Flecainide

[chromuffin]

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I haven't found a good source on this. Does Flecainide cause QT prolongation? I had a discussion with a classmate the other day and he swore up and down that flecainide didn't cause QT prolongation because it was an Ic antiarrhythmic but Flecainide inhibits K+ channels....

Would love to have a source for this..

 

[baclofen]

Class I drugs are Na+ blockers, not K+ blockers, although Ia has the additional effect of blocking K+, which increases QT. Flecainide is a Ic, and does not block K+ channels, thus it will not prolong QT.

 

[chromuffin]

Class I drugs are Na+ blockers, not K+ blockers, although Ia has the additional effect of blocking K+, which increases QT. Flecainide is a Ic, and does not block K+ channels, thus it will not prolong QT.

My class notes state flecainide "blocks a K+ current involved in depolarization and prolongs action potential duration in the ventricles"

 

[baclofen]

By definition, Class I antiarrhythmic's primary mechanism of action is Na+ channel blockade. Some also block the K+ channel significantly (i.e. Class Ia), while other do to a much lesser extent, if at all (i.e. Class Ic).

Here's a link to an article where someone felt that it was rare enough to get torsades with flecainide, that it warranted a case report: http://onlinelibrary.wiley.com/doi/10.1002/phar.1403/abstract

Also, see here:
http://emedicine.medscape.com/artic...i3V2zxLFOu9AF/HZt4/lJoichrzF/7vlnSF6AEX/09M8=
"Ia - Quinidine, procainamide, disopyramide (depress phase 0, prolonging repolarization)
Ib - Lidocaine, phenytoin, mexiletine (depress phase 0 selectively in abnormal/ischemic tissue, shorten repolarization)
Ic - Flecainide, propafenone, moricizine (markedly depress phase 0, minimal effect on repolarization"

In summary, flecainide likely has minimal blockade on K+ channels that in rare cases can cause prolonged QT. For Step I purposes (and as per First Aid), only classes Ia and III have significant K+ channel blockade, and therefore can prolong QT.

 

[chromuffin]

By definition, Class I antiarrhythmic's primary mechanism of action is Na+ channel blockade. Some also block the K+ channel significantly (i.e. Class Ia), while other do to a much lesser extent, if at all (i.e. Class Ic).

Here's a link to an article where someone felt that it was rare enough to get torsades with flecainide, that it warranted a case report: http://onlinelibrary.wiley.com/doi/10.1002/phar.1403/abstract

Also, see here:
http://emedicine.medscape.com/article/2172024-overview?pa=LdlepnQBnb9AIg6HQDBS3zmjLwleUtR6PHr/CdtsVfdmZehiWt2C02zj+ypef3Ni3V2zxLFOu9AF/HZt4/lJoichrzF/7vlnSF6AEX/09M8=
"Ia - Quinidine, procainamide, disopyramide (depress phase 0, prolonging repolarization)
Ib - Lidocaine, phenytoin, mexiletine (depress phase 0 selectively in abnormal/ischemic tissue, shorten repolarization)
Ic - Flecainide, propafenone, moricizine (markedly depress phase 0, minimal effect on repolarization"

In summary, flecainide likely has minimal blockade on K+ channels that in rare cases can cause prolonged QT. For Step I purposes (and as per First Aid), only classes Ia and III have significant K+ channel blockade, and therefore can prolong QT.

I'm aware of the classes and their typical presentation. This is precisely why I made the post. Flecainide CAN induce torsades, so should it be contraindicated in, say, a patient with congenital long QT? Perhaps I don't understand what qualifies as step question..