The American journal of cardiology
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Randomized Controlled Trial Clinical Trial
Göteborg Metoprolol Trial: design, patient characteristics and conduct.
The Göteborg Metoprolol Trial was a double-blind, placebo-controlled, stratified trial aimed at evaluating the effect of the beta 1-selective blocker, metoprolol, in suspected acute myocardial infarction and during 2 years of follow-up. The primary end-point was 3-month mortality (blind treatment period). Secondary end-points were 2-year mortality, indirect signs of infarct size, chest pain, arrhythmias and tolerability. ⋯ Treatment started as soon as possible after arrival in hospital with intravenous administration followed by oral treatment for 3 months. All patients were randomized 48 hours or less after estimated onset of infarction and 69% were randomized at 12 hours or less. The blind treatment had to be withdrawn in 19% of all randomized patients before the end of the 3-month follow-up.
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Randomized Controlled Trial Clinical Trial
Göteborg Metoprolol Trial: effects on chest pain.
The effect of metoprolol on chest pain was compared with that of placebo in all randomized patients. The pain score before and 15 minutes after the injection of trial medication was registered and a reduction in chest pain was observed in the metoprolol group. Increasing chest pain after blind injection was observed in only 16 and 9 patients from the placebo and metoprolol groups, respectively. ⋯ Either metoprolol does not induce coronary vasospasm or spasm does not play a role in these patients with definite and suspected acute myocardial infarction as well as unstable angina pectoris. Metoprolol reduced the need for analgesics during the first 4 days and shortened the duration of pain. The effects were similar in patients with early and late treatment, but may depend on initial heart rate, blood pressure and site of infarction.
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During the 3-month blind treatment period there were 40 deaths in the metoprolol group compared with 62 deaths in the placebo group (p = 0.024). During the first year (after 3 months the 2 groups were treated similarly) there were 64 deaths in the metoprolol group vs 93 in the placebo group (p = 0.017) and during 2 years 92 patients died in the metoprolol group vs 120 in the placebo group (p = 0.043). The relative incidence of different causes of death did not differ significantly between the 2 treatment groups, indicating that metoprolol reduced all causes of death to the same extent as its effect on overall mortality.
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Entrainment was attempted during electrophysiologic evaluation of 8 patients with atrioventricular (AV) nodal reentrant tachycardia. Entrainment could be performed while pacing from the high right atrium in 35 of 35 episodes, from proximal coronary sinus in 9 of 21 episodes and from distal coronary sinus in 10 of 20 episodes. The minimal rates required were 8 to 40 beats/min faster than those of the tachycardias. ⋯ Moreover, termination of tachycardia apparently was a function of the pacing site. In some episodes, either because of a proximity effect or because of a preferential input into the upper common pathway, coronary sinus pacing terminated the tachycardia at slower rates or with fewer stimuli than high right atrial pacing. Thus, patients with drug-resistant AV nodal reentrant tachycardias may benefit from recently introduced pacing techniques for termination of tachycardia through entrainment.
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A pericardial effusion is easily recognized by echocardiography, but the diagnosis of cardiac tamponade by echocardiography is controversial. Recently, several reports have indicated that right ventricular (RV) or right atrial (RA) diastolic collapse represent highly specific and sensitive signs of a hemodynamically significant pericardial effusion. This report evaluates the pathophysiologic significance of these findings in 3 patients. ⋯ Increases in wall stiffness of chamber pressures may prevent diastolic collapse in the setting of tamponade. Conversely, extremely low intracardiac pressures may allow diastolic collapse to occur in the absence of overt cardiac tamponade. The extent and timing of the RA or RV collapse, rather than its mere occurrence, are important in the diagnosis of cardiac tamponade by echocardiography.