Flecainide is an oral drug used as a Type 1C antiarrhythmic drug. It is used to treat conditions including sustained ventricular tachycardia, ventricular pre-excitation and cardiac dysrhythmias. Flecainide acts in neurons where it inhibits voltage gated sodium channels in the pre synaptic neurons. In neurons, voltage gated sodium channels allow sodium to come into the neuron triggering the depolarization phase. the potassium channels are responsible for the repolarization phase to bring the neuron back to resting potential. The action potentials created travel down the axon of the neuron and at the nerve terminal, calcium channels open, allowing calcium to enter the cell. Calcium entry causes synaptic vesicles containing neurotransmitters like glutamate to fuse with the membrane and expel the neurotransmitter into the synapse. Glutamate binds to AMPA and NMDA receptor on the post synaptic neurons where they cause excitation of the neuron. By blocking the voltage gated sodium channels, flecainide prevents the depolarization phase, inhibiting action potential generation and the release of excitatory neurotransmitter like glutamate. Pre and post synaptic neuronal firing are therefore reduced. Flecainide works as a “use-dependent” block. This means that it preferentially binds to channels that are being opened. In neurons that are repetitively firing, their sodium channels are being opened more often, and as a result, carbamazepine is able to produce a greater block in these neurons. It also possesses some anticholinergic and local anesthetic properties. Side effects of flecainide include nausea, vomiting, headaches, feeling dizzy, or feeling hot and flushed.

Flecainide Antiarrhythmic Pathway References