Editing Flecainide (section)

==Side effects==
Results of a medical study known as the [[Cardiac Arrhythmia Suppression Trial|Cardiac Arrhythmia Suppression Trial (CAST)]] demonstrated that patients with structural heart disease (such as a history of MI (heart attack), or left ventricular dysfunction) and also patients with ventricular arrhythmias, should not take this drug. The results were so significant that the trial was stopped early and preliminary results were published.<ref name = CAST>{{cite journal | author = Cardiac Arrhythmia Suppression Trial (CAST) Investigators | title = Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction | journal = The New England Journal of Medicine | volume = 321 | issue = 6 | pages = 406–412 | date = August 1989 | pmid = 2473403 | doi = 10.1056/NEJM198908103210629 }}</ref>

The dose may need to be adjusted in certain clinical scenarios. As with all other [[antiarrhythmic agent]]s, there is a risk of [[proarrhythmia]] associated with the use of flecainide. This risk is probably increased when flecainide is co-administered with other class Ic antiarrhythmics, such as [[encainide]]. The risk of proarrhythmia may also be increased by [[hypokalemia]].<ref name = Ohki>{{cite journal | vauthors = Ohki R, Takahashi M, Mizuno O, Fujikawa H, Mitsuhashi T, Katsuki T, Ikeda U, Shimada K | display-authors = 6 | title = Torsades de pointes ventricular tachycardia induced by mosapride and flecainide in the presence of hypokalemia | journal = Pacing and Clinical Electrophysiology | volume = 24 | issue = 1 | pages = 119–121 | date = January 2001 | pmid = 11227957 | doi = 10.1046/j.1460-9592.2001.00119.x | s2cid = 41090195 }}</ref> The risk of proarrhythmia is not necessarily associated with the length of time an individual is taking flecainide, and cases of late proarrhythmia have been reported.<ref name = Morganroth>{{cite journal | vauthors = Morganroth J | title = Early and late proarrhythmia from antiarrhythmic drug therapy | journal = Cardiovascular Drugs and Therapy | volume = 6 | issue = 1 | pages = 11–14 | date = February 1992 | pmid = 1533532 | doi = 10.1007/BF00050910 | s2cid = 22653784 }}</ref> Because of the role of both the liver and the kidneys in the elimination of flecainide, the dosing of flecainide may need to be adjusted in individuals who develop either liver failure or [[kidney failure]].

Because of the negative inotropic effects of flecainide, it should be used with caution in individuals with depressed [[ejection fraction]], and may worsen [[congestive heart failure]] in these individuals. It should be avoided in people with ischaemic heart disease and the elderly.<ref name = Santinelli/>

As with all class I [[antiarrhythmic agents]], flecainide increases the capture thresholds of [[artificial pacemaker|pacemakers]].<ref name = Fornieles-Pérez>{{cite journal | vauthors = Fornieles-Pérez H, Montoya-García M, Levine PA, Sanz O | title = Documentation of acute rise in ventricular capture thresholds associated with flecainide acetate | journal = Pacing and Clinical Electrophysiology | volume = 25 | issue = 5 | pages = 871–872 | date = May 2002 | pmid = 12049386 | doi = 10.1046/j.1460-9592.2002.00871.x | s2cid = 7180036 }}</ref><ref>{{cite journal | vauthors = Suffredini JM, Rutland J, Akpunonu P, Baum R, Catanzaro J, Elayi CS | title = Flecainide Toxicity Resulting in Pacemaker Latency and Intermittent Failure to Capture | journal = The American Journal of Case Reports | volume = 20 | pages = 1279–1283 | date = August 2019 | pmid = 31467262 | pmc = 6735620 | doi = 10.12659/AJCR.916370 }}</ref>

===Heart===
Due to the narrow therapeutic index of flecainide, physicians should be alert for signs of toxicity before life-threatening arrhythmias occur like [[torsades de pointes]]. While the toxic effects of flecainide are closely related to the plasma levels of the drug,<ref name = Winkelmann>{{cite journal | vauthors = Winkelmann BR, Leinberger H | title = Life-threatening flecainide toxicity. A pharmacodynamic approach | journal = Annals of Internal Medicine | volume = 106 | issue = 6 | pages = 807–814 | date = June 1987 | pmid = 3107447 | doi = 10.7326/0003-4819-106-6-807 }}</ref> it is unfeasible to check the plasma concentration in an individual on a regular basis.

Signs of flecainide toxicity include marked prolongation of the PR interval and widening of the QRS duration on the surface ECG. There may be signs and symptoms attributable to overt [[congestive heart failure|heart failure]] secondary to sudden decreased [[myocardial contractility]].

====Treatment====
Treatment of flecainide cardiac toxicity involves increasing the excretion of flecainide, blocking its effects in the heart, and (rarely) institution of cardiovascular support to avoid impending lethal arrhythmias. Modalities that have had success include administration of a beta-sympathomimetic agent,<ref name = Winkelmann/> and administration of a sodium load<ref name = Winkelmann/>(often in the form of [[Tonicity#Hypertonic solution|hypertonic]] [[sodium bicarbonate]]). Placing the individual on [[cardiopulmonary bypass]] support may be necessary in order to temporarily remove the need for a beating heart and to increase blood flow to the liver.<ref name = Corkeron>{{cite journal | vauthors = Corkeron MA, van Heerden PV, Newman SM, Dusci L | title = Extracorporeal circulatory support in near-fatal flecainide overdose | journal = Anaesthesia and Intensive Care | volume = 27 | issue = 4 | pages = 405–408 | date = August 1999 | pmid = 10470398 | doi = 10.1177/0310057x9902700413 | doi-access = free }}</ref><ref name = Yasui>{{cite journal | vauthors = Yasui RK, Culclasure TF, Kaufman D, Freed CR | title = Flecainide overdose: is cardiopulmonary support the treatment? | journal = Annals of Emergency Medicine | volume = 29 | issue = 5 | pages = 680–682 | date = May 1997 | pmid = 9140253 | doi = 10.1016/S0196-0644(97)70257-9 }}</ref>

===Lungs===
Flecainide has a very high affinity for lung tissue <ref>{{cite journal | vauthors = Latini R, Cavalli A, Maggioni AP, Volpi A | title = Flecainide distribution in human tissues | journal = British Journal of Clinical Pharmacology | volume = 24 | issue = 6 | pages = 820–822 | date = December 1987 | pmid = 3125854 | pmc = 1386410 | doi = 10.1111/j.1365-2125.1987.tb03252.x }}</ref> and is associated with drug-induced [[interstitial lung disease]].<ref>{{cite journal | vauthors = Ozkan M, Dweik RA, Ahmad M | title = Drug-induced lung disease | journal = Cleveland Clinic Journal of Medicine | volume = 68 | issue = 9 | pages = 782–785, 789–795 | date = September 2001 | pmid = 11563482 | doi = 10.3949/ccjm.68.9.782 | doi-broken-date = 22 December 2024 | s2cid = 45036873 }}</ref><ref>{{cite journal | vauthors = Camus P, Fanton A, Bonniaud P, Camus C, Foucher P | title = Interstitial lung disease induced by drugs and radiation | journal = Respiration; International Review of Thoracic Diseases | volume = 71 | issue = 4 | pages = 301–326 | year = 2004 | pmid = 15316202 | doi = 10.1159/000079633 | s2cid = 16315007 }}</ref><ref>{{cite journal | vauthors = Pesenti S, Lauque D, Daste G, Boulay V, Pujazon MC, Carles P | title = Diffuse infiltrative lung disease associated with flecainide. Report of two cases | journal = Respiration; International Review of Thoracic Diseases | volume = 69 | issue = 2 | pages = 182–185 | year = 2002 | pmid = 11961436 | doi = 10.1159/000056325 | s2cid = 72367121 }}</ref><ref>{{cite journal | vauthors = Haas M, Pérault MC, Bonnefoy P, Rodeau F, Caron F | title = [Interstitial pneumopathy due to flecainide] | journal = Presse Médicale | volume = 30 | issue = 21 | pages = 1062 | year = 2001 | pmid = 11471279 }}</ref><ref>{{cite journal | vauthors = Robain A, Perchet H, Fuhrman C | title = Flecainide-associated pneumonitis with acute respiratory failure in a patient with the LEOPARD syndrome | journal = Acta Cardiologica | volume = 55 | issue = 1 | pages = 45–47 | date = February 2000 | pmid = 10707759 | doi = 10.2143/ac.55.1.2005718 | s2cid = 20721407 }}</ref>