1/38. Clinical implications of fetal magnetocardiography.OBJECTIVES: To test the usefulness and reliability of fetal magnetocardiography as a diagnostic or screening tool, both for fetuses with arrhythmias as well as for fetuses with a congenital heart defect. methods: We describe 21 women with either a fetal arrhythmia or a congenital heart defect discovered during prenatal evaluation by sonography. Four fetuses showed a complete atrioventricular block, two an atrial flutter, nine ventricular extrasystole, and one a complete irregular heart rate. Five fetuses were suspected to have a congenital heart defect. In all cases magnetocardiograms were recorded. RESULTS: Nine fetuses with extrasystole showed a range of premature atrial contractions, premature junctional beats or premature ventricular contractions. Two fetuses with atrial flutter showed typical flutter waves and four fetuses with complete atrioventricular block showed an uncoupling of P-wave and QRS complex. One fetus showed a pattern suggestive of a bundle branch block. In three of four fetuses with confirmed congenital heart defects the magnetocardiogram showed abnormalities. CONCLUSION: Fetal magnetocardiography allows an insight into the electrophysiological aspects of the fetal heart, is accurate in the classification of fetal arrhythmias, and shows potential as a tool in defining a population at risk for congenital heart defects.- - - - - - - - - - ranking = 1keywords = bundle (Clic here for more details about this article) |
2/38. Ashman's phenomenon--a source of nonsustained wide-complex tachycardia: case report and discussion.The refractory period of the right bundle branch is increased when the R-R interval between the prior two conducted impulses is long. Thus, an impulse that arrives soon after the second of two impulses separated by a long R-R interval may be aberrantly conducted with a right bundle branch block morphology on electrocardiogram. This aberrant conduction is termed "Ashman's phenomenon" and is often responsible for isolated wide QRS complexes in the presence of underlying atrial fibrillation. This process may also produce runs of wide QRS complexes that must be distinguished from nonsustained ventricular tachycardia. A case of such multibeat Ashman's phenomena is presented, and the characteristics used to identify this phenomenon are discussed. A brief review of several recent studies on the differentiation of sustained ventricular tachycardia from supraventricular tachycardia with aberrancy in the setting of a regular underlying rhythm is given as well.- - - - - - - - - - ranking = 2keywords = bundle (Clic here for more details about this article) |
3/38. Spontaneous onset of ventricular fibrillation in brugada syndrome with J wave and ST-segment elevation in the inferior leads.We report the case of a 52-year-old man with variant brugada syndrome who was successfully resuscitated from ventricular fibrillation (VF). Resting ECG showed J wave and ST-segment elevation in the inferior leads but no coved or saddleback ST-segment elevation in the right precordial leads. Pilsicainide infusion provoked coved-type ST-segment elevation in the right precordial leads and mild ST-segment elevation 80 ms after the J point in the inferior leads. During an emergency, 12-lead ECG showed that spontaneous onset of VF was preceded by left bundle branch block and superior axis-type ventricular extrasystoles. The present case provides additional information on the site of origin of VF in patients with brugada syndrome.- - - - - - - - - - ranking = 1keywords = bundle (Clic here for more details about this article) |
4/38. Suppression of exercise-induced ventricular arrhythmias by propranolol and diltiazem in a woman without organic heart disease--a case report.A thirty-five-year-old woman without organic heart disease who has exercise-induced ventricular arrhythmias suppressed by propranolol and diltiazem is reported. Treadmill exercise provoked reproducibly nonsustained ventricular tachycardia (NSVT) and salvos of ventricular premature contraction (VPC). QRS morphology of these ventricular arrhythmias showed left bundle branch block pattern and right axis deviation. Oral propranolol (20 mg) and diltiazem (90 mg) prevented exercise provocation of NSVT and VPC. However, oral mexiletine (200 mg) and procainamide (500 mg) could not prevent exercise provocation of these ventricular arrhythmias. No ventricular arrhythmias could be induced by any form of ventricular extrastimulations. Right ventricular pacing at a rate of 210 beats/minute provoked NSVT of which the QRS morphology was similar to that of exercise-induced NSVT. Triggered activity may be a possible electrophysiologic mechanism for exercise-induced ventricular arrhythmias in this patient, although other mechanisms such as reentry and enhanced automaticity could not be completely excluded.- - - - - - - - - - ranking = 1keywords = bundle (Clic here for more details about this article) |
5/38. Demonstration of accessory pathway interaction by computerized mapping in preexcitation syndrome.While interaction between the normal conduction system and an accessory pathway (AP) has been reported, interaction between two APs has not been well documented. With the assistance of computerized mapping techniques, we recently operated on a patient with two APs. One of these two APs had slow anterograde conduction velocity and was concealed during sinus rhythm and atrial pacing. Intraoperative computerized mapping studies revealed that the interaction between the APs was responsible for the anterograde conduction block of the slow AP during sinus rhythm and atrial pacing. This is the first direct demonstration of inhibition of conduction of one AP by the other AP in a patient with preexcitation syndrome.- - - - - - - - - - ranking = 0.030207254229213keywords = accessory (Clic here for more details about this article) |
6/38. Two cases of bi-ventricular dysplasia associated with ventricular tachycardia and familial occurrence of sudden death.Two strikingly similar patients with arrhythmogenic right ventricular dysplasia which severely impaired not only the right ventricle but also the left ventricle are described in association with familial occurrence of sudden death. A 49-year-old man experienced syncope which was due to ventricular tachycardia. electrocardiography revealed a first degree atrioventricular block, incomplete right bundle-branch block, T wave inversions in leads II, III, a VF and V1 to V5, and multiformal ventricular extrasystoles. echocardiography and ventricular cineangiography showed not only the right ventricular dilatation with an aneurysm in the right ventricular apex, inflow and outflow tracts, but also mild dilatation of the left ventricle with left ventricular apical and posterior aneurysms. radionuclide angiography also disclosed dysfunction of both ventricles, especially during exercise. His family history revealed that 3 members of his family died of sudden deaths. A 56-year-old woman experienced syncope secondary to ventricular tachycardia, with left bundle-branch block. electrocardiography showed complete right bundle-branch block, left axis deviation, and T wave inversions in leads V1 to V4. echocardiography and ventricular cineangiography revealed not only marked right ventricular dilatation with the "triangle of dysplasia", but also a left ventricular aneurysm in the apex and posterior portion. Her elder brother died of a sudden death, and electrocardiograms of 2 members of her family showed ventricular extrasystoles and T wave inversions. These 2 cases may well be termed "familial bi-ventricular dysplasia".- - - - - - - - - - ranking = 3keywords = bundle (Clic here for more details about this article) |
7/38. Atrioventricular nodal reentry in the wolff-parkinson-white syndrome.Although supraventricular tachycardia in the Wolff-Parkinson-White (WPW) syndrome is generally due to atrioventricular reentry, the presence of the accessory pathway does not preclude other mechanisms of tachycardia. We observed AV nodal reentry in three of 95 consecutive patients (3.1%) referred for assessment of arrhythmias associated with WPW syndrome. The unique observation of spontaneous transition from atrioventricular reentry to AV nodal reentry at a similar cycle length was observed in one patient and is the subject of this report.- - - - - - - - - - ranking = 0.0060414508458427keywords = accessory (Clic here for more details about this article) |
8/38. 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.- - - - - - - - - - ranking = 0.018124352537528keywords = accessory (Clic here for more details about this article) |
9/38. Alternating left and right bundle branch block aberration of atrial extrasystoles in bigeminal rhythm.We report two cases of atrial extrasystolic bigeminy manifesting with alternating right and left bundle branch block aberration. The manifestation is explained on the basis of cycle-dependent variations of the bundle branch refractory period with alternate resetting of bundle branch refractoriness.- - - - - - - - - - ranking = 7keywords = bundle (Clic here for more details about this article) |
10/38. Periodic changes in cycle length of ventricular tachycardia: a Wenckebach type exit block?A 55-year-old female developed ventricular tachycardia (VT) which showed a Wenckebach periodicity in cycle length. She had had a myocardial infarction about ten years previous and, at age 51, felt fatigability and palpitations. The ECG showed VT. Thereafter, she had had palpitations of short duration two to three times a year. On the last admission she developed fatigability; the ECG showed VT. lidocaine (100 mg i.v.) did not terminate VT. procainamide (600 mg) could not terminate the VT, but the rate became slower. Programmed stimulation was given at bedside which effectively terminated VT. Electrophysiologic study induced VT in a reproducible manner. Ventricular tachycardia showed initial fluctuation in cycle length which stabilized at 270 msec. disopyramide therapy (400 mg/day p.o.) was begun and electrophysiologic study was repeated one week later. VT was again induced but the cycle length was a little longer. A periodic change in cycle length from 328 to 442 msec was repeated. The change in cycle length was uniformly found in surface leads (I, II, V1) and intracardiac electrograms from the right ventricular apex and the His bundle region. No change in QRS complex was found and the periodicity was unrelated to atrial activity. A Wenckebach type exit block was therefore suggested; disopyramide might be responsible for the development of the block. We could not find another such case in the literature.- - - - - - - - - - ranking = 1keywords = bundle (Clic here for more details about this article) |
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