Coffee and Arrhythmias
Data linking coffee consumption to increased risk of arrhythmias are inconsistent. Early animal studies indicated that coffee appeared to cause arrhythmias in a canine model. Yet, more recent studies have suggested that coffee appears not to increase arrhythmias; to the contrary, long-term coffee drinking might actually reduce the risk of abnormal cardiac rhythms. In a Kaiser Permanente study of 130,054 adults living in California, an inverse relationship between habitual coffee consumption and risk of hospitalization for arrhythmia was observed during long-term follow-up. A total of 3,137 persons were hospitalized over a mean follow-up period of 17.6 years. Coffee intake correlated inversely with cardiac arrhythmia (Fig. 4). The relationship was consistent in men, women, whites, blacks, and persons younger than or older than 60 years of age. The authors concluded that people who drank 4 cups of coffee per day tended to have fewer cardiac arrhythmias, including less atrial fibrillation (AF).
(Enlarge Image)
Figure 4.
Coffee Consumption and Risk of Arrhythmias
Adjusted hazard ratio (no coffee take is referent = 1) of arrhythmia diagnoses by coffee intake. Error bars indicate 95% confidence interval (CI). Adapted from Klatsky et al. AF = atrial fibrillation; SVT = supraventricular tachycardia.
Considering the effects of caffeine in isolation, controlled interventional studies show that in normal adults, even high-dose caffeine does not affect prevailing cardiac rhythm and rate, and, moreover, does not cause clinically significant ventricular or supraventricular arrhythmias. In 5 placebo-controlled trials, caffeine in doses as high as 500 mg/day (equivalent to 4 or 5 cups of coffee) did not increase the frequency or severity of ventricular arrhythmias. In a prospective interventional electrophysiological study, ingestion of 275 mg of caffeine did not significantly alter inducibility or severity of arrhythmias.
The mechanisms conferring potential protection against arrhythmias are still largely unknown, but according to 1 hypothesis, caffeine inhibits adenosine in the heart, as it does in the brain. Endogenously secreted adenosine affects cardiac electrical conduction and cardiomyocyte repolarization and may cause shortening of the atrial and ventricular refractory periods, thereby predisposing to arrhythmias. Caffeinated coffee intake could theoretically confer cardioprotection by attenuating these negative effects of endogenous adenosine.
On the other hand, caffeine acting as an adenosine receptor blocker might reduce the efficacy of exogenously administered adenosine for the treatment of paroxysmal supraventricular tachycardia. One case-control study found that ingestion of caffeine within 4 h before a 6-mg adenosine bolus significantly reduced its effectiveness for the conversion of supraventricular tachycardia to normal sinus rhythm. A large prospective, observational study found that drinking coffee, even ≥6 cups/day, was not associated with any QT interval abnormalities that might predispose to serious arrhythmias.
In the Women's Health Study, 33,638 women older than 45 years of age and free of CV disease and AF at baseline were prospectively followed for incident AF from 1993 through 2009. During a median follow-up of 14.4 years in this large cohort of initially healthy women, caffeine consumption was not associated with an increased risk of incident AF. In the Danish Diet, Cancer, and Health study, 47,949 participants 50 to 64 years of age were followed for a mean of 5.7 years. Caffeine consumption in the form of coffee, tea, and cola was not associated with the risk of the development of AF or flutter. These results were replicated in the Framingham Heart Study cohort of 4,526 participants; during a prospective follow-up of 4 years, no significant association between coffee consumption and AF risk was noted.