No-reflow and platelet reactivity in diabetic patients with ST-segment elevation myocardial infarction: is there a link?

Introduction

The no-reflow phenomenon in percutaneous coronary intervention (PCI) is defined classically as the absence of flow after restoration of arterial patency. Further research has shown that despite flow restoration in myocardial infarction (MI) there is still a considerable percentage of patients with a lack of perfusion at the level of the microvasculature caused by microvascular obstruction (MVO) [1]. This has a deleterious effect on outcomes and should be considered as a form of no-reflow [2]. It can be diagnosed with angiography or as the absence of ST-segment normalization in ECG after PCI, but the reference method for MVO diagnosis is contrast-enhanced cardiac magnetic resonance (CMR) [3]. Causes of MVO are thought to include peripheral embolism caused by debris originating in and flushed from the atherosclerotic plaque, ischemia/reperfusion injury, and individual predispositions such as diabetes [4]. Recently, increased platelet reactivity was proposed as one of the reasons for MVO occurrence [5–7]. Increased platelet reactivity is present in diabetes and together can increase MVO. Nevertheless, there is still a considerable lack of data regarding platelet reactivity and MVO assessed with the reference method of CMR in diabetic patients with ST-segment elevation MI (STEMI).

Aim

The aim of the study was to assess the link between platelet reactivity and the occurrence of MVO in diabetic patients with STEMI.

Material and methods

This is a sub-study of a larger series of patients included in the previously reported data [8]. In brief the previous study included patients with STEMI treated with PCI and diagnosed with diabetes before hospital admission. To have a closer look into MVO we included patients with Thrombolysis In Myocardial Infarction (TIMI) flow grade 3 after PCI and defined MVO when myocardial perfusion grade (MPG) assessed with angiography was 0–1 while normal microvascular flow was defined when MPG was 2 or 3 [1]. Study exclusion criteria were cardiogenic shock, platelet count below 100 000/m3 or above 450 000/m3, known allergy to acetylsalicylic acid or thienopyridine derivatives, and use of GP IIb/IIIa blockers during PCI. Patients included in the study were treated according to guidelines [9]. Antiplatelet treatment included a loading dose of 600 mg clopidogrel and a loading dose of 300 mg aspirin given by the paramedics before hospital admission. Blood for platelet reactivity was collected...


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