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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the findings in a patients with the Wolff-Parkinson-White syndrome (type A) who initially had recurrent fainting episodes. It appeared that they were caused by prolonged posttachycardiac depression of the sinus node, which was induced by treatment with propranolol. The possibility of covert dysfunction of the sinus node in patients with Wolff-Parkinson-White syndrome should be considered before commencing therapy with beta-adrenergic blocking agents.
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PMID:Propranolol-induced dysfunction of the sinus node in Wolff-Parkinson-White syndrome. 65 66

A 7-year-old black boy with sickle cell disease, Wolff-Parkinson-White syndrome, mild left ventricular dysfunction, and normal coronary arteries developed angina pectoris five months after cessation of hypertransfusion therapy. Exercise-induced ECG ST segment depression associated with angina disappeared following transfusion therapy.
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PMID:Angina pectoris in a child with sickle cell anemia. 67 56

Diagnostic and therapeutic problems in 14 year old patient with concealed WPW syndrome were presented. Paroxysms of atrio-ventricular reentrant tachycardia 180-220/min were frequently recurring, usually with normal QRS pattern. Tachycardias often had to be terminated by intravenous administration of antiarrhythmic drugs. Long term treatment with various antiarrhythmic agents did not prevent recurrence of tachycardias but they became sustained and were recurring more often. Their other side effects manifested with sinus node disfunction and depression of the heart muscle. The electrophysiologic study revealed right anterior septal accessory pathway. Epicardial dissection of the accessory pathway was urgently performed. The control electrophysiologic study revealed no evidence of conduction through the accessory pathway. The patient did not require antiarrhythmic treatment. During the 12 months follow up no tachycardia occurred.
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PMID:[Emergency epicardial dissection of the accessory pathway in a patient with atrioventricular nodal reentrant tachycardia]. 143 78

These findings permit the following conclusions on cardiac changes induced by high-performance sports and high levels of training. Sinus bradycardia and AV block can frequently be observed in athletes, but they do not require attention as long as they are asymptomatic or do not produce pauses exceeding 4 seconds. Persistent rather than transient second-degree AV block or Mobitz second- or third-degree AV block is an extremely unusual finding even in athletes and should be considered a sign of organic lesions until proved otherwise. Supraventricular and AV node ectopic beats are not more frequent in athletes than in the general population except for atrial fibrillation. WPW syndrome is of particular importance, since rapid conduction to the ventricle via the accessory AV pathway is possible, especially if there is a tendency toward atrial fibrillation. Likewise caution is required in athletes with hypertrophic cardiomyopathy. Here hemodynamic deterioration must be anticipated with the occurrence of supraventricular tachycardia. Simple ventricular arrhythmias occur among athletes with the same frequency as in the general population, but they usually disappear with exercise. The occurrence of complex ventricular forms of arrhythmia should always prompt cardiologic examination in search of underlying cardiac disease, particularly hypertrophic or dilated cardiomyopathy. The presence of ventricular arrhythmias without evidence of underlying heart disease does not indicate a special or increased risk of sudden cardiac death. A higher incidence of right and/or left ventricular hypertrophy, exercise-reversible ST elevation, and exercise-reversible changes in T waves (T negativity, sharp and/or excessive T waves) can be considered physiologic changes in the ECGs of athletes. These changes correlate closely with the type of sports activity and degree of training and are reversible when the activity is stopped. Horizontal ST segment depression are by contrast very rare in athletes and should always be clarified by cardiologic examination. Exercise-induced sudden cardiac death in athletes is unusual without preexisting heart disease. The cause of sudden cardiac death among athletes less than 40 years of age can be predominantely ascribed to congenital heart diseases (such as hypertrophic cardiomyopathy or coronary anomalies). In athletes more than 40 years of age and with increasing age, coronary heart disease is the most frequent autopsy finding. A corresponding risk stratification should take these partial dangers into account.
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PMID:ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance. 219 78

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

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

The electrophysiologic properties of bepridil, a calcium channel blocker with additional effects on fast response tissues, were investigated in 10 patients with atrioventricular accessory pathways. Seven patients had Wolff-Parkinson-White syndrome, and three had concealed atrioventricular pre-excitation. A dose of 4 mg/kg was administered intravenously over five minutes. Bepridil increased the AH interval and the functional refractory period of the atrioventricular node. The effective refractory periods of the right atrium and right ventricle were also increased. Bepridil prolonged refractoriness in the accessory pathway both in the anterograde and retrograde direction. After bepridil administration it was impossible to induce reciprocating tachycardia electrically in two patients because of conduction block in the normal pathway. On the other hand, the zone of tachycardia was often increased after bepridil. Nevertheless, the heart rate during tachycardia was slowed by depression of conduction in both the normal and accessory pathways. The findings of this study provide a basis for the antiarrhythmic action of bepridil in patients with atrioventricular accessory pathways.
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PMID:Electrophysiological action of bepridil on atrioventricular accessory pathways. 349 24

Ventricular preexcitation, as seen in Wolff-Parkinson-White syndrome, results in a high frequency of positive exercise electrocardiographic responses. Why this occurs is unknown but is not believed to reflect myocardial ischemia. Exercise thallium testing is often used for noninvasive assessment of coronary artery disease in patients with conditions known to result in false-positive electrocardiographic responses. To assess the effects of ventricular preexcitation on exercise thallium testing, 8 men (aged 42 +/- 4 years) with this finding were studied. No subject had signs or symptoms of coronary artery disease. Subjects exercised on a bicycle ergometer to a double product of 26,000 +/- 2,000 (+/- standard error of mean). All but one of the subjects had at least 1 mm of ST-segment depression. Tests were terminated because of fatigue or dyspnea and no patient had chest pain. Thallium test results were abnormal in 5 patients, 2 of whom had stress defects as well as abnormally delayed thallium washout. One of these subjects had normal coronary arteries on angiography with a negative ergonovine challenge, and both had normal exercise radionuclide ventriculographic studies. Delayed thallium washout was noted in 3 of the subjects with ventricular preexcitation and normal stress images. This study suggests that exercise thallium testing is frequently abnormal in subjects with ventricular preexcitation. Ventricular preexcitation may cause dyssynergy of ventricular activation, which could alter myocardial thallium handling, much as occurs with left bundle branch block. Exercise radionuclide ventriculography may be a better test for noninvasive assessment of coronary artery disease in patients with ventricular preexcitation.
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PMID:Exercise thallium testing in ventricular preexcitation. 357 50

In 58 patients with Wolff Parkinson White syndrome (WPW), we performed exercise stress testing in order to investigate the incidence of normalization of the auriculo-ventricular conduction and the ST-segment changes. For a more accurate evaluation of the latter, exercise and redistribution radionuclide images with Thallium-201 were obtained in 18 cases. Forty-nine had type A and nine had type B of WPW. Forty-eight had permanent, four had alternant and six had no pre-excitation (PE) when they started the test. Mean maximal functional capacity, mean maximal heart rate and mean maximal double product were not different when compared to an age-matched control group. Of the 48 patients who began the test with PE, in 23 (48%) it disappeared while PE persisted in 25 (52%). In 16 cases the disappearance of the PE was sudden and in seven it was progressive. Pre-excitation persisted in 39.5% of patients with type A and in 88.8% with type B (p less than 0.01). ST-segment depression was observed in 76.6% of patients with PE and in 28.6% of cases without PE (p less than 0.01). ST-segment depression occurred in 44.8% of patients with type A and in 100% of cases with type B (p less than 0.05). Transient abnormal Thallium-201 scans were observed in 62.5% of patients without PE and in 20% with PE. No patients showed exertional arrhythmias. This study suggests the possibility of measuring the duration of the refractory period of the accessory pathway in those patients in which the PE disappears suddenly, at a given heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exercise testing and thallium-201 myocardial perfusion scintigraphy in the clinical evaluation of patients with Wolff Parkinson White syndrome. 379 71

Lorcainide is a type I antiarrhythmic drug of the local anesthetic type. It can be given either intravenously or orally, and its pharmacokinetic properties allow relatively long (12 hours) dosing intervals with oral administration. A slowly eliminated metabolite, norlorcainide, probably contributes to the effects of orally administered lorcainide in chronically treated patients. In mainly short term studies, lorcainide has been shown to suppress ventricular ectopy in about 80% of patients treated either orally or intravenously. Preliminary evidence suggests that its efficacy in suppressing ectopy in the setting of acute myocardial infarction is comparable with that of lignocaine (lidocaine). It is of variable efficacy in preventing recurrent ventricular tachycardia and has been shown to be effective in some patients who have failed to respond to other antiarrhythmic drugs. Experience is limited in treating supraventricular arrhythmia, but initial results in patients with Wolff-Parkinson-White syndrome have been favourable. Adverse cardiac effects are infrequent. Abnormal sinus node function may be exacerbated by lorcainide treatment, however, and bundle branch block may be precipitated in patients with pre-existing conduction system disease. Exacerbation of pre-existing arrhythmias is uncommon, and clinically important myocardial depression has not been observed. The most frequent side effect is disturbed sleep during the initiation of oral treatment, which may occur in the majority of patients but usually responds to treatment with a benzodiazepine and subsides with time. Thus, lorcainide appears useful against a variety of arrhythmias. With its convenient dosage schedule and apparently low incidence of serious side effects it should become a useful addition to the antiarrhythmic agents available, although longer term studies are needed to confirm its continued efficacy and lack of unexpected side effects when used for long periods.
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PMID:Lorcainide. A preliminary review of its pharmacodynamic properties and therapeutic efficacy. 637 22


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