These results suggest that levetiracetam is an effective and well-tolerated adjunctive treatment for patients with previously uncontrolled idiopathic generalized epilepsy with myoclonic seizures.

Polymorphic ventricular tachyarrhythmias occurred spontaneously during bradycardia in dogs given the inotropic polypeptide anthopleurin-A (AP-A).The arrhythmia was investigated in in vitro and in vivo experiments. In in vitro experiments, AP-A (50 /ig/1) produced bradycardiadependent prolongation of action potential duration that was more pronounced in Purkinje than in muscle fibers. Only Purkinje fibers developed early afterdepolarizations (EAD) and triggered activity. These effects could be abolished by rapid pacing, lidocaine (4 mg/1), or tetrodotoxin (1 mg/1). In vivo experiments were conducted in anesthetized healthy dogs with simultaneous recording of surface ECG, monophask action potentials from the endocardia! and epicardial surface of the left ventricle by contact electrode catheter technique, and transmembrane action potentials from the epicardial surface of the left ventricle with a floating microelectrode technique. AP-A in a dose comparable to that used in vitro (4 /ig/kg, i.v. bolus) resulted in bradycardia-dependent marked prolongation of both monophasic and transmembrane action potentials. An EAD gradually appeared on both recordings but was more marked in endocardia! monophasic action potentials. Eventually, a premature ventricular depolarization arose from or very close to the peak of the EAD. The prolongation of action potentials was associated with similar prolongation of the QTU interval hi surface ECG, and in some experiments, the EAD corresponded to a distinct prominent U wave. A ventricular premature depolarization arose from the U or TU complex and initiated polymorphic ventricular tachyarrhythmias that terminated spontaneously or degenerated into ventricular fibrillation. These effects were reversed by rapid pacing or lidocaine (1 mg/kg). The present study provides evidence in support of the hypothesis that AP-A-induced ventricular tachyarrhythmias are due to bradycardia-dependent EAD and triggered activity.

Isochronal maps of ventricular activation were analyzed in dogs 3-5 days after ligation of the left anterior descending coronary artery utilizing a 64-channel multiplexer. Isochronal maps of the effective refractory period were determined from 62 epicardial sites and correlated with the activation maps. The ischemia occurring in the surviving epicardial layer prolonged refractoriness in a spatially nonuniform manner. The resulting pattern of refractoriness on the epicardial surface resembled concentric rings of isorefractoriness which increased in duration from the normal zone to the center of the ischemic zone. The formation of an arc of functional unidirectional conduction block occurred along the gradient of refractoriness and the exact location of the arc depended on the S1-S2 interval. When a short S1-S2 failed to induce reentry, fewer adjacent sites with sufficiently disparate refractoriness formed a smaller arc of block. A subsequent S3 encountered further nonuniformly shortened refractoriness (normal areas had shortened refractoriness greater than ischemic areas) and the arc of block was lengthened. This required a longer time for the wavefront to circulate around the arc. When it then reached the distal side of the arc, refractoriness had expired proximal to the arc and reentry occurred. Similarly, nonuniform shortening of refractoriness explained why one reentrant beat may or may not produce successive reentrant beats. Therefore, the spatial pattern of refractoriness forms the substrate for the arc of unidirectional conduction block that is fundamental to the development of ventricular reentry in this experimental model.

SUMMARY A 58-year-old man with hypertensive cardiovascular disease and atrial flutter underwent electrophysiologic studies, including multiple intra-atrial recordings and atrial stimulation. Although the surface ECG suggested the presence of atrial flutter, intra-atrial recordings demonstrated the presence of (1) sinus-like rhythm localized to an area of approximately 5 mm in and around the region of the sinus node, which was protected by entrance block; (2) flutter and/or fibrillation of the remaining parts of the right atrium; (3) fibrillation of the left atrium; and (4) transient degeneration of flutter into fibrillation at right atrial sites, with predominant flutter activity. Although a major part of the right atrium was in flutter and/or fibrillation, we could assess sinus node function by overdrive stimulation of the area of sinus node activity. Sinus node function studies revealed an underlying sick sinus syndrome.THE DIAGNOSIS of atrial arrhythmias is essentially based on the analysis of the configuration, timing, and rate of P waves on the surface ECG. However, recent studies in selected patients have demonstrated dissimilar atrial rhythms with direct intra-atrial recordings otherwise not discernible on the surface ECG."3 In this paper we report the electrophysiologic findings in a patient in whom the ECG revealed atrial flutter and intra-atrial recordings demonstrated the presence of sinus-like rhythm in and around the region of the sinus node, flutter and/or fibrillation of the remaining parts of the right atrium and fibrillation of the left atrium. We also assessed sinus node function, although a major part of the right and left atria were in flutter and/or fibrillation. Assessment of sinus node function revealed an underlying sick sinus syndrome.Case Report A 58-year-old man with hypertensive cardiovascular disease was admitted to the Medical Service of the Brooklyn Veteran's Administration Medical Center for uncontrolled hypertension, congestive heart failure and atrial flutter of recent onset. A 12-lead ECG suggested the presence of atrial flutter at a rate of 240 beats/min, with a ventricular response of 120 beats/min and poor R-wave progression from V1 to V3 ( fig. 1). Chest x-ray film showed cardiomegaly and pulmonary congestive changes. Echocardiogram revealed left atrial and left ventricular enlargement. The patient's hypertension and congestive heartfailure responded promptly to medical therapy. He was then referred to the cardiology service for elective electrical conversion of the atrial flutter after medical conversion with digitalis and quinidine had failed. Electrophysiologic StudiesThe patient underwent electrophysiologic studies to convert the atrial flutter by overdrive atrial stimulation. The procedure was explained to the patient, who gave signed consent. The electrophysiologic studies were performed after withholding digitalis and quinidine for 2 days. Serum digoxin level was 0.5 ng/ml on the day of the study. Two quadripolar #6FUSCI catheters with 10-mm interelectrode distance ...

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