Dataset Information

Alcohol and the risk of all-cause death, atrial fibrillation, ventricular arrhythmia, and sudden cardiac arrest.

ABSTRACT: The risk of having atrial fibrillation (AF) is associated with alcohol intake. However, it is not clear whether sudden cardiac arrest (SCA) and ventricular arrhythmia (VA) including ventricular tachycardia, flutter, or fibrillation have similar associations with alcohol. We aimed to evaluate the association of alcohol intake with all-cause death, new-onset AF, VA, and SCA using single cohort with a sufficient sample size. A total of 3,990,373 people without a prior history of AF, VAs, or SCA was enrolled in this study based on nationwide health check-up in 2009. We classified the participants into four groups according to weekly alcohol consumption, and evaluated the association of alcohol consumption with each outcome. We observed a significant association between mild (hazard ratio [HR] = 0.826; 95% confidence interval [CI] = 0.815-0.838) to moderate (HR = 0.930; 95% CI = 0.912-0.947) drinking with decreased risk of all-cause mortality. However heavy drinking (HR = 1.108; 95% CI = 1.087-1.129) was associated with increased all-cause death. The risk of new-onset AF was significantly associated with moderate (HR = 1.129; 95% CI = 1.097-1.161) and heavy (HR = 1.298; 95% CI = 1.261-1.337) drinking. However, the risk of SCA showed negative association with all degrees of alcohol intake: 20% (HR = 0.803; 95% CI = 0.769-0.839), 15% (HR = 0.853; 95% CI = 0.806-0.902), and 8% (HR = 0.918; 95% CI = 0.866-0.974) lower risk for mild, moderate, and heavy drinkers, respectively. Mild drinking was associated with reduced risk of VA with moderate and heavy drinking having no associations. In conclusion, the association between alcohol and various outcomes in this study were heterogeneous. Alcohol might have different influences on various cardiac disorders.

SUBMITTER: Kim YG

PROVIDER: S-EPMC10904378 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Alcohol and the risk of all-cause death, atrial fibrillation, ventricular arrhythmia, and sudden cardiac arrest.

Kim Yun Gi YG Kim Dong Yun DY Roh Seung-Young SY Jeong Joo Hee JH Lee Hyoung Seok HS Min Kyongjin K Choi Yun Young YY Han Kyung-Do KD Shim Jaemin J Choi Jong-Il JI Kim Young-Hoon YH

Scientific reports 20240229 1

The risk of having atrial fibrillation (AF) is associated with alcohol intake. However, it is not clear whether sudden cardiac arrest (SCA) and ventricular arrhythmia (VA) including ventricular tachycardia, flutter, or fibrillation have similar associations with alcohol. We aimed to evaluate the association of alcohol intake with all-cause death, new-onset AF, VA, and SCA using single cohort with a sufficient sample size. A total of 3,990,373 people without a prior history of AF, VAs, or SCA was ...[more]

PMID: 38424149

Similar Datasets

Project description:ObjectivesThis study aimed to develop a novel clinical prediction algorithm for avertable sudden cardiac death.BackgroundSudden cardiac death manifests as ventricular fibrillation (VF)/ ventricular tachycardia (VT) potentially treatable with defibrillation, or nonshockable rhythms (pulseless electrical activity/asystole) with low likelihood of survival. There are no available clinical risk scores for targeted prediction of VF/VT.MethodsSubjects with out-of-hospital sudden cardiac arrest presenting with documented VF or pulseless VT (33% of total cases) were ascertained prospectively from the Portland, Oregon, metro area with population ≈1 million residents (n = 1,374, 2002-2019). Comparisons of lifetime clinical records were conducted with a control group (n = 1,600) with ≈70% coronary disease prevalence. Prediction models were constructed from a training dataset using backwards stepwise logistic regression and applied to an internal validation dataset. Receiver operating characteristic curves (C statistic) were used to evaluate model discrimination. External validation was performed in a separate, geographically distinct population (Ventura County, California, population ≈850,000, 2015-2020).ResultsA clinical algorithm (VFRisk) constructed with 13 clinical, electrocardiogram, and echocardiographic variables had very good discrimination in the training dataset (C statistic = 0.808; [95% CI: 0.774-0.842]) and was successfully validated in internal (C statistic = 0.776 [95% CI: 0.725-0.827]) and external (C statistic = 0.782 [95% CI: 0.718-0.846]) datasets. The algorithm substantially outperformed the left ventricular ejection fraction (LVEF) ≤35% (C statistic = 0.638) and performed well across the LVEF spectrum.ConclusionsAn algorithm for prediction of sudden cardiac arrest manifesting with VF/VT was successfully constructed using widely available clinical and noninvasive markers. These findings have potential to enhance primary prevention, especially in patients with mid-range or preserved LVEF.

Project description:Atrial fibrillation (AF) has an estimated prevalence of 1.5–2%, making it the most common cardiac arrhythmia. The mechanisms that cause and sustain AF are still not completely understood. An association between AF and systemic as well as local inflammatory processes has been reported, however, the exact mechanisms underlying this association have not been established. While it is understood that tissue resident macrophages can influence cardiac electrophysiology, the effects of activated pro-inflammatory macrophages have not been described yet. This study investigated the pro-arrhythmic effects of activated macrophages (M1) on human induced pluripotent stem cell (hiPSC)-derived atrial cardiomyocytes (aCM), to propose a mechanistic link between inflammation and AF. Two hiPSC lines from healthy individuals were differentiated to aCMs and M1 macrophages. Electrophysiology characteristics of M1 and aCM cocultures were analysed for beat rate irregularity, electrogram amplitude and conduction velocity. M1 cocultures resulted in a significant increase in beat rate irregularity and decrease in electrogram amplitude compared to other conditions tested, including aCMs treated with activated M1 supernatant, which did not produce an increase in irregularity. Conduction analysis further showed significantly lower conduction homogeneity in M1 cocultures. Immunosuppression through glucocorticoids significantly decreased beat irregularity in aCM+M1 cocultures compared to vehicle. RNA sequencing performed in aCMs, revealed downregulation of various ion channels (SCNA5, KCNA5, ATP1A1), as a result of the M1 coculture. Electrophysiology related transcription changes were reversed by glucocorticoid treatment. This study establishes a causal relationship between M1 activation and the development of subsequent atrial arrhythmia, documented as irregularity in spontaneous electrical activation in aCM cocultured with activated macrophages. Further, beat rate irregularity could be alleviated using anti-inflammatory steroidal glucocorticoids. These results strongly support the relevance of the proposed hiPSC-derived coculture model and point at macrophage mediated inflammation as a potential AF mechanism.

Dataset Information

Alcohol and the risk of all-cause death, atrial fibrillation, ventricular arrhythmia, and sudden cardiac arrest.

Publications

Alcohol and the risk of all-cause death, atrial fibrillation, ventricular arrhythmia, and sudden cardiac arrest.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets