Division of Cardiology, Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong SAR
* Corresponding author. Tel: +852 28554244; fax: +852 28551143. E-mail address: cplau{at}hkucc.hku.hk
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 that involved 787 patients with acute myocardial infarction, the predictive value of SAECG was compared in patients with and without reperfusion therapy by either thrombolysis or angioplasty. The authors reported that reperfusion therapy reduced the incidence of late potentials, and an abnormal SAECG was predictive of an increased incidence of arrhythmic events in all patients regardless of prior reperfusion therapy.2 However, more recent studies demonstrated a low predictive value of SAECG in post-infarct patients who received reperfusion therapy.3,4
The use of beta-blockers in post-myocardial infarction patients is associated with reduced sudden death. The underlying mechanisms may be multiple. Apart from neurohumoral modulation, beta-blockers have important anti-ischaemic and anti-arrhythmic properties. It has been demonstrated that the use of beta-blockers reduced the incidence of late potentials in patients with acute myocardial infarction who received reperfusion therapy.5 In a prospective study involving 700 post-infarct patients taking beta-blockers, it was reported that common arrhythmia risk variables including standard ECG markers and late potentials had limited predictive power in identifying patients at risk of sudden cardiac death.6
Revascularization has multiple effects on ventricular arrthymogenesis, including removal of ischaemic burden and remodelling of the substrate. In the Coronary Artery Bypass Graft Patch Trial, patients with coronary artery disease scheduled for coronary artery bypass surgery, a depressed left ventricular ejection fraction and presence of late potentials were randomized to receive conventional treatment or prophylactic defibrillator implantation at the time of surgery.7 Total mortality was identical in both treatment groups. The lack of survival improvement in the defibrillator arm was thought to be due to a low incidence of sudden death in the study population. This is supportive of the notion that, in patients undergoing complete revascularization, the incidence of fatal ventricular arrhythmia is minimized. Several other studies have also confirmed that abnormal SAECG was not a strong predictor of sudden cardiac death after surgical revascularization.8
Bauer et al.9 reported on reduced prognostic power of ventricular late potentials in patients who received revascularization therapy. The authors retrospectively analysed the predictive values of late potentials, left ventricular ejection fraction, and heart rate turbulence in a cohort of patients who survived a recent myocardial infarction from January 1996 to December 2000. The majority of these patients received contemporary post-myocardial infarction treatment, namely, revascularization, beta-blockers, aspirin, ACE inhibitors, and statins. The authors found that the incidence of late potentials was low (9.3%), and that the presence of late potentials was not predictive of cardiac death and serious arrhythmic events. However, this study has to be interpreted with a number of considerations. The study patients involved were young (mean age of 58 years), the enzyme rise of the index myocardial infarction was small (mean peak creatine kinase of 556 U/L), and the left ventricular function was mostly preserved (mean ejection fraction of 57%). SAECG was either not performed or not suitable for analysis in almost half of the patients. Lastly, the study was a retrospective analysis and some patients were lost to follow-up. Despite these limitations, the findings are consistent with what others have shown on the effect of revascularization and the use of beta-blockers on late potentials. This study is particularly remarkable in that it involved a large number of post-infarct patients with a revascularization rate of 99%. Indeed, in this study population, the extent of myocardial damage was limited and predictive of a better prognosis. To examine if the loss of predictive power of SAECG is due to a low risk cohort, it will be helpful to analyse the discriminative value of late potentials in those patients with a depressed left ventricular function.
With contemporary treatment for acute myocardial infarction targeting early reperfusion and infarct size reduction, the overall outcome is improved. Beta-blockers that are widely used after acute myocardial infarction have anti-ischaemic, anti-arrhythmic, and neurohumoral effects. Standard post-myocardial infarction pharmacological therapies including ACE-inhibitors, statins, and anti-platelet agents also result in significant reduction in long-term mortality and morbidity. As a consequence, acute myocardial infarction survivors managed according to modern treatment guidelines are at a lower risk of recurrent ischaemic or arrhythmic event. In this relatively low risk population, the SAECG appears to have lost its predictive power on mortality and arrhythmic events.
The use of SAECG has significant limitations pertaining to risk stratification in post-infarct patients. There are uncertainties regarding the best time and technique for collection of the SAECG and the optimal criteria of classification.10 The interaction of modern pharmacotherapy and reperfusion strategies modifies the arrhythmogenic trigger, substrate, and neurohumoral milieu extensively. The prognostic power of late potentials is diminished. With contemporary aggressive treatment for acute myocardial infarction, the routine use of SAECG for risk stratification is not recommended.
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