During a double-blind trial in which patients with suspected myocardial infarction received metoprolol or placebo, we analyzed the occurrence of ventricular tachyarrhythmias. Metoprolol (15 mg intravenously) was given as soon as possible after admission, and thereafter 200 mg was given daily for three months. Antiarrhythmic drugs were given only for ventricular fibrillation and sustained ventricular tachycardia (greater than 60 beats per second). Definite acute myocardial infarction developed in 809 of the 1395 participants, and probable infarction in 162. Metoprolol did not influence the occurrence of premature ventricular contractions or short bursts of ventricular tachycardia. However, there were 17 cases of ventricular fibrillation in the placebo group (697 patients) and only 6 in the metoprolol group (698 patients, P less than 0.05). During the hospital stay significantly fewer patients receiving metoprolol (16) than placebo (38) (P less than 0.01) required lidocaine. In a separate analysis of 145 patients, metoprolol did not influence the occurrence of premature ventricular contractions or short bursts of ventricular tachycardia during the first 24 hours of treatment. Despite a lack of effect on less serious ventricular tachyarrhythmias, metoprolol had a prophylactic effect against ventricular fibrillation in acute myocardial infarction.
Previous comparisons of physiological and single-rate ventricular pacing are mostly based on open studies. The present investigation was designed to control possible biases of such a study design with the aim to investigate effects of the two pacing modes on maximal and submaximal exercise tolerance and the subjective feeling of well-being of the patients. Forty-four patients treated with atrioventricular synchronous pacemakers for more than 12 months participated in the study. Their pacemakers were randomly programmed to one 3-week long period of ventricular inhibited and a similar period of atrioventricular synchronous ventricular inhibited pacing. Thereafter, they went through echocardiography, symptom-limited maximal exercise test and answered a questionnaire on subjective symptoms. The study was blind since neither the patients nor the physician conducting the exercise tests were informed of pacing mode. The mean maximal exercise tolerance increased 14% (p less than 0.01) on atrioventricular synchronous pacing. Arterial lactate, respiratory rates and perceived exertion ratings during submaximal levels of exercise were higher on ventricular inhibited pacing, as well as symptoms scored during the two 3-week periods. A majority of patients improved their functional class during atrioventricular synchronous pacing and preferred the physiological pacing mode.
The clinical applicability of rate-responsive pacing (RRP) by means of activity sensing has been tested in 15 patients. The patients (ages 24-85) had sinus node dysfunction (2), atrial fibrillation (7), or sinus rhythm (6) combined with complete atrioventricular block. Exercise capacity was investigated on a bicycle ergometer and on a treadmill in a double-blind cross-over study design following one week each of fixed rate ventricular pacing (70 bpm) and rate-responsive pacing (60/125-150 bpm). The patients answered a questionnaire concerning subjective symptoms. A Holter ECG was recorded during 24 hours of all day activity on rate-responsive pacing. During exercise in the rate-responsive mode, heart rate increased more on the treadmill than on the bicycle. A majority of the patients (13 of 15) preferred rate-responsive pacing mainly due to less dyspnea and tiredness. Exercise capacity improved significantly both on bicycle (+7%; p less than 0.01) and on treadmill (+19%; p less than 0.01) during rate-responsive pacing. There were no complications during the follow-up period. In conclusion, the activity-sensing pacemaker is a valuable supplement to existing types of pacemakers. It should be used in patients in whom an atrial electrogram cannot be used for rate triggering.
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