Antiarrhythmic agents blockers

Class I Antiarrhythmic Agents The Sodium Channel Blockers... 

ICDs have been found to be significantly more effective than antiarrhythmic agents such as amiodarone or sotalol for reducing the risk of sudden cardiac death 45,46 therefore, ICDs are preferred therapy.44 However, many patients with ICDs receive concurrent antiarrhythmic drug therapy to reduce the frequency with which patients experience the discomfort of shocks and to prolong battery life of the devices. Combined pharmacotherapy with amiodarone and a 3-blocker is more effective than monotherapy with sotalol or (i-blockers for reduction in the frequency of ICD shocks.47... 

Proarrhythmia refers to development of a significant new arrhythmia (such as VT, ventricular fibrillation [VF], or TdP) or worsening of an existing arrhythmia. Proarrhythmia results from the same mechanisms that cause other arrhythmias or from an alteration in the underlying substrate due to the antiarrhythmic agent. TdP is a rapid form of polymorphic VT associated with evidence of delayed ventricular repolarization due to blockade of potassium conductance. TdP may be hereditary or acquired. Acquired forms are associated with many clinical conditions and drugs, especially type la and type III IKr blockers. 

In addition to being used as antianginal and antiarrhythmic agents, calcium channel blockers are used to treat weak and moderate hypertension. These drugs prevent calcium ions from entering into the smooth muscle cells of peripheral vessels, and they cause relaxation of peripheral vessels, which leads to lowering of arterial blood pressure. In clinically used doses, calcium channel blockers relax smooth musculature of arteries and have little effect on veins. In doses that relax smooth musculature, calcium channel blockers have relatively little effect on cardiac contractility. 

Sotalol [SOE ta lol], although a class III antiarrhythmic agent, also has potent p-blocker activity. It is well established that p-blockers reduce mortality associated with acute myocardial infarction. 

The p adrenoceptor antagonists (beta blockers) are class II antiarrhythmic agents. They prolong phase 4 of the cardiac action potential (pacemaker potential), slowing the heart rate. There are three subtypes of P adrenoceptors Pi, P2 and P3. Stimulation of Pi adrenoceptors in the heart increases the force and rate of cardiac contraction, as well as increasing automaticity of the pacemaker sites and conduction through the AV node. The P2... 

The roule (raveled by a Ca channel blocker, such as verapamil, (o its receptor site parallels (hat observed with many local aneslhetic-like antiarrhythmic agents. It i.s believed that verapamil, like mo.sl of (he Ca channel blockers. crosses the cell membrane in an uncharged form to gain access to its site of action on the intracellular side of the membrane. Data show a greater affinity of verapamil and other Ca- channel hlockers to the inactivated. state of the channel. ... 

ANTIARRHYTHMIC agents (Class I agents, e.g. disopyramide, flecainide. lignocaine. procainamide, quinidine) are sodium-channel blockers and are mainly used to treat atrial and ventricular tachycardias (see antiarrhythmic agents). ANTIEPILEPTICS have a number of mechanisms of action, but some appear to have a component involving modulation of sodium-channel function, e.g. carbamaxepine and phenytoin (see anticonvulsants). 

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