Percutaneous coronary intervention (PCI) is associated with a 15% to 35% incidence of periprocedural myocardial injury (PMI). Its spectrum ranges from obvious clinical myocardial infarction to subtle myocardial injury manifested by mild rises in cardiac enzymes. Even in the latter case, the resulting myocardial damage is clinically important, as multiple studies have consistently demonstrated that PMI is associated with increased long-term mortality with a graded risk related to the extent of creatine kinase-MB or cardiac troponin elevation. Despite extensive basic and clinical research and multiple therapeutic approaches, its incidence has not substantially decreased over the last 2 decades. Two patterns of PMI have been recognized by magnetic resonance imaging. Type I is near the intervention site consequent to side branch occlusion, and type II is in the downstream territory of the treated artery where perfusion is compromised mainly due to structural and functional mi-crovascular dysfunction (1). PCI can be considered as an iatrogenic form of plaque rupture. It magnifies underlying or pre-existing microvascular disorders. It is thus not surprising that patients with pre-procedural abnormal coronary flow (2), high cardiovascular risk profiles, or high systemic inflammation markers, such as high sensitivity C-reactive protein, are most likely to have PMI and worse long-term outcomes (3).