This study examines the pathology of acute and chronic coronary stenting in humans, focusing on the morphological changes and inflammatory responses following stent placement. Histological analysis of 55 stents in 35 coronary vessels from 32 patients revealed that early after stent deployment (within 11 days), fibrin, platelets, and neutrophils were associated with stent struts. In stents implanted for ≤3 days, only 3% of struts in contact with fibrous plaque had >20 inflammatory cells, compared to 44% of struts embedded in a lipid core and 36% of struts in contact with damaged media. Neointimal growth was a key factor in long-term histological success, with increased neointimal growth correlating with increased stent size relative to the proximal reference lumen area. Neointimal thickness was greater for struts associated with medial damage than those in contact with plaque or intact media. Neointimal cell density in stented arteries was similar to that in unstented arteries that had undergone balloon angioplasty, with similar proteoglycan deposition. The study also found that medial injury and lipid core penetration by stent struts resulted in increased inflammation. Neointimal growth increased as the ratio of stent area to reference lumen area increased. Deployment strategies that reduce medial damage and avoid stent oversizing may lower the frequency of in-stent restenosis. The findings suggest that the morphology after coronary stenting demonstrates an early sequence of thrombus formation and acute inflammation, followed by neointimal growth. Medial injury and lipid core penetration by stent struts are associated with increased inflammation. Neointimal growth is influenced by the ratio of stent area to reference lumen area. The study is the first to compare whole arterial sections and show neointimal cell density and proteoglycan deposition in coronary stents similar to those in matched PTCA coronary vessels. The results indicate that stent deployment strategies that minimize arterial injury may be beneficial in reducing late neointimal growth. The study also highlights the importance of avoiding severe arterial injury during catheter-based interventions with stents to prevent in-stent restenosis.This study examines the pathology of acute and chronic coronary stenting in humans, focusing on the morphological changes and inflammatory responses following stent placement. Histological analysis of 55 stents in 35 coronary vessels from 32 patients revealed that early after stent deployment (within 11 days), fibrin, platelets, and neutrophils were associated with stent struts. In stents implanted for ≤3 days, only 3% of struts in contact with fibrous plaque had >20 inflammatory cells, compared to 44% of struts embedded in a lipid core and 36% of struts in contact with damaged media. Neointimal growth was a key factor in long-term histological success, with increased neointimal growth correlating with increased stent size relative to the proximal reference lumen area. Neointimal thickness was greater for struts associated with medial damage than those in contact with plaque or intact media. Neointimal cell density in stented arteries was similar to that in unstented arteries that had undergone balloon angioplasty, with similar proteoglycan deposition. The study also found that medial injury and lipid core penetration by stent struts resulted in increased inflammation. Neointimal growth increased as the ratio of stent area to reference lumen area increased. Deployment strategies that reduce medial damage and avoid stent oversizing may lower the frequency of in-stent restenosis. The findings suggest that the morphology after coronary stenting demonstrates an early sequence of thrombus formation and acute inflammation, followed by neointimal growth. Medial injury and lipid core penetration by stent struts are associated with increased inflammation. Neointimal growth is influenced by the ratio of stent area to reference lumen area. The study is the first to compare whole arterial sections and show neointimal cell density and proteoglycan deposition in coronary stents similar to those in matched PTCA coronary vessels. The results indicate that stent deployment strategies that minimize arterial injury may be beneficial in reducing late neointimal growth. The study also highlights the importance of avoiding severe arterial injury during catheter-based interventions with stents to prevent in-stent restenosis.