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

Fourteen patients (mean age, 48 +/- 19 years) with left ventricular dysfunction in the absence of underlying organic heart disease underwent catheter ablation (nine with direct-current energy and five with radiofrequency energy) to treat drug-refractory, symptomatic supraventricular reentrant tachycardia (mean duration of tachycardia, 22 +/- 17 years). Clinical tachycardias were accessory pathway-mediated tachyarrhythmia (12 patients) and atrioventricular nodal reentrant tachycardia (two patients). Changes of ventricular function after successful ablation, as assessed by radionuclide ventriculography and echocardiography, showed a decrease in left ventricular end-systolic dimension (39 +/- 6 mm to 34 +/- 6 mm; 32 +/- 6 mm; p < 0.05) and in left ventricular end-diastolic dimension (55 +/- 5 mm to 52 +/- 3 mm; 51 +/- 3 mm; p < 0.05) in the early (2 to 3 months) and late (6 to 8 months) follow-up periods, increase of nuclear ejection fraction (38% +/- 8% to 46% +/- 7%; p < 0.05) and fractional shortening (28% +/- 7% to 36% +/- 8%; p < 0.05) in the late follow-up period. Increase of fractional shortening was mainly due to decrease in the end-systolic dimension. These findings suggest that prolonged attacks of uncontrolled supraventricular tachycardia may result in left ventricular dysfunction, which is reversible after successful catheter ablation of the arrhythmias.
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PMID:Reversibility of left ventricular dysfunction after successful catheter ablation of supraventricular reentrant tachycardia. 146 7

Seven out of 829 pediatric cardiac patients (0.84%) were found to have sinus node dysfunction (SND) over the past seven years. Of the seven patients, three had structurally normal hearts. One of these three patients had long QT syndrome. In four patients, structural heart disease was noted. In three of these four patients the sinus node dysfunction was attributed to cardiac surgery. The age of onset of SND ranged from four months to eight years. Presenting symptoms and signs included syncope, near-syncope, seizure and congestive heart failure. Two patients were asymptomatic. Five patients had episodic sinus pause. Sinus or junctional bradycardia was noted in four patients. Three had tachy-bradycardia. High grade atrioventricular block was noted in one patient. Treadmill exercise test revealed a nonsustained ventricular tachycardia in two patients. All seven patients were found to have prolonged maximal corrected sinus node recovery time. Prolonged intra-atrial conduction time was found in three, prolonged AV nodal conduction time in one, and prolonged His-Purkinje conduction time in one patient during the electrophysiologic study. All seven patients showed abnormal results in intrinsic heart rate study. Anti-arrhythmic drugs were prescribed. During the follow-up study, no patient died, but two patients received a pacemaker implantation. Because of the extent of their conduction system diseases, it is recommended that patients with SND should be thoroughly investigated.
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PMID:Sinus node dysfunction in children. 151 8

It has been previously demonstrated that radiofrequency (RF) energy can be safely applied to successfully eliminate accessory pathways in patients with the Wolff-Parkinson-White syndrome. This technique may also be used to successfully eliminate atrioventricular (AV) nodal reentrant tachycardia by elimination of either the fast or slow AV nodal pathways. However, RF energy has achieved only limited success in eliminating ventricular tachycardia (VT) in patients with structural heart disease, such as coronary artery disease and dilated cardiomyopathy. Direct-current catheter techniques have successfully eliminated VT in patients with and without structural heart disease, but this technique is limited by the risk of barotrauma and proarrhythmia. We used RF catheter ablation techniques to eliminate VT in patients without structural heart disease. Our results from the basis of this report. 16 patients (nine women and seven men; mean age 38; range 18 to 55 years) who did not have any identifiable structural heart disease by echocardiography where included in this study. These patients underwent RF catheter ablation to eliminate VT. Two patients had presented with syncope, nine with presyncope and five with palpitations only. The mean duration of symptoms was 6.7 years (range 0.5 to 20 years). VT was successfully eliminated by RF catheter techniques in 15 of the 16 patients (a 94% success rate). Importantly, successful ablation sites included regions other than the right ventricular outflow tract. Areas of VT origin therefore included the high right ventricular outflow tract (twelve patients), right ventricular septum near the tricuspid valve (three patients), and the left ventricular septum (one patient). The only ablation failure was in a patient whose VT arose from a region near the His bundle. Successful ablation occurred in patients in whom an accurate pace map could be obtained and early local endocardial activation was obtainable. Further, firm catheter contact with endocardium was required for successful elimination of VT. RF ablation did not cause any identifiable arrhythmia and produced a minimal cardiac enzyme rise. It also resulted in no detectable change in cardiac function by Doppler echocardiography. Based on these findings, we conclude that RF catheter ablation of VT in patients without structural heart disease was highly effective and safe. It may therefore be considered as early therapy in these patients.
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PMID:Catheter ablation of ventricular tachycardia using radiofrequency techniques in patients without structural heart disease. 163 37

Since the first successful surgical intervention for Wolff-Parkinson-White syndrome by W. C. Sealy, a surgical electrophysiological intervention has been developed for every single supraventricular arrhythmia. The surgical rationale is based on the site of the mechanism of the arrhythmia and associated pathology which characterizes the "arrhythmogenic substrate". Wolff-Parkinson-White syndrome is a congenital heart disease characterized by an accessory atrioventricular connection distinct from the AV node-His bundle system. It is associated with AV reentrant tachycardia and/or atrial fibrillation with fast ventricular responses via the accessory pathway. The current surgical management is ablation of the accessory pathway using either an endocardial dissection or epicardial approach. Surgical ablation is associated with high efficacy and low morbidity. Epicardial dissection of the accessory pathway on the beating heart has helped to localize variant accessory pathways associated with Coumel's tachycardia or Mahaim's fiber electrophysiological entity. AV nodal reentrant tachycardia can be cured using direct AV nodal dissection (or perinodal cryoablation). Atrial flutter can be interrupted by cryoablation of the arrhythmogenic substrate located in the coronary sinus orifice of the region modifying atrial inputs. Chronotropic atrial function abolished by chronic or paroxysmal idiopathic atrial fibrillation can be restored using the corridor operation (sinus node-AV node insulation). Surgery is an alternative in patients with resistant atrial tachycardias. Currently surgery is indicated only after other non-invasive EP interventions have been either attempted or rejected.
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PMID:Surgery for supraventricular tachyarrhythmias. 176 6

Dependence of QT interval duration on cardiac heart rate has been well established and is considered to be an intrinsic property of ventricular myocardium. Conclusive results of autonomic influences on such phenomena are lacking. To evaluate whether rate-dependent changes of QT interval are conditioned by the autonomic nervous system, 28 normal subjects with no heart disease and a normal QT interval were electrophysiologically assessed. The QT interval was calculated at 6 paced cycle lengths (600, 540, 500, 460, 430 and 400 ms) during the basal state, and after beta blockade (propranolol 0.2 mg/kg) and autonomic blockade (propranolol plus atropine 0.04 mg/kg). Because of atrioventricular nodal conduction limits, intrapatient cross-comparisons were performed in 10 subjects (aged 42 +/- 15 years). Single regression lines, evaluated in each subject, showing correlation between pacing cycle length and QT duration at each of the 3 states were analyzed. The mean slope observed after autonomic blockade (b = 0.10 +/- 0.04) was significantly lower than that seen during the basal state (b = 0.22 +/- 0.12, p less than 0.05) and after beta blockade (b = 0.23 +/- 0.08, p less than 0.05); nonsignificant differences were found between slopes during the basal state and after beta blockade. Results showed that vagal tone increased intrinsic dependence of QT at increasing cycle length, whereas sympathetic tone did not seem to interfere significantly. Since (in each subject) beta blockade was performed--or achieved--before atropine administration, the vagal influences are likely to be directly exerted on the ventricular electrophysiologic substrate.
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PMID:Sympathetic and vagal influences on rate-dependent changes of QT interval in healthy subjects. 195 Oct 79

We investigated the electrophysiological properties of the heart in patients with definite or classical rheumatoid arthritis using programmed electrical stimulation techniques. Twelve patients with rheumatoid arthritis and without evidence of organic heart disease or arrhythmia detectable with serial electrocardiograms and 24-hour ambulatory electrocardiographic monitoring were compared with 12 control subjects. Stimulation was performed from the high right atrium and right ventricular apex at a drive cycle length of 600 msec and the recording sites included high right atrium, atrioventricular junction and distal coronary sinus. There was no statistically significant difference in the corrected sinus node recovery time between the study and control group of patients. Similarly, no differences from normal were found in the AH and HV intervals or in the atrial and ventricular refractoriness, whereas the atrioventricular nodal effective refractory period was higher in patients with rheumatoid arthritis, compared with the control group (338 +/- 38 vs 286 +/- 29, P less than 0.02). The atrial conduction time during basic cycle length had a tendency to increase from high right atrium to atrioventricular junction in the study group and reached statistical significance from high right atrium to coronary sinus (92 +/- 15 vs 74 +/- 14, P less than 0.05). Electrophysiologic differences between the study and control patients also included a greater increase in maximal intraatrial (40 +/- 13 vs 27 +/- 16, P less than 0.05) and interatrial conduction delay (54 +/- 16 vs 31 +/- 12, P less than 0.01) of early premature stimuli in patients with rheumatoid arthritis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiologic studies of the heart in patients with rheumatoid arthritis. 229 20

Fifty patients with supraventricular tachycardia (SVT) underwent clinical electrophysiological studies (EPS), endomyocardial biopsies and cardiac catheterizations. EPS revealed AV nodal reentrant tachycardia (AVNRT) in seven patients, AV reentrant tachycardia utilizing concealed AV bypass tracts (AVR-CBT) in nine patients, AV reentrant tachycardia utilizing AV bypass tracts with ventricular preexcitation (manifest WPW) in 13 patients, sinus nodal or intra-atrial reentrant tachycardia (SNRT or IART) in three patients, atrial flutter (AF) in nine patients, automatic atrial tachycardia (AAT) in five patients, and multifocal atrial tachycardia (MAT) in four patients. According to the clinical observations, three patients with AVNRT (43%), six with AVR-CBT (67%), six with manifest WPW (46%), two with SNRT or IART (67%), eight with AF (89%), two with AAT (40%), and two with MAT (50%) showed other accompanying clinical abnormalities. In all patients who were studied histologically, changes in the myocardium were seen; myocarditic changes, postmyocarditic changes and nonspecific abnormalities were present in six (12%), 15 (30%), and nine (18%) respectively. Myocardial changes were observed in four out of seven cases with AVNRT (57%), in six out of nine with AVR-CBT (67%), in five out of 13 with manifest WPW (38%), in two out of three with SNRT or IART (67%), in six out of nine with AF (67%), in all five cases of AAT (100%), and in two out of four with MAT (50%). Nineteen out of 32 without clinical abnormalities except for arrhythmias (59%) had myocardial changes (six had myocarditic changes, ten had postmyocarditic changes, and three had nonspecific abnormalities). On the other hand, nine out of 21 with myocarditic or postmyocarditic changes were accompanied with various arrhythmias other than SVT (two had SSS, five had AV block or rBBB, and two had VT). Elevated LVEDP was present in 36% of the group with normal myocardium and in 53% of the group with myocardial changes. However, the low EF was shown in no patients with normal myocardium but in 21% of the group with myocardial changes. The low CI was also shown in only 9% of the group with normal myocardium but in 28% of the group with myocardial changes. These results suggest that patients with SVT may exhibit several histopathological changes in the myocardium, even in the absence of any clinical organic heart disease.
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PMID:Clinical, electrophysiological, and histopathological observations in supraventricular tachycardia. 245 68

Encainide is a class IC antiarrhythmic agent having little or no effect on action-potential duration or maximum diastolic potential but decreasing the maximum rate of phase O depolarization as well as increasing atrial and ventricular effective refractory periods. In intact animals or humans, encainide increases the AH, PR, QRS, and H-V intervals while not affecting the sinus node cycle length or JT interval. QT interval increases only by the concomitant increase in the QRS interval. Encainide is metabolized to O-demethyl encainide (ODE) and 3-methoxy-ODE (MODE), both of which are also antiarrhythmics with similar pharmacology to encainide. Encainide and its metabolites have little negative inotropic activity and ancillary pharmacology. Consequently, encainide has little or no effect on hemodynamic variables in patients with either normal or compromised cardiac function. The drug is well tolerated, with side effects being mainly those associated with its local anesthetic activity such as blurred vision and dizziness. Encainide is particularly effective in patients with excessive premature ventricular complexes (PVCs) and less so in patients with sustained ventricular tachycardia (VT). Like all antiarrhythmics, encainide may aggravate or precipitate new arrhythmias (proarrhythmia). The overall incidence of proarrhythmia is about 10%, with less occurring in patients with PVCs and more in those with sustained VT; also, the incidence of proarrhythmia is higher in patients with underlying heart disease. Encainide is also effective for the treatment of supra-ventricular arrhythmias, including atrial fibrillation, PSVT (both PAF as well as reentry of the nodal or W-P-W type), and ectopic atrial tachycardia. Its dosage and role in antiarrhythmic therapy are discussed.
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PMID:Encainide. 251 80

Transesophageal electrophysiologic study has recently been proposed for the evaluation of supraventricular arrhythmias. In this report we present 13 cases, with palpitations occurring only during effort, due to a suspected supraventricular tachycardia, in which the usefulness of the transesophageal electrophysiologic study performed during stress test was evaluated. Of these 13 patients, nine were male and four were female, mean age was 29 yrs. Twelve cases had no heart disease, one had a moderate mitral valve insufficiency. Nine cases had a normal ECG, four had a WPW pattern. In 9/13 cases no significant arrhythmia was ever documented, in 1/13 ventricular premature beats were present in the basal ECG, in 1/13 a atrial fibrillation and in 2/13 a supraventricular reciprocating tachycardia was recorded. In all cases a maximal exercise test and a 24-hour Holter monitoring were performed. In all pts a transesophageal electrophysiologic study was performed both at rest and during extra-stimuli and incremental atrial pacing. The end point of transesophageal study was the induction of a sustained (greater than 30") supraventricular tachycardia. RESULTS. Maximal exercise test was negative in 11/13 cases; it showed ventricular premature beats in one case and initiated a supraventricular tachycardia in one. The 24 hour Holter monitoring was negative in 12/13 cases while it showed frequent ventricular premature beats in one. Resting transesophageal electrophysiologic study revealed dual A-V nodal pathways in six pts: in one of them a junctional re-entry was induced; in two a single echo beat was observed, while in three no reentry was observed. In three cases a supraventricular tachycardia was induced which was sustained in one and unsustained (7" and 24") in two cases. In 4 cases transesophageal electrophysiologic study gave no information. Transesophageal stimulation during exercise induced a greater than 30" reciprocating tachycardia in all patients, at work loads of 30-180 watts. Six pts had an intranodal tachycardia (V-A less than 70 msec) a further six pts had a atrioventricular tachycardia involving a Kent bundle (V-A greater than or equal to 70 msec), which was concealed in two, and one had a atrial tachycardia. In four cases (3 with intranodal and 1 with atrioventricular tachycardia), exercise transesophageal study was repeated after chronic therapy with betablockers (sotalol 240 mg/die or metoprolol 200 mg/die). In all cases, after therapy, the induced tachycardia had a longer cycle and in two cases it was induced at a higher work load. In a further two cases flecainide (200 mg/die) was tested. In one case (with atrial tachycardia), the arrhythmia was no longer inducible after therapy, in another case (with intranodal tachycardia) the drug had no effect. CONCLUSIONS. In patients with paroxysmal supraventricular tachyarrhythmias occurring during effort the basal ECG is normal or shows a WPW pattern. The maximal exercise test and 24 hour Holter monitoring give no information in over 90% of cases.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Usefulness of transesophageal electrophysiological study during the ergometric test in the evaluation of supraventricular paroxysmal tachycardia occurring during exertion]. 257 99

Although electrophysiologic testing accurately delineates abnormalities in patients with fixed cardiac-conduction defects, its sensitivity in identifying transient rhythm disturbances is unknown. We prospectively studied 21 patients who had electrocardiographically documented intermittent atrioventricular block (n = 13) or sinus pauses (n = 8) causing syncope, but whose cardiac rhythm had reverted to normal by the time of referral. There were 14 men and 7 women, with a mean age (+/- SD) of 63 +/- 13 years. Fourteen patients had organic heart disease, and 8 were taking cardioactive medications. Electrophysiologic testing was performed before the implantation of a permanent pacemaker. Only three of the eight patients with documented sinus pauses had abnormalities during their tests that suggested the correct diagnosis (sensitivity, 37.5 percent), including a prolonged sinus-node recovery time in one and carotid-sinus hypersensitivity in two. Three of the eight patients had abnormalities detected that were unrelated to syncope, including atrial flutter, dual atrioventricular nodal pathways, and sustained monomorphic ventricular tachycardia. Of the 13 patients with documented atrioventricular block, only 2 had abnormalities suggesting the correct diagnosis (sensitivity, 15.4 percent). Additional observations unrelated to syncope among these 13 patients included abnormal sinus-node function, atrial flutter, and atrial fibrillation causing hypotension. These preliminary observations suggest that a negative electrophysiologic test in a patient with a normal cardiac rhythm who has experienced syncope does not exclude a transient bradyarrhythmia as a cause of the syncope. Furthermore, electrophysiologic testing may sometimes reveal unrelated rhythm disturbances that may mistakenly be designated as the cause of the syncope.
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PMID:The diagnostic sensitivity of electrophysiologic testing in patients with syncope caused by transient bradycardia. 232 41


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