Cases reported "Tachycardia, Paroxysmal"

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1/22. Paroxysmal supraventricular tachycardia caused by 1:2 atrioventricular conduction in the presence of dual atrioventricular nodal pathways.

    One-to-two atrioventricular conduction, ie, the double response to a single sinus or atrial impulse, resulting in two QRS complexes for one P wave, is a rare manifestation of dual atrioventricular (AV) nodal pathways. This report describes the case of a 61-year-old woman with continuous episodes of supraventricular tachycardia caused by independent conduction to the ventricles of sinus impulses over both the fast and the slow AV nodal pathway, giving rise to a ventricular rate that was twice the sinus rate. A wide spectrum of electrocardiographic manifestations of 1:2 AV conduction was observed on the surface electrocardiogram. The diagnosis was suggested by several elements including evidence of dual AV nodal pathways during sinus rhythm and cycle length alternans during tachycardia. The patient underwent successful slow pathway ablation with complete disappearance of symptoms and electrocardiographic manifestations of 1:2 AV conduction.
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2/22. Shortening of conduction time over arborized atrioventricular accessory pathway with Mahaim fibers physiology just before interruption during radiofrequency ablation.

    A 21-year-old woman had paroxysmal wide QRS tachycardia with a left bundle branch block configuration and a retrograde conducted P wave just behind the QRS complex. An electrophysiological study revealed antidromic atrioventricular tachycardia involving an atrioventricular connection with decremental conduction as the anterograde limb and normal atrioventricular node as the retrograde limb. During constant pacing from the high right atrium (HRA) at the cycle length (CL) of 600 ms, the QRS configurations were not identical to those during the wide QRS tachycardia or constant pacing at the CL of less than 500 ms. The process by which this arborized atrioventricular accessory pathway with the Mahaim fibers physiology was interrupted by radiofrequency catheter ablation is described. Radiofrequency energy was delivered to the site recording a Mahaim potential at the tricuspid annulus during constant pacing from the HRA at the CL of 429 ms. The stimulus-QRS interval gradually shortened as it reached the power plateau without changing the preexcited QRS configuration. Shortening of the conduction time over the Mahiam pathway might have resulted in changing of the propagation from a slow to fast conduction zone or acceleration in response to thermal effect in a node-like structure on the atrial insertion site.
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3/22. A fetal wolff-parkinson-white syndrome diagnosed prenatally by magnetocardiography.

    We report a case of fetal Wolff-Parkinson-White (WPW) syndrome diagnosed prenatally by magnetocardiography (MCG). At 32 weeks' gestation, the fetus was diagnosed to have a paroxysmal supraventricular tachycardia by ultrasonography and direct fetal electrocardiogram (ECG). Transplacental fetal therapy by maternal oral administration of propranolol resolved the fetal tachyarrhythmia. Although the wave forms of the fetal MCG at 32 weeks' gestation were normal, the fetal MCG at 35 weeks' gestation showed a short PR interval and a long QRS complex duration with a delta wave, indicating WPW syndrome. The findings of the fetal MCG were confirmed by the postnatal ECG. MCG made the prenatal diagnosis of WPW syndrome possible.
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4/22. sinoatrial block during lithium treatment.

    lithium is known to produce T wave changes in the ECG, whereas effect upon the conducting system of the heart has not been described. In our patient lithium produced sinoauricular block and possibly tachycardia. The correlation between lithium treatment and tachyarrhythmias is discussed. When during lithium treatment block is found, the treatment should preferably be stopped, but if this is not possible it is important to realize that digitalis should not be used as a prophylactic drug against tachycardia, as it worsens the block and therefore increases the frequency of arrhythmia, even leading to Adams-Stokes attacks.
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5/22. Differential diagnosis of rhythm disturbances induced by endocardial pacing.

    Rhythm disturbances induced by endocardial pacing were studied in 15 patients. Atrial extrasystoles were found in 8, ventricular extrasystoles in 5, ventricular tachycardia in 1 and ventricular fibrillation in 1 patient. In all cases, an implanted pacemaker EKS-222 was used working in VVI regime. The connection of the above-mentioned rhythm disturbances with pacing is deduced from the stability of the coupling interval with the earlier induced complex, and from the presence of a negative P wave in standard leads II and III. A reliable criterion is in the authors' view, the disappearance of rhythm disturbances after the implanted pacemaker has been switched off.
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6/22. Spontaneous termination of paroxysmal supraventricular tachycardia following disappearance of bundle branch block ipsilateral to a concealed atrioventricular accessory pathway: the role of autonomic tone in tachycardia diagnosis.

    We present a case of an 18-year-old man with a history of palpitations in whom episodes of paroxysmal supraventricular tachycardia were easily initiated by administered atrial premature beats. In all 15 control episodes of tachycardia, functional left bundle branch block (LBBB) seen at the onset, resolved within 10-20 cycles (mean, 13.1 /- 0.95). The tachycardia ended with the normalized QRS complex in each episode. Eleven episodes ended because of block within the antegrade pathway (ended with a P-wave), and four episodes stopped because of block within the retrograde pathway (ended without a P-wave). During the administration of isoproterenol (1 mg/min IV) all six episodes of tachycardia had LBBB but these did not end when LBBB disappeared spontaneously. When LBBB subsided, the mean tachycardia cycle interval shortened from 328.5 /- 1.4 to 264.2 /- 2.1 ms (p less than 0.001). Each episode of tachycardia was then terminated by carotid sinus massage. The disappearance of LBBB in control conditions presented the retrograde and antegrade limbs of the reentrant circuit with an early impulse that stopped the tachycardia. After isoproterenol administration, the tachycardia did not end following disappearance of LBBB, thus enabling the tachycardia cycle interval to shorten by a mean of 64.3 /- 1.9 ms. This extent of tachycardia acceleration is diagnostic of the participation of a concealed, left free-wall bypass tract.
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7/22. Paroxysmal supraventricular tachycardia initiated by a swallowing-induced premature atrial beat.

    We report a unique patient in whom electrophysiologic studies elucidated the mechanism of a rare form of swallowing-induced atrioventricular reentrant tachycardia, and for whom successful surgical ablation of an accessory pathway abolished intractable episodes of palpitation. A 64-year-old man was incapacitated by frequent attacks of palpitation following swallowing. Electrocardiograms documented paroxysmal supraventricular tachycardias initiated by a premature atrial beat or beats following swallowing. During electrophysiologic studies swallowing consistently induced premature atrial beats which in turn initiated a sustained atrioventricular reentrant tachycardia incorporating a retrogradely conducting left-sided concealed accessory pathway. The atrial activation sequence related to the premature atrial beats and the morphology of the premature P waves suggested that premature atrial beats originated in the right atrium. The mechanism of induction of premature atrial beats following swallowing remains obscure in our patient. Antiarrythmic drugs failed to prevent induction of sustained tachycardias during sequential electrophysiologic studies. The patient underwent successful surgical ablation of the accessory pathway and is free from palpitation 15 months after the surgery.
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8/22. Swallowing-induced paroxysmal supraventricular tachycardia.

    A 54-year-old man had palpitations on swallowing without any esophageal or heart disease. Electrophysiological findings, including an A wave in the high right atrial leads appearing prior to the A wave on His bundle electrogram, revealed that the arrhythmia was paroxysmal supraventricular tachycardia originating in an ectopic focus of the atrium with intraventricular aberration. Treatment with verapamil, 120 mg/day, reduced his symptoms in spite of an insignificant decrease in the arrhythmia observed with Holter dynamic electrocardiography.
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9/22. disopyramide-induced ventricular fibrillation.

    Three cases are described with documented ventricular fibrillation shortly after the patients received disopyramide in moderate dosage. Electrocardiograms showed markedly prolonged Q-T intervals in two patients and a prominent U wave with a prolonged Q-U interval in one patient, but no change in QRS width. disopyramide-induced ventricular fibrillation appears to be similar to that caused by quinidine and is an indication to discontinue the drug.
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10/22. Atrial reentry in chronic repetitive supraventricular tachycardia.

    Atrial reentrance as a mechanism of the tachycardia was demonstrated in a 28-year-old patient suffering from chronic repetitive supraventricular tachycardia. Criteria for diagnosis included the following: (1) Repetitive supraventricular tachycardia was induced and terminated by properly timed atrial extrastimuli. (2) Return cycles of all atrial extrastimuli not abolishing the tachycardia were fully compensatory. (3) A-H prolongation was not a prerequisite to induce the tachycardia. (4) The contours of P and A waves during tachycardia differed from those in sinus rhythm, but atrial activation remained antegrade. (5) A concealed anomalous pathway could not be proved.
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