Acute coronary syndromes (ACS) represent the clinical manifestations of sudden flow limiting coronary artery disease leading to acute myocardial ischemia or necrosis. Treatment of progressive coronary stenosis or acute thrombotic occlusion by means of percutaneous coronary intervention (PCI) with balloon dilatation and stent placement aims to reduce the risk of myocardial ischemia or necrosis by restoring coronary flow. But, being an invasive technique, it is associated with a periprocedural and also eventually long-term risk of complications. Pathological examination of atherosclerotic coronary arteries after PCI treatment has been shown to be very helpful in providing insights in this iatrogenic pathology. Importantly, the pathological substrate of the treated coronary artery segment in patients with ACS differs significantly from coronary artery segments in patients with stable coronary artery disease. Such studies have shown that besides the physical trauma induced by a balloon or a stent also the specific histomorphological and biological properties of the treated coronary plaques play an important role in the risk of PCI related vascular complications. Major complications, which are thrombosis and restenosis, have reduced significantly over the past years. Still, late stent thrombosis remains a small but clinically important problem after placement of drug eluting stents DES, mainly related to delayed in stent wound healing and early withdrawal of antiplatelet therapy. Moreover, restenosis remains a problem in the still large group of patients treated with bare metal stents (BMS) worldwide. Both in case of BMS and DES emerging evidence from recent histopathological studies on coronary resected stents shows that the outcome of PCI can be influenced by the occurrence of in stent neo- atherosclerosis, in DES more frequent than in BMS, which in turn may stimulate both thrombosis and restenosis on the very long term.