Detecting acute coronary syndrome in the emergency department: the answer is in seeing the heart: why look further?The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.

医学 急诊科 急性冠脉综合征 医疗急救 心脏病学 心肌梗塞 护理部
作者
Roxy Senior,Houman Ashrafian
出处
期刊:European Heart Journal [Oxford University Press]
卷期号:26 (16): 1573-1575 被引量:8
标识
DOI:10.1093/eurheartj/ehi381
摘要

This editorial refers to ‘Regional left ventricular perfusion and function in patients presenting to the emergency department with chest pain and no ST-segment elevation’† by D. Rinkevich et al., on page 1606 The emergent assessment of chest pain continues to represent a major medical challenge. In the USA alone, 6 million patients annually present to emergency departments with chest pain. The time-honoured application of clinical assessment, electrocardiography, and markers of myocardial injury (e.g. troponins) definitively identify only 20–30% of patients with acute coronary syndrome (ACS); indeed, biochemical markers are frequently normal in the early hours of pain. Conversely, many admissions pending normal results are unnecessary and take much of the patient time and cause anxiety as well as costing billions of dollars. Worryingly, ∼5% of patients with ACS are discharged inadvertently, representing a source of significant mortality (∼25%) and litigation. Therefore, there is an urgent demand for effective risk stratification tools. Can pathophysiological principles help identify the ideal test? A direct relationship between myocardial blood flow (MBF) and regional function (RF) is well recognized in acute ischaemia; RF diminishes with diminishing MBF and at 25% of resting MBF, RF abates completely. Importantly, these RF abnormalities persist for hours even after reperfusion (myocardial stunning). Consequently, despite the lack of overt myocardial necrosis as evidenced by normal troponin levels, a significant risk of future events may exist in patients with myocardial stunning owing to flow-limiting coronary disease. In addition, when only ∼20% of the myocardium (especially endocardium) is infarcted, wall thickening is abolished; RF is therefore exquisitely sensitive to perfusion defects and precedes electrocardiographic or biochemical defects.1 As a tribute to the accuracy of … *Corresponding author. Tel: +44 208 869 2548; fax: +44 208 864 0075. E-mail address : roxy.senior{at}virgin.net
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