyopathy in association with a fasciculoventricular pathway and sinus node and atrioventricular conduction abnormalities. Whole exome sequencing revealed a novel variant of uncertain significance in LIM domain-binding protein 3 (LDB3) which has not been heretofore described. This variant was predicted to be deleterious by the computational prediction tools: Polyphen2 and SIFT. The mutated allele was heterozygous in the patient. Segregation analysis revealed that his father carried the same variant in heterozygous form. The case is reported for its rarity.

We appreciate and thank Rasheed et al. very much for their interest in our article [1] and for highlighting important limitations. However, we believe that these authors did not well understand the most unique point in our study compared with previous studies. First of all, the strength of the present study was its focus on amiodarone 50 mg daily. There are no or few organized data on amiodarone 50 mg therapy in previous studies, as we described in detail in the Discussion section. We would encourage Rasheed et al. to correctly recognize that in most previous studies, “low-dose” would actually mean 200 mg daily. Although we agree that our study size was not so large, our focus on a 50 mg dose was still a significant strength of the study, and we believe that our organized data on amiodarone 50 mg therapy are quite novel and worthy of publication.

Rasheed et al. likely misunderstood the results of the previous study by Tsaban et al. that was also cited in our manuscript. Although amiodarone did show a small clinically marginal statistical association with increased risk of interstitial lung disease between 2 and 8 years of follow-up in that study, those authors concluded that this increased risk was clinically negligible and did not significantly affect the patients' overall prognosis because the incidence of interstitial lung disease was low (~2%) and, of note, the mortality risk was lower among patients exposed to amiodarone and remained so for all follow-up years. We truly sympathize with the final description by Tsaban et al. that “the results of this study may encourage an increase in amiodarone use for rhythm control in AF.” Again, the median daily amiodarone dose was approximately 200 mg in that study, much higher than the dose in our study, making direct comparison with our study difficult.

We agree that thyrotoxicosis is a clinically critical side effect of amiodarone use. However, Guðjónsson et al. never emphasized dose-independent risks in thyroid dysfunction in their study. On the contrary, a higher dose of amiodarone was actually associated with an increased risk of thyrotoxicosis [HR 2.0 (95% CI 1.1–3.5)]. The mean daily amiodarone dose of 193 mg in their study—again, much higher than that in our study—makes it difficult to directly compare their study with ours.

We agree that hepatotoxicity may be underdiagnosed in amiodarone use because abnormal liver function and symptoms are not necessarily apparent even if hepatotoxicity is present. In our cohort, no patients had abnormal liver tests or suffered from liver dysfunction. Dual-energy computed tomography may be a useful modality that can contribute to the early detection of hepatotoxicity, but such an assessment was beyond the scope of our retrospective study. Also, the assessment and description of all three of these toxicities (lung, thyroid, and liver) in the manuscript of a study would be difficult due to the word limits imposed by the Journa