Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

Our purpose was to assess the efficacy and safety of intravenous ATP for the acute termination of paroxysmal supraventricular tachycardia. There were 14 women and 10 men, aged 38 +/- 15 years. Three patients had evidence of structural heart disease (Ebstein's anomaly associated to atrial septal defect, operated mitral stenosis with insertion of a mechanical heart valve and CAD respectively). Twelve patients had Wolff-Parkinson-White syndrome and another had undergone surgical ablation of an accessory pathway. At the time of electrophysiologic testing, ATP was administered during episodes of paroxysmal supraventricular tachycardia, via a central vein, in incremental doses of 5, 10 and 20 mg followed by a flush of 10 c.c. of isotonic saline. The mechanism of the arrhythmia was orthodromic AV reentrant tachycardia in 19 (79%), AV nodal reentrant tachycardia in 4 (16.6%) and atrial tachycardia in one patient. The mean frequency of the tachycardia was 174 +/- 33 b.p.m. A dose of 5 mg was effective in 16 patients (66%), 5 required 10 mg and two required 20 mg for termination of the tachycardia. In the patient with atrial tachycardia ATP was not effective. The average time after injection to termination of the arrhythmia was 16 +/- 8 seconds. Orthodromic AV reentrant tachycardia was interrupted in the AV node limb in all but one patient and AV nodal reentry was terminated in the "slow-pathway" in three of the four patients. Nine patients had premature ventricular complexes, isolated or in couplets, after the termination of the SVT. Three patients had immediate recurrence of the SVT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Efficacy and safety of adenosine triphosphate in the control of supraventricular paroxysmal tachycardia]. 804 86

A 1-year-old infant with asplenia syndrome and congenital heart disease consisting of common atrium, common inlet left ventricle with a common atrio-ventricular (AV) valve, pulmonary atresia, and total anomalous pulmonary venous connection was admitted to our hospital for radiofrequency catheter ablation (RFCA) of supraventricular tachycardia (SVT) before total cavo-pulmonary connection. After antiarrhythmic medications were discontinued for RFCA, she suffered from SVT that resulted in the rapid deterioration of hemodynamic status. Antiarrhythmic medications and cardioversion were not effective in terminating SVT. The baseline electrocardiogram confirmed the existence of twin AV nodes; however, this SVT was revealed to be focal atrial tachycardia (AT) with enhanced automaticity. The origin of AT was not related to surgical scar. Emergent RFCA for AT was successful in our case of asplenia syndrome. AT is a life-threatening complication in a single ventricle and delayed treatment can be fatal. It is important to perform RFCA promptly when drug treatment is not effective. We suggest that the AV node is not always the target site for ablation in patients with asplenia syndrome and twin AV nodes. <Learning objective: In the case of supraventricular tachycardia with asplenia and twin atrio-ventricular (AV) nodes, atrial tachycardia (AT) as well as AV reentrant tachycardia could occur. AT is a life-threatening complication in infants with single ventricle. If drug therapy is not effective, emergent catheter ablation should be performed. AV node is not always the target site for ablation in patients with asplenia and twin AV nodes.>.
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PMID:Successful radiofrequency catheter ablation of life-threatening atrial tachycardia in an infant with asplenia syndrome. 3069 48