The American journal of cardiology
-
Randomized Controlled Trial Clinical Trial
Usefulness of heart rate variability in predicting drug efficacy (metoprolol vs diltiazem) in patients with stable angina pectoris.
We investigated whether analysis of heart rate (HR) variability may be used to predict the efficacy of drug treatment of myocardial ischemia. In a double-blind, crossover study, 28 patients with stable angina pectoris, proven coronary artery disease, and myocardial ischemia during Holter monitoring received metoprolol controlled-release 200 mg once daily and diltiazem 60 mg 4 times daily. After a placebo run-in phase and after each treatment period, 72-hour Holter recordings were obtained for HR variability and ST-segment analysis. ⋯ Diltiazem reduced the total duration of ischemia by -4.9 minutes (-9.7 to -0.1), but not the number of episodes. Moreover, in contrast to metoprolol, efficacy of diltiazem was not related to baseline HR variability. In conclusion, patients with reduced HR variability at baseline responded to treatment with metoprolol.(ABSTRACT TRUNCATED AT 250 WORDS)
-
Randomized Controlled Trial Clinical Trial
Interaction of intravenous heparin and organic nitrates in acute ischemic syndromes.
We evaluated whether a drug interaction between intravenous nitroglycerin or isosorbide dinitrate and heparin exists. Ninety-six patients with a diagnosis of acute myocardial infarction, unstable angina, or other thromboembolic disorders were divided into 3 groups: group I (control group, n = 35) received intravenous heparin alone; group II (n = 31) received combined intravenous nitroglycerin and heparin; and group III (n = 30) received combined intravenous isosorbide dinitrate and heparin. We determined the mean of 2 separate measurements of heparin dosage requirement, antithrombin III activity, and the dose of intravenous nitroglycerin or isosorbide dinitrate at the time that the ratio of activated partial thromboplastin time (aPTT) to baseline aPTT was 1.5 to 2.0. ⋯ The mean antithrombin III activity of each group was 22.2, 22.8, and 21.3 mg/dl, respectively. The overall results for groups I, II, and III, and results for the subgroup of patients with acute ischemic syndromes in those groups, did not differ significantly. The heparin dose did not show a significant correlation to the dose of intravenous nitroglycerin (r = -0.26, p > 0.05) nor to that of isosorbide dinitrate (r = 0.30, p > 0.05).
-
Randomized Controlled Trial Comparative Study Clinical Trial
Comparison of sotalol with digoxin-quinidine for conversion of acute atrial fibrillation to sinus rhythm (the Sotalol-Digoxin-Quinidine Trial).
We randomized 61 patients with paroxysmal atrial fibrillation (AF) ( < 48 hours from onset) to either sotalol or quinidine treatment. Conversion of rhythm was recorded by Holter monitoring. The starting 80 mg dose of sotalol was repeated at 2, 6, and 10 hours if AF persisted (heart rate > 80 beats/min), and if systolic blood was > or = 120 mm Hg. ⋯ Asymptomatic wide complex tachycardia (QRS > 0.12 second) was found in 13% and 27% of patients taking sotalol and quinidine, respectively. The longest RR intervals were 6.4 and 3.8 seconds in the sotalol and quinidine groups, respectively. Oral sotalol did not appear as effective as quinidine sulfate treatment in conversion of paroxysmal AF.(ABSTRACT TRUNCATED AT 250 WORDS)
-
Randomized Controlled Trial Clinical Trial
Predictors of non-Q-wave acute myocardial infarction in patients with acute ischemic syndromes: an analysis from the Thrombolysis in Myocardial Ischemia (TIMI) III trials.
Among patients with acute ischemic syndromes, patients with non-Q-wave acute myocardial infarction (AMI) are known to be at higher risk for death, reinfarction, and other morbidity than those with unstable angina. The aim of this study was to develop a clinically useful prediction rule to assist in distinguishing, at the time of presentation, patients with non-Q-wave AMI from those with unstable angina. The TIMI IIIB trial enrolled 1,473 patients presenting with ischemic pain at rest within 24 hours who had either electrocardiographic changes or documented coronary artery disease. ⋯ After performing logistic regression, 4 baseline characteristics independently predicted non-Q-wave myocardial AMI: the absence of prior coronary angioplasty (odds ratio [OR] = 3.3, p < 0.001), duration of pain > or = 60 minutes (OR = 2.9, p < 0.001), ST-segment deviation on the qualifying electrocardiogram (OR = 2.0, p < 0.001), and recent-onset angina (OR = 1.7, p = 0.002). Using these 4 characteristics, a prediction rule for non-Q-wave AMI was developed. For the entire cohort of patients in TIMI III, the percentages of patients with non-Q-wave AMI when 0, 1, 2, 3, and 4 risk factors were present were 7.0%, 19.6%, 24.4%, 49.9%, and 70.6%, respectively (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
-
Randomized Controlled Trial Comparative Study Clinical Trial
Electrophysiologic effects of sotalol and amiodarone in patients with sustained monomorphic ventricular tachycardia.
No prospective studies have compared sotalol and amiodarone during electropharmacologic testing. The purpose of this prospective, randomized study was to compare the electrophysiologic effects of sotalol and amiodarone in patients with coronary artery disease and sustained monomorphic ventricular tachycardia (VT). Patients with coronary artery disease and sustained monomorphic VT inducible by programmed stimulation were randomly assigned to receive either sotalol (n = 17) or amiodarone (n = 17). ⋯ There were no significant differences in the effects of sotalol and amiodarone on the ventricular effective refractory period. In patients with coronary artery disease, amiodarone and sotalol are similar in efficacy in the treatment of VT as assessed by electropharmacologic testing. The effects of the 2 drugs on ventricular refractoriness are similar, but amiodarone slows VT to a greater extent than sotalol.