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23rd December 2021
Increased alcoholic spirit intake is associated with an increased risk of ventricular arrhythmia but this elevated risk is absent for other forms of alcoholic beverages. This was a key finding from a retrospective analysis by a team from the Centre for Heart Rhythm Disorders, University of Adelaide and Royal Adelaide Hospital, Australia.
Higher intakes of alcohol are generally considered to damage the cardiovascular system although light to moderate alcohol intake appears to be protective. The term ‘holiday heart syndrome‘ has been coined to describe any alcohol-induced atrial arrhythmias and/or conduction disturbance associated with heavy consumption in a person without other clinical evidence of heart disease. Whilst the relationship between atrial arrhythmias and alcohol has become well recognised, there is a paucity of data linking alcohol intake with ventricular arrhythmias (VA). In fact, the available evidence is inconsistent, with some data showing a non-significant association whereas other studies suggesting that heavy alcohol consumption is an important contributing factor. Moreover, the influence of the type of alcoholic drink on VA or even sudden cardiac death (SCD) is also uncertain.
For the present study, researchers used information held in the UK Biobank which provides data on approximately half a million community-dwelling individuals aged 40 to 69 years across the UK. For their analysis, the researchers focused on incident cases of VA but excluded those with a previous history of the condition and former drinkers. The amount of alcohol intake was reported in terms of a standard drink, defined as 8g of alcohol and the average number of standard drinks consumed per week. For alcohol intake, the team also considered the type of each beverage consumed and created regression models which adjusted for several covariates such as age, sex, race, education.
Data for a total of 408,712 individuals with an average age of 58.3 years (52.1% female) were included in the analysis and who were followed up for a median duration of 11.5 years. The median alcohol intake for the whole cohort was 8 drinks per week although 5.5% of the group reported having never consumed alcohol.
There were a total of 1733 incident VA events and 2044 SCDs which occurred during the follow-up period. Overall, there was no statistically significant association between total alcohol intake and the risk of VA. However, when considered by type of alcoholic beverage, only alcoholic spirit intake was linearly linked with an increased risk of VA among those consuming greater than 14 drinks per week (hazard ratio, HR = 1.15, 95% CI 0.98 – 1.34) and this became statistically significant with more than 28 drinks per week (HR = 1.33, 95% CI 1.03 – 1.73).
For SCD there was a U-shaped distribution of risk with the lowest risk at around 7 drinks per week.
The authors concluded that they were unable to find an association between total intake of beer, cider and wine and VA and that only increased alcoholic spirit intake was linked to a higher risk. In fact, wine intake was associated with a lower risk of SCD although the authors suggested that these findings require clarification from experimental studies.
1st October 2021
Throughout the COVID-19 pandemic, several important risk factors for more severe disease have become apparent including male sex, increased age and cardiovascular co-morbidities. Whether or not being a current smoker affects COVID-19 outcomes is less clear with some analyses indicating a higher risk of worse outcomes, whereas others reviews suggest a reduced risk . One solution to untangling this ambiguity is the adoption of a dual analytical approach to data analysis, for example, by comparing the results from observational studies with those from a Mendelian randomisation study. In a Mendelian randomisation (MR) study, the underlying assumption is that a genetic variant influences only the variable of interest and since genetic variants are randomly allocated at birth, MR is less susceptible to confounding which is a problem in observational studies. Genetic analysis can be used to identify variants associated with particular traits. For example, tobacco and alcohol use are known to have heritable behaviours and in one study, researchers identified 566 genetic variants in 406 loci associated with multiple stages of tobacco use, e.g., initiation, cessation, and heaviness (i.e., the number of cigarettes smoked per day).
Using a dual analytical approach to examine the relationship between smoking and outcomes in COVID-19, a team from the Nuffield Department of Primary Care Health Sciences, University of Oxford, UK, turned to data held within the UK Biobank. The researchers separately explored the relationship between smoking and COVID-19 using findings from both observational studies and Mendelian randomisation. For the MR study, researchers used established genetic proxies for smoking initiation and smoking heaviness (i.e., the number of cigarettes smoked per day). The results were analysed using multivariate logistic regression analysis adjusted for several variables including age, sex, ethnicity and several co-morbidities.
For the observational analysis, there were 421,469 individuals with a median age of 68.6 years (55.1% female). Current smokers were found to have an overall higher risk of hospitalisation (adjusted odds ratio, aOR = 1.80, 95% CI 1.26 – 2.29) and mortality (aOR = 4.89, 95% CI 3.41 – 7.0).
Similarly, in the Mendelian randomisation analysis, genetic propensity to initiate smoking was associated with a higher risk of hospitalisation (aOR = 1.60, 95% CI 1.13 – 2.27), but not mortality (aOR = 1.35, 95% CI 0.82 – 2.22, p = 0.23). For genetically predicted higher number of cigarettes smoked per day, the risk of hospitalisation was also higher (aOR = 5.08, 95% CI 2.04 – 12.66) and risk of death (aOR = 10.02, 95% CI 2.53 – 39.72).
Discussing their findings, the authors said that this was the first study to adopt a dual analytical approach to assess the relationship between smoking and outcomes from COVID-19. They concluded that the congruence between the two methods indicated that a lifelong predisposition to smoking and smoking heaviness supported a causal effect (found in the observational analysis) of smoking on COVID-19 severity.
Clift AK et al. Smoking and COVID-19 outcomes: an observational and Mendelian randomisation study using the UK Biobank cohort. Thorax 2021