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

Report of attacks of ventricular tachycardia in a 39 year-old man, free from heart disease. Cardiac pacing showed that the tachycardia could be induced by premature supraventricular beats normally propagated to the ventricles, and by atrial acceleration. The same part played by the cardiac rate on triggering of attacks was demonstrated during ventricular pacing. Besides, the possibility to interrupt the tachycardia by one electrically induced ventricular beat, supports the hypothesis of a re-entry machanism. The QRS configuration during the arrythmia suggested a propagation of excitation starting from the posterior-inferior area of the left ventricle. However, the absence of anomalies of the supraventricular beats initiating the tachycardia excluded a circus movement resulting from a unidirectional block on the left anterior hemibranch. More probably there existed an area of micro-reentry, stimulating the left ventricle from the posterior branches of the His-Purkinje system.
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PMID:[Ventricular tachycardia due to premature supra-ventricular beats with a normal QRS complex. Analysis of a case]. 81 98

His bundle electrograms were performed on 10 patients with organic heart disease. Six patients had had a recent myocardial infarction. Recordings were made at various rates utilizing right atrial pacing. Nitroglycerin, 1/150 gr, was administered to all 10 subjects, and the P-A, A-H, H-Q and H-S intervals were determined before, and immediately after the disappearance of the sublingually administered nitroglycerin. A significant decrease in the A-H interval occurred with negligible effects on the P-A, H-Q and H-S intervals. At the atrial pacing rate of 100/min, the average A-H interval fell from the control value of 152 msec to 129 msec after the administration of nitroglycerin (p less than 0.02); at the pacing rate of 130/min, the A-H interval decreased from 194 to 133 msec (p less 0.05). Second degree heart block occurred at higher pacing rates in six patients after nitroglycerin administration as compared to the control value. The average postsuppression sinoatrial recovery time control value of 1,083 msec decreased to 906 msec after nitroglycerin administration (p less than 0.01). These findings demonstrate that nitroglycerin can improve conduction through the A-V node.
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PMID:The effect of nitroglycerin on atrioventricular conduction in man. 82 58

His bundle electrograms were recorded in 348 patients aged 2 months to 24 years following routine diagnostic cardiac catheterization. Among 41 children found to be free of anatomic or hemodynamic abnormality the following mean values were obtained: P-H interval, 93.4 +/- 15.3 msec; P-A time, 21.2 +/- 7.1 msec; A-H interval, 72.2 +/- 15.9 msec; and H-V interval, 39.8 +/- 5.2 msec. The remaining 307 patients were analyzed by diagnosis of congenital heart disease. The mean P-H interval was found to be significantly increased in both ostium primum and secundum atrial septal defect (ASD) with A-H prolongation in primum ASD and P-A prolongation in secundum ASD. The mean H-V interval was significantly prolonged in ostium primum ASD and in patients with severe aortic stenosis, aortic insufficiency. and mitral regurgitation. Grouping of the patients physiologically revealed that patients with moderate-to-severe right ventricular volume overload had P-H prolongation, and patients with severe left ventricular volume or pressure overload had H-V prolongation. The clinical implications of these findings are discussed.
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PMID:Intracardiac conduction intervals in children with congenital heart disease: comparison of His bundle studies in 41 normal children and 307 patients with congenital cardiac defects. 83 44

The conduction system of the heart was carefully examined at necropsy in two cases of rheumatoid arthritis and one of ankylosing spondylitis. All three patients had cardiac electrical instability and two fo the three died suddenly. The electrophysiological abnormalities of the three patients included paroxysmal atrial fibrillation in the first case, sustained atrial fibrillation with complete heart block and escape atrioventricular (A-V) junctional rhythm in the second case, and progressively increasing heart block eventually became complete in the third case. The sinus node exhibited extensive focal degeneration with and without associated inflammation in all three hearts, but the sinus node artery was not remarkably abnormal in any of these. All three hearts had important focal degenerative disease in the A-V node and His bundle, and in each of these there was marked narrowing of the local nutrient arteries, amounting to virtual occlusion in two hearts. The probable relationship of these postmortem histological findings to the electrocardiographic disturbances in each patient is discussed. Abnormalities in the cardiac conduction system of the hearts of these three patients are compared to ones previously reported for disseminated lupus erythematosus, polyarteritis nodosa, and scleroderma heart disease.
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PMID:De subitaneis mortibus. XXIII. Rheumatoid arthritis and ankylosing spondylitis. 83 14

The specialized cardiac conduction tissue was identified quickly and easily at operation in 2 patients with corrected transposition (L-TGV) and 1 with Ebstein's anomaly. In each of the former cases the tissue was located along the upper rim of the VSD, beneath the pulmonary outflow tract; in neither patient was there a disturbance in cardiac rhythm as a result of operation. In the patient with Ebstein's anomaly the bundle of His descended onto the ventricular septum more directly than was anticipated. There was only a transitory disturbance in atrioventricular conduction following tricuspid valve replacement. Accurate identification of the cardiac conduction tissue is a prerequisite to the safe repair of certain forms of complex congenital heart disease.
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PMID:Automated identification of cardiac conduction tissue in L-TGV and Ebstein's anomaly. 84 25

Postmortem findings within the cardiac conduction system are described from the case of a black woman with sarcoid heart disease who died suddenly. Her clinical course had been characterized by recurring ventricular arrhythmias and bouts of syncope. Both the sinus node artery and the atrioventricular (A-V) node artery were sites of focal fibromuscular dysplasia, which thickened slightly the wall of the former but markedly narrowed the lumen of the latter. Small foci of sarcoid infiltration were present in the sinus node and the A-V node. Fatty replacement within the His bundle was attributable to the probable ischemia caused by narrowing of the A-V node artery. Sarcoid granulomata and infiltration with epithelioid cells were present throughout the ventricular myocardium, but were conspicuously less prevalent in the atria. All the large coronary arteries were normal. Many small coronary arteries in the ventricular myocardium were involved by the sarcoidosis and their lumen were narrowed. These findings and analogous ones reported by others are discussed relative to the pathogenesis of syncopal attacks and sudden death which seem to peculiarly prevalent in sarcoid heart disease.
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PMID:Clinicopathologic correlations. De subitaneis mortibus. XXV. Sarcoid heart disease. 87 28

The effects of phentolamine, 0-3 mg/min given intravenously for 15 minutes, on His bundle electrograms were studied in 11 patients with heart disease. Recordings were made at varied heart rates, using atrial pacing. Phentolamine significantly reduced the AH interval in every patient but it had no effect on the HV interval. Functional and effective refractory periods were measured with the use of the atrial extrastimulus technique. The effective refractory period of the atrium and atrioventricular node as well as the functional refractory period of the atrioventricular node all significantly decreased after phentolamine infusion. This improvement in conduction is probably mediated by a release of catecholamines.
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PMID:Electrophysiological properties of phentolamine in man. 90 72

The case of a 22-year-old white male without known heart disease who presented with activity related lightheadedness at age 19 and dizziness and fatigue at age 21 is described. Standard electrocardiograms (ECG's) revealed intermittent complete trifascicular block. Rapid progression of symptoms over the succeeding eight months resulted in increasing incapacity. Holter monitoring demonstrated that symptoms were related to development of second and higher degrees of A-V block. Normal A-H interval and markedly prolonged H-Q interval on His bundle electrograms indicated that block was infranodal and localized to bundle branch system. Conduction problems aside, clinical and laboratory evaluation, including echocardiograms and cardiac catheterization, were unremarkable. Progression of bilateral bundle branch disease in a young patient without other demonstrable heart lesions and a negative family background conforms with criteria for Lenegre's disease. To our knowledge, this represents the youngest reported patient with this entity. Possible electrophysiologic basis of block and of exercise induced improvement in A-V conduction also are considered.
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PMID:Lenegre's disease in youth. 91 Jun 82

A His electrogram was registered with a Castillo tripolar catheter in seven patients with atrio-ventricular discordance and transposition of the great arteries (corrected transposition). They all had ventricular septal defect, six had pulmonary stenosis. two had atrial septal defect, and only one patient presented first degree AV block. The QRS was of normal duration, 4 had RBBB morphology in the left precordials. Two with ASD and VSD had a prolonged P/A interval. In one, the His recording was polyphasic with a prolonged H-V (55 msec) and two others showed a wide polyphasic His potential (25 and 26msec), with a prolonged H-V. These 3 cases with prolonged His had a minor degree of RBBB. The remaining 3 showed normal AV conduction. In all, the Purkinje electrogram was registered. The duration of the Pu potential and the Pu-V were normal. Corrected transposition shows a high incidence of slow AV conduction, frequently not detectable in the usual electrocardiogram in agreement with previous anatomo-pathological studies. The distal block would explain the frequency of complete AV block with low cardiac output and frequent sudden death in this type of heart disease. The distal block would compel us to take e more agressive steps in its treatment. Atrial septal defect with slowing of the intra-arial conduction is not detected in the electrocardiogram.
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PMID:[Study of the heart conduction system in atrioventricular disorders]. 93 45

This report details our total experience with documented chronic His bundle block in 24 patients. Ten patients had second-degree block (eight with 2:1 block and two with type-1 block), and 14 patients had complete heart block. There were 16 women (67 percent) and eight men (33 percent) with ages ranging from 17 to 87 years. Diagnoses were as follows: hypertensive cardiovascular disease, nine patients (38 percent); arteriosclerotic heart disease, six patients (25 percent); aortic valvular disease, three patients (13 percent); primary conduction disease, two patients (8 percent); primary myocardial disease, two patients (8 percent); congenital heart block, one patient (4 percent); and traumatic heart block, one patient (4 percent). Pacing was instituted in 20 patients because of the following; congestive heart failure, seven patients; syncope, seven patients; fatigue, four patients; and recurrent dizziness, two patients. Permanent pacing was indicated within ten days of initial diagnosis in 13 patients, from 20 to 80 days in four patients, and later than 100 days in three patients. An additional two asymptomatic patients were treated with prophylactic pacing.
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PMID:The clinical spectrum of chronic His bundle block. 100 Oct 51


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