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

The purpose of this study was to examine the time course and evaluate the clinical significance of marked left axis deviation (LAD) in airline pilots. The study group consisted of 30 Japan Airlines' pilots with marked LAD, identified from a group of 1,700 who are now 35 years of age or older. The mean age at examination was 48.5 +/- 5.7 years [corrected] and the mean observation period was 22.6 +/- 5.6 years [corrected]. The prevalence rate of marked LAD was 1.8%. In 20%, the axis remained unchanged, and in 70%, LAD progressed either gradually or suddenly. All subjects were examined by exercise testing and 26 had echocardiograms. Two pilots (6.7%) were found to have organic heart disease (hypertension), which was much lower than the rate reported previously. In these individuals, the onset of marked LAD was noted more than 10 years before hypertension was detected. No progression to complete left bundle branch block, nor any form of AV block, was observed among these subjects. No cardiac events or death occurred during the study period.
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PMID:Time course and clinical significance of marked left axis deviation in airline pilots. 189 6

To clarify the mechanisms of ventricular tachycardia (VT) in humans, sixty patients (average age, 43.9 +/- 15.6 years) with life-threatening VT were examined electrophysiologically. Multielectrode catheters were inserted to the heart and programmed electrical stimulation was performed to induce VT. VT was inducible in thirty (50%) of 60 patients. In twenty-nine (93.6%) of these 30 patients VT was induced by ventricular extrastimuli, suggesting that the most important mechanism for the induction of VT is reentry. Background of VT was idiopathic (IDIO) in 36 patients. The remaining 24 patients had underlying heart disease (HD), and only two of them had old myocardial infarction; this was considerably different from that in USA and Europe in which more than 70% of patients with VT have ischemic heart disease. Induction rate VT (IRVT) in IDIO and HD were both 50%. IRVT in 46 sustained VT was 63% and it was significantly higher than that in 14 non-sustained VT (7.1%). The QRS morphology of VT was complete right bundle branch block (RBBB) pattern in 33 patients [with left axis deviation (LAD); 14 and without LAD; 19] and left bundle branch block (LBBB) pattern in 24 patients. IRVT was significantly high in RBBB with LAD (92.9%) compared with RBBB (63.6%), RBBB without LAD (42.1%) and LBBB (37.5%). Both cardiothoracic ratio and ejection fraction had no relationship to IRVT.
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PMID:[Mechanisms of ventricular tachycardia induced by electrophysiological methods in humans]. 191 26

In this paper, we report the cases of 4 male patients (mean age 32.7 yr) with right-ventricular dysplasia, that occurred in familial form. Diagnosis was possible according to the clinical features and to the electrocardiographic, echocardiographic and scintigraphic criteria; at Holter monitoring recorded ventricular arrhythmias with left bundle branch block configuration, associated to sinus arrhythmias (sino-auricular block). In two patients a sustained ventricular tachycardia was recorded. The patients are living and a fourteen-year-old subject is without heart disease. From our data we conclude that: the most serious clinical features occur in extensive form with right atrial and left-ventricle involvement; the clinical features were manifested at a young age and then got worse. A dominant autosomic inheritance is observed (only males were affected).
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PMID:[Arrhythmogenic right ventricular myocardiopathy. A study of a family group]. 195 45

Resting ST segment depression has been identified as a marker for adverse cardiac events in patients with and without known coronary artery disease. To correlate this with exercise testing, coronary angiography, and how it impacts on long-term prognosis, a retrospective study was performed on 476 patients, of whom 223 had no clinical or electrocardiographic evidence of prior myocardial infarction while 253 were survivors of an infarction. All patients performed a standard exercise test and underwent diagnostic coronary angiography within an average of 32 days of their exercise test (range 0 to 90 days). Exclusions were women, those with left bundle branch block, left ventricular hypertrophy, use of digoxin, previous revascularization procedures, or significant valvular or congenital heart disease. Long-term follow-up was carried out for an average of 45 months (+/- 17). Of the patients without prior infarction, 23 (10%) had persistent resting ST segment depression, and of those with a prior history of infarction, 37 (15%) also had resting ST segment depression. Patients with resting ST segment depression and no prior myocardial infarction had a higher prevalence of severe coronary disease (three-vessel and/or left main) (30%) than those without resting ST segment depression (16%) (95% confidence interval [CI] for observed difference -5.0% to 33.9%, p = 0.12). The criterion of greater than or equal to 2 mm of additional exercise-induced ST segment depression was a particularly useful marker in these patients for the diagnosis of any coronary disease (likelihood ratio 3.35, 95% CI 0.56 to 19.93, p = 0.06). Patients with resting ST segment depression and a prior myocardial infarction had a 2.5 times higher prevalence of severe coronary artery disease compared with patients without resting ST segment depression (43% versus 17% prevalence, respectively, 95% CI for observed difference 9.38% to 42.8%, p less than 0.001) and also had larger left ventricles postinfarction (left ventricular end-diastolic volume index 102 ml/m2 compared with 96 ml/m2, p less than 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Correlation between resting ST segment depression, exercise testing, coronary angiography, and long-term prognosis. 195 57

In patients with syncope, ventricular tachyarrhythmias, and sudden death, in the absence of coronary artery disease or dilative and hypertrophic cardiomyopathy, arrhythmogenic right ventricular disease is a common underlying heart disease. It is marked by ventricular tachyarrhythmias of left bundle branch block pattern, often induced by exercise; negative T-waves in the right precordial leads of the surface-ECG, and localized or diffuse right ventricular contraction abnormalities detected by various imaging techniques in a young, apparently healthy population. Congenital disposition with progressive fibrous and lipomatous tissue infiltration of the right ventricular myocardium with hypertrophy and degeneration of surviving myocytes is the pathogenetic factor leading to modification of conduction and resulting in the development of arrhythmogenic zones. This review contains the current knowledge about arrhythmogenic right ventricular disease on the basis of our own experience, and also a review of the literature. Controversial hypotheses concerning etiology and prognosis are discussed. Variant forms and stages of the disease are described, taking differential diagnostic aspects into consideration. Non-invasive and invasive diagnostic methods are evaluated with regard to their diagnostic accuracy, feasibility, and limitations. Pharmacological and alternative therapeutic concepts are presented, including catheter ablation and surgical intervention.
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PMID:[Arrhythmogenic right ventricular disease]. 205 43

Right ventricular arrhythmogenic dysplasia (RVAD) is a typical asymptomatic arrhythmogenic cardiopathy in athletes, which is occasionally concurrent with normal ventricular function and life-threatening arrhythmias. A total of 32 athletes (28 males and 4 females, mean age, 23 years, mean follow-up, 6.7 years) were examined for severe cardiac arrhythmias with left bundle branch block. The conclusive diagnosis of RVAD was established from clinical, echocardio-, and angiographic evidence. The protocol of the examination involved Holter monitoring, loading tests, electrophysiological study, two-dimensional echocardiography, cardiac angiography of the right and left ventricles, coronary angiography. The most severe arrhythmias were observed in athletes whose mean age was 23.4 years, 20 patients had sustained ventricular tachycardia (it occurred only in 19 who were indulging in sports), 6 presented with transient ventricular tachycardia, and 1 had ventricular fibrillation. They all had been considered fit for sports. The disease proceeded severely in 16 of 32 athletes (in 13 of 16 while indulging in sports), the conditions close to syncope were seen in 9 patients (8 had sustained ventricular tachycardias and 1 had transient ventricular tachycardias), syncopes were observed in 5 patients (sustained ventricular tachycardias).
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PMID:[Stable ventricular tachycardia in arrhythmogenic dysplasia of the right ventricle in sportsmen]. 208 39

Ten consecutive patients with recurrent episodes of symptomatic, idiopathic, sustained monomorphic ventricular tachycardia (VT) originating in the right ventricle underwent an attempt at catheter ablation of the ventricular tachycardia. There were seven women and three men, with a mean age of 39 +/- 14 years (+/- SD). None of the patients had any evidence of structural heart disease. The VT had a left bundle branch block configuration and an inferior axis in each patient, and the mean cycle length was 313 +/- 75 msec. Based on the methods of induction of the VT and the response of the VT to verapamil, the VT mechanism was presumed to be reentry in six patients, triggered activity in three patients, and catecholamine-sensitive automaticity in one patient. Sites for ablation were guided by pace mapping, and an appropriate target site was identified in the right ventricular outflow tract in each patient. From one to three shocks of 100-360 J (mean total, 336 +/- 195 J) were delivered from a defibrillator between the tip of the ablation catheter (cathode) and a patch electrode on the anterior chest (anode). An electrophysiology test 7-9 days after ablation demonstrated that VT was still inducible in only one patient, who was treated with amiodarone. One other patient had a recurrence of VT 3 weeks after ablation and was treated with verapamil. Eight of 10 patients were not treated with antiarrhythmic medications and have had no episodes of symptomatic VT during 15-68 months of follow-up (mean follow-up, 33 +/- 18 months). There were no acute or long-term complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term results of catheter ablation of idiopathic right ventricular tachycardia. 224 52

We studied 20 patients with a confirmed diagnosis of Chagas heart disease. Clinical and electrocardiography examinations at baseline documented that all patients had chronic PVC's and that 40% of them also had supraventricular extrasystoles. Also 80% of the patients had RBBB's, 70% had LBBB's and 35% had 1st. degree AV blocks. Flecainide (F) completely suppressed the arrhythmias in 85% of the patients and did partially so in 98% of the patients. Flecainide did not affect sinus node function except in one patient who developed a sinus node atrial block. PR and QRS intervals were prolonged after F but there no 2nd or 3rd degree AV blocks. Flecainide demonstrated to be highly effective with a comfortable margin of safety in the management of these patients with marked alterations of their pace-making and conduction functions.
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PMID:[Electrophysiological changes of the excitoconduction system in patients with Chagas cardiomyopathy and their modification by flecainide]. 245 50

A 51-year-old woman was admitted to the hospital for further elucidation of a syncope of unknown origin and exercise-induced tachycardias with broad QRS-complex. The tachycardia was induced by bicycle exercise stress testing, had a frequency of 165/min, showed an inferior axis and left bundle branch block. Organic heart disease was excluded by right and left heart catheterization and selective coronary angiography. A nodoventricular bundle or an atrio-ventricular bundle was excluded by an extensive electrophysiologic study, therefore the documented tachycardia was probably of ventricular origin. However, it was not possible to induce a ventricular tachycardia by programmed ventricular stimulation with up to three extrastimuli even after the infusion of isoprenaline. Sotalol (2 x 160 mg/die) and the combined treatment with mexiletine (2 x 360 mg/die) and disopyramide (2 x 250 mg/die) did not prevent the induction of the tachycardia by exercise testing. The combination of sotalol and flecainide (2 x 100 mg/die) evoked complex ventricular arrhythmias at rest not noted before, and it was therefore withdrawn as well. After all antiarrhythmic drugs were withdrawn verapamil was given in a dose of 3 x 120 mg and this therapy reproduceably prevented the induction of ventricular tachycardia by exercise testing.
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PMID:[Successful treatment of stress-induced therapy refractory ventricular tachycardia with verapamil]. 247 23

Cardiac function at the time of ventricular premature contractions (VPC) is influenced by the coupling interval or the site of those origin. Clinical and experimental studies of the effects of VPC on intracardiac pressure dynamics have been performed; however, little is known about left ventricular blood flow dynamics. This study was attempted to determine the characteristics of blood flow dynamics in respect to the site of origin of VPC using pulsed Doppler echocardiography. The subjects consisted of 18 cases with VPC but without apparent organic heart disease. Seven cases had VPCs with a left bundle branch block pattern suggesting possible origin in the right ventricle. The other 11 cases had VPCs with a right bundle branch block pattern indicating the left ventricular origin. With the probe in the apical position, the blood flow patterns of the left ventricular outflow, central and inflow tracts were examined. The results were as follows; 1. Except for one case with shortened coupling interval, all six cases with VPCs originated from the right ventricle showed preservation of left ventricular ejection flow. 2. In two of the three cases with VPC which originated from the left ventricle and with left axis deviation, systolic flow in the left ventricular central area showed "back flow" to the apex. Ejection flow at the outflow tract was markedly diminished or disappeared in all three cases. 3. In all eight cases with VPC which originated from the left ventricle and with right axis deviation, ejection flow was slightly disturbed both in the left ventricular outflow and in the central area. 4. Ejection flow volume assessed by velocity integral indicated similar dynamics as did the ejection flow velocity. 5. In left ventriculography, asynchrony due to dyskinetic motion of the anteroapical wall was observed at the times of VPCs with left axis deviation. In conclusion, the patterns of left ventricular ejection flow dynamics depend on the site of origin of VPCs. This disturbed flow is more apparent in VPCs originating from the left ventricle compared to the right ventricle. This is especially true in cases with left axis deviation, in which VPCs arise from the posterior site of the left ventricle.
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PMID:[Left ventricular blood flow dynamics caused by ventricular premature contraction: pulsed Doppler echocardiographic study]. 247 91


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