Cardiology: Accessory Pathways =============================== þ Amiodarone: - controversial, but will slow both pathways; British literature suggests it is safe and effective - can give procainamide - no beta blockers or calcium channel blockers or digoxin - adenosine reported to make patients worse þ Wolff-Parkinson-White syndrome (WPW) - "slurrred upstroke" of the QRS (delta wave) - in regular tachycardia, even with WPW the AV node is part of the circuit and limits the top rate to about 250 in normal individuals. þ Lown-Ganong-Levine syndrome (LGL) - no delta wave on EKG > Once a cardiologist told me that lidocaine > can be misleading as a "diagnostic test" when given to someone with a > wide-QRS tachycardia of ?? origin -- if the person has underlying WPW and SVT > with aberrant ventricular conduction, lidocaine can also suppress the > accessory pathway, normalizing the rhythm, and breaking the re-entrant cycle > (if you believe that re-entry really exists). Thus, there is obviously some > type of activity on the ventricular myocardium. Antidromic (antegrade accessory pathway, retrograde AVN with wide QRS) SVT in WPW is rare (5%) compared to orthodromic SVT (opposite path and thus narrow complex). Lidocaine does indeed increase refractoriness (see below, however) in accessory pathways (AP). Kent bundles, however are embryologically derived from atrial and not ventricular muscle. > Another thing I've been taught -- but can't look up the references now > (looking for work, Harv??:-)) is that lidocaine can accelerate conduction > through the AV node -- the times when this is especially problematic is when > a person is in AF. If we give lido for "wide QRS" beats in AF, many of which > are actually aberrancies, we can accelerate the ventricular response to the > 350-500 impulses bombarding the AV node per minute, leading to very rapid AF > which often degenerates into VF. I've seen this happen, and I know that it's > reported (somewhere) in the literature. I think that what you are referring to is the rare reported cases of lidocaine accelerating accessory pathway conduction in cases of WPW with atrial fibrillation. In general lidocaine is considered safe and effective as a second line drug to procainamide for wide QRS tachycardias (1,2). Digoxin (3), verapamil (4) and propranolol (5) are contraindicated in that setting. Digoxin can, of course, _increase_ conduction down the AP and verapamil may do so as well. Although beta-blockers, in general do not adversely effect the conduction properties of the AP they too may accelerate conduction by blocking the AVN and thus decreasing concealed retrograde conduction in the AP. Amiodarone has also been implicated in occasional acceleration of AP conduction (6). Of course, verapamil is also contraindicated in wide QRS tachycardias not only because of its possible acceleration of rate in WPW with AF but also as a result of its adverse hemodynamic effects in VT unrelated to WPW. H. Louzon MD (1) Li P [Electrophysiological properties of atrial fibrillation with WPW syndrome and the role of procainamide in conversion] Chung Hua Hsin Hsueh Kuan Ping Tsa Chih 1991 Apr;19(2):65-6, 123 ABSTRACT: Fifty one patients with recurrent episodes of atrial fibrillation associated with WPW syndrome were studied by pre-operative clinical electrophysiogical testing. The results showed that: these patients had an markedly prolonged intra-atrial conduction time (PA intervals: 42.22 +/- 10.93 ms) than the patients only with attack of atrioventricular reentry tachycardia (AVRT) (PA intervals: 17.21 +/- 9.68ms, P less than 0.001). The attack of atrial fibrillation related to an markedly prolonged atrial vulnerable phase and the retrograde conduction of accessory pathway (AP). The clinical results of atrial fibrillation were decided by the antegrade effective refractory period (AERP) of AP. When the shortest R-R (V-V) intervals during attack of atrial fibrillation was shorter than 180ms, the atrial fibrillation spontaneously turned to the ventricular fibrillation. The conversion of atrial fibrillation to sinus rhythm showed that procainamide not only prolonged AERP of AP, which were 248.57 +/- 15.74ms and 388.57 +/- 63.9 ms (P less than 0.001) respectively before and after intravenous procainamide infusion, but also prolonged intra-atrial conduction time significantly, the PA interval before and after intravenous procainamide infusion were 42.22 +/- 10.93 ms and 57.14 +/- 11.12 ms (P less than 0.025) respectively. (2) Sager et. al. Narrow Complex Tachycardias: Differential Diagnosis and Management. Card Clin 1991;9(4):619- (3) Sellers TD Jr, Bashore TM, Gallagher JJ Digitalis in the pre-excitation syndrome. Analysis during atrial fibrillation. Circulation 1977 Aug;56(2):260-7 ABSTRACT: The effect of digitalis in 21 patients with Wolff-Parkinson-White syndrome was anlayzed with respect to the ventricular response during atrial fibrillation and antegrade and retrograde refractory periods of accessory pathways. Digitalis shortened the cycle length of the most rapid ventricular response (shortest R-R) (i.e., increased the ventricle response) in 6/21 patients, increased the cycle length in 7/21 patients, had no effect on the cycle length in 5/21, and could not be determined in 3/21. Digitalis could be directly related to the onset of ventricle fibrillation resulting from atrial fibrillation in 9/21 patients. Each of these patients had shortest R-R intervals (220 msec or less) during atrial fibrillation in the control data. The results of this study indicate that no a priori prediction about the effect of digitalis on the antegrade conduction of accessory pathways can be made. By elective induction of atrial fibrillation it is possible to separate WPW patients into groups at high and low risk for developing ventricular fibrillation with the administration of digitalis. (4) Michel B, Goy JJ, Kappenberger L [Wolff-Parkinson-White syndrome and verapamil: apropos of a case of ventricular fibrillation] Schweiz Med Wochenschr 1989 May 13;119(19):630-4 ABSTRACT: Numerous highly effective antiarrhythmic agents are now available which have a powerful anti-arrhythmia action but may cause severe side effects in the case of inappropriate use. We report the case of a patient with WPW syndrome in whom inappropriate administration of verapamil during an episode of atrial fibrillation and rapid ventricular response caused ventricular fibrillation. (5) Morady F, DiCarlo LA Jr, Baerman JM, De Buitleir M Effect of propranolol on ventricular rate during atrial fibrillation in the Wolff-Parkinson-White syndrome. PACE Pacing Clin Electrophysiol 1987 May;10(3 Pt 1):492-6 ABSTRACT: Atrial fibrillation was induced during an electrophysiology study in 10 patients with the Wolff-Parkinson-White (WPW) syndrome, after determination of baseline properties of the accessory atrioventricular (AV) connection; intravenous propranolol (0.2 mg/kg) was then administered. Atrial fibrillation terminated during the drug infusion in three patients, allowing determination of propranolol's effects on conduction and refractoriness during sinus rhythm, before atrial fibrillation was reinduced. In these three patients propranolol had no effect on refractoriness or conduction properties of the accessory AV connection during sinus rhythm. The mean ventricular rate during atrial fibrillation was slowed by 15-56 beats/min in six patients, had no effect on the mean rate in three patients, and markedly increased the ventricular rate (203 to 267 beats/min) in one patient. In this patient, 54% of QRS complexes during atrial fibrillation were narrow, compared to 0-25% in the other patients. Propranolol reduced the percentage of QRS complexes that were narrow from 13 +/- 16% to 1 +/- 2% (mean +/- standard deviation, p less than 0.05). We conclude that propranolol may slow the ventricular rate during atrial fibrillation in some patients with the WPW syndrome, probably by blocking the effects of adrenergic activation. However, propranolol should not be used in patients with the WPW syndrome who have atrial fibrillation, if most QRS complexes during atrial fibrillation are preexcited. When a large percentage of QRS complexes are narrow, propranolol may increase the ventricular rate, probably by eliminating concealed retrograde conduction in the accessory AV connection. (6) Perticone F, Cuda G, Spadea F, Pintaudi C, Tropea R Malignant ventricular arrhythmia in the Wolff-Parkinson-White syndrome during amiodarone treatment. Clin Cardiol 1987 Aug;10(8):477-80 ABSTRACT: The ventricular rate during rapid atrial rhythms is related in Wolff-Parkinson-White (WPW) syndrome to antegrade effective refractory period of the accessory pathways. Among the many antiarrhythmic drugs available, amiodarone is most commonly used for its large therapeutic window and very long half-life. We report a case of cardiac pre-excitation syndrome in a young male patient in whom amiodarone therapy (3000 mg/weekly) was instituted to modify the dangerous ventricular response during atrial fibrillation (shortest R-R interval 190 ms, ventricular rate 210 beats/min). Four months later, starting pharmacological treatment, a new electrophysiological study documented a malignant ventricular arrhythmia: during atrial fibrillation the minimum R-R interval was 160 ms and the ventricular rate 280 beats/min. Finally, the possible mechanism of paradoxical effect observed in our patient is hypothesized. Amiodarone could favor conduction over the accessory pathways by slowing or blocking conduction into the atrioventricular node and decreasing concealed retrograde conduction into the accessory bypass tract by normally conducted beats.