Journal of electrocardiology
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Lightning strike is a natural phenomenon with potentially devastating effects and represents one of the leading causes of cardiac arrest and death from environmental phenomena. Almost every organ system may be impaired as lightning passes through the human body preferring the pathways that the lowest resistance between the contact points. ⋯ The victim may develop hypertension, tachycardia, nonspecific electrocardiographic changes (including prolongation of the QT interval and transient T-wave inversion), and myocardial necrosis with release of creatine phosphokinase-MB fraction. We present the case of a 13-year-old boy with acute myocardial infarction secondary to an indirect lightning strike.
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Patients presenting to the emergency department with chest pain are triaged to early reperfusion therapies based on their initial 12-lead electrocardiogram (ECG). The standard 12-lead ECG lacks sensitivity to detect acute myocardial infarction (AMI). Electrocardiographic diagnosis of non-ST-elevation myocardial infarction (non-STEMI) is especially difficult and is delayed until cardiac biomarkers turn positive, indicating onset of myocardial necrosis. ⋯ Patients diagnosed with non-STEMI have distinct distribution of K-L coefficients compared with non-ACS cardiac patients. Coefficients from the first 50 samples of the ST-T wave (ST segment) better predict diagnostic category than do coefficients derived from the entire ST-T wave. Karhunen-Loève coefficient feature analysis may provide early diagnostic information to distinguish patients with non-STEMI vs non-ACS cardiac patients.
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QT surveillance of neonatal patients, and especially premature infants, may be important because of the potential for concomitant exposure to QT-prolonging medications and because of the possibility that they may have hereditary QT prolongation (long-QT syndrome), which is implicated in the pathogenesis of approximately 10% of sudden infant death syndrome. In-hospital automated continuous QT interval monitoring for neonatal and pediatric patients may be beneficial but is difficult because of high heart rates; inverted, biphasic, or low-amplitude T waves; noisy signal; and a limited number of electrocardiogram (ECG) leads available. Based on our previous work on an automated adult QT interval monitoring algorithm, we further enhanced and expanded the algorithm for application in the neonatal and pediatric patient population. ⋯ Mean and standard deviation of the error were both low (TRN = -3 +/- 8 milliseconds; TST = 1 +/- 20 milliseconds); regression slope (TRN = 0.94; TST = 0.83) and correlation coefficients (TRN = 0.96; TST = 0.85) (P < .0001) were fairly high. Performance on the TST was similar to that on the TRN with the exception of 2 cases. These results confirm that automated continuous QT interval monitoring in the neonatal intensive care setting is feasible and accurate and may lead to earlier recognition of the "vulnerable" infant.
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To study the effect of electrical neurostimulation on the ST segment shift in patients with ST elevation myocardial infarction (STEMI) with residual ST elevation after primary percutaneous coronary intervention (PCI). ⋯ Electrical neurostimulation may result in significant additional reduction of ST elevation in STEMI after reperfusion treatment, in particular in patients with marked ST elevation on the first ECG after successful primary PCI.
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Recent reports have highlighted the importance of a family history of sudden death as a risk for ventricular fibrillation (VF) in patients experiencing acute myocardial infarction (AMI), pointing to the possibility of a genetic predisposition. This report briefly reviews 2 recent studies designed to examine the hypothesis that there is a genetic predisposition to the development of arrhythmias associated with AMI. Ventricular tachycardia and VF (VT/VF) complicating AMI as well as arrhythmias associated with Brugada syndrome, a genetic disorder linked to SCN5A mutations, have both been linked to phase 2 reentry. ⋯ Expression of this polymorphism has previously been shown to cause a loss of function in HERG current consistent with the long-QT phenotype. These observations suggest a genetic predisposition to the development of long-QT intervals and torsade de pointes in the days after an AMI. These preliminary studies provide support for the hypothesis that there is a genetic predisposition to the type and severity of arrhythmias that develop during and after an AMI, and that additional studies are warranted.