The American journal of cardiology
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Survival rates and antiarrhythmic drug use were determined in 941 consecutive patients resuscitated from prehospital cardiac arrest due to ventricular fibrillation between March 7, 1970, and March 6, 1985. Of these patients, 18.7% were treated for at least a portion of the period with quinidine, 17.5% with procainamide, and 39.4% received no antiarrhythmic agent. Beta blockers were prescribed for 28.3% of the patients. ⋯ Beta-blocker therapy was associated with improved (p less than 0.001) survival. Thus, although neither procainamide nor quinidine appear to have had a benefit on mortality, the effect of procainamide appears to be significantly worse than that of quinidine. The use of antiarrhythmic drug therapy in patients resuscitated from prehospital ventricular fibrillation should be regarded as not only unproved, but potentially hazardous, and should probably be restricted to testing in randomized clinical trials.
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Propafenone was administered to 58 patients with a mean age of 3.2 years (range 0.1 to 16). Mean intravenous dose was 1.2 mg/kg body weight (range 0.3 to 1.5 mg). The final mean oral maintenance dose was 308 mg/m2 body surface area (range 200 to 600 mg/m2, 16.8 mg/kg body weight). ⋯ Chaotic atrial tachycardia (n = 3) and junctional ectopic tachycardia (n = 2) were controlled after successful intravenous therapy. Systemic side effects were rare. Two patients developed a proarrhythmic effect, and 1 patient with ventricular ectopy after repair of tetralogy of Fallot died suddenly during propafenone maintenance therapy.
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Withdrawal of beta-blocker therapy has been associated with the development of adrenergic hypersensitivity and adverse clinical effects in patients with coronary artery disease and hypertension. The aim of this study was to establish the occurrence and clinical significance of adrenergic hypersensitivity after abrupt withdrawal of long-term beta blockade in hypertrophic cardiomyopathy. Beta-adrenergic sensitivity was measured using the isoprenaline chronotropic dose25. ⋯ Of 3 patients with inducible outflow tract gradients, 2 developed resting gradients greater than 30 mm Hg during the acute withdrawal period. There was an increase in peak late filling velocity of mitral inflow after beta-blocker withdrawal. In conclusion, transient beta-adrenergic hypersensitivity occurs after beta-blocker withdrawal in hypertrophic cardiomyopathy and is associated with significant physiologic changes and adverse clinical consequences.