Caffeine did not trigger arrhythmias in heart failure patientsLiterature - Zuchinali P, et al, JAMA, 2016
Short-term Effects of High-Dose Caffeine on Cardiac Arrhythmias in Patients With Heart Failure: A Randomized Clinical Trial
Zuchinali P, Souza GC, Pimentel M, et al.
JAMA Intern Med 2016; published online ahead of print
BackgroundWhether caffeine consumption causes arrhythmias or not, is disputed [1,2]. However, in clinical practice, HF patients are advised to avoid caffeine consumption . On the other hand, sudden cardiac death due to arrhythmias, remains a major cause of mortality and morbidity in HF patients .
In this study, the effect of high-dose caffeine intake compared with placebo on the rate of supraventricular and ventricular ectopy at rest and during a symptom-limited exercise test was evaluated in a double-blinded, randomised, cross-over, clinical trial of 51 Brazilian HF patients with reduced left ventricular ejection fraction (≤45%) at high risk for ventricular arrhythmias.
During this trial, patients started with a washout period of 7 days, than received each hour 5 doses of 100 mL decaffeinated coffee, mixed with 100 mg of either caffeine or lactose powder, which was followed by another 7-day washout period and subsequent crossing-over.
- No significant differences in mean heart rate, ventricular premature beats (VPBs) or supra ventricular premature beats (SVPBs) (isolated, couplets, or non-sustained tachycardia) were observed between groups, with 185 and 239 VPBs in the caffeine and placebo groups, respectively (P = 0.47) and 6 SVPBs in each group.
- The OR for at least 1 non-sustained ventricular tachycardia episode was 0.76 (95% CI: 0.31-1.80) and the OR for non-sustained supraventricular tachycardia was 0.69 (95% CI: 0.30-1.61).
- An additional analysis compared rates of arrhythmic end points stratified by plasma caffeine concentrations. There were no increased arrhythmias in patients with higher plasma levels of caffeine compared with lower levels or with the placebo group.
- During the treadmill test, there were no differences in VPBs (caffeine 19 and placebo group 11, P=0.57) or SVPBs (caffeine 3 and placebo 1, P=0.39). Exercise duration caffeine group 10 min, placebo group 9.4 min, P=0.56) and estimated peak oxygen consumption (caffeine group 19.5, placebo group 18.4 mL/kg/min, P=0.53) were similar between groups. The only significant differences were higher values of peak systolic (SBP) and diastolic blood pressure (DBP) in the caffeine group. Peak SBP was 147 vs. 136 mmHg, P = 0.004 and peak DBP was 78.2 vs. 72 mmHg, P = 0.001.
- Subgroup analysis stratified by patients with the ICD for primary or for secondary prevention, or those with previous ICD therapy, did not demonstrate any effect of caffeine ingestion on arrhythmic outcomes.
ConclusionsThe acute ingestion of high doses of caffeine in 51 HF patients did not induce arrhythmias neither at rest, nor during exercise. These data do not support the recommendation to limit caffeine consumption in patients at risk for arrhythmias.
Editorial comment In their invited commentary, Kelly and Granger mention that the limitations of the study, which include the short-term nature of the exposure and the small number of patients, prevent from making any definite conclusions regarding the safety of caffeine consumption in HF patients on high risk of arrhythmias. They conclude: ‘In summary, the findings of Zuchinali et al that modest caffeine consumption does not increase ventricular or atrial ectopy in patients with heart failure are reassuring, including in the context of epidemiologic data that suggests safety in broader populations. However, the longer-term safety of moderate- and high-dose consumption of caffeine, including in popular energy drinks and in patients at high risk for arrhythmias, remains unknown. For the time being, it seems reasonable to reassure our patients that modest caffeine consumption appears to be safe, including for most patients with heart failure.’
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