[Stratification of arrhythmic risk].
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Humans↗
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Results for “Arrhythmic risk”
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[Evaluation of the risk of arrhythmia after infarction].
Evaluation of the risk of arrhythmias after myocardial infarction involves identification of those patients at a high risk of arrhythmic events, i.e. those who fall victim to ventricular tachycardia or sudden death. Such identification is an essential first stage before any treatment can be proposed. It has been clearly shown that the existence of premature ventricular contractions following infarction is an indicator of poor prognosis. In addition to evaluation of premature ventricular contractions, a Holter record can identify sinus variability, a parameter which the prognostic importance is currently being increasingly emphasized. Electrocardiography with averaging and high amplification has now been shown to be of value in the evaluation of arrhythmic risk after infarction. The negative predictive value of this investigation is very high, of the order of 90 percent. In addition to Holter and electrocardiography with averaging, two other non-invasive investigations can be used to determine arrhythmic risks after infarction. Stress testing can seek the presence of premature ventricular contractions related to exercise, while isotope ventriculography measures the value of ejection fraction which, in itself, has a high predictive value in terms of arrhythmic events. Mortality after infarction is proportional to the lowering of ejection fraction and among deaths approximately half are probably due to arrhythmias. Programmed ventricular pacing also has a role to play in evaluation of arrhythmic risk after infarction, but should not be routine. It may be indicated in those patients showing all of the signs of risk, i.e. repetitious forms by Holter, late potentials and low ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)
Arrhythmias, Cardiac↗
Identification of patients at risk for arrhythmic death: role of Holter ECG recording.
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Adolescent↗
Risk stratification in short QT syndrome: Findings from a pooled analysis.
BACKGROUND: In long QT syndrome, longer QT intervals indicate increased arrhythmic risk, and a rate-corrected QT interval (QTc) of ≥500 ms denotes high risk. Establishing similar associations in short QT syndrome (SQTS) remains elusive. OBJECTIVE: This study aimed to demonstrate that shorter QT intervals denote a higher risk of malignant arrhythmias in SQTS and to define the "high-risk" QTc value in SQTS. METHODS: Pooled analysis of patients treated in our institutions or those reported in the literature revealed 162 patients with SQTS and known symptomatic status; 57 of them (35.2%) had arrhythmic symptoms (sudden death, cardiac arrest, or malignant syncope). RESULTS: There was a significant inverse association between the QTc and arrhythmic symptoms (with a median QTc of 315.0 ms [interquartile range 300.5-338.0] among symptomatic patients vs 330.0 ms [interquartile range 312.5-355.0] among asymptomatic patients; P = .0023). Receiver operator characteristics analysis showed that shorter QTc values were associated with a higher risk (area under the curve 0.64 ± 0.04; P = .0024). When patients were grouped by QTc range, most of those with a QTc of ≤320 ms had malignant arrhythmic symptoms, whereas the reverse was true for those with a QTc of ≥320 ms. Male patients were overrepresented in the SQTS cohort and more so in the subgroup with malignant symptoms. CONCLUSION: This pooled analysis of patients with SQTS demonstrates that, among patients with congenital SQTS, a shorter QTc is associated with a higher risk of malignant ventricular arrhythmias. A QTc shorter than 320 ms correlates with a higher arrhythmic risk. Men seem to be at higher risk.
Humans↗
Diagnosis and management of very rare primary arrhythmia syndromes in children and adults: a Clinical Consensus Statement of the European Heart Rhythm Association of the ESC and the Association of Cardiovascular Nursing & Allied Professions of the ESC, endorsed by the Association for European Paediatric and Congenital Cardiology.
Very rare and ultra-rare primary inherited arrhythmia syndromes (IAS) represent a heterogeneous group of disorders associated with a significant risk of sudden cardiac death, often manifesting from foetal life to early adulthood. Current guidelines primarily address more common IAS and provide limited, non-specific recommendations for these rare entities, particularly in paediatric populations. This European Heart Rhythm Association Clinical Consensus Statement, developed in collaboration with the Association of Cardiovascular Nursing and Allied Professions and endorsed by the Association for European Paediatric and Congenital Cardiology, integrates available evidence with expert opinion. Recommendations were formulated through structured discussion and voting, following ESC consensus methodology, with a focus on clinically actionable gene-disease associations. The document provides a comprehensive framework for the diagnosis and management of very rare IAS, including calmodulinopathies, Andersen-Tawil syndrome, Timothy syndrome, TRDN-related disease, calcium release deficiency syndrome, and other atypical channelopathies. It highlights age-specific clinical presentations, the importance of genetic testing, and tailored therapeutic strategies, including pharmacological treatments, left cardiac sympathetic denervation, and selective use of implantable cardioverter-defibrillators. Special attention is given to paediatric considerations, foetal diagnosis, and the role of multidisciplinary care. The document also addresses arrhythmic risk in metabolic and cardiomyopathic conditions, as well as the importance of molecular autopsy and family screening in sudden unexplained death. This consensus document fills a critical gap by providing expert-driven, pragmatic guidance for the management of very rare IAS across the lifespan. It underscores the need for specialized care, international collaboration, and prospective registries to improve evidence generation, risk stratification, and patient outcomes in this vulnerable population.
Humans↗
RNA splicing and cardiovascular disease: a guide for cardiologists.
Alternative splicing (AS) is a fundamental RNA processing mechanism, which generates different RNA transcripts and consequently different protein isoforms from a single gene. This increases the diversity of proteins within an organism and can fine-tune biological processes. This review examines how cardiac-enriched RNA-binding proteins establish heart-specific splicing programs governing aspects of cardiac development, function, and disease. Developmentally, coordinated sarcomeric isoform switches underpin the foetal-to-adult transition and further isoform rewiring in ion channel and kinase genes determine electrophysiology and excitation-contraction coupling. AS contributes to the pathogenesis of several cardiomyopathies and emerging datasets suggest that pathological hypertrophy engages distinct splicing signatures compared with physiological hypertrophy. This review summarizes diagnostic and prognostic opportunities arising from bulk, long-read, and single-cell/nucleus transcriptomics, which resolve cell type-specific isoforms and disease-associated switches. Circulating RNA biomarkers (including splice ratios and circularRNAs) may signify myocardial remodelling and arrhythmic risk. Integrative approaches that link AS with proteomics and genomics improve variant interpretation, reveal previously unannotated protein isoforms, and enable tracking of disease progression and therapy response. Finally, an outline of therapeutic strategies to modulate AS in cardiovascular disease (CVD), including antisense oligonucleotides, small molecules, and genome-editing modalities (CRISPR, base, and prime editing), is provided. The major challenges that remain before splice-targeting therapeutics can be targeted to treat cardiovascular disease are highlighted. Lessons from neuromuscular indications establish clinical feasibility of splicing correction and motivate translation to cardiology. Together, mechanistic insight, biomarker development, and therapeutic innovation position RNA splicing as a tractable axis for precision cardiovascular medicine.
Humans↗
[Preventive drug therapy of recurrence of atrial fibrillation].
Without treatment, about 60% of atrial arrhythmia patients suffer a relapse within 3 months and 70% within one year. Antiarrhythmic treatment intended to reduce this percentage is therefore justified, on condition that it is well tolerated. Several preliminary questions have to be settled before this medical prophylaxis: 1) Justification of antiarrhythmic treatment (sometimes pointless to deal with very occasional episodes); 2) Treatment of the underlying heart disease (valve disease, cardiothyrotoxicosis, etc.) or promoting factors (potassium depletion etc.); 3) Accurate assessment of any associated conduction abnormalities, which may constitute a contraindication to antiarrhythmic treatment (WPW syndrome in the case of verapamil and the digitalis-like drugs) or require additional treatment (pacemaker); 4) Definition of the mechanism (vagal or sympathotonic) inducing arrhythmia; 5) Evaluation of the hemodynamic parameters of the underlying heart disease (size of the atria, ventricular function, coronary or valvular lesions) which may limit the efficacy of the treatment. Once these parameters have been identified, the primary treatment should be type la or lb antiarrhythmics, which have been shown to be effective, despite the fact that they are not without arrhythmic risks (the Ib antiarrhythmics are less effective and have a poor safety profile). The beta-blockers have preferential indications (hypersympatheticotonia, hyperthyroidism, hypertrophic myocardiopathy, mitral prolapse, angina etc.) and can be replaced by verapamil or bepridil if there are non-cardiac contraindications (ulcers, asthma, diabetes). Amiodarone is extremely effective, but its poor extracardiac safety restricts its long-term use. Complementary treatments (digitalis-like, anticoagulants or anti-PAF and cardiostimulant drugs) should be added if necessary. Recurrences (to be confirmed by ECG or Holter) should lead to rigorous confirmation of therapeutic compliance and observance of simple hygienic and dietary measures (no excessive exertion, elimination of stimulants etc.). With strict clinical and ECG monitoring, it would then be possible either to increase the dose levels (accompanied by plasma determinations if possible) or to switch to a treatment with more effective, but more aggressive drugs (amiodarone, flecainide) or to use drug associations (la and lb, la and II etc.). Repeated failure of such attempts should lead to a non-medical approach to treatment.
Anti-Arrhythmia Agents↗
Evaluation of severe ventricular arrhythmias in chronic Chagas' heart disease by effort test and Holter monitoring.
The objective of the present study was to evaluate the ability of the gradual effort test (GET) to detect ventricular extrasystoles (VE), and, in particular, to identify patients with high arrhythmic risk in Chagas' heart disease, as well as to compare the results to those obtained by 24 h ambulatory electrocardiographic monitoring (Holter monitoring). A total of 103 Chagasic patients aged 20 to 55 years who exhibited no clinical signs of heart failure or complex arrhythmias under resting conditions were submitted to 24 h Holter monitoring and to a GET with discontinuous loads first applied to reach 120 bpm and then submaximal or maximal heart rate. The results of 24 h ambulatory electrocardiographic monitoring demonstrated that 52.4% of patients had no VE, 20.4% had few isolated VE (Grade I), 1.9% had frequent monomorphic VE (grade II), 4.8% very frequent polymorphic VE (grade III), and the remaining 20.4% had repetitive forms (doubles or bursts of 3 or more) classified as grade IV. In 68% of these patients, the GET did not detect VE. These were the patients who showed no arrhythmias or isolated VE during the Holter test. The 32% of patients who exhibited VE when submitted to the GET included all patients shown to have grade III and grade IV arrhythmia (27 cases) and 5 patients shown to have grade I arrhythmia by the Holter test. The GET showed 100% sensitivity in the detection of pathological (greater than 100 VE daily) and high-risk arrhythmias (greater than 1000 VE per 24 h, polymorphism or repetitive forms), with a specificity of 93 and 92%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Risk stratification for arrhythmic events in postinfarction patients based on heart rate variability, ambulatory electrocardiographic variables and the signal-averaged electrocardiogram.
The value of heart rate variability, ambulatory electrocardiographic (ECG) variables and the signal-averaged ECG in the prediction of arrhythmic events (sudden death or life-threatening ventricular arrhythmias) was assessed before hospital discharge in 416 consecutive survivors of acute myocardial infarction. During the follow-up period (range 1 to 1,112 days), there were 24 arrhythmic events and 47 deaths. The initial relation between several prognostic factors and arrhythmic events was explored with use of the Kaplan-Meier product limit estimates of survival function. Impaired heart rate variability less than 20 ms (p less than 0.0000), late potentials (p less than 0.0000), ventricular ectopic beat frequency (p less than 0.0000), repetitive ventricular forms (p less than 0.0000), left ventricular ejection fraction less than 40% (p less than 0.02) and Killip class (p less than 0.02) were identified as significant univariate predictors of arrhythmic events. When these variables were analyzed by using a stepwise Cox regression model, only impaired heart rate variability, followed by late potentials and repetitive ventricular forms remained independent predictors of arrhythmic events. The combination of impaired heart rate variability and late potentials had a sensitivity of 58%, a positive predictive accuracy of 33% and a relative risk of 18.5 for arrhythmic events and was superior to other combinations including those incorporating left ventricular function, exercise ECG, ventricular ectopic beat frequency and repetitive ventricular forms. These results suggest that a simple method of assessment based on heart rate variability and the signal-averaged ECG can select a small subgroup of survivors of myocardial infarction at high risk of future life-threatening arrhythmias and sudden death.
Arrhythmias, Cardiac↗
Risk stratification for arrhythmic events in postinfarction patients based on heart rate variability.
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Arrhythmias, Cardiac↗
The Cardiac Arrhythmia Suppression Trial: background, interim results and implications.
The Cardiac Arrhythmia Suppression Trial (CAST) was designed to test the hypothesis that suppression of ventricular premature complexes (VPCs) in survivors of acute myocardial infarction would reduce arrhythmic death risk. Instead, a preliminary finding from the CAST was that the encainide and flecainide groups had a 3.6-fold increase in arrhythmic death compared with their placebo group. These unfortunate results were especially surprising in that the CAST population represented patients in whom the risk of arrhythmic death was only moderate and the risk of proarrhythmia was thought to be low. In contrast, the arrhythmic death rate of the CAST placebo group was unusually low, to the extent that it paralleled the arrhythmic death rate in previous clinical trials of patients surviving myocardial infarction with no ventricular arrhythmia. The excessive arrhythmic death rate in patients taking encainide and flecainide occurred over the duration of the CAST, implying a proarrhythmic effect that may be due to mechanisms that are unique in this population, and thus challenging traditional concepts of proarrhythmia. The existing knowledge regarding the proarrhythmic and negative inotropic effects of encainide and flecainide are reviewed. The previous pharmaceutical database experience with these 2 antiarrhythmic drugs exceeded 3,000 patients; however, there was no indication of this serious proarrhythmic effect. In contrast, the CAST population taking encainide and flecainide totaled only 725 patients who were followed for 10 months and had an extremely high proarrhythmic event rate. The reasons for this discrepancy are discussed. The results of the CAST emphasize the power of a randomized, placebo-controlled clinical trial to uncover previously unsuspected benefits or liabilities of traditional therapies.
Anilides↗
Inability of the signal-averaged electrocardiogram to determine risk of arrhythmia recurrence in patients with implantable cardioverter defibrillators.
Signal-averaged electrocardiography has been used to identify patients at risk for arrhythmic death after myocardial infarction. Since patients with implantable cardioverter defibrillators (ICDs) are at high risk for arrhythmic events, they should also be expected to have a high incidence of abnormal signal-averaged electrocardiograms (SAECGs). However, whether the SAECG can discriminate patients who will have arrhythmia recurrence and receive appropriate ICD shocks from those who will have no recurrence and no shocks is unknown. This study examines the usefulness of the SAECG to separate appropriate users from non-users of the ICD. Fifty patients with ICDs participated in this study. Those who received a shock preceded by symptoms, a shock without preceding symptoms but with electrocardiographic documentation of ventricular fibrillation or ventricular tachycardia, or a shock while asleep were classified as ICD users. All other patients were classified as nonusers. The SAECG was classified as normal if the QRS duration on the standard electrocardiogram was less than or equal to 110 msec and if the total filtered QRS duration was less than 120 msec, the root-mean square voltage of the terminal 40 msec was greater than 25 muV, and the terminal low amplitude signal duration measured less than 38 msec. The SAECG was classified as abnormal if the QRS duration on the standard electrocardiogram was less than or equal to 110 msec and any one of these three criteria were outside the "normal range." The SAECG was classified as indeterminate if the QRS duration on the standard 12-lead electrocardiogram was greater than 110 msec. For the entire group of 50 patients, 8 (16%), 12 (24%), and 30 (60%) had normal, abnormal, and indeterminate SAECGs, respectively. Of the 22 ICD users, 1 (5%), 5 (23%), and 16 (73%) patients had normal, abnormal, and indeterminate SAECGs, respectively. Of the 28 ICD nonusers, 7 (25%), 7 (25%), and 14 (50%) patients had normal, abnormal, and indeterminate SAECGs, respectively. ICD users had lower left ventricular ejection fractions (P = 0.0002), a higher incidence of ventricular tachycardia (P = 0.04), prior exposure to a greater number of antiarrhythmic drugs (P = 0.04), and a lower likelihood for survival (P = 0.02) compared to the ICD nonusers. There was no statistically significant difference between the ICD users and nonusers as stratified by SAECG classification regardless of whether or not the interminate studies were included or excluded from the analysis.(ABSTRACT TRUNCATED AT 400 WORDS)
Arrhythmias, Cardiac↗
Multifactorial prediction of arrhythmic events after myocardial infarction. Combination of heart rate variability and left ventricular ejection fraction with other variables.
Autonomic dysfunction has recently been shown to identify postinfarction patients at a high risk of arrhythmic events. Therefore, the predictive characteristics of heart rate variability and the left ventricular ejection fraction in combination with other prognostic variables--mean heart rate, late potentials, and ventricular ectopic beat frequency greater than 10/hour (VE10)--were examined in 417 postinfarction patients. The heart rate variability index was the most important factor for the stratification of patients at high risk of arrhythmic events after myocardial infarction and optimum stratification was based on the combination of the heart rate variability index with late potentials or with frequent ventricular ectopic beats.
Death, Sudden, Cardiac↗
Events in the cardiac arrhythmia suppression trial: baseline predictors of mortality in placebo-treated patients.
Patients randomized to placebo in the encainide and flecainide arms of the Cardiac Arrhythmia Suppression Trial (CAST) have been found to have a relatively low 1-year mortality rate of 3.9% in comparison with previous studies of patients in the postmyocardial infarction period. To determine the comparability of CAST with previous studies, baseline variables were examined in the 743 patients randomized to placebo in the flecainide and encainide arms of CAST. Twenty-three baseline characteristics were correlated with major outcome events: arrhythmic death (16 events), total mortality (26 events) and congestive heart failure (51 events). On multivariate analysis the risk of new or worsening congestive heart failure was significantly associated with diuretic use, diabetes, high New York Heart Association functional class, age, prolonged QRS duration and low ejection fraction. The risk of arrhythmic death or resuscitated cardiac arrest was significantly associated with an index Q wave myocardial infarction, history of heart failure, use of digitalis, diabetes and prolonged QRS duration. Total mortality or resuscitated cardiac arrest was significantly associated with an index Q wave myocardial infarction, diabetes, ST segment depression, high functional class, prolonged QRS duration and low ejection fraction. The variables at baseline associated with mortality from all causes or arrhythmic death or resuscitated cardiac arrest and heart failure in the CAST placebo-treated patients are similar to those identified in previous postmyocardial infarction studies. Thus, the observation of increased mortality in CAST associated with the administration of encainide and flecainide for suppression of ventricular premature depolarizations is probably applicable to any comparably defined group of patients in the postmyocardial infarction period.
Aged↗
Surgery for control of recurrent life-threatening ventricular tachyarrhythmias within 2 months of myocardial infarction.
Twenty-seven patients (mean age 57 +/- 7 years) underwent surgery for control of recurrent drug-refractory ventricular tachyarrhythmias (uniform ventricular tachycardia alone in 9 patients, ventricular tachycardia and ventricular fibrillation in 15 and ventricular fibrillation alone in 3) within 2 months of acute myocardial infarction. The mean number of major arrhythmic episodes per patient was 15 (range 2 to 200) and of drug failures 4 +/- 2. Left ventricular function was severely impaired in the majority (ejection fraction 29%; range 14% to 47%) and 18 patients (66%) had a left ventricular aneurysm. Endocardial resection guided by a combination of endocardial activation mapping during tachycardia and fragmentation mapping during sinus rhythm was performed in all patients. All electrically abnormal left ventricular endocardium was excised. Eight patients (29.6%) died within 30 days of surgery. Death was not related to age, time of surgery after infarction, ventricular function, bypass time or type of arrhythmia. Patients requiring emergency surgery had a higher early postoperative mortality rate than did those undergoing planned surgery (43% versus 15%). During a follow-up period of 32 +/- 20 months, there have been no arrhythmic deaths and only three patients (16%) have required antiarrhythmic drug therapy. When required in the early weeks after infarction, surgery for ventricular arrhythmias offers a high cure rate at a risk related to the patient's preoperative arrhythmia frequency, which in turn relates to the risk of arrhythmic death.
Adult↗
Early and late proarrhythmia from antiarrhythmic drug therapy.
Antiarrhythmic drug therapy is used with the hope of suppressing arrhythmias and therefore decreasing their associated symptoms or prolonging life. Unfortunately, many antiarrhythmic drugs have the opposite effect of exacerbating or provoking arrhythmias, a phenomenon that is termed proarrhythmia when such an event is specifically due to the drug in use. Early proarrhythmic events (within 30 days of initiation of drug use) have been reasonably well characterized and are predicted by either type of drug employed or the nature of the patient's cardiac disease and arrhythmia type. Late proarrhythmic events, as defined by placebo-controlled trials, have now been recognized as an increased risk of arrhythmic death in patients on antiarrhythmic drugs after many months of therapy. Initially, this late proarrhythmic event was identified with encainide and flecainide, but now several new studies have demonstrated that the risk of late proarrhythmia of comparable magnitude may be present in patients subjected to commonly used drugs, such as quinidine, mexelitine, etc. At present, only moricizine and the class II drugs (beta-adrenergic blockers) appear not to have this potential late proarrhythmic response. Therefore, before instituting antiarrhythmic drug therapy, the physician must be able to quantitate the degree of proarrhythmia and other risks of such therapy, as compared to their potential benefit, to define the proper indications for these agents.
Anti-Arrhythmia Agents↗
Prognostic significance and evolution of late ventricular potentials in the first year after myocardial infarction: a prospective study.
We performed a prospective study of the high-frequency components of the terminal portion of the QRS complex in 220 patients who survived acute myocardial infarction. Signal-averaged electrocardiograms (SA-ECGs) were performed before hospital discharge (16 +/- 6 days) and then serially at regular intervals over the following year. SA-ECGs were processed using a 40 Hz high-pass bidirectional filter. Duration of "filtered" QRS (D-normal value less than 120 ms), duration of the low-amplitude signals (D40 - n.v. less than 39 ms) and last 40 ms voltage of the QRS complex (V40 - n.v. greater than 20 microV) were measured. Late potentials (LPs) were defined as the presence of two or more abnormal values. In addition, 24-hour Holter monitoring was performed in 208 patients and left ventricular ejection fraction (LVEF) was determined by scintigraphy in 111. Sixty-two patients (group 1) had LPs, 158 had normal SA-ECGs (group 2). Spontaneous normalization of SA-ECGs occurred in 20% of patients after 6 months, although the mean values of D, D40 and V40 did not change significantly and the reproducibility was very good for all the indexes during all the follow-up controls. Three patients had sudden death and three presented again with spontaneous, sustained ventricular tachycardia. Five of 62 (8%) group 1 patients had an arrhythmic event compared with one of 158 patients (0.6%) in group 2. The sensitivity of SA-ECGs as a predictor of arrhythmic events was 83% with a specificity of 73%. Patients with subsequent arrhythmic events had longer filtered QRS (133 +/- 19 vs 104 +/- 16 ms; P less than 0.001), longer duration of the low-amplitude signals (54 +/- 15 vs 33 +/- 14 ms; P less than 0.01), and lower voltages in the last 40 ms of the filtered QRS (11 +/- 3 vs 36 +/- 25 microV; P less than 0.02) and, moreover, higher peak CK values and lower LVEF than those without such events. In conclusion, SA-ECGs provide important prognostic information in identifying patients at risk of arrhythmic events after myocardial infarction although dynamic changes of LPs are observed during the first year after myocardial infarction.
Arrhythmias, Cardiac↗
Late potentials after acute myocardial infarction. Performance of different criteria for the prediction of arrhythmic complications.
In order to compare different criteria for the definition of late potentials in patients after myocardial infarction, three signal averaged ECG variables, duration of the signal-averaged QRS complex (QRS), root-mean-square voltage of the terminal 40 ms (RMS-40), and the duration of low amplitude signals less than 40 microV (LASD-40), were assessed in 332 survivors of acute myocardial infarction who were followed-up for at least 6 months, during which 12 patients died suddenly and 14 suffered symptomatic sustained ventricular tachycardia. The associations of the three variables with arrhythmic events were analysed in the total population, in infarct site and age-specific subgroups. The sensitivity and specificity for the prediction of arrhythmic events was computed (for all dichotomy points) and compared with nine published criteria for late potentials based on the same three variables. Analysis showed that (a) the total signal averaged QRS duration was a better predictor of arrhythmic events than the other two variables, (b) for arrhythmic events in cases of anterior infarctions, higher RMS-40 dichotomy limits and lower QRS and LASD-40 dichotomy limits were needed for cases of inferior infarction, (c) a multivariate stratification of arrhythmic events based on all three variables performed better in the anterior infarction population than in the inferior infarction population, (d) the strategy defining late potentials, which requires that two variables reach critical values, is better than the strategies that require that any one or all three variables reach critical values, (e) all the definitions of late potentials performed differently in the populations with anterior as compared to inferior infarctions; to identify groups at similar risk of arrhythmic events, different criteria defining late potentials should be used in these subpopulations.
Action Potentials↗