Prevalence Of Late Potentials Research Articles

Electrocardiographic parameters among beta-thalassemia major patients

Abstract Background/Introduction The majority of beta thalassemia major (β-TM) patients suffer from cardiac disorders, while a significant proportion of them die suddenly. Twelve-lead and signal-averaged electrocardiography are simple, inexpensive, readily available tools for identifying an unfavorable arrhythmiological substrate by detecting the presence of arrhythmias, conduction abnormalities and late potentials (LPs) in these patients. Methods 47 β-TM patients and 30 healthy controls were submitted to twelve-lead and signal-averaged electrocardiography. Basal rhythm, heart rate, PR interval duration, QRS complex duration and morphology, QTc interval duration and prevalence of LPs were recorded. Results β-TM patients demonstrated a more prolonged PR segment (167.74 msec vs. 147.07 msec) (p=0.043), a higher prevalence of PR prolongation (21.05% vs. 0%) (p=0.013) and a higher prevalence of LPs (18/47, 38.3% vs. 2/30, 6.7%) (p=0.002) compared with controls. In particular, every single SAECG parameter significantly differed among patients compared with controls. Among patients, left ventricular ejection fraction was marginally lower and QTc more prolonged among LPs positive subgroup compared with LPs negative subgroup. The prevalence of atrial fibrillation among b-TM patients was estimated at 10.64%. Conclusions β-TM patients have a higher prevalence of a prolonged PR segment, atrial fibrillation and LPs. Twelve-lead and SAECG performance was feasible in all subjects and constitutes a readily available tool for assessing myocardial electrophysiological alterations in this patient group, that could have significant impact on survival and quality of life with timely application of appropriate treatment. Funding Acknowledgement Type of funding source: None

P460Increased prevalence of late potentials on signal-averaged electrocardiogram in psychiatric patients

P460Increased prevalence of late potentials on signal-averaged electrocardiogram in psychiatric patients

Prevalence of late potentials on signal-averaged ECG in patients with psychiatric disorders

BackgroundSudden cardiac death (SCD) occurs three times more often in psychiatric patients than in the general population. QRS fragmentation (QRSfr) and signal-averaged electrocardiography (SAECG) are simple, inexpensive, readily available tools for detecting the presence of abnormal depolarization and late potentials (LPs) in these patients, a result of either the underlying disease or treatment. MethodsFrequency of LP detection by SAECG and QRSfr was studied in 52 psychiatric patients and compared with 30 healthy (without known structural heart disease or occurrence of ventricular arrhythmia) controls. Patients were then prospectively followed up and incidence of SCD was recorded. ResultsLP prevalence was significantly higher in patients than in controls (16/52–31% vs 2/30–7%, p=0.012), while QRSfr was similar between these two groups (p=0.09). Of the LP presence criteria, the root mean square value at terminal 40msec of the QRS (RMS40) was significantly lower in patients (32μV, SD=19μV, vs 46μV, SD=32μV, p=0.015). Among patients, no differences were noted between the LP positive and negative groups regarding age, sex, number of medications, class of antipsychotics and defined daily doses. Mean follow-up was 46months (SD=11) and during it 3 patients suffered SCD. Although 2 SCD victims had both LPs and QRSfr concurrently present, neither of them, nor their simultaneous presence could definitely account for the events. ConclusionsLP prevalence in psychiatric patients was significantly higher than in controls. SAECG performance was feasible in all cases and constitutes a readily available tool for assessing myocardial electrophysiological alterations in this patient group.

Prevalence and significance of the early repolarization pattern in inferolateral leads in patients with Brugada syndrome: A single-center study

In this study, the prevalence and prognostic significance of the early repolarization (ER) pattern in the inferolateral leads in patients with Brugada syndrome were investigated. Clinical, genetic, and electrophysiological data were collected and analyzed from 69 individuals with either a spontaneous or drug-induced Brugada type 1 electrocardiogram (ECG) pattern. An ER pattern was defined as J-point elevation at least 0.1mV from the baseline in at least 2 inferior or lateral leads. The presence of late potentials and inducibility of ventricular fibrillation (VF) by programmed stimulation were compared between patients with and without a J wave. Follow-up data, including outcome events, were obtained for all patients. An ER pattern was observed in the inferolateral leads in 6 patients with a spontaneous Brugada type 1 ECG pattern and in 1 patient with a drug-induced Brugada type 1 ECG pattern. There was no significant intergroup difference in symptoms, family history of sudden cardiac death, prevalence of late potentials, or inducibility of VF. No patient with the ER pattern developed a cardiac event during the mean follow-up period of 73.6±38.1 months. The ER pattern in the inferolateral leads is not uncommon in Brugada syndrome; however, the presence of a J wave does not appear to be associated with subsequent arrhythmic events in patients with Brugada syndrome.

Criteria to predict carriers of a novel SCN5A mutation in a large Portuguese family affected by the Brugada syndrome

Brugada syndrome (BrS) is a life-threatening arrhythmia disorder associated with autosomal-dominant mutations in the SCN5A gene. We aimed to characterize the diagnostic challenges and clinical manifestations of a novel SCN5A mutation associated with BrS. From a novel SCN5A mutation (c.664C>T; p.Arg222X) identified in a proband with the characteristic electrocardiographic pattern and the history of sudden collapse, 122 family members were studied including 40 carriers of the mutation. The electrocardiographic diagnosis of BrS requires type 1 Brugada electrocardiogram (ECG) pattern in >1 right precordial lead (V1-V3), but recently an isolated lead with coved-type ECG was proposed to be enough for the diagnosis. In this family, these proposed criteria (PC) were more sensitive in detecting mutation carriers than the conventional criteria without repercussion on the specificity. Carriers had, on average, longer P-wave duration, PR, and QRS intervals and higher transmural dispersion of repolarization. The prevalence of late potentials was higher in carriers, and individual signal average ECG (SAECG) parameters (QRSf, LAS, and RMS40) also were related to SCN5A gene mutation. Three non-carriers were found to be affected by BrS, two with a spontaneous type 1 ECG with alternative placement of the precordial electrodes, and one only after the pharmacological provocative test, suggesting that other genes may play a role in the pathophysiology of this disease. The PC for BrS diagnosis should be implemented. Some parameters from the spontaneous ECG and the SAECG are more effective tools than the characteristic repolarization pattern to discriminate between carriers of SCN5A mutations.

Young Investigator Abstract Session

Young Investigator Abstract Session

Reconciling the Protean Manifestations of Arrhythmogenic Cardiomyopathy

Medical conception of a disease begins with in vivo observation and develops with recognition of cognate findings on gross anatomy, histology, and cellular pathology. It was histopathology that established myocyte disarray as the cardinal feature of hypertrophic cardiomyopathy, present even in cases where left ventricular (LV) hypertrophy is subtle or absent. To this day, clinical-pathological association retains its historical value as the primary means of gaining insight into underlying disease processes. Enhancing its appeal is its accessibility to physicians, most of whom are familiar with histopathology from medical school and attuned to visual diagnosis. Article see p 632 With the advent of molecular genetics, however, the limitations of clinical-pathological association have become apparent and nowhere more so than in the inherited arrhythmia syndromes. In the long-QT and Brugada syndromes and catecholaminergic polymorphic ventricular tachycardia, a structurally normal heart belies the propensity to ventricular arrhythmia and sudden cardiac death (SCD). How this might be possible began to unravel with the isolation of mutations in genes encoding ion channels, transporters, and binding proteins. Genetic studies also have provided fresh insights into diseases with an obvious pathological substrate, such as hypertrophic cardiomyopathy, in which sarcomeric mutations predominate. Families with a high incidence of SCD and myocyte disarray but minimal LV hypertrophy were found to have mutations in troponin T,1 lending further support to the inclusion of this phenotype within the spectrum of hypertrophic cardiomyopathy. Redefining diseases according to their genetic etiology, while attractive, is less straightforward than immediately obvious. Defects in sarcomeric components, for example, have been implicated in both hypertrophic cardiomyopathy and dilated cardiomyopathy. In some heritable disorders, such as dilated cardiomyopathy, marked locus heterogeneity precludes delineation of a single genetic determinant. The ultimate solution to disease classification involves going 1 step further and identifying a unifying molecular mechanism, which may …

Characterization of the Arrhythmogenic Substrate in Ischemic and Nonischemic Cardiomyopathy: Implications for Catheter Ablation of Hemodynamically Unstable Ventricular Tachycardia

The purpose of this study was to compare the characteristics and prevalence of late potentials (LP) in patients with nonischemic cardiomyopathy (NICM) and ischemic cardiomyopathy (ICM) etiologies and evaluate their value as targets for catheter ablation. LP are frequently found in post-myocardial infarction scars and are useful ablation targets. The relative prevalence and characteristics of LP in patients with NICM is not well understood. Thirty-three patients with structural heart disease (NICM, n = 16; ICM, n = 17) referred for catheter ablation of ventricular tachycardia were studied. Electroanatomic mapping was performed endocardially (n = 33) and epicardially (n = 19). The LP were defined as low voltage electrograms (<1.5 mV) with onset after the QRS interval. Very late potentials (vLP) were defined as electrograms with onset >100 ms after the QRS. We sampled an average of 564 +/- 449 points and 726 +/- 483 points in the left ventricle endocardium and epicardium, respectively. Mean total low voltage area in patients with ICM was 101 +/- 55 cm(2) and 56 +/- 33 cm(2), endocardial and epicardial, respectively, compared with NICM of 55 +/- 41 cm(2) and 53 +/- 28 cm(2), respectively. Within the total low voltage area, vLP were observed more frequently in ICM than in NICM in endocardium (4.1% vs. 1.3%; p = 0.0003) and epicardium (4.3% vs. 2.1%, p = 0.035). An LP-targeted ablation strategy was effective in ICM patients (82% nonrecurrence at 12 +/- 10 months of follow-up), whereas NICM patients had less favorable outcomes (50% at 15 +/- 13 months of follow-up). The contribution of scar to the electrophysiological abnormalities targeted for ablation of unstable ventricular tachycardia differs between ICM and NICM. An approach incorporating LP ablation and pace-mapping had limited success in patients with NICM compared with ICM, and alternative ablation strategies should be considered.

Effects of Reperfusion Obtained Two to Six Months After Acute Myocardial Infarction on Myocardial Electrical Stabilization in Patients With an Occluded Infarct-Related Coronary Artery

To assess the changes in electrical stability markers in patients with previous myocardial infarction after very late reopening of the infarct-related artery, we studied QT dispersion, corrected-QT dispersion, and late potentials before and 1, 3, and 6 months after an attempt at late percutaneous coronary intervention (PCI) in 31 consecutive patients with single-vessel disease (infarct-related artery occlusion or subocclusion) diagnosed > or = 4 weeks after the ST-elevation myocardial infarction. Patients underwent PCI 3.9 +/- 2 months after ST-elevation myocardial infarction. PCI was successful in 24 patients (group A) and unsuccessful in 7 (group B). The 2 groups were similar in clinical and angiographic characteristics, as well as the prevalence of basal late potentials, average QT dispersion, and corrected-QT dispersion. One month after PCI, the successful reperfusion group had a significant 67% decrease in the prevalence of late potentials and average QT dispersion and corrected QT dispersion (51 +/- 9 vs 72 +/- 11 ms, p <0.00001, and 51 +/- 10 vs 76 +/- 15 ms, p <0.00001, respectively). These benefits remained stable at 3 and 6 months after PCI. Conversely, the unsuccessful group did not show any improvement in electrical stability markers after PCI failed. Thus, reperfusion obtained very late after ST-elevation myocardial infarction confers significant electrical stabilization that may contribute to a better outcome in patients with patent infarct-related arteries.

The use of signal-averaged electrocardiogram in risk stratification after acute myocardial infarction in the modern era

This editorial refers to ‘Reduced prognostic power of ventricular late potentials in post-infarction patients of the reperfusion era’† by A. Bauer et al. , on page 755 Signal-averaged electrocardiogram (SAECG) reveals presence of late potentials that are low-amplitude high-frequency waveforms within the terminal portion of the QRS complex. Late potentials reflect the presence of slow conduction within the ventricular myocardium that may serve as a substrate for arrhythmogenesis. The underlying histology is hypothesized to be areas of fibrosis interspersed among areas of viable myocardium. Early studies showed that the presence of late potentials predicted inducibility of ventricular arrhythmias during programmed electrical stimulation in patients with remote myocardial infarction. Although the presence of late potentials was not a highly sensitive or specific marker for sudden death, it was regarded as having a good negative predictive value for arrhythmic events in post-infarction patients in the 1980s. Currently, it is well established that beta-blockers and successful thrombolysis/revascularization reduce the prevalence of late potentials after acute myocardial infarction.1 However, less data were published on the effect of reperfusion and/or beta-blocker therapy on the prognostic value of SAECG in post-infarct risk stratification. In the Cardiac Arrhythmia Suppression Trial Substudy … *Corresponding author. Tel: +852 28554244; fax: +852 28551143. E-mail address : cplau{at}hkucc.hku.hk

Late potentials in female triathletes before and after prolonged strenuous exercise.

The objectives of this study were to evaluate the prevalence of late potentials (LP) in female triathletes before and after prolonged strenuous exercise (PSE), and to determine whether LP are related to greater left ventricular (LV) dimensions and/or mass. Thirteen female triathletes were examined immediately before (Pre), one hour after (Post), and 24 to 48 hours after PSE (Recovery) using signal-averaged electrocardiography (SAECG). Late potentials were evaluated by two or more standard SAECG anomalies. Left ventricular dimensions and mass were measured Pre using two-dimensional echocardiography. Results revealed that no significant differences existed between Pre, Post, and Recovery in the SAECG parameters. Four athletes displayed LP during Pre. The incidence of LP during did not increase Post. There were no significant relationships between LV dimensions or mass and SAECG parameters. In conclusion, a small portion of female triathletes display LP before and after PSE, which are not worsened by PSE nor related to increased LV dimensions and/or mass.

Occurrence of ventricular late potentials in patients with active acromegaly.

Patients with acromegaly have an increased risk of ventricular dysrhythmias and sudden death. Late potentials in a signal-averaged electrocardiogram (SAECG), a predictor of ventricular dysrhythmias, are frequently seen in patients after previous myocardial infarction, but little is known about the prevalence of late potentials in acromegaly. The aim of our study was to investigate the prevalence of late potentials in patients with acromegaly and their relation to the activity of the disease and to myocardial hypertrophy. The study included 48 patients with acromegaly [27 males, 21 females, mean age 52.3 +/- 14.2 years, 16 active disease, 32 cured or 'well controlled', under treatment with sandostatin analogues (12/32)] and 38 healthy volunteers as a control group. Late potentials were detected in 9/16 (56%) patients with active acromegaly vs. 2/32 (6%) with cured/well controlled acromegaly (P = 0.001), defined as normal age-related IGF-1 levels and GH levels suppressible below 1 microg/l after an oral glucose load (75 g). Late potentials were not related to muscle mass index (127 +/- 35 active vs. 123 +/- 34 g/m2 cured/well controlled). The association of disease activity with the detection of late potentials was independent of age, gender, duration of the disease and body mass index. In comparison to the control group, the prevalence of late potentials was significantly higher in patients with acromegaly (23%) than in the control group (0%; P < 0.001). Late potentials in the SAECG are frequently seen in active acromegaly and may represent an early and sensitive parameter to detect myocardial injury in acromegaly.

Prevalence of late potentials in a sample of 487 healthy, middle-aged men from southwestern France.

Late potentials (LPS) have been shown to be predictive of ventricular tachycardia in coronary artery disease subjects, but the prevalence of LP in the general population is not as well-known. The study included 487 men without a history of cardiovascular disease (aged 50-59) living in Southwestern France. Standard-averaged high resolution electrocardiogram was performed using Butterworth filtering at 40-250 Hz. LPS were defined as two or more of the following criteria: QRS > 114 ms, duration of the low amplitude signals in the terminal portion of QRS > 38 ms, root mean square (RMS) voltage of the last 40 ms < 20 microV. The mean QRS duration was 97 +/- 12 ms (mean +/- SD), duration of the low amplitude signals in the terminal portion of QRS was 32 +/- 10 ms, and RMS voltage in the last 40 ms was 39 +/- 27 microV. Eight percent of subjects (95% confidence interval [CI]: 6%-11%) had a QRS duration > 114 ms; 22% (95% CI: 18%-26%) had a duration of low amplitude signals > 38 ms, and 25% (95% CI: 22%-29%) had RMS voltage in the last 40 ms < 20 microV. Finally, the prevalence of LP was 21% (95% CI: 18%-25%). In conclusion, according to commonly used criteria, the prevalence of LP in this healthy population of middle-aged men is 21%, close to the values found in the literature for myocardial infarction patients. Those findings indicate the need for reconsidering the definition of LPS.

Temporal properties of high frequency intra-QRS signals in myocardial infarction and healthy hearts.

The prevalence of late potentials after myocardial infarction depends on the site of the infarction. This may be caused by the different activation onsets of the anterior and inferior myocardial segments. Therefore, in anterior infarcts the high frequency signals may be concealed within the QRS whereas in the inferior infarcts they last beyond the end of the QRS. We compared the timing and the spatial patterns of high frequency intra-QRS signals (IQSs) in the different infarction sites. We investigated 14 patients with anterior infarcts, 17 patients with inferior infarcts, and 10 healthy subjects. 31-lead magnetocardiograms were recorded in left precordial position and averaged. The QRS signals were smoothed with a Savitzky-Golay filter. The smoothed QRS signals were subtracted from the measured ones. The difference of the signals (frequency band of about 60-200 Hz) representing the high frequency components was quantified. The percentage of the high frequency signals was calculated for the entire QRS, for the first and for the second half, respectively. We found that in patients with anterior infarcts the high frequency components predominantly appeared in the first half of the QRS whereas in inferior infarcts these components predominantly appeared in the second half of the QRS. The different infarction sites were associated with different spatial patterns of the high frequency signals on the body surface. In healthy subjects there was not such a preferential association of time intervals and high frequency signals. Late potentials are the special case of high frequency signals appearing in the terminal QRS. It is the general property of the myocardium to generate high frequency signals associated with the depolarization of infarcted tissue. The timing of such signals and the spatial distribution patterns on the body surface may help to identify the location of the sources.

Late coronary angioplasty and ventricular late potentials

To assess the effect of successful late coronary angioplasty of an occluded infarct-related artery on the prevalence of ventricular late potentials, signal-averaged electrocardiograms were recorded in 123 consecutive patients surviving a first acute myocardial infarction (58 with and 65 without mechanical reperfusion of the occluded coronary artery). Multivariate analysis showed that successful reperfusion by late angioplasty of the infarct artery contributes to a decrease in the prevalence of late potentials.

Late Potentials in Healthy Subjects

Objective: Criteria for detection of late potentials have not yet been standardized, but the criteria recommended by ESC/AHA/ACC are widely used. In this investigation, the prevalence of late potentials is studied in an age stratified healthy population with likelihood of coronary artery disease &lt; 5%. Relation between signal‐averaged variables and clinical variables was studied.Methods: Signal‐averaged ECGs were recorded using Butterworth filters at 40 and 250 Hz. The following three time‐domain parameters were evaluated: QRS duration (duration of the amplified, filtered QRS complex); LPD (duration of the late potentials, i.e., duration from the point of time when the magnitude of the main complex becomes lower than 40 μV); and RMS40 (root mean square of the activity within the last 40 ms of the amplified, filtered QRS complex).Results: QRS duration was significantly longer in men than in women, and was correlated to the mass of the left ventricle (LVM). The combination LPD and RMS40 gave the highest prevalence of late potentials. The prevalence of late potentials was 25%.Conclusion: Standard criteria should be used with great caution, and normal limits should be established in each laboratory to a preselected noise level. QRSD should be included within the definition of reference limits and should be gender matched. Even though there is correlation between LVM and the QRSD, the upper normal limit of QRSD based on LVM matching is unchanged.

Signal-averaged ECG prior to and serially after thrombolytic therapy for acute myocardial infarction.

Signal averaging has been performed to evaluate late potentials following infarction and the administration of thrombolytic therapy. Most studies have recorded signal-averaged electrocardiograms (SAECGs) at least 12 hours after the onset of the infarction. In this study, SAECGs were recorded before thrombolytic therapy and serially over 7-10 days following infarction in 21 patients. The high frequency QRS duration was significantly shortened at 1 and 24 hours compared to presentation (96.8 +/- 11.3 ms and 93.4 +/- 8.0 ms vs 103.3 +/- 14.3 ms, respectively, P < 0.05) and there was an increase in the terminal voltage over time, significant at 1 hour and 3 days (57.3 +/- 29.1 microV and 58.6 +/- 44.7 microV vs 44.4 +/- 35.5 microV, respectively, P < 0.01). Five patients met criteria for ventricular late potentials on at least one SAECG. The prevalence of late potentials was higher in patients with Q wave infarctions, or with occluded infarct related arteries. These changes in myocardial activation may be related to ischemia and reperfusion, and may not correlate with the development of a fixed substrate for reentry.

Prognosis and risk stratification after myocardial infarction.

In order to assess prognosis after myocardial infarction, various methods have been used: estimation of ejection fraction, Holter monitoring, detection of ventricular late potentials using signal-averaging techniques, programmed ventricular stimulation of the heart to test the inducibility of ventricular tachyarrhythmias, and parameters that assess heart rate variability. Left ventricular dysfunction is the major determinant for prognosis after myocardial infarction, but left ventricular end-systolic volume may be better than overall ejection fraction. The presence of an 'arrhythmogenic substrate' may be detected by recording low-amplitude, fractionated activity or by artificially introducing premature ventricular extrasystoles using programmed ventricular stimulation. The signal-averaged ECG represents an independent tool for risk assessment. In some studies, signal-averaging and programmed ventricular stimulation proved to be more sensitive for the prediction of sustained ventricular tachycardia than for sudden death. The risk of an arrhythmic event in patients with an abnormal signal-averaged ECG or an abnormal result of programmed ventricular stimulation is increased, although the majority of these patients still do not experience a fatal or life-threatening arrhythmia. This high number of false-positive results limits the practical applicability of the signal-averaged ECG but also of other techniques such as long-term ECG recording. Recent interest has focussed on heart rate variability, which is considered an index of sympatho-vagal interaction after acute myocardial infarction. Patients with decreased heart rate variability have a poorer prognosis than those with normal parameters. Patency of the infarct-related artery is a major factor that governs the potentially beneficial effects of thrombolytic therapy. Many, but not all, studies have shown a reduced prevalence of late potentials after successful thrombolysis or in the presence of an open infarct-related artery. Effective thrombolytic therapy may prevent the development of an abnormal electrophysiological milieu after myocardial infarction. Finally, neurological factors such as depression have been shown to be independent risk factors for mortality after acute myocardial infarction. The role of psycho-social factors and their mechanisms of action need further attention since they open the door for behavioural modification. In conclusion, there are several promising new techniques for identification of patients at risk of ventricular tachyarrhythmias. These techniques seem to be superior to more conventional methods such as long-term ECG monitoring as well as exercise testing. Methods which determine the arrhythmogenic substrate might be combined with a parameter of left ventricular ejection fraction because of the paramount importance of left ventricular pump function. However, due to the large proportion of false-positive results obtained with any of these methods, it seems unlikely that they will clearly surpass the others and be sufficiently accurate for risk assessment in the individual patient.

Late potentials in arrhythmogenic right ventricular dysplasia. Prevalence, diagnostic and prognostic values.

A time-domain signal-averaged ECG was performed in 52 patients with arrhythmogenic right ventricular dysplasia (ARVD) proven by angiography, in 45 control subjects with normal hearts, and in 132 patients with various types of ventricular arrhythmias and no evidence of cardiac disease during routine cardiac examination. Based on the results of control subjects, patients with at least 2/3 abnormal parameters (QRS > or = 113 ms, LAS > or = 38 ms, RMS 40 < or = 16 microV) were considered as having late potentials (LP). Prevalence of LP was 75% (39/52) in patients with ARVD, 19% (25/132) in patients with apparently idiopathic ventricular arrhythmias, and 4% (4/45) in controls (P < 0.01). In ARVD, no relationship was found between LP and age, type of ventricular arrhythmia (sustained or not), or extent of the disease on angiography. A significant correlation was found between the values of two parameters (QRS and LAS length) and the delay between the first ventricular arrhythmia and the examination (r = 0.39 and 0.42 respectively, P < 0.01). Further examinations (echo and/or angiography) revealed underlying heart disease in 26/132 patients with apparently normal hearts, including 13 with ARVD. LP were present in 21/26 patients (81%) with diseased heart vs 4/106 (4%) in those with normal hearts after complete examination, giving a sensitivity of 86%, and a specificity of 96% for detecting underlying heart disease. During a follow-up of 3.1 +/- 1.2 years after signal-averaged ECG, only one patient died from heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of infarct-related artery patency on the indexes of parasympathetic activity and prevalence of late potentials in survivors of acute myocardial infarction

Objectives. The purpose of this study was to determine whether infarct-related coronary artery patency influence myocardial electrical stability as measured by the prevalence of late potentials or heart rate variability.Background. Several studies have suggested that loss of vagal activity is associated with an increased incidence of arrhythmic death after myocardial infarction.Methods. A short-duration, high resolution electrocardiogram (ECG) was performed before hospital discharge in 175 patients with a first myocardial infarction. Seventy-three patients received thrombolytic therapy. All patients underwent coronary angiography. Coronary occlusion was defined as minimal or no anterograde flow. Eighty-eight patients (50.3%) had an occluded infarct-related artery. Sixty-two healthy subjects served as control subjects to determine the normal range of heart rate variability.Results. Comparison between the control group and patients without patency of the infarct-related artery in the time domain and spectral analyses revealed in the latter patients a reduced heart rate variability (p < 0.0001) and a lower power spectrum density in both the 0.05- to 0.15-Hz band (p < 0.0001) and the 0.15- to 0.35-Hz band (p < 0.0001). The heart rate variability in patient with late potentials was lower than in those with a normal signal-averaged ECG. Those patients with spontaneous or thrombolysis-induced reperfusion have less occurrence of late potentials and higher parasympathetic activity than do patients with a closed artery.Conclusions. This study suggests that the patency of the infarct-related artery determines both the absence of late potentials and the preservation of vagal tone and may explain the reduction in mortality induced by thrombolytic therapy in myocardial infarction.