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Coronary artery disease (CAD) mortality has declined substantially over the past decades thanks to advancing medical and interventional/surgical treatments; therefore, the prognostic value of the heart rate variability in CAD in the current treatment era is not well established. We evaluated the prognostic significance of baseline heart rate variability in 1,757 ARTEMIS study patients with angiographically verified CAD. During an average follow-up time of 8.7 ± 2.2 years, a total of 285 (16.2%) patients died. Of the patients, 63 (3.6%) suffered sudden cardiac death or were resuscitated from sudden cardiac arrest (SCD/SCA), 60 (3.4%) experienced non-sudden cardiac death (NSCD), and death attributable to non-cardiac causes (NCD) occurred in 162 (9.2%) patients. For every 10 ms decrease in standard deviation of normal to normal intervals the risk for SCD/SCA, NSCD and NCD increased significantly: HR 1.153 (95% CI 1.075–1.236, p<0.001), HR 1.187 (95% CI 1.102–1.278, p<0.001) and HR 1.080 (95% CI 1.037–1.125, p<0.001), respectively. The natural logarithm of the low-frequency component of the power spectrum and the short-term scaling exponent of the detrended fluctuation analysis also had significant association with all modes of death (p<0.001). After relevant adjustment, standard deviation of normal-to-normal intervals retained its association with NSCD and NCD (p<0.01), the natural logarithm of the low-frequency component of the power spectrum with all modes of death (p from <0.05 to <0.01), and the short-term scaling exponent of the detrended fluctuation analysis with SCD/SCA (p<0.05) and NCD (p<0.001). In conclusion, impairment of many measures of heart rate variability predicts mortality but is not associated with any specific mode of death in patients with stable CAD during the current treatment era, limiting the clinical applicability of heart rate variability to targeting therapy.

Background The aim of this study was to investigate the clinical implication of incidentally induced atrial fibrillation (AF) during programmed electrical stimulation (PES) in patients with left ventricular systolic dysfunction (≤40%) after an acute myocardial infarction (MI). Methods In this study, we included 231 patients from the Cardiac Arrhythmias and RIsk Stratification after Myocardial InfArction (CARISMA) study with left ventricular ejection fraction ≤40% and no prior history of AF. These patients underwent PES 6 weeks post‐MI as part of the study protocol. Patients all received an implantable cardiac monitor (ICM) 3–21 days post‐MI and were continuously monitored for cardiac arrhythmias for 2 years. Induction of AF was unwanted but reported if this incidentally occurred. Results A total of 61 patients (26%) developed AF within 2 years of follow‐up, in which n = 10 (29%) had incidental AF during PES at baseline. The overall risk of AF was not significantly increased in patients with incidental AF (n = 34) during PES compared to patients without incidental AF (n = 197) (HR 1.6 [0.9–3.0], p = 0.14). The risk of bradyarrhythmia (HR = 0.2 [0.0–1.2], p = 0.07), ventricular arrhythmias (HR = 0.7 [0.1–5.8], p = 0.77), and major cardiovascular events (MACE) (HR 0.5 [0.2–1.7], p = 0.28) was not significantly different in patients with versus without incidental AF. Conclusions Incidentally induced AF during PES in post‐MI patients with reduced LVEF was not significantly associated with a higher risk of long‐term atrial fibrillation, other cardiac arrhythmias, or major cardiac events. Trial Registration NCT00145119 Two hundred and thirty‐one patients post‐acute myocardial infarction (AMI) underwent programmed electrical stimulation (PES) and 34 patients had incidental induced atrial fibrillation (AF). An implantable cardiac monitor (ICM) was implanted in all patients. Through 2 years of follow‐up, 61 patients in total (26%) and 10 patients with incidental AF during PES (29%) developed AF.

ObjectiveWe investigated whether combining several ECG abnormalities would identify general population subjects with a high sudden cardiac death (SCD) risk.MethodsIn a sample of 6830 participants (mean age 51.2±13.9 years; 45.5% male) in the Mini-Finland Health Survey, a general population cohort representative of the Finnish adults aged ≥30 years conducted in 1978–1980, we examined their ECGs, following subjects for 24.3±10.4 years. We analysed the association between individual ECG abnormalities and 10-year SCD risk and developed a risk score using five ECG abnormalities independently associated with SCD risk: heart rate >80 beats per minute, PR duration >220 ms, QRS duration >110 ms, left ventricular hypertrophy and T-wave inversion. We validated the score using an external general population cohort of 10 617 subjects (mean age 44.0±8.5 years; 52.7% male).ResultsNo ECG abnormalities were present in 4563 subjects (66.8%), while 96 subjects (1.4%) had ≥3 ECG abnormalities. After adjusting for clinical factors, the SCD risk increased progressively with each additional ECG abnormality. Subjects with ≥3 ECG abnormalities had an HR of 10.23 (95% CI 5.29 to 19.80) for SCD compared with those without abnormalities. The risk score similarly predicted SCD risk in the validation cohort, in which subjects with ≥3 ECG abnormalities had HR 10.82 (95% CI 3.23 to 36.25) for SCD compared with those without abnormalities.ConclusionThe ECG risk score successfully identified general population subjects with a high SCD risk. Combining ECG risk markers may improve the risk stratification for SCD.

The risk for sudden cardiac death (SCD) increases with ageing. We evaluated causes and characteristics of unexpected SCD in SCD victims aged ≥ 80 years in a consecutive series of 5,869 SCD victims in Northern Finland. All the victims underwent medico-legal autopsy as medico-legal autopsy is mandatory in cases of unexpected sudden death in Finland. All the non-cardiac deaths such as pulmonary embolism and cerebral hemorrhage were excluded from the study, as were unnatural deaths such as intoxications. Among SCD victims ≥ 80 years, 91.0% of SCDs were due to ischemic heart disease (IHD) determined in autopsy and 9.0% due to non-ischemic heart disease (NIHD), whereas among those < 80 years, only 72.6% of SCDs were due to IHD and 27.4% due to NIHD (P < .001). Severe fibrosis in myocardium was more common whereas heart weight and liver weight, body mass index and abdominal fat thickness, were lower among SCD victims aged ≥ 80 years than among victims aged < 80 years. In those with IHD as etiology of SCD, at least 75% stenosis in one or more major coronary vessels was more common in SCD victims aged ≥ 80 years than among victims aged < 80 years (P = .001). SCD victims 80 years or older were less likely to die during physical activity than those under 80 years old (5.6% vs. 15.9%, P < .001). Dying in sauna was more common among those ≥ 80 years than among those < 80 years (5.5% vs. 2.6%, P < .001). In victims of unexpected SCD aged ≥ 80 years, the autopsy-based etiology of SCD was more commonly IHD than in those aged < 80 years. In SCD victims aged ≥ 80 years, severe fibrosis in myocardium, representing arrhythmic substrate, was more common than in the younger ones.

Fragmented QRS (fQRS) is an electrocardiographic (ECG) marker of myocardial conduction abnormality, characterized by additional notches in the QRS complex. The presence of fQRS has been associated with an increased risk of all-cause mortality and arrhythmia in patients with cardiovascular disease. However, current binary visual analysis is prone to intra- and inter-observer variability and different definitions are problematic in clinical practice. Therefore, objective quantification of fQRS is needed and could further improve risk stratification of these patients. We present an automated method for fQRS detection and quantification. First, a novel robust QRS complex segmentation strategy is proposed, which combines multi-lead information and excludes abnormal heartbeats automatically. Afterwards extracted features, based on variational mode decomposition (VMD), phase-rectified signal averaging (PRSA) and the number of baseline-crossings of the ECG, were used to train a machine learning classifier (Support Vector Machine) to discriminate fragmented from non-fragmented ECG-traces using multi-center data and combining different fQRS criteria used in clinical settings. The best model was trained on the combination of two independent previously annotated datasets and, compared to these visual fQRS annotations, achieved Kappa scores of 0.68 and 0.44, respectively. We also show that the algorithm might be used in both regular sinus rhythm and irregular beats during atrial fibrillation. These results demonstrate that the proposed approach could be relevant for clinical practice by objectively assessing and quantifying fQRS. The study sets the path for further clinical application of the developed automated fQRS algorithm.

We wanted to evaluate the prevalence and prognostic value of the fragmented QRS (fQRS) complex, defined as changes in QRS morphology with various RSR′-patterns in 12-lead electrocardiogram (ECG) in a middle-aged general population. We evaluated the 12-lead ECGs of 10,904 Finnish middle-aged subjects (52% men, mean age 44 ± 8.5 years) with (n = 2,543) and without (n = 8,361) an evidence of cardiac disease drawn from general population and followed them for 30 ± 11 years. Fragmentation of the QRS complex was defined as various RSR′-patterns in at least 2 consecutive leads within the same territory (inferior II, III, aVF; lateral I, aVL, V4 to V6; anterior V1 to V3). Primary end points were death from any cause, cardiac, and arrhythmic deaths. In the total population, fQRS was present in 19.7% (n = 2,147) of subjects, including 15.7% (n = 1714) in inferior leads, 0.8% (n = 84) in lateral leads, and 2.9% (n = 314) in anterior leads. Fragmentation was not associated with increased mortality in subjects without a known cardiac disease. However, fQRS observed in lateral leads in subjects with an evidence of cardiac disease was associated with an increased risk of all-cause (p = 0.001), cardiac (p = 0.001), and arrhythmic (p = 0.004) mortalities. In conclusion, fQRS reflecting minor intraventricular conduction defect is a common finding, especially in the inferior leads, but it is not a sign of increased risk of mortality in subjects without a known cardiac disease. Lateral fQRS, which is less commonly observed in the ECG, is associated with a worse outcome in patients with a known cardiac disease.

Patients after an acute coronary syndrome (ACS) with preserved left ventricle ejection fraction (LVEF) (n = 45, 10 female) were guided by exercise training for 6 months after percutaneous coronary intervention. Exercise capacity, LVEF, standard resting ECG, and 24‐h Holter recording were measured at baseline. Time and frequency domain heart rate variability were analyzed over 24 h. Sokolow–Lyon index, as a marker of left ventricular hypertrophy and P wave Terminal Force in lead V1 (PTF), a marker of left atrial dilatation, along with the standard parameters were analyzed from ECG. A training load of over 6 months (TRIMP) was calculated. Subjects were categorized according to training responses in exercise capacity as low (−3 ± 4%), average (6 ± 2%), and high (15 ± 6%) responders. PTF and P wave duration at baseline differed between the groups: 0.051 ± 0.018, 0.028 ± 0.023, and 0.016 ± 0.015 ms (p < 0.0001) and 120 ± 11, 113 ± 12 and 104 ± 13 ms (p = 0.002) for low, average, and high groups, respectively. Other ECG variables, or any clinical parameters (e.g., sex, age, baseline fitness, LVEF) at baseline or TRIMP were not associated with the training response. Left atrial dilatation, as indicated by PTF on surface ECG, is associated with a low training response in exercise capacity in patients after ACS.

Heart rate variability (HRV) has been conventionally analysed with time- and frequency-domain methods, which measure the overall magnitude of RR interval fluctuations around its mean value or the magnitude of fluctuations in some predetermined frequencies. Analysis of heart rate dynamics by novel methods, such as heart rate turbulence after ventricular premature beats, deceleration capacity of heart rate and methods based on chaos theory and nonlinear system theory, have gained recent interest. Recent observational studies have suggested that some indices describing nonlinear heart rate dynamics, such as fractal scaling exponents, heart rate turbulence and deceleration capacity, may provide useful prognostic information in various clinical settings and their reproducibility may be better than that of traditional indices. For example, the short-term fractal scaling exponent measured by the detrended fluctuation analysis method has been shown to predict fatal cardiovascular events in various populations. Similarly, heart rate turbulence and deceleration capacity have performed better than traditional HRV measures in predicting mortality in post-infarction patients. Approximate entropy, a nonlinear index of heart rate dynamics, which describes the complexity of RR interval behaviour, has provided information on the vulnerability to atrial fibrillation. There are many other nonlinear indices which also give information on the characteristics of heart rate dynamics, but their clinical usefulness is not as well established. Although the concepts of nonlinear dynamics, fractal mathematics and complexity measures of heart rate behaviour, heart rate turbulence, deceleration capacity in relation to cardiovascular physiology or various cardiovascular events are still far away from clinical medicine, they are a fruitful area for research to expand our knowledge concerning the behaviour of cardiovascular oscillations in normal healthy conditions as well as in disease states.

Biomarkers have shown promising results in risk assessment of cardiovascular events. Their role in predicting the risk of sudden cardiac death (SCD) is not well established. We tested the performance of several biomarkers in risk assessment for SCD in patients with coronary artery disease (CAD) and preserved left ventricular function. The study population consisted of 1,946 CAD patients (68% male; mean age 66.9±8.6 yrs; type 2 diabetes (T2D) 43%) enrolled in the ARTEMIS study. The study subjects underwent examinations with echocardiography and measurement of several biomarkers. The primary endpoint of the study was SCD. During the mean follow up of 76±20 months 50 patients experienced SCD. Elevated high sensitive CRP (hs-CRP, p = 0.001), soluble ST2 (sST2, p<0.001), B-type natriuretic peptide (BNP, p<0.001), and highly sensitive TroponinT (hs-TnT, p<0.001) predicted the occurrence of SCD in univariate analysis. Using the optimal cutoff points, elevated sST2 (≥27.45ng/mL; hazard ratio [HR] 2.7; 95%CI 1.4-5.1, p = 0.003) and hs-TnT (≥15 ng/mL; HR 2.9; 95% CI 1.5-5.6, p = 0.002) were the strongest predictors of SCD followed by hs-CRP (HR 2.4; 95% CI 1.3-4.4, p = 0.004) and BNP (HR 1.9; 95% CI 1.0-3.7, p = 0.046) in adjusted analysis. Combination of elevated hs-TnT and sST2 resulted in adjusted HR of 6.4 (95% CI 2.6-15.5, p<0.001). Elevated sST2 and hs-TnT predict the occurrence of SCD among patients with CAD and preserved left ventricular function. The association between sST2, hs-TnT and SCD may be explained by an ongoing myocardial apoptosis followed by fibrosis leading to vulnerability to malignant arrhythmias.

The contribution of genetic variants to non-ischemic sudden cardiac death (SCD) due to acquired myocardial diseases is unclear. We studied whether SCD victims with hypertension/obesity related hypertrophic myocardial disease harbor potentially disease associated gene variants. The Fingesture study has collected data from 5869 autopsy-verified SCD victims in Northern Finland. Among SCD victims, 740 (13%) had hypertension and/or obesity as the most likely explanation for myocardial disease with hypertrophy and fibrosis. We performed next generation sequencing using a panel of 174 cardiac genes for 151 such victims with the best quality of DNA. We used 48 patients with hypertension and hypertrophic heart as controls. Likely pathogenic variants were identified in 15 SCD victims (10%) and variants of uncertain significance (VUS) were observed in additional 43 SCD victims (28%). In controls, likely pathogenic variants were present in two subjects (4%; p = 0.21) and VUSs in 12 subjects (25%; p = 0.64). Among SCD victims, presence of potentially disease-related variants was associated with lower mean BMI and heart weight. Potentially disease related gene variants are common in non-ischemic SCD but further studies are required to determine specific contribution of rare genetic variants to the extent of acquired myocardial diseases leading to SCD.