This review article summarizes important changes in our approach to the serious public health problem of sudden death from ventricular arrhythmias.

Early repolarization, which is characterized by an elevation of the QRS–ST junction (J point) in leads other than V₁ through V₃ on 12-lead electrocardiography, has been associated with vulnerability to ventricular fibrillation, but little is known about the prognostic significance of this pattern in the general population.

Background —Preliminary data suggest that the analysis of R-R interval variability by fractal analysis methods may provide clinically useful information on patients with heart failure. The purpose of this study was to compare the prognostic power of new fractal and traditional measures of R-R interval variability as predictors of death after acute myocardial infarction. Methods and Results —Time and frequency domain heart rate (HR) variability measures, along with short- and long-term correlation (fractal) properties of R-R intervals (exponents α ₁ and α ₂ ) and power-law scaling of the power spectra (exponent β), were assessed from 24-hour Holter recordings in 446 survivors of acute myocardial infarction with a depressed left ventricular function (ejection fraction ≤35%). During a mean±SD follow-up period of 685±360 days, 114 patients died (25.6%), with 75 deaths classified as arrhythmic (17.0%) and 28 as nonarrhythmic (6.3%) cardiac deaths. Several traditional and fractal measures of R-R interval variability were significant univariate predictors of all-cause mortality. Reduced short-term scaling exponent α ₁ was the most powerful R-R interval variability measure as a predictor of all-cause mortality (α ₁ <0.75, relative risk 3.0, 95% confidence interval 2.5 to 4.2, P <0.001). It remained an independent predictor of death ( P <0.001) after adjustment for other postinfarction risk markers, such as age, ejection fraction, NYHA class, and medication. Reduced α ₁ predicted both arrhythmic death ( P <0.001) and nonarrhythmic cardiac death ( P <0.001). Conclusions —Analysis of the fractal characteristics of short-term R-R interval dynamics yields more powerful prognostic information than the traditional measures of HR variability among patients with depressed left ventricular function after an acute myocardial infarction.

To determine whether risk stratification tests can predict serious arrhythmic events after acute myocardial infarction (AMI) in patients with reduced left ventricular ejection fraction (LVEF ≤ 0.40). A total of 5869 consecutive patients were screened in 10 European centres, and 312 patients (age 65 ± 11 years) with a mean LVEF of 31 ± 6% were included in the study. Heart rate variability/turbulence, ambient arrhythmias, signal-averaged electrocardiogram (SAECG), T-wave alternans, and programmed electrical stimulation (PES) were performed 6 weeks after AMI. The primary endpoint was ECG-documented ventricular fibrillation or symptomatic sustained ventricular tachycardia (VT). To document these arrhythmic events, the patients received an implantable ECG loop-recorder. There were 25 primary endpoints (8.0%) during the follow-up of 2 years. The strongest predictors of primary endpoint were measures of heart rate variability, e.g. hazard ratio (HR) for reduced very-low frequency component (<5.7 ln ms²) adjusted for clinical variables was 7.0 (95% CI: 2.4–20.3, P < 0.001). Induction of sustained monomorphic VT during PES (adjusted HR = 4.8, 95% CI, 1.7–13.4, P = 0.003) also predicted the primary endpoint. Fatal or near-fatal arrhythmias can be predicted by many risk stratification methods, especially by heart rate variability, in patients with reduced LVEF after AMI.

—Low heart rate (HR) variability is associated with increased risk of cardiovascular morbidity and mortality, but the causes and mechanisms of this association are not well known. This prospective study was designed to test the hypothesis that reduced HR variability is related to progression of coronary atherosclerosis. Average HR and HR variability were analyzed in 12-hour ambulatory ECG recordings from 265 qualified patients participating in a multicenter study to evaluate the angiographic progression of coronary artery disease in patients with prior coronary artery bypass surgery and low high-density lipoprotein cholesterol concentrations (<1.1 mmol/L). Participants were randomized to receive a placebo or gemfibrozil therapy. The progression of coronary atherosclerosis was estimated by quantitative, computer-assisted analysis of coronary artery stenoses from the baseline angiograms and from repeated angiograms performed an average of 32 months later. The progression of focal coronary atherosclerosis of the patients randomized to placebo therapy was more marked in the tertile with the lowest standard deviation of all normal to normal R-R intervals (SDNN, 74±13 ms; mean decrease in the per-patient minimum luminal diameter −0.17 mm; 95% confidence interval [CI], −0.23 to −0.12 mm) than in the middle tertile (SDNN, 107±7 ms; mean decrease −0.05 mm; 95% CI, −0.08 to −0.01 mm) or highest tertile (SDNN, 145±25 ms; mean change 0.01 mm; 95% CI, −0.04 to 0.02 mm) ( P <0.001 between the tertiles). This association was abolished by gemfibrozil. SDNN was lower ( P <0.001) and minimum HR was faster ( P <0.01) in the patients with marked progression than in those with regression of focal coronary atherosclerosis. In multiple regression analysis including HR variability, minimum HR, demographic and clinical variables, smoking, blood pressure, glucose, lipid measurements and lipid-modifying therapy, progression of focal coronary atherosclerosis was independently predicted by the SDNN (β=0.24; P =0.0001). Low HR variability analyzed from ambulatory ECG predicts rapid progression of coronary artery disease. HR variability provided information on progression of focal coronary atherosclerosis beyond that obtained by traditional risk markers of atherosclerosis.