MYLAN-VERAPAMIL TABLET

Valsts: Kanāda

Valoda: angļu

Klimata pārmaiņas: Health Canada

Nopērc to tagad

Produkta apraksts Produkta apraksts (SPC)
24-07-2009

Aktīvā sastāvdaļa:

VERAPAMIL HYDROCHLORIDE

Pieejams no:

MYLAN PHARMACEUTICALS ULC

ATĶ kods:

C08DA01

SNN (starptautisko nepatentēto nosaukumu):

VERAPAMIL

Deva:

120MG

Zāļu forma:

TABLET

Kompozīcija:

VERAPAMIL HYDROCHLORIDE 120MG

Ievadīšanas:

ORAL

Vienības iepakojumā:

100/500/1000

Receptes veids:

Prescription

Ārstniecības joma:

MISCELLANEOUS CALCIUM-CHANNEL BLOCKING AGENTS

Produktu pārskats:

Active ingredient group (AIG) number: 0113846001; AHFS:

Autorizācija statuss:

APPROVED

Autorizācija datums:

2009-07-03

Produkta apraksts

                                PRODUCT MONOGRAPH
MYLAN-VERAPAMIL TABLETS
(Verapamil Tablets, BP)
80 and 120 mg
Antianginal/Antiarrhythmic/Antihypertensive Agent
Mylan Pharmaceuticals ULC
Date of Preparation:
85 Advance Rd.
July 7, 2009
Etobicoke, Ontario M8Z 2S6
Control#: 131047
1
PRODUCT MONOGRAPH
MYLAN-VERAPAMIL TABLETS
(Verapamil Tablets, BP)
80 and 120 mg
THERAPEUTIC CLASSIFICATION
Antianginal/Antiarrhythmic/Antihypertensive Agent
ACTIONS AND CLINICAL PHARMACOLOGY
ANGINA AND ARRHYTHMIA
Verapamil hydrochloride is a calcium ion influx inhibitor (calcium
entry blocker or calcium ion
antagonist). The mechanism of the antianginal and antiarrhythmic
effects of verapamil is believed to be
related to its specific cellular action of selectively inhibiting
transmembrane influx of calcium in cardiac
muscle, coronary and systemic arteries and in cells of the
intracardiac conduction system. Verapamil
blocks the transmembrane influx of calcium through the slow channel
(calcium ion antagonism) without
affecting, to any significant degree the transmembrane influx of
sodium through the fast channel. This
results in a reduction of free calcium ions available within cells of
the above tissues.
Verapamil's antiarrhythmic effects are believed to be brought about
largely by its action on the sinoatrial
(S-A) and atrioventricular (A-V) nodes. Verapamil depresses A-V nodal
conduction and prolongs
2
functional refractory periods. Verapamil does not alter the normal
atrial action potential or
intraventricular conduction time, but depresses amplitude, velocity of
depolarization and conduction in
depressed atrial fibers. Through this action, it interrupts re-entrant
pathways and slows the ventricular
rate.
Verapamil may shorten the antegrade effective refractory period of the
accessory bypass tract.
Acceleration of ventricular rate and/or ventricular fibrillation has
been reported in patients with atrial
flutter or atrial fibrillation and a coexisting accessory A-V pathway
following administration of verapamil
(see WARNINGS).
Verapamil is a potent smooth muscle relax
                                
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