The American journal of medicine
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For the greater part of the 20th century, the pathophysiology of acute myocardial infarction regarding whether thrombosis was either present or primary was debated until 1973 when pathologists and clinicians met and by consensus, finally decided that the data supported that transmural infarction (what we now refer to as ST elevation myocardial infarction or STEMI) was caused by thrombus in the vessel supplying the infarcted territory. As the data for this consensus came from pathological analysis, it took another 7 years until angiographic and interventional data in humans with acute presentations of transmural infarction convincingly indicated that thrombus was indeed responsible. Subsequently, in patients presenting with either syndromes of unstable angina or nontransmural (later called non-ST elevation) myocardial infarction, it was established through angiographic and other interventional approaches that thrombus formation was also causative in a substantial proportion of these patients. This article reviews the history and this search for causation of myocardial infarction that now has resulted in present therapies that have saved innumerable lives over the last 30 to 40 years.
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Patients presenting to the emergency department with consideration of an acute coronary syndrome (ACS) are risk-stratified with sensitive troponin assays. Among many patients who present with symptoms other than chest pain, they are admitted for observation if the troponin assay is above the upper reference limit of that specific assay. ⋯ As such, the clinician is often confused about the optimal treatment at hospital discharge. More studies should address the value of specific known therapies in this cohort that have been shown to improve outcomes in patients with an acute coronary syndrome or type 1 myocardial infarction.