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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. [ABSTRACT FROM AUTHOR]

Aims: The Cardiac Arrhythmias and RIsk Stratification after Myocardial infArction (CARISMA) study was an observational trial including 312 patients with acute myocardial infarction (MI) and left ventricular ejection fraction (LVEF) <40%. Primary percutaneous intervention (pPCI) was introduced 2 years after start of the enrolment, dividing the population into two groups: pre- and post-pPCI. This substudy sought to describe the influence of the mode of revascularization on long-term risk of new-onset atrial fibrillation (AF), bradyarrhythmia, and ventricular tachycardia and the subsequent risk of relevant major cardiovascular events (MACE).Methods and Results: The study included the 268 patients without a history of AF. All patients received an implantable cardiac monitor (ICM) and were followed for 2 years. The choice of revascularization was made by the treating team independently of the trial and retrospectively divided into pPCI, subacute PCI, primary thrombolysis, or no revascularization. Endpoints were new-onset arrhythmia and MACE.A total of 77 patients received no revascularization, whereas 49 received thrombolysis only and 142 received any PCI. The adjusted hazard ratio (HR) for developing any arrhythmia and the subsequently risk of MACE were increased in non-revascularized or thrombolysed patients compared with PCI-patients (any arrhythmia, non-revascularization: HR = 1.7, P = 0.01 and thrombolysis: HR = 1.6, P = 0.05; MACE, non-revascularization: HR = 3.1, P = 0.05 and thrombolysis: HR = 3.1, P = 0.08). All HRs were adjusted for significant baseline and clinically considered covariates and stratified for calendar year.Conclusion: This study is the first to demonstrate that the long-term risk of arrhythmia documented by an ICM and the subsequent risk of MACE were increased in non-revascularized or thrombolysed patients compared with PCI-patients in a post-MI population with LVEF <40%. [ABSTRACT FROM AUTHOR]

Introduction: The prognostic significance of beat-to-beat variability of spatial heterogeneity of repolarization measured from standard 12-lead ECG is not well-understood. Methods: We measured the short-term variability of repolarization parameters, such as T-wave heterogeneity in leads V4–V6 (TWH) and QT interval (QT), from five consecutive beats of previously recorded standard 12-lead ECG in 200 victims of unexpected sudden cardiac death (SCD) confirmed to be due to complicated atherosclerotic coronary artery disease (CAD) in medico-legal autopsy and 200 age- and sex-matched controls with angiographically confirmed CAD. The short-term variability of repolarization heterogeneity was defined as the standard deviation (SD) of the measured repolarization parameters. All ECGs were in sinus rhythm, and no premature ventricular contractions were included in the measured segment. Results: TWH-SD and QT-SD were significantly higher in SCD victims than in subjects with CAD (6.9 ± 5.6 μV vs. 3.8 ± 2.6 μV, p = 1.8E-11; 8.3 ± 13.1 ms vs. 3.8 ± 7.1 ms, p = 0.00003, respectively). After adjusting in the multivariate clinical model with factors, such as diabetes, RR interval, and beta blocker medication, TWH-SD and QT-SD retained their significant power in discriminating between the victims of SCD and the patients with CAD (p = 0.00003, p = 0.006, respectively). TWH-SD outperformed QT-SD in identifying the SCD victims among the study subjects (area under the curve in the receiver operating characteristics curve 0.730 vs. 0.679, respectively). Conclusion: Increased short-term variability of repolarization heterogeneity measured from standard 12-lead ECG is associated with SCD. [ABSTRACT FROM AUTHOR]

The article highlights the association of heart rate variability (HRV) with autonomic nervous system (ANS). Topics discussed include study on the ANS control of sinus node periodicity; long-term HRV that provide powerful risk prediction mainly in cardiac patients; and the function of ANS to maintain the homeostasis of organism.

Introduction: Previous studies have documented that day-to-day variability of heart rate (HR) has prognostic significance for cardiovascular (CV) events in general population. It is unknown how HR dynamics variate before imminent CV event in patients with coronary artery disease (CAD). Our aim was to study day-to-day variation in HR dynamics before the occurrence of CV event in patients with initially stable CAD. Methods: Forty-four patients with angiographically documented CAD from ARTEMIS study measured R-R intervals on a weekly basis at home for 2 years. Home measurements were performed in controlled conditions (3 min at supine and sitting) 1–2 times per week. Eleven patients had a CV event (7 acute coronary syndromes, 1 cardiac death, 2 new onset of arrhythmia needing hospitalization and 1 stroke), which occurred 11 ± 7 months after enrolment. Mean R-R interval was analyzed prospectively from the home measurements. For the patients with new CV event, average, and standard deviation (SD) of the mean R-R interval over 8 weeks preceding the CV event were calculated. For the patients without new CV event, corresponding period was determined by the median follow-up at the occurrence of new CV event. Results: There were no differences in the mean R-R interval analyzed over 8 weeks between the patients with and without new CV event. The variability of mean R-R interval over 8 weeks was greater in the patients with new CV event compared to the patients without new CV event at the supine (95 ± 34 vs. 59 ± 26 ms, p < 0.001) and sitting positions (92 ± 28 vs. 62 ± 24 ms, p < 0.001). Conclusion: Day-to-day variability of mean R-R interval is greater before the new CV event in CAD patients suggesting to a more unstable cardiac autonomic regulation preceding these events. [ABSTRACT FROM AUTHOR]

Aims: 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. Methods and results: 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). Conclusion: 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. [ABSTRACT FROM AUTHOR]

Sudden cardiac death (SCD) causes a high burden of premature deaths in the population affecting subjects of all ages. The identification of subjects at high risk for SCD is of great importance as the prevention of many of these events would be possible with the treatment of underlying cardiac diseases and the use of implantable cardioverter-defibrillators (ICD). However, the current selection of patients for ICD therapy is based solely on left ventricular ejection fraction, and thus a substantial portion of patients at high risk does not qualify for the therapy. Role of the standard electrocardiogram (ECG) in SCD risk stratification has been under active research during the last decade and multiple abnormalities of depolarization and repolarization on the ECG associated with an increased risk of SCD have been identified. In this review, we describe the basic pathophysiological principles behind these changes. We also review the current knowledge of the prognostic significance of ECG predictors of SCD in the general population, and in patients with coronary heart disease (CHD), heart failure, cardiomyopathies, and in inheritable arrhythmia syndromes. Also, insights into the novel digital ECG signal processing techniques are provided. [ABSTRACT FROM AUTHOR]

Aims: Dyx is a new heart rate variability (HRV) density analysis specifically designed to identify patients at high risk for malignant ventricular arrhythmias. The aim of this study was to test if Dyx can improve risk stratification for malignant ventricular tachyarrhythmias and to test if the previously identified cut-off can be reproduced.Methods and Results: This study included 248 patients from the CARISMA study with ejection fraction ≤40% after an acute myocardial infarction and an analysable 24 h Holter recording. All patients received an implantable cardiac monitor, which was used to diagnose the primary endpoint of near-fatal or fatal ventricular tachyarrhythmias likely preventable by an implantable cardioverter defibrillator (ICD), during a period of 2 years. A Dyx ≤ 1.96 was considered abnormal. The secondary endpoint was cardiovascular death. At enrolment 59 patients (24%) had a Dyx ≤ 1.96 and 20 experienced a primary endpoint. A Dyx ≤ 1.96 was associated with a significantly increased risk for malignant arrhythmias [hazards ratio (HR) = 4.36 (1.81-10.52), P = 0.001] and cardiovascular death [HR = 3.47 (1.38-8.74), P = 0.008]. Compared with important clinical risk parameters (age >70 years and QRS > 120 ms), Dyx ≤ 1.96 significantly added predictive value (P = 0.0066).Conclusions: Dyx was a better predictor of ventricular tachyarrhythmias than the traditional measures of HRV and heart rate turbulence, particularly in the elderly. Dyx might be a useful tool for better selection of ICD candidates in the elderly population, since a normal Dyx in this group was associated with a very low risk for malignant ventricular arrhythmias.ClinicalTrials.gov Identifier NCT00145119. [ABSTRACT FROM AUTHOR]

Presence of J-point elevation with rapidly ascending ST segment in the anterior leads of the 12-lead electrocardiogram has been generally considered a benign phenomenon. The concept of benign nature of J-waves has changed as data emerged on variants of J-waves that were associated with the increased risk of sudden cardiac death. Two specific inherited arrhythmia syndromes, such as Brugada syndrome and early repolarization syndrome, have been recognized that carry an increased risk for ventricular fibrillation. The current review is aimed at discussing the clinical aspects of these syndromes and the implications of incidental recognition of the J-waves in a randomly recorded electrocardiogram of asymptomatic subjects. [ABSTRACT FROM AUTHOR]

Objectives: The aim of our study was to assess the effect of short-term cold exposure, typical in subarctic climate, on cardiac electrical function among untreated middle-aged hypertensive men. Methods: We conducted a population-based recruitment of 51 hypertensive men and a control group of 32 men without hypertension (age 55–65 years) who underwent whole-body cold exposure (15 min exposure to temperature −10°C, wind 3 m/s, winter clothes). Conduction times and amplitudes, vectorcardiography, arrhythmias, and heart rate variability (autonomic nervous function) were assessed. Results: Short-term cold exposure increased T-peak to T-end interval from 67 to 72 ms (p<0.001) and 71 to 75 ms (p<0.001) and T-wave amplitude from 0.12 to 0.14 mV (p<0.001) and from 0.17 to 0.21 mV (p<0.001), while QTc interval was shortened from 408 to 398 ms (p<0.001) and from 410 to 401 ms (p<0.001) among hypertensive men and controls, respectively. Cold exposure increased both low (from 390 to 630 ms2 (p<0.001) and 380 to 700 ms2 (p<0.001), respectively) and high frequency heart rate variability (from 90 to 190 ms2 (p<0.001) and 150 to 300 ms2 (p<0.001), respectively), while low-to-high frequency-ratio was reduced. In addition, the frequency of ventricular ectopic beats increased slightly during cold exposure. The cold induced changes were similar between untreated hypertensive men and controls. Conclusions: Short-term cold exposure with moderate facial and mild whole body cooling resulted in prolongation of T-peak to T-end interval and higher T-wave amplitude while QTc interval was shortened. These changes of ventricular repolarization may have resulted from altered cardiac autonomic regulation and were unaffected by untreated hypertension. Trial Registration: ClinicalTrials.gov NCT02007031 [ABSTRACT FROM AUTHOR]

The article discusses a study which examined the association between early repolarization (ER) and sudden cardiac death (SCD) during an acute coronary event. The researchers observed higher prevalence of ER in a standard 12-lead electrocardiogram (ECG) in victims of SCD than in survivors of an acute coronary event. A plausible mechanistic link between the ECG pattern and higher arrhythmic mortality of middle-aged/elderly subjects is also noted.

Aims: The aims of this study were to describe arrhythmias documented with an implantable loop recorder (ILR) in post-acute myocardial infarction (AMI) patients with left ventricular dysfunction at the time of death and to establish the correlation to mode of death. [ABSTRACT FROM PUBLISHER]

Background: Brugada syndrome predisposes some subjects to ventricular tachyarrhythmias and sudden cardiac death. Mutations in SCN5A gene have been associated with ∼25% of Brugada syndrome patients. A common variant in SCN5A, H558R has shown to improve sodium channel activity in mutated channels. We studied whether common variant H558R has any clinical implications in the phenotype of Brugada syndrome. Methods: Our study population consisted of Brugada syndrome subjects 75 with SCN5A mutation and 92 without SCN5A mutation. Their mean age was 39 ± 15 and 42 ± 17 years, and 65% and 86% were male, respectively. We measured PR-, QRS-, QTc-intervals from leads II and V2 of the 12-lead ECG. We also evaluated J-point amplitude from lead V2 and R‘/S ratio from lead aVR (the “aVR sign”). The H558R (A→G) genotype was detected with direct sequencing of the SCN5A gene. Results: The AA genotype carriers had longer QRS duration in lead II (P = 0.017) and higher J-point elevation in lead V2 (P = 0.013), higher “aVR sign” (P = 0.005) and a trend toward more subjects with symptoms (P = 0.067) than G allele carriers. None of the results were significant in Brugada syndrome subjects without SCN5A mutation. Conclusion: The common variant H558R seems to be a genetic modulator of Brugada syndrome among carriers of a SCN5A mutation, in whom the presence of the less common allele G improves the ECG characteristics and clinical phenotype. [ABSTRACT FROM AUTHOR]

: ObjectivesThis study assessed the predictive power of arrhythmia risk markers after an acute myocardial infarction (AMI).: BackgroundSeveral risk variables have been suggested to predict the occurrence of sudden cardiac death (SCD), but the utility of these variables has not been well established among patients using medical therapy according to contemporary guidelines.: MethodsA consecutive series of 700 patients with AMI was studied. The end points were total mortality, SCD, and nonsudden cardiac death (non-SCD). Nonsustained ventricular tachycardia (nsVT), ejection fraction (EF), heart rate variability, baroreflex sensitivity, signal-averaged electrocardiogram (SAECG), QT dispersion, and QRS duration were analyzed (n = 675). Beta-blocking therapy was used by 97% of the patients at discharge and by 95% at one and two years after AMI.: ResultsDuring a mean (±SD) follow-up of 43 ± 15 months, 37 non-SCDs (5.5%) and 22 SCDs (3.2%) occurred. All arrhythmia risk variables differed between the survivors and those with non-SCD (e.g., the standard deviation of N-N intervals was 98 ± 32 vs. 74 ± 21 ms [p < 0.001] and the QRS duration was 103 ± 22 vs.89 ± 16 ms [p < 0.001]). Sudden cardiac death was weakly predicted only by reduced EF (<0.40; p < 0.05), nsVT (p < 0.05), and abnormal SAECG (p < 0.05), but not by autonomic markers or standard ECG variables. The positive predictive accuracy of EF, nsVT, and abnormal SAECG as predictors of SCD was relatively low (8%, 12%, and 13%, respectively).: ConclusionsThe common arrhythmia risk variables, particularly the autonomic and standard ECG markers, have limited predictive power in identifying patients at risk of SCD after AMI in the beta-blocking era. [Copyright &y& Elsevier]

Introduction: Adenosine is an endogenous nucleoside that has an important role in the diagnosis and treatment of several cardiac arrhythmias. However, its effects on inappropriate sinus tachycardia (IST) are not well established. Methods and Results: In this study, the response to intravenous adenosine (0.1 to 0.15 mg/kg) was studied in 18 patients (age 46 ± 15 years) with IST. In a subset of patients (n = 5), the direct effects of adenosine were assessed during pharmacologic beta-adrenergic and cholinergic blockade. Atrial cycle length (ACL) was measured before adenosine injection, at the time of the greatest cycle length prolongation, and during the maximum rebound acceleration of heart rate. Eighteen subjects (age 46 ± 11 years) with normal sinus rhythm undergoing clinically indicated electrophysiologic study served as controls. Adenosine did not terminate IST in any patient. The maximum dose of adenosine prolonged the sinus interval significantly, from 780 ± 128 msec to 985 ± 225 msec (P < 0.001) in the control subjects. In contrast, adenosine caused no significant lengthening of atrial cycle length (527 ± 69 msec vs 590 ± 148 msec; P = NS) in the patients with IST. Similar difference in the response to adenosine was seen during the pharmacologic autonomic blockade. The reflex increase of the sinus rate (rebound effect) was greater in the control subjects than in the patients with IST (21.2% ± 9.7% vs 8.5% ± 8.8%; P < 0.001). Conclusion: The usual negative chronotropic effect of adenosine was impaired in the patients with 1ST. This may have important diagnostic implications and provide new insight into the mechanism(s) of IST. [ABSTRACT FROM AUTHOR]

Focuses on sudden death due to cardiac arrhythmias. Rates of death from cardiovascular causes in developed countries; Mechanisms of sudden death from arrhythmia, including ventricular tachycardia degeneration; Epidemiology; Risk factors, including cardiovascular dysfunction and ambient ventricular arrhythmias; Prevention.

Abstract: Background: Previous studies have shown substantially increased risk of cardiac arrhythmias and sudden cardiac death in post-myocardial infarction (MI) patients. However it remains difficult to identify the patients who are at highest risk of arrhythmias in the post-MI setting. The purpose of this study was to investigate if CHADS2 score (congestive heart failure, hypertension, age ≥75years, diabetes and previous stroke/TCI [doubled]) can be used as a risk tool for predicting cardiac arrhythmias after MI. Methods: The study included 297 post-MI patients from the CARISMA study with left ventricular ejection fraction (LVEF) ≤40%. All patients were implanted with an implantable cardiac monitor (ICM) within 5 to 21days post-MI and followed every three months for two years. Atrial fibrillation, bradyarrhythmias and ventricular tachycardias were diagnosed using the ICM, pacemaker or ICD. Patients were stratified according to CHADS2 score at enrollment. Congestive heart failure was defined as LVEF ≤40% and NYHA class II, III or IV. Results: We found significantly increased risk of an arrhythmic event with increasing CHADS2 score (CHADS2 score=1–2: HR=2.1 [1.1–3.9], p=0.021, CHADS2 score≥3: HR=3.7 [1.9–7.1], p<0.001). This pattern was identical when dividing the arrhythmias into subgroups of atrial fibrillation, ventricular tachycardias and bradyarrhythmias. CHADS2 score was similarly associated with the development of major cardiovascular events defined as reinfarction, stroke, and hospitalization for heart failure or cardiovascular death. Conclusion: In the post-MI setting, CHADS2 score efficiently identifies populations at high risk for cardiac arrhythmias. [Copyright &y& Elsevier]

Background-Early repolarization (ER) in inferior/lateral leads of standard ECGs increases the risk of arrhythmic death. We tested the hypothesis that variations in the ST-segment characteristics after the ER waveforms may have prognostic importance. Methods and Results-ST segments after ER were classified as horizontal/descending or rapidly ascending/upsioping on the basis of observations from 2 independent samples of young healthy athletes from Finland (n = 62) and the United States (n503), where ascending type was the dominant and common form of ER. Early repolarization was present in 27/62 (44%) of the Finnish athletes and 151/503 (30%) of the US athletes, and all but! of the Finnish (96%) and 91/107 (85%) of US athletes had an ascending/upsloping ST variant after ER. Subsequently, ECGs from a general population of 10 864 middle-aged subjects were analyzed to assess the prognostic modulation of ER-associated risk by ST-segment variations. Subjects with ER≥0.1 mV and horizontal/descending ST variant (n=412) had an increased hazard ratio of arrhythmic death (relative risk 1.43; 95% confidence interval 1.05 to 1.94). When modeled for higher amplitude ER (>0.2 mV) in inferior leads and horizontal/descending ST-segment variant, the hazard ratio of arrhythmic death increased to 3.14 (95% confidence interval 1.56 to 6.30). However, in subjects with ascending ST variant, the relative risk for arrhythmic death was not increased (0.89; 95% confidence interval 0.52 to 1.55). Conclusions-ST-segment morphology variants associated with ER separates subjects with and without an increased risk of arrhythmic death in middle-aged subjects. Rapidly ascending ST segments after the J-point, the dominant ST pattern in healthy athletes, seems to be a benign variant of ER. [ABSTRACT FROM AUTHOR]

Background: 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. Methods: We assessed the prevalence and prognostic significance of early repolarization on 12-lead electrocardiography in a community-based general population of 10,864 middle-aged subjects (mean [±SD] age, 44±8 years). The primary end point was death from cardiac causes, and secondary end points were death from any cause and death from arrhythmia during a mean follow-up of 30±11 years. Early repolarization was stratified according to the degree of J-point elevation (=0.1 mV or >0.2 mV) in either inferior or lateral leads. Results: The early-repolarization pattern of 0.1 mV or more was present in 630 subjects (5.8%): 384 (3.5%) in inferior leads and 262 (2.4%) in lateral leads, with elevations in both leads in 16 subjects (0.1%). J-point elevation of at least 0.1 mV in inferior leads was associated with an increased risk of death from cardiac causes (adjusted relative risk, 1.28; 95% confidence interval [CI], 1.04 to 1.59; P=0.03); 36 subjects (0.3%) with J-point elevation of more than 0.2 mV in inferior leads had a markedly elevated risk of death from cardiac causes (adjusted relative risk, 2.98; 95% CI, 1.85 to 4.92; P<0.001) and from arrhythmia (adjusted relative risk, 2.92; 95% CI, 1.45 to 5.89; P=0.01). Other electrocardiographic risk markers, such as a prolonged QT interval corrected for heart rate (P=0.03) and left ventricular hypertrophy (P=0.004), were weaker predictors of the primary end point. Conclusions: An early-repolarization pattern in the inferior leads of a standard electrocardiogram is associated with an increased risk of death from cardiac causes in middle-aged subjects. N Engl J Med 2009;361:2529-37. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Heart rate variability (HRV) is the most frequently used noninvasive diagnostic method in the assessment of cardiac autonomic control. The clinical relevance of HRV, especially nonlinear HRV in CPB patients has not been well studied. Short brief myocardial ischemia has been reported to influence HRV. We therefore hypothesis that the protective mechanism of ischemic preconditioning (IP) may involve in cardiac autonomic regulation. Methods: Eighty-six CABG patients were randomized into a control and an IP group. The IP patients received two periods of 2-min ischemia followed by 3-min reperfusion by aortic cross-clamped. Holter data were collected in 86 CABG patients before and after surgery. Arrhythmias, linear and nonlinear HRV measures were analyzed. Results: All time and frequency domain HRV variables as well as nonlinear indexes of HRV, the short-term (4–11 beats) scaling exponent α1, were suppressed significantly after surgery in both study groups. The lower pre- and postoperative exponent α1 predict the higher incidence of postoperative AF and worse postoperative outcome. The suppressed exponent α1 was attenuated in the IP group as compared to controls (P=0.008). No other differences were observed in the changes in linear HRV measures between the groups. IP significantly reduced the incidence of postoperative arrhythmias and improved postoperative outcome. Conclusions: The present findings show that cardiac autonomic regulation is impaired after CABG. Nonlinear HRV exponent α1 is a more sensitive measure to predict the postoperative outcome in CABG patients. IP alleviates the extreme autonomic reactions after surgery, suggesting that cardiac autonomic regulation is involved in the IP protective mechanism. [Copyright &y& Elsevier]