Journal of electrocardiology
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Uncomplicated left bundle branch block (LBBB) is characterized by true ST-segment shifts resulting from delayed repolarization in the left ventricle with respect to the right ventricle. When acute coronary occlusions develop in the setting of previous or new LBBB, 12-lead eCG manifestations of injury may also appear. They consist of a more pronounced ST-segment elevation, of ST-segment deviations opposite to those of uncomplicated LBBB, or both. ⋯ Similar values applied to a subgroup of patients with serial ECGs. We propose that thrombolysis among patients with chest pain and LBBB be decided on the basis of a systematic ECG review to "rule patients in". This provision may result in both a significant reduction in the number of patients without infarction who receive thrombolysis and in timely treatment of those who do have MI.
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A genetic origin in diseases like the long QT syndrome, the Brugada syndrome, or hypertrophic cardiomyopathy have been identified over the past years. These diseases have in common that they may result in sudden cardiac death of the patient. Recognition of patients based on their phenotype and application in clinical practice of the knowledge acquired on the genetic basis may have a major impact on how we approach them. ⋯ The results are electrophysiologically opposite to the ones observed in the long QT syndrome. Thus different mutations in the same gene lead to different functional consequences. Again, identification and study of the right mutation may lead to a more rational treatment directed to correct the malfunction of the channel.
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A variety of tachycardias originate from the right ventricle or use right ventricular structures as part of their circuit. They are characterized by a left bundle branch block pattern. Many of these tachycardias are relatively easy targets for radiofrequency catheter ablation. ⋯ Atriofascicular (so-called Mahaim) fibers can sustain antidromic AV reentrant tachycardia. They represent an accessory AV node and His-Purkinje-like conduction system with atrial insertion in the right free wall near the tricuspid annulus and distal insertion directly into the right bundle branch. The accessory connection is ablated at the level of the tricuspid ring.
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Analysis of the 12-lead electrocardiogram (ECG) provides important diagnostic and prognostic information in the long QT syndrome. The clinical diagnosis of long QT syndrome is determined by the presence of a QTc > or = 0.44 sec. A normal QTc does not exclude a family member from being a genetic carrier. ⋯ This abnormality can be dormant and elicited by administration of drugs that cause Na channel blockade, such as ajmaline or type 1a or 1C antiarrhythmic drugs. Individuals who do not have the Brugada ECG findings at baseline but have this pattern induced by antiarrhythmic drugs are also at risk for sudden death. Further risk stratification may be obtained in the asymptomatic patients if ventricular fibrillation is induced at electrophysiological study.
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This article outlines the up-to-date understanding of the molecular basis of primary ventricular arrhythmias. Two disorders have recently been well described at the molecular level, the long QT syndromes and Brugada syndrome, and this article reviews the current scientific knowledge of each disease. A third disorder, arrhythmogenic right ventricular dysplasia, which is on the cusp of understanding, will also be described.