Introduction

Caffeine is a methylxanthine compound that has pleiotropic cardiovascular effects, including stimulation of the sympathetic nervous system. Caffeine is ingested daily by a large percentage of the global population (in the form of tea, coffee and cola), and is the most widely consumed vasoactive substance in the world.1

The relationship of caffeine to cardiovascular disease has been debated and investigated for decades. Considered a stimulant, caffeine had long been postulated to be proarrhythmic. Initial physiologic measurements in humans showed that acute caffeine ingestion in caffeine naïve subjects increased heart rate and blood pressure, and correlated with increases in plasma renin and catecholamine levels.2 Electrophysiological studies performed in the 1980s during acute caffeine loading (both oral and intravenous) demonstrated a heterogeneous pattern of effect in cardiac tissue, with caffeine prolonging the myocardial refractory period in the left atrium and shortening the refractory period in the right atrium.3 In these experiments, patients seemed to have an increased proclivity to develop supraventricular arrhythmia after caffeine loading.

The results of these early studies suggested a deleterious effect of caffeine on cardiovascular health. Importantly, however, these studies investigated the acute effects of caffeine ingestion and not the chronic effects of daily exposure in a habituated subject. The keen interest in identifying potential ill effects of caffeine consumption led to high-profile publications, including one linking coffee drinking to pancreatic cancer—a finding later debunked, as it resulted from the use of flawed statistical and study design methods.4

Recently, interest in identifying risk factors for supraventricular arrhythmias has increased—particularly with respect to atrial fibrillation (AF), given the high prevalence of this dysrhythmia and the risk of …