Caffeine: No Downside, Hint of Benefit in Atrial Fibrillation

A meta-analysis from Chinese researchers has concluded that there is an inverse relationship between regular caffeine consumption and atrial fibrillation risk.

"It is unlikely that habitual caffeine intake increases AF risk," write Dr Min Cheng (State Key Laboratory of Cardiovascular Disease, Beijing, China) and colleagues in their study, published online January 6, 2014 in the Canadian Journal of Cardiology.

In fact, they conclude, habitual caffeine consumption may actually reduce AF risk.

"The finding of this study is meaningful. First, there is no need for concern that habitual caffeine intake may increase AF risk. Second, as atrial fibrosis is an important substrate for AF and caffeine has an antifibrosis property, the finding may pave the way for seeking effective antifibrosis agents for AF management or prompt development of caffeine as an agent for preventing AF," Cheng et al write.

Commenting on this study, Dr Stanley Nattel (University of Montreal, QC) called the findings "reassuring" for patients, many of whom have felt they need to steer clear of coffee and other caffeinated drinks.

Caffeine and AF: Link Unclear 

Caffeine is a major component of some of the most widely consumed beverages, and the link between regular caffeine intake with incident AF was unknown. The aim of this meta-analysis was to investigate the association between chronic exposure to caffeine and AF risk and also to evaluate the potential dose-response relationship.

Cheng et al"s analysis consisted of six prospective cohort studies that included 228 465 participants. Three of these studies were done in the US, two in Sweden, and one in Denmark.

During a mean follow-up of from four to 25.2 years, 4261 participants suffered from AF.

Participants" mean age at baseline ranged from 53 to 63 years. The prevalence of smoking ranged from 5.8% among participants with the lowest caffeine intake to 76.8% among participants with the highest caffeine intake.

All of the studies documented the incidence of AF by electrocardiography; three studies estimated daily caffeine intake by the frequency of caffeine or coffee consumption during the previous year, and three studies estimated caffeine consumption according to reported daily coffee consumption. In addition, three studies summed the daily intake of coffee, tea, 
cola, cocoa, or chocolate for each subject.

The pooled relative risk (RR) for the incidence of AF from habitual caffeine exposure was 0.90 (95% CI 0.81–1.01; p=0.07) in the primary analysis. There was also significant heterogeneity among the six studies (I2=73%; p=0.002).

The researchers also found an inverse relationship between the amount of caffeine consumed and the risk of AF.

Pooled results from studies that adjusted for potential confounders showed an 11% reduction for low doses of caffeine (RR 0.89, 95% CI 0.80–0.99; p=0.032), and a 16% reduction for high doses (RR 0.84, 95% CI 0.75–0.94; p=0.002).

Similarly, an inverse relation was found between habitual caffeine intake and AF risk (p=0.015 for overall trend), and the incidence of AF decreased by 6% (RR 0.94, 95% CI 0.90–0.99) for every 300-mg/day increment in habitual caffeine intake.

A Second Cup? 

In their discussion, the authors suggest that habitual caffeine consumption may offer a moderate protective effect against AF for a variety of reasons.

The studies in this meta-analysis showed that 400 mg of caffeine did not induce change in P-wave indices compared with the baseline electrocardiography, and one showed that 400 mg of caffeine did not change PR interval, QRS duration, corrected QT interval, RR interval, or corrected QT-interval dispersion.

Nor, in another study, did 300 mg of caffeine increase the occurrence or severity of ventricular arrhythmias during the healing phase of acute MI. Even in patients with clinical ventricular arrhythmias, caffeine did not significantly alter inducibility or severity of arrhythmias, the authors noted.

Further, in people who habitually consumed caffeine, the adrenergic effects of caffeine were greatly attenuated and its possible acute proarrhythmia effect reduced.

Habitual caffeine intake may also reduce AF risk because of its antifibrosis effect, Cheng et al write.

Harm vs Benefit 

"AF is a very common condition, affecting about one in four people over their lifespan. 

Patients with AF are often told to avoid stimulants like caffeine, but the evidence for deleterious effects of caffeine is quite weak," Nattel, who was not part of the current study, pointed out. He also applauded the rigorous criteria investigators used in their meta-analysis.

But, unlike the authors, Nattel stopped short of saying that patients should actually consider "using" caffeine to treat AF.

"Even though the study suggested a dose-related protective effect of caffeine against AF, I would not recommend using caffeine to treat AF on this basis. But the results do reassure us that AF patient can enjoy their cup of coffee with a clear conscience," he said.

The study was supported by the National Natural Science Foundation of China and the National Basic Research Program of China. Cheng reports no relevant financial relationships. Nattel is editor in chief of the Canadian Journal of Cardiology.


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