Journal of electrocardiology
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Comparative Study
Comparison of model-based and expert-rule based electrocardiographic identification of the culprit artery in patients with acute coronary syndrome.
Culprit coronary artery assessment in the triage ECG of patients with suspected acute coronary syndrome (ACS) is relevant a priori knowledge preceding percutaneous coronary intervention (PCI). We compared a model-based automated method (Olson method) with an expert-rule based method for the culprit artery assessment. ⋯ The automated model-based Olson method performed at least at the level of expert cardiologists using a manual rule-based method.
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Several studies have investigated the ability of the twelve-lead electrocardiogram (ECG) to reliably distinguish Takotsubo cardiomyopathy (TC) from an acute anterior ST-segment elevation myocardial infarction (STEMI). In these studies, only ECG changes were required - ST-segment deviation and/or T-wave inversion - in TC whereas in acute anterior STEMI, ECGs had to meet STEMI criteria. In the majority of these studies, patients of both genders were used even though TC predominantly occurs in women. The aim of this study is to see whether TC can be distinguished from acute anterior STEMI in a predominantly female study population where all patients meet STEMI-criteria. ⋯ Given the consequences of missing the diagnosis of an acute anterior STEMI the diagnostic accuracy of the ECG criteria investigated in this retrospective study were insufficient to reliably distinguish patients with TC from patients with an acute anterior STEMI. To definitely exclude the diagnosis of an acute anterior STEMI coronary angiography, which remains the gold standard, will need to be performed.
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A case of torsade de pointes (TdP) with complete atrioventricular block and pacemaker failure that was misdiagnosed as epilepsy is presented herein. An 82-year-old female with recurrent seizure-like attacks showed epileptiform discharge during an electroencephalogram recording. ⋯ After a DDD pacemaker with a new ventricular lead was replaced, there was no recurrence of any seizure-like attacks. Bradycardia-mediated TdP associated with complete atrioventricular block should not be missed in patients with recurrent seizure-like attacks even after pacemaker implantation.
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The J-wave pattern on 12-lead ECG is traditionally defined as a positive deflection at junction between the end of the QRS and the beginning of the ST-segment. This pattern has recently been associated with increased risk for idiopathic ventricular fibrillation in the absence of cardiovascular disease. The interest for the clinical significance of J-wave pattern as a potential ECG hallmark of high risk for cardiac arrest has recently been reinforced by the growing practice of ECG screening, such as occurs in large population of young competitive athletes. ⋯ Furthermore the J-wave pattern has been demonstrated to be a dynamic phenomenon related to the training status, with the larger prominence at the peak of training and with an inverse relation between magnitude of J-wave and heart rate. In addition the J-wave pattern is usually associated with other ECG changes, such as increased QRS voltages and ST-segment elevation, as well as LV remodeling, suggesting that it likely represents another expression of the physiologic athlete's heart. Finally the scientific data available demonstrated that during a medium follow-up period the J-wave pattern does not convey risk for adverse cardiac events, including sudden death or ventricular tachyarrhythmias.
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Case Reports
Wellens syndrome caused by spasm of the proximal left anterior descending coronary artery.
Electrocardiographic characteristics of Wellens syndrome (WS) consist of deeply inverted T waves or biphasic T waves in anterior precordial leads. Studies have shown that patients with WS have critical stenosis or complete obstruction of the proximal left anterior descending coronary artery (LAD) and high risk for the development of extensive anterior myocardial infarction. Here, we reported a case presenting with WS and with a small plaque in the proximal LAD and slow flow in the LAD other than significant stenosis of the proximal LAD detected by coronary angiography. The mechanisms for WS of our case are discussed.