We read the article by Kurtul et al. The authors investigated the usefulness of platelet-to-lymphocyte ratio (PLR) in predicting angiographic no-reflow after primary percutaneous coronary intervention (PCI) in acute ST-elevation myocardial infarction (STEMI). We have some comments about the presented study.

PLR has recently emerged as a prognostic marker that integrates the predictive risk of these 2 parameters into 1. It gives an idea about both aggregation and inflammation pathways, and it may be more valuable than either platelet or lymphocyte counts alone in prediction of adverse cardiovascular events. As PLR is a derivation of routine complete blood count parameters, it does not require any additional expense and is a readily available marker. Additionally, neutrophil-to-lymphocyte ratio has been extensively researched in recent years, especially in cardiovascular diseases. In our previous study, high preprocedural neutrophil-to-lymphocyte ratio and PLR levels were shown to be significant and independent predictors of no-reflow in patients undergoing primary PCI.

There was no information in the study by Kurtul et al about the rates of predilatation and/or postdilatation during primary PCI. There are conflicting data about the role of predilatation and postdilatation during primary PCI on no-reflow development. The data from EUROTRANSFER (European Registry on Patients with ST-Elevation MI Transferred for Mechanical Reperfusion with a Special Focus on Upstream Use of Abciximab) registry showed a lower risk of no-reflow in patients presented with acute myocardial infarction and treated with direct stenting compared with conventional stenting (stent deployment after predilatation). Predilatation was reported to increase the risk of microvascular injury in the setting of acute myocardial infarction although final Thrombolysis In Myocardial Infarction 3 flow grade rates were comparable between direct stenting and conventional stenting techniques and with similar corrected Thrombolysis In Myocardial Infarction frame counts. Electrocardiographic analysis after reperfusion showed no ST-segment resolution in 20% and 38% of the patients after direct and conventional stenting, respectively (p = 0.01).

As the stent underexpansion is an important cause of stent thrombosis and restenosis after stent implantation, postdilatation is widely recommended. Aggressive postdilatation of the stent however may cause further distal embolization and microvascular injury, especially for patients presented with STEMI. In the study by Tasal et al, postinterventional angiographical parameters such as Thrombolysis In Myocardial Infarction flow, corrected Thrombolysis In Myocardial Infarction frame counts, and myocardial blush grade were not different between the groups who underwent postdilatation or not. The study conducted by Zhang et al revealed nonsignificantly higher no-reflow rates in the postdilatation group than in non–postdilatation group. The 1-year cumulative incidence of death, myocardial infarction, and death and/or myocardial infarction were significantly higher in patients with STEMI who underwent postdilatation compared with patients with STEMI not receiving postdilatation. Neither predilatation nor postdilatation had significant effect on no-reflow development in our study.