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  • asymptomatic  (1)
  • atrioventricular node  (1)
  • implantable cardioverter defibrillator  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of interventional cardiac electrophysiology 4 (2000), S. 369-382 
    ISSN: 1572-8595
    Keywords: atrial fibrillation ; asymptomatic ; atrial arrhythmias
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Although first described about 100yr ago, atrial fibrillation (AF) is now recognized as the most common of all arrhythmias. It has a substantial morbidity and presents a considerable health care burden. Improved diagnosis and an ageing population with an increased likelihood of underlying cardiac disease results in AF in more than 1% of population. AF is associated with an approximately two-fold increase in mortality, largely due to stroke which occurs at an annual rate of 5–7%. Another risk to survival is heart failure, which is aggravated by poor control of the ventricular rate during AF. Usually AF is associated with a variety of symptoms: palpitations, dyspnea, chest discomfort, fatigue, dizziness, and syncope. Paroxysmal AF is likely to be symptomatic and frequently presents with specific symptoms, while permanent AF is usually associated with less specific symptoms. However, in at least one third of patients, no obvious symptoms or noticeable degradation of quality of life are observed. This asymptomatic, or silent, AF is diagnosed incidentally during routine physical examinations, pre-operative assessments or population surveys. Recently, a very large incidence of generally short paroxysms of AF has been seen in patients with implantable pacemakers or defibrillators and these arrhythmias are often silent. Pharmacological suppression of arrhythmia may be associated with a conversion from a symptomatic to an asymptomatic form of AF. Holter monitoring and transtelephonic monitoring studies have demonstrated that asymptomatic episodes of AF exceed symptomatic paroxysms by twelve-fold or more. Although symptoms may not stem directly from AF, the risk of complications is probably the same for symptomatic and asymptomatic patients. AF is found incidentally in about 25% of admissions for a stroke. Studies in patients with little or no awareness of their arrhythmia condition indicate that unrecognized and untreated AF may cause congestive heart failure. In patients with coronary bypass, AF may not only represent risk for immediate postoperative morbidity and increase hospital resource utilization, but being unrecognized, may produce a significant impact on long-term survival and quality of life. Although silent AF merits consideration for anticoagulation and rate control therapy according to standard criteria, whether antiarrhythmic therapy is relevant in this condition remains unclear.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cardiovascular drugs and therapy 4 (1990), S. 531-534 
    ISSN: 1573-7241
    Keywords: antiarrhythmic drugs ; implantable cardioverter defibrillator ; ablation ; amiodarone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cardiac arrhythmias are commonplace in the Western world and vary in their degree of seriousness from benign to life threatening. In general, arrhythmias may be managed in one of five ways: reassurance only, physical maneuvers, antiarrhythmic drugs, implantable electronic devices, and surgical or transvascular ablation. Treatment is designed to terminate ongoing arrhythmias, to prevent recurrence of arrhythmias, or to control the rate of the arrhythmia. Occasionally, the propensity to arrhythmia may be cured by abolition of the anatomic substrate for the arrhythmia. Which of these modalities and approaches to the management of cardiac arrhythmia will be chosen by the physician for any individual patients is very much dependent on the character of the arrhythmia and the patient's underlying disease.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Cardiovascular drugs and therapy 7 (1993), S. 139-147 
    ISSN: 1573-7241
    Keywords: adenosine ; nucleoside ; antiarrhythmic ; supraventricular tachycardia ; junctional tachycardia ; atrioventricular node ; preexcitation ; Wolff-Parkinson-White syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Adenosine is a purine nucleoside with a rapid onset and brief duration of action after intravenous bolus administration. Its most prominent cardiac effect is impairment or blockade of atrioventricular nodal conduction, but other effects are depression of automaticity of the sinus node and attenuation of catecholamine-related ventricular after-depolarizations. The cardiac cell surface receptor is the A1 purinoceptor. The therapeutic value of adenosine is predominantly in those arrhythmias in which the atrioventricular node forms part of a reentry circuit, as clearly demonstrated by the high success rate for termination of atrioventricular nodal reentry tachycardia and of atrioventricular reentry tachycardia involving an accessory pathway in the Wolff-Parkinson-White syndrome. Ventricular tachycardias are generally unresponsive, with the exception of right ventricular outflow tract tachycardia. A diagnostic role has emerged for adenosine. The transient blockade of the atrioventricular node that it causes can reveal important electrocardiographic features in arrhythmias, such as atrial flutter, or can unmask latent preexcitation. In wide-QRS tachycardias, adenosine can help to distinguish ventricular tachycardia from supraventricular tachycardia with QRS aberration. Unlike verapamil, adenosine is safe in ventricular tachycardia. A suggested dosing scheme is to give incremental doses at 1-minute intervals, starting at 0.05 mg/kg and continuing until complete atrioventricular block is induced or a maximum of 0.25 mg/kg is reached. Side effects are transient, sometimes uncomfortable, and not hazardous; dyspnea and chest discomfort are most frequent. A history of asthma is a relative contraindication. Aminophylline antagonizes and dipyridamole potentiates the effects of adenosine.
    Type of Medium: Electronic Resource
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