A Study of Caffeine on Cardiac Arrhythmias

• Status: Completed
• Trial end date: 2015-08-01
• Target enrollment: 0
• Participant gender: All

Summary

Stimulants and drugs are often associated with cardiac effects. Caffeine, a therapeutic xanthine, has been described as a sympathomimetic and has shown to have stimulatory effects on the heart. Patients with symptomatic cardiac arrhythmias are generally informed by their physician to stop or significantly reduce caffeine intake. However, in spite of numerous reports that have reviewed the cardiac effects of caffeine, it remains unclear to what extent this stimulant may be detrimental, and what subgroups of patients may be most vulnerable. The investigators propose to evaluate the effects of caffeine in patients with previously diagnosed cardiac arrhythmias. The results of our report will provide important new information for physicians and patients regarding the effects of caffeine on symptomatic cardiac arrhythmias.

• Phase: N/A
• Accepts Healthy Volunteers?: No

Details

• Lead Sponsor: Ottawa Heart Institute Research Corporation
• Treatments: Caffeine

Criteria

Inclusion Criteria:

• Age 18-80 years.

• Document cardiac arrhythmia, consisting of either:

i. Patients with SVT: Patients with documented narrow complex tachycardia on a twelve lead ECG or on ambulatory monitoring ii. Patients with AF, paroxysmal (self-terminating AF within 7 days), documented on a twelve lead ECG or on ambulatory monitoring

Exclusion Criteria:

• Failure to provide informed consent

• Pregnancy as determined by a pre-procedure pregnancy test, or women who are breastfeeding

• Class III or IV congestive heart failure

• Myocardial infarction within the last 6 months

• Coronary stenting or cardiac surgery within the last 6 months

• History of unstable angina

• Uncontrolled hypertension

• Intolerance to caffeinated beverages or chocolate

• Dependency on medications that may severely react with caffeine: substrate for Cytochrome P450 1A2 (CYP1A2) (tizanidine), inhibit CYP1A2 (fluvoxamine, ketoconazole, and rofecoxib), induce CYP1A2 (aminoglutethimide, carbamazepine, phenobarbital, and rifampin)

• Enrolment in another study at University of Ottawa Heart Institute (UOHI), unless approved by the Human Ethics Review Board (HREB).