Primary percutaneous coronary intervention (PCI) is established as optimal therapy for patients with ST-elevation myocardial infarction (STEMI).¹ The goal of primary PCI is to achieve a thrombolysis in myocardial infarction (TIMI) 3 flow and also to restore adequate perfusion at the myocardial level. However, visible thrombus embolization to the distal circulation during primary PCI occurs in up to 14% of patients, and outcomes in these patients are compromised.² Furthermore, even in patients without such macroembolization, myocardial reperfusion is often suboptimal, w

B-type natriuretic peptide (BNP) and serum unbound free fatty acid (FFAu) are novel cardiac markers. BNP is a polypeptide secreted by the cardiac ventricles in response to volume and pressure overload. Measurement of BNP levels has demonstrated diagnostic value in heart failure and has evolved to be a powerful prognostic marker in acute coronary syndromes, stable coronary heart disease, diabetes and heart failure.^1–3 FFAu is a sensitive marker of myocardial ischemia.⁴ A previous study conducted prior to the era of routine coronary stenting demonstrated a rise in

Stent thrombosis (ST), while infrequent, is a serious complication of percutaneous coronary intervention (PCI) resulting in myocardial infarction (MI) or death.^1–4 While drug- eluting stents (DES) have reduced the rate of restenosis and target lesion revascularization by 50–70% as compared to baremetal stents (BMS), there have been some concerns regarding ST.^5,6,9–12 Systematic reviews of randomized trials revealed no overall differences relative to death with DES during longterm follow up to 5 years, but did show an increase in very late ST with DES.