Journal of electrocardiology
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The American College of Cardiology recommends that patients with high risk acute myocardial infarction (AMI) be triaged to hospitals with percutaneous transluminal coronary angioplasty capability. However, there are no prehospital triage criteria to select candidates for bypassing community hospitals and being taken directly to "cardiac centers." This article assesses which independent variables predict death within 7 days in patients with suspected AMI transported by EMS. This is a retrospective study of 291 AMI patients transported by ambulance to 3 hospitals during 1996-1997. ⋯ The overall model was 86% sensitive and 53% specific with an area under the receiving operating characteristic curve of 0.8 (P < or = .001). A triage rule based on a multivariate model can identify the group at high risk of early cardiac death. This decision rule needs to be prospectively validated.
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Prehospital triage of cardiac patients for bypass from community hospitals to cardiac centers may improve survival. This article determines if electrocardiogram (ECG)-based scoring triage methods (Aldrich MI scoring, QRS distortion, and the TIMI classification) and location of infarct (via 12 lead ECG) are associated with mortality before and after adjusting for age, sex, and race. It is a retrospective study of 291 AMI adult patients transported by ambulance to community hospitals or cardiac centers. ⋯ Patients classified as a "high risk" for AMI per TIMI status were almost 3 times more likely to die than those at "low risk" and reached borderline statistical significance (P = .06) after adjusting for the covariates. Having an anterior infarct, as opposed to an inferior infarct, was significantly associated with death before and after adjusting for the covariates (Unadjusted OR = 2.6, Adjusted OR = 2.8). Properly training emergency medical system professionals in this area may prove useful for identifying higher risk AMI patients in the prehospital setting.
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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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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.