17 research outputs found
Implications of precordial ST segment depression during acute inferior myocardial infarction. Arteriographic and ventriculographic correlations during the acute phase.
No full textSignificance of reciprocal ST depression in acute myocardial infarction: a study of 258 patients treated by thrombolysis.
No full textIs transluminal coronary angioplasty mandatory after successful thrombolysis? Quantitative coronary angiographic study.
No full textEffect of hyaluronidase on mortality and morbidity in patients with early peaking of plasma creatine kinase MB and non-transmural ischaemia. Multicentre investigation for the limitation of infarct size (MILIS).
No full text
Changes in Doppler indices of cardiac function during and after percutaneous transluminal coronary angioplasty.
No full textAnatomic versus physiologic assessment of coronary artery disease: Guiding management decisions using positron-emission tomography (PET) as a physiologic tool
Full text linkAngiographic severity of coronary artery stenosis has historically been the primary guide to revascularization or medical management of coronary artery disease. However, physiologic severity defined by coronary pressure and/or flow has resurged into clinical prominence as a potential, fundamental change from anatomic- to physiologically-guided management. This review addresses clinical coronary physiology - pressure and flow - as clinical tools for treating patients. We clarify the basic concepts that hold true for whatever technology measures coronary physiology directly and reliably, here focusing on positron emission tomography (PET) and its interplay with intracoronary measurements
Enzyme tests in the evaluation of thrombolysis in acute myocardial infarction.
No full textThe activity of alpha-hydroxybutyrate dehydrogenase, creatine kinase, creatine kinase MB and aspartate aminotransferase was measured on serial plasma samples from patients with acute myocardial infarction. The study was part of a multicentre randomised trial of the effect of thrombolytic treatment in the acute phase of acute myocardial infarction. The applicability and comparability of enzyme tests for the estimation of myocardial injury were studied in 76 control patients and 74 patients treated with streptokinase. Treatment with streptokinase caused a considerable acceleration of enzyme release after acute myocardial infarction, both in patients with persistent coronary occlusion and in those with successful reperfusion. But this changed pattern of enzyme release did not affect the rate of enzyme elimination from plasma or the released proportions of different enzymes. Thus the assessment of infarct size by measurement of these enzyme activities can also be applied to patients treated with streptokinase. Moreover, the enzymes measured in the present study are all equally valid markers of myocardial injury
