Titlebook: Cardiac Arrhythmias: New Therapeutic Drugs and Devices; Proceedings of the S Joel Morganroth,E. Neil Moore Conference proceedings 1985 Mart

Fatten

Is There a Rational Basis for the Modified Classification of Antiarrhythmic Drugs?ties, their electrophysiologic properties in the intact heart (where studies could determine thresholds of conduction), and their clinical use in specific syndromes. Most of these attempts did not increase our knowledge of antiarrhythmic drugs or their clinical application. Since quinidine, introduc

monogamy

廚房里面

Mexiletine, Tocainide and Ethmozine: Newer Class I Antiarryhthmic Agentsesults in impaired conduction velocity in myocardial tissue.. Overall clinical antiarrhythmic efficacy in this group is dependent upon the ability of these agents to alter conduction and refractoriness, and suppress diastolic depolarization, thereby interfering with reentrant circuits and suppressin

Servile

Class IC Antiarrhythmic Agents: Status — 1984ysfunction can be identified as being at high risk for sudden cardiac death, protocols have been implemented to determine whether this endpoint can be eliminated. The group of antiarrhythmic agents, which are known as Vaughan Williams Class IC agents have demonstrated particularly unique clinical ch

釘牢

Pudendal-Nerve

Status of Class III Antiarrhythmic Drugs: Amiodarone, Bretylium and SotalolIn addition to their pharmacologic property of prolonging myocardial repolarization they were all introduced for clinical use and study for indications unrelated to cardiac arrhythmias. Therefore, it is important to remember that their development was not guided by the intention to develop an ideal

apiary

Spinous-Process

Sudden Cardiac Death — Failure or Effect of Antiarrhythmic Drug Therapy?units. and from chance events captured on dynamic ECG recorders. show that ventricular tachyarrhythmias (ventricular tachycardia, ventricular flutter and ventricular fibrillation) are the commonest arrhythmias implicated.

Promotion

Sudden Death as an End-Point for the Clinical Evaluation of Antiarrhythmic Drugshythmia induced death rather than alleviating symptomatology. The major dilemma facing the clinician is that the use of easily quantifiable total or partial pharmacologic suppression of ventricular arrhythmia during a period of electrocardiographic monitoring has not been shown to be associated with

設(shè)施

Holter/Exercise and Electrophysiologic Methods for Evaluating Drug Therapy for Malignant Ventricularbrillation (VF). Routine clinical evaluation usually reveals ample evidence for the existence of heart disease in patients with these arrhythmias. Coronary heart disease is by far the most frequently occurring etiologic form of heart disease (about 80%) followed by cardiomyopathy and valvular heart