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

A rare phenomenon of escape rhythm and paroxysmal tachycardia originating in the right bundle branch, in a young female without any organic heart disease, is presented.
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PMID:Escape rhythm and paroxysmal tachyarrhythmia originating from the right bundle. 374 55

In an attempt to define more clearly the hemodynamic effects of paroxysmal tachycardia in their time sequence not only for the normal heart, we monitored coronary sinus flow (CSF), aortic mean pressure (AOMP), and coronary vascular resistance in 42 patients. They underwent stress testing of left ventricular function by paced ventricular tachycardia (VT 170/min); 13 patients had no heart disease (controls), 10 patients left ventricular hypertrophy, and 19 patients coronary artery disease (CAD). Up to the 6th s after the sudden start of VT, CSF was maintained during a 50% decrease in AOMP, while controls and hypertrophy patients with less pressure reduction (of 33 and 42%, respectively) showed a tendency to increase CSF. From the 12th to the 26th s of VT, a slight recovery of the low AOMP values took place, while CSF remained at or slightly below baseline levels. The steady state VT was characterized by further improved pressures and a CSF slightly above baseline even in CAD. Up to the 12th s after sudden stop of VT, aortic systolic pressure showed a steep increase (by 17, 13, and 8% for the three groups, respectively), while CSF dropped temporarily and after an upswing between the 12th and 26th s reached baseline levels together with AOMP. We conclude: (1) The rapidity of coronary response and its initial lag after changes of perfusion pressure are similar for normal and impaired myocardium; slight differences exist in quantity. (2) While with VT initiation perfusion pressure drops precipitously, CSF is maintained at baseline levels or slightly below even in CAD. (3) The quality of coronary hemodynamic adaptation to tachycardiac paroxysms in the impaired myocardium warrants the presence of additional operative mechanisms other than a reduced reduction in coronary vascular reserve capacity known in CAD and left ventricular hypertrophy.
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PMID:Alterations in aortic pressure and coronary blood flow: their time sequences with induced paroxysms of ventricular tachycardia in normal and impaired myocardium. 621 73

A long term follow-up study of arrhythmic graduates from junior or senior high schools under the Heart Disease Program in Osaka was performed by mailing questionnaires. The age of the total 515 subjects ranged from 20 to 38 years, 26.9 years on an average. From 397 graduates (77%), answers to questionnaires were obtained. We could confirm 92 graduates were alive (18% of total subjects) among the 118 graduates who did not return their answers to the questionnaires. The following is what we could confirm through the present study: The prognoses of simple premature beats, Wenckebach type heart block and complete right bundle branch block are good in young adults. The prognosis of sick sinus syndrome does not warrant an optimistic prognosis even in young adults. The prognosis of WPW syndrome in young adults is not always fair if they have a history of paroxysmal tachycardia. From 95 to 97% of the graduates with arrhythmia as a whole answered that their daily lives are quite similar to those of healthy people. Attitudes toward daily life and medical checks were also studied.
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PMID:Follow-up study of the arrhythmic graduates from the schools under the heart disease program for students in Osaka. 651 48

Since January 1984, 120 patients (78 male, 42 female; aged 3 to 66 years) with the Wolff-Parkinson-White (WPW) syndrome have been operated upon. The indication for surgery was documented recurrent, paroxysmal tachycardia refractory to medical treatment in 118 cases. Twenty-two patients (18%) had additional heart disease. One hundred and twenty patients had a total of 140 accessory pathways (AP). AP were localized at the left free wall in 63% (87 AP), at the right free wall in 24% (35 AP), and septally in 13% (18 AP). Sixteen patients (13%) had multiple AP (12 patients had two and four patients had three AP), 124 AP were known pre-operatively (88%), 133 were localized intra-operatively (94%) and seven were diagnosed during re-operation (6%). Surgery in 28 patients with left lateral AP was via the epicardial approach and the endocardial approach in 59. Of 15 patients with right lateral AP, the surgical approach was epicardial in two and transmural in 13. A cryosurgery was also used in 117 patients. Fifteen patients suffered recurrences, in 12 of whom repeat surgery was required. One hundred and thirty-six AP (97%) were dissected successfully, of which 14 (10%) were ablated during re-operation. All patients survived the initial operation, but two patients died after re-operation. One patient is pacer-dependent due to persisting postoperative atrioventricular (AV) block. We conclude that surgical dissection of accessory pathways can be offered as an alternative to non-surgical treatment modes, at a low risk and with a high success rate.
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PMID:Surgical treatment of the Wolff-Parkinson-White syndrome--experiences in 120 patients. 822 64

It is well known that the incidence of cardiac arrhythmia is particularly high in patients with chronic respiratory insufficiency (CRI). This study examines the prevalence, incidence and prognostic clinical importance of arrhythmia occurring during the course of CRI on the basis of data taken from the literature and the authors' personal experience using dynamic electrocardiographic diagnosis (24-hour Holter monitoring). The majority of arrhythmias observed in these patients appeared to take the form of premature ventricular and/or supraventricular beats and less frequently of atrial fibrillation and/or attacks of supraventricular paroxysmal tachycardia. Cardiac rhythm alterations were observed using Holter monitoring in 70-90% of patients. No cardiac rhythm disorder is specific to this pathological condition. The aim of this study was to formulate, as far as was possible, a rational therapeutic approach which took account of the electrogenesis of arrhythmic phenomena, variations in the type of arrhythmia and the hemodynamic conditions under which they occur. The etiopathogenesis of arrhythmias within the framework of CRI is relatively complex and probably multifactorial since there are a number of concomitant pathological conditions able to trigger off arrhythmogenic processes both inducing the onset of reflux circuits and enhancing cardiac automatism centres. Many studies correlate the presence of arrhythmia with hypoxemia, hypercapnia and both respiratory and metabolic alkalosis. Even the combined effect of hypoxia with respiratory acidosis and the integrity or otherwise of cardiac function (chronic pulmonary heart, right ventricular hypertrophy, ischemic cardiopathy) have a notable pro-arrhythmic effect. Hypokalemia induced by both respiratory alkalosis and by drugs used during the course of CRI (eg diuretics and/or steroids) may induce a marked dispersion of refractory periods of the various fibrocells thus encouraging the onset of arrhythmia. With regard to drugs, it has been observed that both digitalis and theophylline and beta-2 stimulants if frequently used during the course of CRI may possibly induce arrhythmia. It is therefore important to underline that they should be used with particular caution. As far as concerns the use of beta-2 adrenergic compounds, it is advised that they be administered using an aerosol rather than systemic route. Digitalis has limited indications; the molecules of the methylxanthine classes require careful pharmacological dose monitoring. Arrhythmic therapy should also be seen in terms of prophylaxis and the correction of predisposing and decisive factors such as hypoxemia, hypercapnia, hemoglobin and electrolyte levels, and alterations in blood pH following the obstruction of small airways.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Respiratory insufficiency and cardiac arrhythmia: the rationale of treatment]. 833 38

The purpose of this study was to determine the frequency of atrioventricular (AV) node reentry tachycardia in infants undergoing transesophageal electrophysiological study for paroxysmal tachycardia. The records of all 52 infants < 1-year-old with structurally normal hearts who underwent transesophageal study for paroxysmal tachycardia over a 3-year period were reviewed. Those with a diagnosis of AV node reentry tachycardia underwent complete data review, and follow-up of > 12 months was obtained. Six of 52 infants had a diagnosis of the common type of AV node reentry tachycardia. Tachycardia was diagnosed at a mean age of 2.1 months (range 1 day to 10 months), and 3 of 6 underwent transesophageal study within the first month. Although no patient had structural heart disease, three patients had significant noncardiac disease. Follow-up of 15-38 months (mean 24 +/- 7.8) revealed recurrences in 2 of 6 patients. The mean tachycardia cycle length was 240 ms (range 200-310 ms), and the transesophageal ventriculoatrial intervals ranged from < 30 to 55 ms. All patients had a inducible reentrant tachycardia with a ventriculoatrial interval that remained constant even when tachycardia cycle length increased following verapamil or adenosine administration, or decreased following isoproterenol infusion. Five of 6 had evidence for discontinuous AV node conduction curves. In our patients the substrate for AV node reentry tachycardia was present early in life, and AV node reentry tachycardia can be a clinical problem even in the newborn period.
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PMID:AV node reentry tachycardia in infants. 877 Nov 25

A case of two: 21 years and 39 years old male patients with congenital heart disease: Single Ventricle with pulmonary valve stenosis and L-malposition of the great vessels. In the first case the diagnosis of congenital pulmonic stenosis & tricuspid regurgitation was established after birth and during the previous period. In the second case the diagnosis of VSD was established during the recruiting checkup, when he was 18 years old. Detailed non-invasive cardiologic examination was performed (transthoracic & transoesophageal echocardiography) and the diagnosis of Single Ventricle with pulmonary valve stenosis & L-malposition of the great vessels: Double-Inlet Left Ventricle with severe symptoms (21 years old & supraventricular paroxysmal tachycardia) with middle symptoms (39 years old) were established in both cases.
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PMID:[Congenital heart defects: single ventricle with pulmonary valve stenosis and malposition of the great blood vessels]. 1093 36

The objectives of this study were to: (1) define the incidence of presyncope and/or syncope in patients with paroxysmal junctional tachycardias, (2) determine their causes, and (3) determine the outcome of symptoms. Syncope is a frequent problem and is often caused by paroxysmal tachycardia. The mechanism of hemodynamic instability is unknown. The population study consisted of 281 patients, consecutively recruited because they had paroxysmal tachycardia and a sinus rhythm on a normal electrocardiogram. Fifty-two patients (group I) had presyncope and/or syncope associated with tachycardia. The remaining patients (group II) had no loss of consciousness. Transesophageal programmed atrial stimulation used 1 and 2 atrial extrastimuli, delivered in a control state, and if necessary, after infusion of 20 to 30 microg of isoproterenol. Arterial blood pressure was monitored. Vagal maneuvers and echocardiogram were performed in all patients. Paroxysmal tachycardia was induced in 51 group I patients and 227 group II patients. Comparisons of groups I and II revealed that age (50 +/- 21 vs 49 +/- 17 years), presence of heart disease (10% vs 10%), mechanism of tachycardia with a predominance of atrioventricular nodal reentrant tachycardia (70.5% vs 76%), and rate of tachycardia (196 +/- 42 vs 189 +/- 37 beats/min) did not differ between the groups. However, there were differences in both groups with regard to significantly higher incidences of positive vasovagal maneuvers (35% vs 4%, p <0.01), isoproterenol infusion required to induce tachycardia (55% vs 17%, p <0.001), and vasovagal reaction at the end of tachycardia (41% vs 4%, p <0.05). Thirty-seven group I patients underwent radiofrequency ablation of the reentrant circuit, which suppressed presyncope and/or syncope in 36 of the 37 patients. Thus, presyncope and/or syncope frequently complicated the history of patients with paroxysmal junctional tachycardia (18.5%). Several mechanisms are implicated, but vasovagal reaction was the most frequent cause. Treatment of the tachycardia typically suppressed presyncope and/or syncope.
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PMID:Incidence and mechanism of presyncope and/or syncope associated with paroxysmal junctional tachycardia. 1144 9

The starting point for evaluation of syncope is the "Initial evaluation" that consists of history, physical examination including orthostatic blood pressure measurements and standard electrocardiogram. Differentiating true syncope from other 'non-syncopal' conditions associated with real or apparent transient loss of consciousness is generally the first diagnostic challenge and influences the subsequent diagnostic strategy. The initial evaluation may lead to certain diagnosis or suspected that need to be confirmed by appropriate diagnostic tests or no diagnosis (here termed as unexplained syncope). The strategy of evaluation varies according to the severity and frequency of the episodes and the presence or absence of heart disease. The absence of suspected or certain heart disease excludes a cardiac cause of syncope with the exception of syncope accompanied by palpitations which could be due to paroxysmal tachycardia. Conversely, the presence of heart disease at the initial evaluation is a strong predictor of cardiac cause of syncope and virtually includes all cardiac syncopes, but its specificity is low as about half of patients with heart disease has a non-cardiac cause of syncope. The Implantable Loop Recorder is indicated in some cases in which diagnosis remains unexplained despite a complete work-up.
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PMID:[Current concepts on syncope of uncertain etiology]. 1461 90

Several different mechanisms are responsible for paroxysmal supraventricular tachycardia in children. Different forms of tachycardia occur at different age. Atrio-ventricular reentry tachycardia results from the presence of congenital atrio-ventricular bypass tracts and is frequently encountered at all ages. Infants may present with ectopic atrial tachycardia or atrial flutter. Atrio-ventricular node reentry tachycardia becomes more frequent in adolescence. Atrial scarring resulting from open heart surgery predisposes to complex intra-atrial reentry. Certain forms of congenital and acquired heart disease are associated with specific types of arrhythmia. Many children with paroxysmal supraventricular tachycardia do not require any therapy. The decision to proceed with treatment should be based on the frequency and severity of symptoms and on the effect of arrhythmia on the quality of life. Infants require medical treatment because of the difficulty to recognize symptoms of tachycardia and a risk of heart failure. Patients with Wolff-Parkinson-White syndrome as well as those with significant heart disease are at risk of sudden death. Syncope in children with paroxysmal tachycardia may indicate a severe fall in cardiac output from extremely rapid heart rate. Patients with potentially life-threatening arrhythmia should not participate in competitive physical activities. Treatment options have undergone significant evolution over the past decade. Indications for the use of specific antiarrhythmic medications have been refined. Contemporary catheter ablation procedures employ different forms of energy allowing for safe and effective procedures. Catheter ablation is the treatment of choice for symptomatic paroxysmal tachycardia in school children and in some infants who failed medical treatment. Surgery is the preferred treatment in few selected cases. The goal of this review is to present the state of the art approach to the diagnosis and management of paroxysmal supraventricular tachycardia in infants, children and adolescents.
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PMID:Supraventricular tachycardia in children. 1607 47


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