Possible arrhythmiogenic mechanism produced by ibuprofen.

Area of Science:

• Cardiovascular Electrophysiology
• Pharmacology

Background:

• Nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen are widely used.
• Potential cardiac side effects of NSAIDs require thorough investigation.

Purpose of the Study:

• To investigate ibuprofen's electrophysiological effects on cardiac action potentials (AP) and electrocardiograms (ECG).
• To elucidate the mechanism underlying ibuprofen-induced cardiac arrhythmias.

Main Methods:

• Intracellular microelectrode recordings of fast- and slow-response AP in guinea pig papillary muscles.
• In vivo and in vitro electrocardiogram (ECG) monitoring of cardiac responses to ibuprofen.

Main Results:

• Ibuprofen induced arrhythmias, including fatal ventricular fibrillation in vitro.
• Dose-dependent shortening of AP duration and effective refractory period (ERP).
• Decreased V(max) of phase 0, prolonged QRS duration, and decreased QTc interval.

Conclusions:

• Ibuprofen inhibits cardiac Na+ and Ca2+ channels, slowing V(max).
• Shortened ERP and decreased excitation propagation may promote re-entry circuits.
• Improper use of ibuprofen poses a risk for cardiac arrhythmias in susceptible patients.