Journal of electrocardiology
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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.
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A 63-year-old diabetic man was admitted with general fatigue. Electrocardiogram (ECG) on admission showed complete atrioventricular (AV) blockade associated with prominent bifid T waves. The second component of the bifid T waves was distinguished from U waves by the beat-to-beat varying bifidity and the nadir between the two components located at > or = 1 mm above the isoelectric line. ⋯ Hypokalemia (3.6 mEq/L) was noted at admission. Partial restoration of the potassium level (3.9 mEq/L) prior to temporary ventricular demand pacing obscured the bifid T waves and attenuated the QT prolongation and dispersion to some extent (absolute QT interval ranging 520 to 620 ms). It was concluded that marked bradycardia caused by complete AV blockade (ie, a junctional escaped rhythm at a rate of 42 beats/min), hypokalemia, and underlying diabetes mellitus contributed in concert to the QT prolongation and dispersion leading to the prominent bifid T waves.
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Case Reports Comparative Study
Severe hyperkalemia with minimal electrocardiographic manifestations: a report of seven cases.
Severe hyperkalemia with minimal or nonspecific electrocardiographic (ECG) changes is unusual. We report data on seven patients with renal failure, metabolic acidosis, and severe hyperkalemia (K+ > or =8 mmol/L) without typical ECG changes. ⋯ QRS intervals were slightly prolonged in two patients (110 ms), and incomplete right bundle branch block was evident in one. Thus, the absence of typical ECG changes does not preclude severe hyperkalemia.