Verapamil Diltiazem

Sinoatrial node

Decreases automaticity of nodal tissue Decreases conduction velocity Increases refractory period

a Sotalol exhibits additional beta-blocking activity.

b Amiodarone also has Na+-,beta-, and calcium channel-blocking activity.

a Sotalol exhibits additional beta-blocking activity.

b Amiodarone also has Na+-,beta-, and calcium channel-blocking activity.

4.7. Drug Interactions With Pacing Systems

It is important to note that certain drug therapies have been reported to have an impact on pacing system performance. Although it is rare for antiarrhythmic drugs to affect pacing thresholds significantly, they have been found to alter stimulation thresholds by inducing changes in the lead-myocardial interfacial conductivity and excitability. In addition, they can slow the intrinsic sinus rate, which necessitates pacing for resultant bradycardia. In general, class Ic drugs are most likely to increase pacing thresholds. Class Ia drugs can increase pacing thresholds at toxic dosages, and sotalol and amiodarone can increase pacing thresholds at therapeutic levels, but it is rarely clinically significant. A summary of the more common drugs and their impact on pacing thresholds, action potentials, and the physiological consequences of their action are found in Tables 5 and 6 (13).

4.8. New Indications/Clinical Trials

Today, single- and dual-chamber pacing systems have become the standard method of treating many bradyarrhythmias. Clinical evidence has raised interest in the selection of both the frequency at which patients are paced and the optimal site of stimulation (14). It has long been known that pacing produces a nonphysiological contraction pattern, but recent research has also indicated that potentially detrimental effects may result from long-term pacing (15-18).

Currently, alternate choices in ventricular stimulation sites are of particular interest because of their presumed physiological and hemodynamic benefits. For example, pacing of the bundle of His is thought to produce a more physiological contraction pattern; additional evidence exists that there may also be hemodynamic benefits associated with right ventricular septal and outflow tract pacing (15,19-24).

In patients with heart failure and associated wide QRS complexes, biventricular pacing has been adopted (25,26) (see resync1.mpg on the Companion CD). Finally, current research in atrial pacing has largely focused on reducing atrial fibrillation, improving methods of pace-terminating atrial tachycardias, and improving ventricular filling and atrial hemodynam-ics (27-29). Researchers are even investigating the possibility of genetically engineering a biological pacemaker (30).

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