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

The fitness of patients with Wolff-Parkinson-White syndrome to indulge in sporting activities is a practical cardiology problem. The major risk is sudden death due to atrial fibrillation deteriorating to ventricular fibrillation. This risk is small or even theoretical, but signing a fitness certificate engages the clinician's responsibility. Non invasive complementary examinations are useful. Echocardiography may detect a heart disease that would preclude any sport. Exercise tests explore the behaviour of the accessory pathway and rarely trigger off arrhythmias. Holter recordings mainly investigate disorders of the atrial rhythm. The decision concerning fitness may be based on clinical symptoms. Exercise-induced tachycardia is a classical contra-indication to competitive sports. In patients whose tachycardia is unrelated to exercise, fitness may be discussed according to the results of exercise tests and of the electrophysiological study. A refractory period which would be considered as rather prolonged at rest does not protect against fast ventricular rate during passage to atrial fibrillation. If pre-excitation disappears during the exercise test in an asymptomatic patient, then competitive sports can be authorized without limitations. If not, only surgical excision or fulguration would provide full protection against a potentially dangerous fibrillation. It is concluded that Wolff-Parkinson-White syndrome contra-indicates competitive sports in most cases. Games played outside competitions remain possible in the absence of symptoms or when arrhythmias are well controlled by medical treatment.
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PMID:[Fitness for sports of patients with Wolff-Parkinson-White syndrome]. 311 45

Thirty-three patients with concurrent supraventricular (SVT) and ventricular tachycardia (VT) were treated with class IC antiarrhythmic agents. Twenty-two patients had atrial fibrillation (17 with paroxysmal and 5 with chronic fibrillation), 1 patient had ectopic atrial tachycardia and 11 patients had reentrant paroxysmal SVT (8 with atrioventricular node reentrant tachycardia, 3 with atrioventricular reentrant tachycardia). Of 5 patients with Wolff-Parkinson-White syndrome, 2 had only atrial fibrillation. Six patients had sustained VT and 27 had nonsustained VT. Twenty-nine patients had organic heart disease (16 with coronary artery disease, 8 with cardiomyopathy and 5 with valvular heart disease) and 4 had primary electrical disease. The mean ejection fraction was 40 +/- 14% (range 15 to 66%). The study population's arrhythmias were not controlled despite having received 2 to 5 (mean 3.1) previous drug trials. Eighteen patients were referred for treatment of SVT and 15 were referred for treatment of VT (mean symptom duration 107 months). Efficacy was determined in 13 of 33 patients with sustained SVT or VT by programmed electrical stimulation and in 20 of 33 by telemetry and 24-hour Holter response. Twenty-two flecainide and 15 encainide trials were conducted in the 33 patients. Four patients underwent trials with both drugs. Of 33 patients with coexisting SVT and VT, 15 (45%) were controlled with an IC agent alone and 3 continued therapy with an IC agent plus additional therapy (2 drugs, 1 antitachycardia pacing). During the follow-up period (mean 10.4 months), flecainide produced a complete response in 9 patients and encainide in 9 patients. SVT was not controlled in 7 patients and VT was not controlled in 7 patients. One patient had neither arrhythmia controlled. Atrial or ventricular proarrhythmia was seen in 9 of 33 patients (27%) (5 with ventricular and 4 with atrial arrhythmia). Noncardiac side effects were uncommon. Oral class IC agents may be effective therapy for some patients with coexisting VT and SVT of different mechanisms. Patients with such complex arrhythmias should be evaluated carefully because there is a potential for both atrial and ventricular proarrhythmia.
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PMID:Efficacy and safety of class IC antiarrhythmic agents for the treatment of coexisting supraventricular and ventricular tachycardia. 313 36

The fate of 31 children (18 boys, 13 girls) whose Wolff-Parkinson-White syndrome (WPW) had been diagnosed before they were 2 years' old (mean 3.4 months) was investigated. The circumstances in which WPW was discovered were: evaluation of a heart disease in 9 cases, attack of orthodromic tachycardia in 16 cases (including one with cardiopathy), and routine electrocardiography in 6 cases. Type A WPW was the most frequent, being found in 20 patients of whom only 3 had a heart disease; type B WPW was present in 11 patients, and 7 of these had a heart disease. Mean follow-up was 5.9 years; 3 children died of other causes than WPW. In patients followed up for more than one year WPW disappeared in 65 p. 100 of the cases (11/17) in the absence of cardiopathy, and in only 14 p. 100 of the cases (1/7) in the presence of cardiopathy. In children who had suffered attacks of tachycardia WPW disappeared in 64 p. 100 of the cases (9/14). When WPW disappeared it was before the age of 1 year in 8 out of 12 cases. Only one child whose WPW had disappeared had further attacks of tachycardia (11 p. 100), while 3 children whose WPW persisted had short and widely spaced attacks (60 p. 100). This study confirms the high rate of spontaneous disappearance of WPW and the excellent prognosis of this syndrome in the absence of heart disease.
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PMID:[Prognosis of Wolff-Parkinson-White syndrome in infants. Apropos of 31 cases]. 313 32

Thirty-six patients with a history of atrial fibrillation and Wolff-Parkinson-White syndrome were treated with oral encainide, 175 +/- 44 mg/day, after undergoing baseline drug-free electrophysiologic studies. The mean age was 38 +/- 15 years, with structural heart disease present in only 3 patients. Nine patients had only paroxysmal atrial fibrillation and 27 patients had both atrial fibrillation and atrioventricular reciprocating tachycardia (AVRT). Symptoms were present for a mean of 195 +/- 168 months and were treated with an average of 2.7 +/- 1.6 drugs before encainide. Anterograde block in the accessory pathway occurred in 12 of 30 patients (40%) and retrograde block accessory pathway occurred in 10 of 24 patients in whom comparison could be made. AVRT was initiated in 29 of 36 patients during the control study and could be initiated in 19 of 29 patients while receiving encainide. Drug efficacy was determined by the clinical response judged completely effective, partially effective or ineffective. During a mean follow-up of 30.1 +/- 25 months, 24 patients (67%) continued to take encainide. Encainide was completely effective in 14 of 24 patients and partially effective in another 7 patients. Noncardiac side effects were mild and generally resolved, and required discontinuance in only 1 patient. More frequent AVRT occurred in 2 patients, but was managed with dose reduction and the addition of a beta blocker. Three patients had ventricular tachycardia requiring discontinuance; however 2 of 3 patients had a history of ventricular tachycardia before receiving encainide. Encainide is an effective and safe agent for treating atrial fibrillation in patients with Wolff-Parkinson-White syndrome.
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PMID:Encainide for atrial fibrillation associated with Wolff-Parkinson-White syndrome. 314 64

In order to study the etiologies and mechanisms in sports-related sudden death, the author selected 198 cases from the world literature which met the following criteria: subjects were less than 40 years of age and in good physical condition, death occurred at the latest 1 hour after the physical activity, there was no known heart disease, and an autopsy had been performed. In spite of the heterogeneous character of those subjects included in this study and numerous biases, the following results were obtained: in some cases, the mechanism underlying the sudden death could be confirmed by autopsy (massive myocardial infarction, rupture of the aorta, cerebral hemorrhage), and in others it appeared highly probable (atheromatous or congenital coronary artery lesions, hypertrophic cardiomyopathies). Finally, in a certain number of cases, the observed abnormalities could only be seen as presumptive evidence (mitral prolapse, sequelae of myocarditis, or the presence of toxic agents). Failure to establish a precise diagnosis at autopsy occurred in only 22 cases (11%), however, amphetamine drug presence was discovered in 7 of these cases. Approximately one-half of the group studied revealed atheromatous coronary artery lesions (29% of cases) or congenital lesions (17.5%) especially involving the origin of the left coronary artery. These were followed in frequency by the hypertrophic cardiomyopathies. Mitral valve prolapse and WPW syndrome were rarely encountered. Extracardiac causes included rupture of the aorta (4.5%) and cerebral vascular accidents (5%).
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PMID:[Sudden death in athletes]. 315 27

Prevention of sudden arrhythmic cardiac death must be preceded by identification of the high-risk patient to whom appropriate therapy can be given. The most common disease state associated with sudden cardiac death is coronary artery disease. Factors which identify a high-risk subset include: left ventricular dysfunction; frequent and complex arrhythmias on Holter monitoring; abnormal signal-averaged electrocardiograms; angina, ST depression, and exertional hypotension or ventricular arrthythmias on exercise testing; inducible sustained arrhythmias at electrophysiologic testing, or a combination of these factors. Other conditions which are known to be associated with sudden death include: dilated or congestive cardiomyopathy, hypertrophic cardiomyopathy, mitral valve prolapse, valvular heart disease, Wolff-Parkinson-White syndrome, myocarditis, congenital heart disease, electrolyte abnormalities, long QT syndromes, proarrhythmic effects of drugs, and less common conditions such as myocardial tumors and pulmonary hypertension. If the primary abnormality responsible for the tendency toward arrhythmias cannot be corrected, appropriate therapy should be administered to attempt to reduce the patient's risk of sudden arrhythmic cardiac death.
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PMID:Definition of patients at high risk of sudden arrhythmic cardiac death. 327 Nov 94

Every year, individuals with no history of heart disease succumb to sudden cardiac death (SCD). Pathologic examination of the hearts usually reveals various forms of heart disease as hypertrophic cardiomyopathy or coronary artery disease. In other cases, however, there is no obvious structural heart disease, and it is possible that some of these individuals died because of a cardiac arrhythmia involving an accessory pathway. If this were the case, the most likely scenario would be onset of atrioventricular reciprocating tachycardia (AVRT), degeneration of the AVRT into atrial fibrillation with a rapid ventricular response over the accessory pathway, and subsequent death caused by the development of ventricular fibrillation. Although these events have been documented, albeit rarely, during intracardiac electrophysiologic studies, in reality very little is known about the natural history of asymptomatic and untreated patients with Wolff-Parkinson-White (WPW) syndrome. In fact, SCD in a previously asymptomatic patient with WPW syndrome is probably relatively rare. Whether asymptomatic WPW patients should undergo electrophysiologic or pharmacologic testing to determine their 'potential' to develop serious cardiac arrhythmias is controversial. The present paucity of data concerning the natural history of WPW syndrome in asymptomatic patients militates against successful identification of those patients who are at risk for sudden death. Long-term prospective studies are necessary to clarify which asymptomatic patients with WPW syndrome require treatment.
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PMID:Wolff-Parkinson-White syndrome and sudden cardiac death. 362 Dec 80

Recent data suggest that the prominent anterior QRS forces (R greater than or equal to S in V1 and/or V2 leads), in the absence of posterior myocardial infarction, right ventricular hypertrophy, or WPW syndrome, are related to an intraventricular conduction disturbance, at times rate-dependent. We followed 240 subjects with prominent anterior QRS forces and without the above mentioned diseases (study group), (mean age: 44.6 +/- 16 years, mean follow-up: 8 +/- 2 years) and 240 subjects without the anterior displacement (control group), (mean age: 44.4 +/- 14 years, mean follow-up: 7.9 +/- 1.9 years). The age distribution, sex, prevalence of organic heart disease, and follow-up period did not show significant differences between the two groups. QRS duration, prevalence of left ventricular hypertrophy pattern, S1 S2 S3 morphology, terminal r wave in AVR and s wave in V6 were similar in the two groups. During the follow-up period the incidence of right and left bundle branch block and fascicular block was very similar in the two groups of patients. These data suggest that prominent anterior QRS forces do not appear to be related to an initial involvement of the main bundle branches and fascicles and do not increase the likelihood of appearance of an intraventricular block of more advanced degree. The clinical, ECG and prospective data are not helpful in localizing either the ventricle or the area of the ventricle affected by conduction disturbance responsible for the anterior displacement. Our data suggest that the prominent anterior QRS forces express a normal variant of ventricular depolarization and that this finding does not have, per se, any unfavourable clinical implication.
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PMID:Prominent anterior QRS forces: clinical, electrocardiographic and prospective study. 365 94

A patient affected by dextrocardia and WPW syndrome with atrio-ventricular bypass connecting the left sided atrium to the left ventricle (located to the right) is described. Signs of organic heart disease were not present. Electrocardiogram showed, in addition to typical features of ventricular pre-excitation, a QS pattern in leads V4-V6. During exercise testing the pre-excitation disappeared and the electrocardiogram recorded with inverted peripheral cables and right precordial leads, did not show alterations. The analysis of this case and of another previously published suggests that a QS pattern in left precordial leads is highly suggestive for dextrocardia, even in presence of ventricular pre-excitation.
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PMID:[Dextrocardia and Wolff-Parkinson-White syndrome. Electrocardiographic diagnosis]. 371 51

Flecainide acetate (Flecaine) is a new antiarrhythmic which has recently become available; its efficacity in treatment of ventricular rhythm disorders has been amply demonstrated. In this study we have evaluated its efficacity per os in treatment of auricular rhythm disorders refractory to the usual therapies, and its effects on the accessory routes of atrioventricular conduction. The results are very promising and better than those obtained with amiodarone in auricular disorders. They show that flecainide is a drug of importance among therapeutic agents used in treatment of auricular arrhythmia, and its action on Kent's bundle makes it a drug of choice in management of Wolff-Parkinson-White syndrome, especially as it seems equally efficacious in its action on the accessory routes with a short refractory period. Most of our patients did not present organic cardiopathy and the side-effects were generally benign. A non-negligible number of cases of paroxysmal hypertension were noted, in disagreement with literature data, and this point needs to be clarified by further study.
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PMID:[Value of flecainide in supraventricular arrhythmias]. 374 Jul 79


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