The chromatographic behavior of some antiarrhythmic compounds has been studied on commercially available TLC plates coated with octylsilane and octadecylsilane silica gel (RP-C8 and RP-C18, respectively) with organic-aqueous mobile phases containing citrate or acetate buffers at different pH. The best separations of individual and mixed drug standards were achieved on both RP-C8 and RPC18 with 3:7 (
) tetrahydrofuran-citrate buffer pH 4.45 as mobile phase. To determine the usefulness of these chromatographic systems for analysis of tablet samples, flecainide acetate was identified and quantified by UV densitometry at two wavelengths, 225 and 310 nm. Linear relationships were obtained between peak height or peak area and amount in the range 6.0 to 12.0 μg per spot, the correlation coefficient,
, was ∼0.990. The method was successfully applied to the analysis of flecainide in a pharmaceutical preparation, with satisfactory precision (RSD 1.14–5.93%) and accuracy (96.19–103.59%).
Authors:Rafał Pietraś, Hanna Hopkała, Dorota Kowalczuk and Agnieszka Małysza
A normal-phase (NP) TLC method has been established for separation of the five antiarrhythmics — disopyramide, flecainide, mexiletine, tocainide, and verapamil. The analysis was performed in horizontal chambers on aluminum oxide 60 F
and silica gel 60 F
TLC plates. The best mobile phases for separation of the compounds were tetrahydrofuran-hexane-25% ammonia, 5 + 4.8 + 0.2 (
), on the alumina plates and chloroform-tetrahydrofuran-ethanol-25% ammonia, 8.1 + 1.9 + 2 + 0.1 (
), on the silica plates. The substances were identified by use of different reagents and under UV irradiation at
= 254 nm. Quantification of mexiletine hydrochloride in Mexicord capsules was performed densitometrically at
= 210 nm. A good correlation coefficient (
= 0.9974) was obtained for the calibration plot constructed in the concentration range 20–45 μg per band. The active substance was extracted from the formulation with methanol (recovery 97.01 ± 2.39%, mean ±
expressing the precision of the proposed method was 5.23%. The procedure was simple and rapid and the results were reliable.
Authors:László Gellér, Szabolcs Szilágyi, Endre Zima, Marianna Srej, Gábor Szűcs, Levente Molnár and Béla Merkely
defibrillátor és reszinkronizációs kezelés. Kardiológiai Útmutató, Klinikai Irányelvek Kézikönyve, 2008, II, 32–37.
Schron, E. B., Exner, D. V., Yao, Q. és mtsai:
Quality of life in the antiarrhythmics versus
There is hardly a symptom that has impressed patients and physicians since ancient times more than an irregular heartbeat. In most cases, atrial fibrillation is the cause of the rhythm disturbance. However, it took many centuries before we were able to clearly understand fibrillation and to counteract it efficiently. The history of arrhythmia therapy with drugs is long and fascinating. Digitalis was probably the first “antiarrhythmic”. It was discovered by Leonhart Fuchs in the 16th century and introduced in the clinical practice by William Withering from Birmingham. Today's rhythm agents are of a much later date. Quinidine, an optical isomer of quinine, became clinically available in 1918. Other antiarrhythmic drugs were only developed in the 60s and 70s of the previous century, e.g. disopyramide, beta-receptor blockers, propafenone, flecainide, amiodarone, adenosine, ibutilide, and dofetilide. Among the latest commercially available antiarrhythmic substances are dronedarone and vernakalant, which were clinically introduced in 2009 and 2010, respectively. Thanks to the further development of innovative pharmaceuticals and modern electrotherapeutic methods, it can be expected that the previously therapy-resistant cases of atrial fibrillation will be lastingly reduced.
Authors:B. Cuparencu, C. Tomus, Manuela Gozariu and Alina Cuprian
Winslow, E., Walke, R. G., Mason, R.: Antiarrhythmic effects of selective beta 1- and nonselective beta-adrenoceptor blokade in normokalaemic and dietary-induced hypokalaemic rats. J. Cardiovasc. Pharmacol. 14 , 673-680 (1989