Posted by Jack Drum on November 09, 2002 at 00:18:42:
In Reply to: Verelan-7 months post Maze posted by Don Haynsworth on November 08, 2002 at 21:50:05:
Don, here is some information, and a web site for drug information on it. You can read more there.
http://www.rxlist.com/cgi/generic/verapsr_cp.htm
Its great to see you back on the board. Your doctor is not talking about ablating the AV node is he. I wouldn't want that done.
Best wishes
Jack
Arrhythmia: Electrical activity through the AV node depends, to a significant degree, upon calcium influx through the channel. By decreasing the influx of calcium, verapamil HCl prolongs the effective refractory period within the AV node and slows AV conduction in a rate-related manner. This property accounts for the ability of verapamil HCl to slow the ventricular rate in patients with chronic atrial flutter or atrial fibrillation.
Normal sinus rhythm is usually not affected, but in patients with sick sinus syndrome, verapamil HCl may interfere with sinus-node impulse generation and may induce sinus arrest or sinoatrial block. Atrioventricular block can occur in patients without preexisting conduction defects (see WARNINGS). Verapamil HCl decreases the frequency of episodes of paroxysmal supraventricular tachycardia.
Verapamil HCl does not alter the normal atrial action potential or intraventricular conduction time, but in depressed atrial fibers it decreases amplitude, velocity of depolarization, and conduction velocity. Verapamil HCl 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 AV pathway following administration of verapamil HCl (see WARNINGS).
Verapamil HCl has a local anesthetic action that is 1.6 times that of procaine on an equimolar basis. It is not known whether this action is important at the doses used in man.
In Vitro: Verapamil binding is voltage-dependent with affinity increasing as the vascular smooth muscle membrane potential is reduced. In addition, verapamil binding is frequency dependent and apparent affinity increases with increased frequency of depolarizing stimulus.
The L-type calcium channel is an oligomeric structure consisting of five putative subunits designated alpha-1, alpha-2, beta, tau, and epsilon. Biochemical evidence points to separate binding sites for 1,4-dihydropyridines, phenylalkylamines, and the benzothiazepines (all located on the alpha-1 subunit). Although they share a similar mechanism of action, calcium channel blockers represent three heterogeneous categories of drugs with differing vascular-cardiac selectivity ratios.
Essential Hypertension: Verapamil HCl exerts antihypertensive effects by decreasing systemic vascular resistance, usually without orthostatic decreases in blood pressure or reflex tachycardia; bradycardia (rate less than 50 beats/min) is uncommon (1.4%). During isometric or dynamic exercise verapamil HCl does not alter systolic cardiac function in patients with normal ventricular function.
Verapamil regularly reduces the total systemic resistance (afterload) against which the heart works both at rest and at a given level of exercise by dilating peripheral arterioles.
Verapamil HCl does not alter total serum calcium levels. However, one report suggested that calcium levels above the normal range may alter the therapeutic effect of verapamil HCl
- Re: Verelan-7 months post Maze Don Haynsworth 21:19:11 11/09/2002 (0)