Page 136 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Chapter 8
Introduction
It is well recognised that even after rapid and successful revascularisation of ST- segment elevation myocardial infarction (STEMI), myocardial tissue perfusion remains compromised in 30–40% of patients despite restored epicardial patency.1,2 This phenomenon is attributed to microvascular dysfunction in the setting of acute STEMI,3 which is observed in both the perfusion territory of the culprit artery, and in non-ischaemic regions remote from the infarcted myocardial tissue.4 Whereas culprit vessel flow abnormalities have been ascribed to numerous pathophysiological mechanisms, it has partly been ascribed to metabolic consequences of the acute ischemic event.5,6
Major stress-related metabolic changes occur during the early hours of STEMI, which include the release of stress hormones such as noradrenaline and cortisol, increased concentration of free fatty acids, and the occurrence of glucose intolerance.7 As a result, elevated glucose levels are frequently observed in (non-diabetic) STEMI patients, which have been associated with an increased risk of in-hospital mortality, congestive heart failure and cardiogenic shock in patients with and without diabetes.8,9 Notably, in patients with STEMI, hyperglycaemia is associated with the no-reflow phenomenon in the culprit vessel, postulated to be a proxy of microvascular dysfunction.10 It suggests that the acute metabolic changes in STEMI may contribute to microvascular dysfunction in this setting through alterations in glucose homeostasis.
The aim of this study was to assess the relationship between admission glucose levels and microvascular function in non-diabetic patients with first anterior- wall STEMI.
Methods
A total of 100 consecutive patients with a first anterior-wall STEMI treated by primary percutaneous coronary intervention (PPCI) were enrolled. The initial results were reported previously.4,11 STEMI was defined as chest pain lasting >30 minutes in the presence of persistent ST-segment elevation in ≥2 precordial leads. PPCI was performed within 6 hours after onset of symptoms according
134