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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In clinical arrhythmias, the main therapeutic role of calcium channel entry blockers is related to their effect on the sinus and atrioventricular (AV) node. Consequently, in cardiac arrhythmias where the AV node is part of the reentry circuit, a beneficial effect of diltiazem and verapamil can be demonstrated. These include AV nodal reentry and orthodromic tachycardia in patients with Wolff-Parkinson-White syndrome. In addition, the ventricular response by the AV node during atrial tachycardias can also be controlled with these agents. A specific type of ventricular tachycardia seen in the absence of structural heart disease has also been reported to respond to intravenous and oral verapamil. Calcium channel blockers have no proven depressant effect on accessory pathway conduction. Similarly, the value of these agents in the treatment of ventricular tachycardia in association with chronic coronary artery disease and idiopathic dilated cardiomyopathy is rather limited. The use of calcium entry blockers in patients with wide QRS tachycardia, therefore, is to be discouraged unless it can be proved that supraventricular tachycardia with aberrant conduction is the underlying basis.
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PMID:Use of calcium channel entry blockers in the treatment of cardiac arrhythmias. 268 83

Between April 1984 and December 1987, electrophysiological studies and endomyocardial biopsy were performed in 14 pediatric patients, aged from 7 to 15 years, with idiopathic ventricular arrhythmias in whom diagnostic evaluation had revealed no structural heart disease. They were 8 boys and 6 girls. Cardiac catheterization revealed regional wall motion abnormalities of the left ventricle in 3 patients, one of whom showed decreased ejection fraction (EF). Electrophysiologic examination showed sinus node dysfunction in 21%. AV nodal dysfunction in 14% and dual AV nodal pathway in 21%. Histopathologic examination by endomyocardial biopsy showed myocellular hypertrophy, degeneration of myocytes, interstitial fibrosis and endomyocardial thickness in 86%, 36%, 35% and 14%, respectively. Since idiopathic ventricular arrhythmias in pediatric age group included relatively high electrophysiologic and histopathologic abnormalities, which were suggestive of occult myocardial disease and might be the early stage of cardiomyopathy, careful follow-up should be required.
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PMID:[Electrophysiologic and histopathologic investigations in children with idiopathic ventricular arrhythmias]. 272 7

The efficacy of amiodarone was evaluated in 85 patients with supraventricular tachycardia (SVT) refractory to several antiarrhythmic agents (mean 3.8 +/- 1.0). All but six patients had organic heart disease. Patients were followed for 19 months (range 2-60 months). Response to amiodarone treatment was considered excellent (no recurrence of SVT) in 22 of 52 patients with paroxysmal atrial fibrillation (PAF), in four of 13 patients with chronic atrial fibrillation (CAF), and in three of 15 patients with Wolff-Parkinson-White syndrome-related circus movement tachycardia (WPW-CMT). Response was improved (marked improvement in symptoms with partial suppression of SVT) in 22 patients with PAF, in seven patients with CAF, in 10 patients with WPW-CMT, and in four patients with atrioventricular nodal reentry tachycardia. Response was considered poor (insignificant or no suppression of SVT) in three patients with PAF, in one patient with CAF, and in one patient with WPW-CMT. Seven patients required discontinuation of amiodarone due to adverse effects. We conclude that amiodarone is efficacious and relatively safe for control of SVT refractory to conventional antiarrhythmic agents irrespective of the underlying electrophysiologic mechanism.
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PMID:The usefulness of amiodarone in management of refractory supraventricular tachyarrhythmias. 274 45

Although beta-blockers have established efficacy in treating ventricular ectopy and PSVT, their applicability for acute antiarrhythmic interventions in patients with organic heart disease or COPD, is frequently limited by negative inotropic or bronchospastic side effects. The development of an ultrashort acting beta-blocker with rapid reversibility of its side effects would widen their applicability. Therefore, we tested the electrophysiologic properties of such a new short acting beta-blocker, esmolol, in 14 patients (10 with organic heart disease) with a mean EF of 47.6 +/- 17%, undergoing standard clinical electrophysiologic studies for various indications. Like most other beta-blockers, esmolol's major direct effects were on sinus node function and AV nodal conduction characteristics; significantly prolonging sinus cycle length, cycle length to Wenckebach and AH interval in sinus rhythm and at a paced cycle length of 600 ms. In contrast to most other beta-blockers, following termination of its infusion, esmolol shortened parameters of sinus node function and AV nodal refractoriness, with respect to the control values, suggesting a possible rebound phenomena. These effects occurred within 5 min of terminating the intravenous drug infusion. Esmolol had no significant effect on systolic blood pressure, electrocardiographic intervals and had rare adverse reactions. We conclude that esmolol is an ultra-short acting beta-blocker, with typical direct electrophysiologic effects on sinus node and AV nodal function, and a possible rebound phenomena following its discontinuation that may make it particularly suited to acute antiarrhythmic interventions in patients susceptible to adverse beta-blocker side effects.
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PMID:The electrophysiologic properties of esmolol, a short acting beta-blocker. 290 Feb 17

To assess the incidence and clinical characteristics of carotid sinus hypersensitivity and the relationship to electrophysiologic findings, 76 patients with unexplained syncope underwent carotid sinus massage during electrophysiologic studies for syncope evaluation. Twenty-one patients (28%) were found to have carotid sinus hypersensitivity. Of these 21 patients, 11 (52%) had coronary artery disease, two (10%) had hypertensive heart disease, and eight (38%) had no organic heart disease. During electrophysiologic studies, abnormal sinus node function was found in three patients (14%), abnormal atrioventricular (AV) node function was noted in four (19%), and combined abnormal sinus node and AV node functions were seen in three (14%). Eleven patients (53%) had a normal electrophysiologic study. During carotid sinus massage, sinus arrest alone was observed in 12 patients (57%), and combined sinus arrest and AV nodal block was seen in nine (43%). Thirteen patients were treated with a permanent pacemaker, in whom either carotid sinus massage reproduced the symptom or concomitant sinus node or AV node abnormality, or organic heart disease was present. With a mean follow-up of 42 +/- 19 months, none of these 13 patients had recurrent syncope. However, one of eight patients (13%) who did not receive a pacemaker had recurrence of syncope. Subsequently, this patient has done well after implantation of a pacemaker. These observations suggest that there is a significant incidence of carotid sinus hypersensitivity in patients with unexplained syncope. Permanent pacing appears to be beneficial in selected patients based on clinical and electrophysiologic findings.
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PMID:Carotid sinus hypersensitivity in patients with unexplained syncope: clinical, electrophysiologic, and long-term follow-up observations. 317 98

Electrophysiologic studies were performed in 51 patients with syncopes of unexplained origin. 25 patients (49%) had organic heart disease. Electrophysiologic testing included determination of corrected sinus node recovery time, AV-nodal effective refractory period, AH- and HV-intervals, and AV-nodal Wenckebach rate. During programmed right ventricular stimulation, 1-3 premature stimuli were used. 26 patients (53%) had an abnormal outcome that strongly suggested an arrhythmogenic cause of the reported syncopes. In ten patients (20%), corrected sinus node recovery time was prolonged; AV-nodal conduction disturbance was manifest in two patients (4%); reversibility with atropine was shown in one patient. Six patients (12%) had an infrahisian conduction delay with an HV-interval longer than 70 ms. Eight patients (15.6%) had either symptomatic ventricular tachycardias (n = 4), AV-nodal reentry tachycardias (n = 2), or inducible symptomatic rapid atrial fibrillation (n = 2). In one additional patient, ventricular tachycardias could not be reinitiated after ending tricyclic antidepressant drug medication. The diagnostic yield of the electrophysiologic study was not influenced by the presence of organic heart disease. Patients with prolonged corrected sinus node recovery time, prolonged HV-interval, and irreversible AV-conduction delay underwent pacemaker implantation (n = 17). Patients with rapid response to programmed stimulation received antiarrhythmic medication, the efficacy of which was assessed by serial electrophysiologic testing until non-inducibility was obtained. The mean follow-up period was 11 months (1-31 months). Overall 2-year mortality was 17%. In 4/5 patients, death was unrelated to the cause of syncope.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Electrophysiologic study in patients with syncope of unknown cause]. 321 47

We present 4 patients aged 51, 19, 22 and 16 years respectively, with no overt heart disease. They complained of recurrent episodes of paroxysmal sustained tachycardia with QRS morphology of right bundle branch block and left fascicular hemiblock. The analysis of the electrocardiogram during the tachycardia and, in two cases, the electrophysiologic study showed a complete a-v dissociation and capture beats confirming the ventricular origin of the arrhythmia. In all the patients the interruption of the tachycardia was obtained by the vagal maneuvers; in two of them the tachycardia was also sensitive to verapamil iv. These cases demonstrate the efficacy of the vagal maneuvers in the termination of fascicular tachycardia and support the hypothesis of slow-response nodal-like fibers, distally displaced, as the anatomical substrate of this arrhythmia.
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PMID:[Termination of idiopathic ventricular tachycardia with QRS morphology of right bundle branch block and anterior fascicular hemiblock (fascicular tachycardia) by vagal maneuvers. Presentation of 4 cases]. 323 56

Parenteral magnesium has been used for several decades in the empiric treatment of various arrhythmias, but the data on its electrophysiologic effects in man are limited. We evaluated the electrophysiologic effects of magnesium sulfate (MgSO4) administration in eight normomagnesemic patients with normal mononuclear cell magnesium content, who had no clinically significant heart disease and had normal baseline electrophysiologic properties. After administration of intravenous MgSO4, serum magnesium rose significantly from 1.9 +/- 0.1 to 4.4 +/- 1.7 mg/dl (p less than 0.02). During a maintenance magnesium infusion, we observed significant prolongation of the ECG PR interval (145 +/- 18 to 155 +/- 26 msec, p less than 0.05), AH interval (77 +/- 27 to 83 +/- 26 msec, p less than 0.002), antegrade atrioventricular (AV) nodal effective refractory period (278 +/- 67 to 293 +/- 67 msec, p less than 0.05), and sinoatrial conduction time (60 +/- 34 to 76 +/- 32 msec, p less than 0.02). No significant effect was observed on sinus cycle length, sinus node recovery time, intra-atrial or intraventricular conduction times, QRS duration (during both sinus rhythm and ventricular pacing), QT interval, HV interval, paced cycle length resulting in AV nodal Wenckebach block, AV nodal functional refractory period, retrograde ventriculoatrial (VA) effective refractory period, or atrial and ventricular refractory periods. These findings, in conjunction with the demonstrated ability of magnesium to block slow channels for sodium movement, may provide an explanation of the mechanism by which magnesium exerts its effect in the treatment of atrial and junctional arrhythmias.
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PMID:Electrophysiologic effects of intravenous magnesium in patients with normal conduction systems and no clinical evidence of significant cardiac disease. 334 Nov 71

There is little data on cardiac electrophysiological assessment and long term follow-up of unexplained syncope from Australasia. We present 94 patients with unexplained syncope who underwent such assessment and followup for an average of 52 months in 92 patients. Of the 94 investigated 57 were male, the average age was 61 years and average number of syncopal episodes prior to study was 8 (minimum 2). Forty-two patients had heart disease. Patients were divided into 3 groups on results of electro physiological testing. Normal (31 patients), group 1 with intermediate abnormalities of sinus node function or atrioventricular conduction (37 patients) and group 2 in whom the abnormalities were felt likely to represent the cause of syncope (26 patients). Abnormalities detected in group 2 were sinus node dysfunction in 12, abnormal atrioventricular nodal conduction in 8, abnormal infranodal conduction in 2, vagal hypersensitivity in 3 and ventricular tachycardia in two. Follow-up for a mean of 52 months was obtained in 92 patients. Recurrent syncope occurred in 37% of the patients. Treatment reduced recurrent syncope to a level approaching statistical significance in group 2 patients (50% to 13%; 0.01 greater than p greater than 0.05) but had little influence on recurrent syncope in group 1 or normal patients. There were 14 deaths over the follow-up period. Mortality was predicted by group 2 electrophysiological abnormality (p less than 0.02) and the presence of heart disease (p less than 0.05) and was not reduced by specific therapy. Sudden death occurred in 3 patients, all with heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac electrophysiological assessment and the natural history of unexplained syncope. 338 Apr 45

The role of i.v. verapamil in the management of atrioventricular (AV) nodal reentrant tachycardias is well established (Schamroth et al., 1980). Generally however the drug is not very effective in recurrent ventricular tachycardia (VT) (Singh et al., 1983). Verapamil was recently demonstrated to be successful in terminating VT induced by programmed stimulation in only 1 out of 8 patients tested (Wellens et al., 1980). Conversely a few recent cases of verapamil responsive VT, mostly occurring in young people without obvious organic heart disease, have been reported (Belhassen, 1984; Klein, 1984; Delise, 1985; Ward, 1984; Lin 1983; German, 1983; Mason, 1983; Wu, 1981). We describe 3 clinical examples of idiopathic recurrent sustained VT responsive to verapamil. A careful analysis of our cases support the hypothesis of different pathophysiologic mechanism involved in the genesis of this unique arrhythmic entity.
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PMID:Idiopathic recurrent sustained ventricular tachycardia responsive to verapamil. 349 43


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