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The test the effects of digitalis and angiotensin-converting enzyme inhibition on the RR interval variability in an electrocardiogram, 20 normal subjects were given digoxin 0.25 mg, enalapril 10 mg, and placebo twice daily in a randomized, double. blind, crossover study. Continuous 24-hour electrocardiographic recordings obtained on day 5 of each treatment were analyzed and several time domain and power spectral measures of heart period variability were calculated. Digoxin markedly increased (up to 51%) indexes of vagal modulation of heart period without changing mean RR interval. Enalapril did not changing any measure of heart period variability despite a modest hypotensive effect. To determine the effect of each treatment on the response to orthostatic stress, 10 subjects also underwent 15 minutes of 60 [degrees] head-up tilt; power spectra were calculated for 15 minutes at 0 [degrees] and at 60 [degrees] of tilt. Neither active treatment affected the response to head-up tilt. (Am J Cardiol 1993;72:95-99)

Seven hundred fifteen participants from a multicenter natural history study of acute myocardial infarction were studied (1) to determine the correlations among time and frequency domain measures of heart period variability, (2) to determine the correlations between the measures of heart period variability and previously established postinfarction risk predictors, and (3) to determine the predictive value of time domain measures of heart period variability for death during follow-up after acute myocardial infarction. Twenty-four hour electrocardiographic recordings obtained 11 [plus or minus] 3 days after acute myocardial infarction were analyzed and 11 measures of heart period variability were computed. Each of 4 bands in the heart period power spectrum had 1 or 2 corresponding variables in the time domain that correlated with it so strongly (r [is greater than or equal to] 0.90) that the variables were essentially equivalent: ultra low frequency power with SDNN(*) and SDANN index,(*) very low frequency power and low-frequency power with SDNN index,(*) and high-frequency power with r-MSSD(*) and pNN50.(*) As expected from theoretical considerations, SDNN and the square root of total power were almost perfectly correlated. Correlations between the time and frequency domain measures of heart period variability and previously identified postinfarction risk predictors, e.g., left ventricular ejection fraction and ventricular arrhythmias, are remarkably weak. Time domain measures of heart period variability, especially those that measure ultra low or low-frequency power, are strongly and independently associated with death during follow-up. (*)Defined in Table II.

To determine the reproducibility of frequency domain measures of heart period variability in patients with previous myocardial infarction, 2 random samples of 40 patients each (1 from the Cardiac Arrhythmia Pilot Study [CAPS] [unsustained ventricular arrhythmias], and 1 from the electro-physiologic Studies Versus Electrocardiographic Monitoring [ESVEM] [sustained ventricular arrhythmias] trial]) were studied. For each patient, two 24-hour continuous electrocardiographic recordings were analyzed, and the average normal RR interval, total power and 4 components of total power were calculated. Group means and standard deviations for each sample were virtually identical for the pairs of 24-hour recordings. Furthermore, measurements for individual patients were stable from day to day, as measured by the intraclass correlation coefficients and the standard errors of measurement. Reproducibility of heart period variability measurements is excellent in patients with previous myocardial infarction and ventricular arrhythmias, and is comparable to the high stability previously found in a small group of normal subjects. The stability of measures of heart period variability facilities distinguishing real changes due to progression or regression of cardiac disease or to drug effects from apparent changes due to random variation.

To determine if the signal-averaged (SA) electrocardiogram (ECG) predicts the occurrence of sustained ventricular arrhythmia and sudden death after acute myocardial infarction, 182 consecutive patients underwent systematic noninvasive testing, including the SAECG. Seventy-one patients (39%) had an abnormal SAECG. The presence of an abnormal SAECG was not related to underlying left ventricular dysfunction or any other clinical or measured variable. There were 16 end points (sustained ventricular arrhythmia or sudden cardiac death) during 14-month follow-up. The SAECG was a significant predictor of these events (p

The a priori hypothesis that diltiazem would reduce the frequency and repetitiveness of ventricular arrhythmias was tested 3 months after myocardial infarction in patients participating in the Multicenter Diltiazem Postinfarction Trial. After 3 months of follow-up, 1,546 of the 2,466 patients enrolled had a 24-hour continuous electrocardiographic recording that contained [greater than or equal to] 12 hours of analyzable data. They were similar to the patients who survived 3 months but chose not to have a 24-hour electrocardiographic recording (i.e., they were representative of the entire group that survived 3 months). After 3 months of follow-up, there were no significant differences between the diltiazem and placebo groups in the prevalence of atrioventricular block, the frequency of atrial arrhythmias or the frequency or repetitiveness of ventricular arrhythmias. Heart rate was significantly lower (67 +/- 12 vs 71 +/- 12 beats/min) and there was a significantly greater proportion of patients with sinus pauses >2 seconds in duration in the diltiazem group (6%) than in the placebo group (3%). Comparison with placebo revealed no evidence either for an anti- or proarrhythmic effect of diltiazem. There was no reduction in sudden or arrhythmic death attributable to diltiazem treatment; the fraction of total deaths that were arrhythmic by the Hinkle classification was 41% in the placebo group and 42% in the diltiazem group. It may be that the lack of effect of diltiazem on ventricular arrhythmias is partially responsible for its lack of effect on mortality after myocardial infarction. (Am J Cardiol 1990;6S:539-546), The entry of calcium into cells triggers important changes in cellular functions. Calcium antagonists, drugs which block calcium entry, have been useful in the treatment of angina, supraventricular arrhythmias (abnormal heartbeats), and high blood pressure. Calcium antagonists have also been used to treat ischemia (reduced blood flow) and ischemia-related ventricular arrhythmias, including fibrillation (rapid and ineffectual heart contractions). Following a heart attack (myocardial infarction, MI), ventricular arrhythmias can arise spontaneously, and are a significant cause of death. The effect of diltiazem, a calcium antagonist, was tested in patients following MI to determine if it would reduce the incidence of arrhythmias and related deaths. Baseline continuous 24-hour ECG (electrocardiograph) recordings were made on 2,164 of the 2,466 study participants, and 95 percent of these were done before the start of medication. Half of the patients received diltiazem, and 24-hour ECG recordings were obtained from treated and untreated groups after three months. Treated patients had a slower heart rate (an expected effect), but there was no difference in the frequency or prevalence of atrial premature complexes, atrioventricular heart block, or spontaneous ventricular arrhythmias, and these results were not expected. Beta-blockers are another type of drug frequently used to treat heart disease, and among the subgroup of patients receiving beta-blockers, there was a greater decrease in heart rate and a reduced frequency of atrial and ventricular arrhythmias. No interaction (either beneficial or harmful) between treatment with beta-blockers and diltiazem was observed. Certain patients had baseline ECGs with significant occurrences of ventricular arrhythmias, and diltiazem treatment had no effect on their frequency. There was no difference in death rate (whether sudden, not sudden, or identifiably cardiac) between the diltiazem-treated and untreated groups. The results of this and other studies suggests that beta-blockers more effectively prevent the type of arrhythmias that occur following MI, and effectively decrease the death rate in arrhythmic patients. (Consumer Summary produced by Reliance Medical Information, Inc.)