Standards for the function of an academic 12-lead electrocardiographic core laboratory.

An academic 12-lead electrocardiogram (ECG) core laboratory aims to provide the highest possible quality ECG recording, measurement, and storage to aid clinicians in research into important cardiovascular outcomes and to maximize the credibility of scientific results based solely, or in part, on ECG data. This position paper presents a guide for the structure and function of an academic ECG core laboratory. The key functional aspects are: 1) Data collection, 2) Staff composition, 3) Diagnostic measurement and definition standards, 4) Data management, 5) Academic considerations, 6) Economic consideration, and 7) Accreditation. An ECG Core Laboratory has the responsibility for rapid and accurate analysis and responsible management of the electrocardiographic data in multicenter clinical trials. Academic Laboratories, in addition, provide leadership in research protocol generation and production of research manuscripts for submission to the appropriate peer-review journals.

Thrombolysis-induced coronary reperfusion causes acute and massive interstitial release of cardiac muscle cell proteins.

OBJECTIVE: Reperfusion of the infarct-related artery in patients with acute myocardial infarction limits infarct size, but also causes accelerated release into plasma of cardiac tissue proteins. The latter effect could reflect either enhanced protein washout from the heart or abrupt disruption of myocyte membranes. The present study indicates that the latter mechanism prevails. METHODS: In 26 patients, patency of the infarct-related artery was determined by coronary angiography 90 min and 5-7 days after thrombolytic treatment. Continuous electrocardiography was performed during the first 24 h after admission. Cumulative release of myoglobin (Mb) and creatine kinase (CK) into plasma was calculated from frequently sampled plasma concentrations. RESULTS: In patients with a patent infarct-related artery after 90 min, onset of a rapid (> 50%) decrease in ST-vector magnitude coincided with an equally rapid increase in QRS-vector magnitude, and with a sudden onset of release into plasma of Mb as well as CK. In these patients, a maximal initial release rate was observed and cumulative release conformed closely to a simple model for sudden interstitial liberation of proteins. In contrast, protein release started more gradually and could not be fitted to this model, in patients with persistent occlusion of the infarct-related artery at 90 min and absence of ST-vector normalisation. CONCLUSIONS: Previous studies have demonstrated significant myocardial salvage by timely reperfusion therapy. Nevertheless, this study indicates that the moment of recanalisation of the infarct-related artery coincides with sudden and massive disruption of myocyte membranes. Attenuation of this effect, if possible, could further improve the benefits of reperfusion therapy.