New research from UC San Francisco that tested possible triggers of a common heart condition, including caffeine, sleep deprivation and sleeping on the left side, found that only alcohol use was consistently associated with more episodes of the heart arrhythmia.
The authors conclude that people might be able to reduce their risk of atrial fibrillation (AF) by avoiding certain triggers.
The study is published in JAMA Cardiology and was presented Nov. 14, 2021, at the annual Scientific Sessions of the American Heart Association.
Researchers were surprised to find that although most of the things that participants thought would be related to their AF were not, those in the intervention group still experienced less arrhythmia than the people in a comparison group that was not self-monitoring.
“This suggests that those personalized assessments revealed actionable results,” said lead author Gregory Marcus, MD, MAS, professor of Medicine in the Division of Cardiology at UCSF. “Although caffeine was the most commonly selected trigger for testing, we found no evidence of a near-term relationship between caffeine consumption and atrial fibrillation. In contrast, alcohol consumption most consistently exhibited heightened risks of atrial fibrillation.”
Atrial fibrillation contributes to more than 150,000 deaths in the United States each year, reports the federal Centers for Disease Control and Prevention, with the death rate on the rise for more than 20 years.
To learn more about what patients felt was especially important to study about the disease, researchers held a brainstorming session in 2014. Patients said researching individual triggers for AF was their top priority, giving rise to the I-STOP-AFib study, which enabled individuals to test any presumed AF trigger. About 450 people participated, more than half of whom (58 percent) were men, and the overwhelming majority of whom were white (92 percent).
Participants in the randomized clinical trial utilized a mobile electrocardiogram recording device along with a phone app to log potential triggers like drinking alcohol and caffeine, sleeping on the left side or not getting enough sleep, eating a large meal, a cold drink, or sticking to a particular diet, engaging in exercise, or anything else they thought was relevant to their AF.
Although participants were most likely to select caffeine as a trigger, there was no association with AF. Recent research from UCSF has similarly failed to demonstrate a relationship between caffeine and arrhythmias – on the contrary, investigators found it may have a protective effect.
The individualized testing method, known as n-of-1, did not validate participant-selected triggers for AF. But trial participants did report fewer AF episodes than those in the control group, and the data suggest that behaviors like avoiding alcohol could lessen the chances of having an AF episode.
“This completely remote, siteless, mobile-app based study will hopefully pave the way for many investigators and patients to conduct similar personalized ‘n-of-1’ experiments that can provide clinically relevant information specific to the individual,” said Marcus.
Atrial fibrillation (AF) is an arrhythmia with a major impact on public health due to its increasing prevalence in ageing populations and its association with adverse outcomes, including stroke and heart failure (HF), with more than a doubling of mortality risk.1,2 The effect of alcohol on AF risk has remained ambiguous.
For diseases predisposing to AF such as coronary artery disease3 or HF4,5 low to moderate alcohol consumption seems to be related to a lower incidence, while higher levels of consumption are associated with an increased risk.6 The reported associations with AF range from null associations at lower regular alcohol intake,5,7 rather linearly increasing in large meta-analyses8,9 to a more J-shaped relation in women.1 In particular, the association at low levels of alcohol consumption is less clear.
From a pathophysiological perspective, alcohol may exhibit direct effects on arrhythmogenesis as observed for the holiday heart syndrome.10–13 Acute alcohol consumption induces autonomic imbalance reflected by sinus tachycardia, predisposing to arrhythmia.10
Electrolyte disturbance and alterations of the acid-base balance are further pro-arrhythmic triggers. Chronic alcohol consumption is known to be correlated with changes in cardiac structure and function including cardiomyopathy.4,11–13
Habitual alcohol intake has been related to atrial remodelling as an intermediate AF phenotype in the community.12,13 At the same time, alcohol intake is also associated with the most prevalent risk factors of AF. Increased alcohol intake is accompanied by higher frequency of hypertension and obesity.14
In younger individuals with low-risk factor burden and heart disease, acute excessive alcohol consumption was not associated with higher AF burden.10 Furthermore, alcohol consumption is predictive of incident HF, which itself is a risk factor for new-onset AF4,6 and may help explain known associations.
Circulating cardiac biomarkers are quantitative measures which shed light on current cardiac pathophysiology. Troponin reflects myocardial injury, while N-terminal pro-B-type natriuretic peptide (NT-proBNP) indicates often chronic, subclinical wall stress.15 A recent study demonstrated that both biomarkers showed distinct patterns in relation to alcohol consumption.15 Whereas troponin concentrations decreased with higher alcohol consumption, NT-proBNP increased.15 Whether this pattern is related to AF risk remains to be shown.
A strong controversy remains for the relation of alcohol consumption with AF in individuals with low alcohol consumption. Therefore, we examined the association of alcohol consumption with incident AF while accounting for classical risk factors, HF and cardiac biomarkers across European cohorts.
reference link : https://academic.oup.com/eurheartj/article/42/12/1170/6090248
More information: Gregory M. Marcus et al, Individualized Studies of Triggers of Paroxysmal Atrial Fibrillation, JAMA Cardiology (2021). DOI: 10.1001/jamacardio.2021.5010