Propranolol Flecainide

Antiarrhythmics (e.g., disopyramide, flecainide, and others) P-Blockers (e.g., propranolol, metoprolol, atenolol, and others) Calcium channel blockers (e.g., verapamil and others)... 

Antiarrhythmics encainide, flecainide, mexiletine Beta-blockers alprenolol, metoprolol, propranolol, timolol Opiates codeine, dextromethorphan, ethylmorphine... 

Drugs that may affect flecainide include amiodarone, cimetidine, cisapride, disopyramide, propranolol, ritonavir, urinary acidifiers/alkalinizers, and verapamil. Smoking may also have an effect. Drugs that may be affected by flecainide include cisapride, propranolol, and digoxin. 

Classes I, III, and IV all involve transmembrane ion channels Classes I and III involve Na+ channels. Class I compounds are designed to block cardiac Na channels in a voltage-dependent manner, similar to local anesthetics. Not surprisingly, many of these Class I agents are either local anesthetics or are structurally based on local anesthetics. Class I compounds include procainamide (7.15), disopyramide (7.16), amiodarone (7.17), lido-caine (7.5), tocainide (7.18), mexiletine (7.19), and flecainide (7.20). The majority of these compounds possess two or three of the fundamental structural building blocks found within local anesthetics. Propranolol (7.21) is the prototypic Class II agent. Class III compounds include molecules that block outward K channels, such as sotalol (7.22) and dofetilide (7.23), and molecules that enhance an inward Na current, such as... 

Propafenone has some structural similarities to propranolol and possesses weak 3-blocking activity. Its spectrum of action is very similar to that of quinidine, but it does not prolong the action potential. Its sodium channel-blocking kinetics are similar to that of flecainide. Propafenone is metabolized in the liver, with an average half-life of 5-7 hours. The usual daily dosage of propafenone is 450-900 mg in three divided doses. The drug is used primarily for supraventricular arrhythmias. The most common adverse effects are a metallic taste and constipation arrhythmia exacerbation can also occur. 

Menthyl chloroformate, [17], is commercially available and has been used in several applications. For example, Seeman et al. (72) carried out the preparative chromatographic resolution of nornicotine using [17] as a CDA. The diastereomeric carbamates formed via the reaction of racemic nornicotine with [17] were separated by preparative silica gel LC, and the pure enantiomers of nornicotine were liberated by acid-catalyzed hydrolysis of the carbamates (72). Several reports have described the use of [17] in the enantiospecific determination of drug concentrations in biological fluids thus, the reagent has been used in the analysis of encainide and some of its metabolites (73), flecainide (74), and propranolol (75), and other drugs (76). 

Lewis GP, Holtzman JL. Interaction of flecainide with digoxin and propranolol. Am J Cardiol 1984 53(5) B52-7. 

In 33 patients with sjmptomatic and inducible supraventricular tachycardias single doses of placebo, flecainide 3 mg/kg, or dUtiazem 120 mg plus propranolol 80 mg were used to terminate the dysrhythmia (5). Conversion to sinus rhythm was achieved within 2 hours in 17 patients with placebo, in 20 with flecainide, and in 31 with diltiazem plus propranolol. Time to conversion was shorter with diltiazem plus propranolol (32 minutes) than with flecainide (74 minutes) or placebo (77 minutes). Of those who were given flecainide, two had hypotension and one had sinus bradycardia. 

The combination of flecainide with propranolol results in additive hjrpotensive and negative inotropic effects (71). 

These principles are important in understanding additive drug combinations (e.g., quinidine and mexiletine), antagonistic combinations (e.g., flecainide and lidocaine), and potential antidotes to excess sodium channel blockade (e.g., sodium bicarbonate or propranolol). They also explain a number of clinical observations, such as why lidocaine-like drugs are relatively ineffective for supraventricular tachycardia. The type Ib drugs are fast on/off, inactivated sodium blockers atrial cells, however, have a very brief inactivated phase relative to ventricular tissue. 

C flecainide a blockers prazosin, doxazosin, etc. P blockers propranolol, etc. 

Ajmaline, alprenolol, amiflamine, amphetamine, aprindine, captopril, chlorpheniramine, cinnarizine, citalopram, clomipramine, clozapine, codeine, desipramine, dolasteron, encainide, flecainide, fluoxetine, fluphenazine, haloperidol, hydrocordone, imipramine, loratidine, methoxyphenamine, 3,4-methylenedioxymethamphetamine, metoprolol, mexiletine, (S)- and (i )-mianserin, nifedipine, olanzapine, omeprazole, oxycodone, perhexiline, phenformin, propaphenone, propranolol, remoxipride, ritonavir, saquinavir, selegiline, tamsulosin, timolol, tomoxetine, tramadol, trifluperidol, zolpidem... 

Extracted acetazolamide, amitriptyline, chlordiazepoxide, chlorpromazine, desipramine, dextromethorphan, diphenhydramine, doxepin, encainide, fentanyl, flecainide, fluoxetine, flurazepam, haloperidol, hydroxyethylflurazepam, ibuprofen, imipramine, lidocaine, ma-protiline, methadone, methaqualone, mexiletine, norchlorimipramine, nordoxepin, norfluoxetine, nordiazepam, nortriptyline, norverapamil, pentazocine, promazine, propafenone, propoxyphene, propranolol, protriptyline, quinidine, temazepam, trazodone, tri-mipramine, verapamil... 

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