60 patients with chronic atrial fibrillation and flutter were randomly allotted to two groups and treated alternately with two different therapy regimes. 30 patients (group I) received lidoflazine in increasing dosage up to 480 mg/24 h and in cases where there was no conversion to sinus rhythm propafenon in a maximal daily dosage of 1800 mg orally. The duration of treatment was limited to 4 days for each substance. 30 patients (group II) were treated in the reverse order, i.e. propafenon and in cases of ineffectiveness with lidoflazine. Atrial fibrillation could be overcome in 21 patients in group I and in 23 patients in group II. The combined success rate in both groups was 73%. The conversion rates for the individual substances were 41% for propafenon (17 out of 41 patients) and 59% for lidoflazine (27 out of 46 patients). The difference was not statistically significant. Successive use of both substances leads to an increased conversion rate. Dangers arising from therapy are a conduction inhibitory action and depression of sinus node function as far as propafenol is concerned and the risk of ventricular ectopy and tachyarrhythmia in lidoflazine.
Haemodynamic investigations were performed before and after oral ingestion of nitroglycerine and isosorbide dinitrate, both in depot form, in eleven and nine patients, respectively, with coronary heart disease. Nitroglycerine (5 mg) led to a significant decrease in arterial and pulmonary artery mid-pressure over one to two hours. Heart rate and mean pulmonary capillary pressure as well as cardiac output and stroke volume hardly changed. After ingestion of isosorbide dinitrate (20 mg) there was a continuous and significant fall in mean arterial, pulmonary artery, and pulmonary capillary pressure already demonstrable during the first hour. Cardiac output and left ventricular work decreased accordingly for up to four hours. At the same time the cardiac output remained constantly lowered over four hours despite the significant increase in frequency. Isosorbide dinitrate has thus a more complete and longer lasting protective haemodynamic effect than nitroglycerine.
Forty-seven patients with chronic atrial fibrillation and (or) flutter in whom the clinical picture and the length of arrhythmia indicated that drug-mediated cardioversion should be tried were treated with a combination of lidoflazine and propafenon. The average daily dosage was 600 mg for propafenon and 180 mg for lidoflazine. Duration of treatment was limited to 8 days. Return to sinus rhythm was achieved in 34 patients. In comparison with monotherapy combined use of the drugs thus led to a clear-cut increase of the conversion rate. Dosage reduction of these differently acting substances decreases the risk of toxic side effects, particularly as both substances have different side effects which in part cancel each other out. It can be assumed that ventricular extrasystoles seen during treatment with lidoflazine as precursor of malignant tachycardia can be suppressed or eliminated by propafenon.
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