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Cardiovascular Drugs during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Another lidocaine-related antiarrhythmic medication that is structurally similar to encainide and procainamide, Flecainide has not been studied in human pregnancy. According the manufacturer, Flecainide is associated with an increased incidence of birth defects and embryotoxic effects in certain strains of rabbits given four times the usual human therapeutic dose. However, congenital anomalies were not increased in frequency in rats, mice, and other strains of rabbits given in the usual human dose (Manufacturer insert). A case report suggested an association with birth defects with flecainide. Flecainide has been used to treat fetal arrhythmias, but fetal deaths have occurred with this treatment. Efficacious alternative but related medications available with a better safety profile are available. Thus, flecainide should be avoided, or at least used only as the drug of last resort when others have failed. It is an old FDA category C drug.
Nonimmune Hydrops Fetalis
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Chelsea DeBolt, Katherine Connolly, Mary E. Norton, Joanne Stone
For parvovirus B19 and arrhythmias, treatment is feasible and effective. Intrauterine transfusion of fetuses with severe hydrops because of parvovirus B19 infection reduces the risk of fetal death. When heart failure and hydrops are associated with supraventricular tachycardia, historically, the first-line drug has been digoxin. Alternatives are flecainide, sotalol, amiodarone, verapamil, and adenosine. However, in fetuses with NIH, the bioavailability of digoxin is decreased compared to non-hydropic fetuses, while flecainide has increased bioavailability in hydropic fetuses. In fetuses with NIH and SVT, digoxin had lower rates of tachycardia resolution compared with flecainide (OR 0.412, 95% CI 0.268–0.632; I2 0%) [9]. In patients with any type of fetal tachycardia, flecainide remained superior to digoxin for conversion to sinus rhythm in hydropic fetuses (OR 5.0, 95% CI 2.5–10, I2 0%, p <0.001) [53]. Maternal side effects and rate of fetal demise were not increased in those that were treated with flecainide [9, 53]. Difficulties derived from placental enlargement may render maternal administration unpredictable and direct administration to the umbilical cord is an alternative.
Pneumonitis induced by non-cytotoxic agents
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Umair A Gauhar, J Allen D Cooper
Flecainide is a class 1C antiarrhythmic agent used for the treatment of ventricular and supraventricular arrhythmias. Dyspnoea and chest pain can occur in 4–7 per cent of the patients on flecainide therapy but pulmonary toxicity is much less rare.119 Five cases of suspected flecainide-induced pneumonitis have been described.120–123 Cell-mediated immune responses are thought to be the causative mechanism.120 Withdrawal of the drug and corticosteroid therapy has been helpful. Tocainide, another class 1C antiarrhythmic with a similar structure, has also been reported to cause interstitial pneumonitis.124,125 Amiodarone toxicity is discussed in Chapter 22.
Cardiac arrhythmias in pregnant women: need for mother and offspring protection
Published in Current Medical Research and Opinion, 2020
Theodora A. Manolis, Antonis A. Manolis, Evdoxia J. Apostolopoulos, Despoina Papatheou, Helen Melita, Antonis S. Manolis
Although both flecainide and propafenone cross the placental barrier, previous case reports have shown that pregnant women who received these drugs did not experience adverse effects on the fetus related to the drug34,118. Neither of these agents is known to have teratogenic potential in humans or laboratory animals. However, use of these agents should be approached cautiously because they have not been studied extensively in pregnant women. Flecainide has been used safely to treat preexcited AF during pregnancy124. Caution is advised with use of IC drugs, as these agents are potent sodium-channel blockers and cause marked slowing of conduction, as depicted by a prolonged QRS complex. Most importantly, these agents have been shown to be pro-arrhythmic in the setting of SHD111.
Flecainide toxicity in renal failure
Published in Baylor University Medical Center Proceedings, 2018
Rogin Subedi, Ryan K. Dean, Arbind Chaudhary, Tamas Szombathy
Flecainide is approved by the Food and Drug Administration for the prevention of paroxysmal supraventricular tachycardia, paroxysmal atrial fibrillation/flutter, and sustained ventricular tachycardia.1–3 However, use of flecainide has been limited because of its proarrhythmic effects and increase in mortality in patients with prior myocardial infarction, structural heart disease, and left ventricular dysfunction.3,4 Because of its negative ionotropic effect, it may cause or worsen congestive heart failure, particularly in patients with cardiomyopathy, preexisting severe heart failure (New York Heart Association functional class III or IV), or an ejection fraction <30%.3 Flecainide is primarily metabolized by the hepatic cytochrome P450 CYP2D6 system; however, approximately 30% of an oral dose is excreted in urine as unchanged drug.5–9 Though the elimination half-life of flecainide ranges from 7 to 23 hours, in patients with renal impairment it can be prolonged to 58 hours, and the total clearance of this drug might fall by approximately 40%.5–7 Therefore, the recommended starting dose is 100 mg daily or 50 mg twice a day in those with a creatinine clearance ≤35 mL/min/1.73 m2. Whenever feasible, plasma flecainide levels should be monitored to keep the trough plasma level from <0.7 to 1 µg/mL.3 Our patient continued to receive flecainide 150 mg twice a day without any adjustment for her renal function. In addition, the failure to monitor the plasma flecainide level might have contributed to her adverse outcomes.
What the internist should know about hereditary muscle channelopathies
Published in Acta Clinica Belgica, 2018
Véronique Bissay, Sophie C. H. Van Malderen
In HyperPP, the acute attacks respond to inhaled salbutamol or glucose and insuline therapy. The attacks of hypoPP are usually treated with oral or, if necessary, intravenous potassium supplements [10]. Additional lifestyle/dietary modifications to avoid known triggers, the use of carbonic anhydrase inhibitors (acetazolamide 250–500 mg/1–2x/day) and daily use of slow-release potassium supplements (in case of hypoPP) further reduce the frequency and severity of the episodic attacks. Acquired forms need to be excluded by checking e.g. thyroid and renal function. In case of ATS, annual screening including a 12-lead ECG and 24-h Holter monitoring [33] is recommended. An implantable cardioverter-defibrillator is required for those with a tachycardia-induced syncope. Empiric treatment with flecainide might be considered for significant, frequent ventricular arrhythmias in the setting of reduced left ventricular function. Hypokaliemia inducing drugs (diuretics) and salbutamol inhalers need to be avoided because they can exacerbate cardiac arrhythmias [33].