SUMMARY Intracardiac electrophysiologic studies were performed in two patients who had recurrent sustained ventricular tachycardia. In both, the tachycardia was repeatedly terminated by carotid massage. In one patient, intracardiac electrophysiologic studies revealed ventricular tachycardia with 2: 1 retrograde ventriculoatrial (VA) block. Carotid massage resulted in alternate Wenckebach retrograde VA conduction terminated by ventricular echo beats. When ventricular echo beats occurred at a coupling interval of 340-400 msec, the tachycardia was terminated. Similarly, induced atrial depolarizations (during ventricular tachycardia) produced ventricular capture and terminated the tachycardia when the resultant ventricular coupling interval was 330-395 msec. In the second patient, progressively premature atrial or ventricular depolarizations did not terminate the tachycardia. Carotid massage had no consistent effect on retrograde VA conduction during ventricular tachycardia, but usually resulted in gradual increases in the tachycardia cycle length (50-100 msec) before abrupt termination of the tachycardia. This is the first report documenting termination of ventricular tachycardia by carotid massage alone (i.e., without prior drug intervention); hence, tachycardia termination by simple carotid sinus massage does not prove a supraventricular origin. The mechanism of tachycardia termination was due to ventricular echo beats from retrograde atrioventricular nodal reentry in one patient and to direct vagal effects on either the ventricular muscle or the ventricular specialized conduction system in the other.DIFFERENTIATION of ventricular from supraventricular tachycardia with aberrant conduction traditionally includes the application of maneuvers that either enhance vagal or inhibit sympathetic tone.' 3 These include the Valsalva maneuver, carotid sinus massage, and the administration of edrophonium hydrochloride or phenylephrine. Termination of a regular wide-QRS-complex tachycardia using these techniques suggests a supraventricular origin. However, ventricular tachycardia can be terminated by either phenylephrine administration or by application of carotid sinus massage after pretreatment with edrophonium hydrochloride.' 6 We studied two patients with recurrent ventricular tachycardia who could terminate their wide-complex tachyarrhythmias by carotid sinus massage alone. Documentation of this phenomenon in the absence of pharmacologic manipulations is reported and adds to the growing evidence that changes in autonomic tone can significantly influence ventricular arrhythmias. Materials and MethodsAll studies were performed in a cardiac catheterization laboratory. Both patients gave informed consent. Patient 1 had been taking quinidine, but the medication was discontinued 48 tion. During the study, four quadripolar electrode catheters were inserted into the right femoral vein. Catheters were positioned in the high lateral right atrium, across the tricuspid valve, in the apex of the right ventricle, and across a patent...
SUMMARY Thirty-two patients were studied before and after i.v. administration of 0.150.20 mg/kg of propranolol. Twenty-one of the 32 underwent combined autonomic blockade with the additional infusion of 0.04 mg of atropine. Twenty other patients with sinus node disease underwent electrophysiologic studies both before and after i.v. administration of 0.04 mg of atropine alone. Spontaneous cycle length, maximal corrected sinus node recovery time, sinoatrial conduction time, secondary pauses and intrinsic heart rate were measured. Secondary pauses were more common in those with abnormal intrinsic heart rates, and they did not correlate with changes in maximal corrected sinus node recovery time or sinoatrial conduction time. In patients with normal intrinsic heart rate, abnormal test measurements usually returned to normal after combined blockade (hypervagotonia); however, some patients showed a new abnormality after propranolol that was not reversible with atropine (catecholamine-dependent). Abnormal test responses in patients with abnormal intrinsic heart rate persisted or increased after combined blockade. We conclude that patients with sinus node disease may be categorized as (1) those with intrinsic sinus node disease; (2) those with normal intrinsic sinus node function but either relative hypervagotonia or catecholamine dependency; and (3) those with abnormal intrinsic sinus node function affected by vagal or catecholamine factors.CLINICAL EVALUATION of patients with electrocardiographic evidence of sinus node dysfunction is difficult because of the interplay of intrinsic sinus node disease and autonomic nervous system tone.'-6 Jordan et al.? suggested that measurement of the intrinsic heart rate might be of value for distinguishing patients with disturbances of autonomic nervous system tone from those with intrinsic sinus node dysfunction. One of the objectives of our report is to extend their observations of the relative contribution of sympathetic and vagal influences in patients with symptomatic sinus node disease.Recently, Benditt et al.6 described the secondary pause (2°P) phenomenon or abnormal prolongation of postpacing cycles 2-10 in patients with sinus node disease. They demonstrated that evaluation of postpacing cycles 2-10 increased the value of atrial pacing tests in that patients with sinus node dysfunction may show the 2°P phenomenon in the presence of normal sinus node recovery time and sinoatrial conduction time (SACT). The role of autonomic tone in unmasking or suppressing this phenomenon has not been studied in detail, and such information might clarify the mechanisms of the 2°P phenomenon.
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