Intracoronary Adenosine versus Intravenous Adenosine during Primary PCI for ST-Elevation Myocardial Infarction: Which One Offers Better Outcomes in terms of Microvascular Obstruction?
Aims. Previous studies have suggested that intravenous administration of adenosine improves myocardial reperfusion and reduces infarct size in ST-elevation myocardial infarction (STEMI) patients. Intracoronary administration of adenosine has shown conflicting results. Methods. In this retrospective, single-centre, blinded clinical study, we assessed whether selective intracoronary administration of adenosine distal to the occlusion site immediately before initial balloon inflation reduces microvascular obstruction (MVO) as assessed with cardiac magnetic resonance imaging (MRI). Using contrast-enhanced sequences, microvascular obstruction (MVO) was calculated. We found 81 patients presenting with STEMI within 12？h from symptom onset who were eligible for the study. In 80/81 (100%) patients receiving the study drug, MRI was performed on Day 1 after primary angioplasty. Results. The prevalence of MVO was reduced in the patients treated with intracoronary adenosine, (45%) compared to 85% of patients who were administered intravenous adenosine ( ). We found that the size of MVO in patients receiving intracoronary adenosine was significantly reduced compared to 0.91？g in the intravenous-treated group ( ). There was no statistically significant difference in TIMI flow and clinical outcomes after primary PCI. Conclusion. We found significant evidence that selective high-dose intracoronary administration of adenosine distal to the occlusion site of the culprit lesion in STEMI patients results in a decrease in microvascular obstruction. 1. Introduction The concept of “no reflow” refers to a state of myocardial tissue hypoperfusion in the presence of a nonoccluded epicardial coronary artery. The underlying cause of no reflow is microvascular obstruction, which may be produced by various mechanisms [1, 2]. “Reperfusion no reflow” [2] occurs after primary percutaneous coronary intervention (PCI) for reperfusion of an infarct artery in the setting of acute myocardial infarction (AMI) and may be asymptomatic or may present clinically with continued chest pain and ST-segment elevation [3]. Reperfusion no reflow is an independent predictor of adverse clinical outcome after AMI, regardless of infarct size. Despite successful recanalization, perfusion of the ischaemic myocardium is either unrestored or incompletely restored in up to 30% of patients as a result of microvascular obstruction (MVO) [4], which is associated with higher incidence of left ventricular (LV) dysfunction, complications, and death. Multiple therapies [5] for no reflow have been tested in animals and
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