BACKGROUND: Neointimal formation can protect against thrombosis after sirolimus-eluting stent (SES) implantation; however, promoters of neointimal formation are unknown. METHODS: Six-month follow-up angioscopy was performed in 141 consecutive patients with SES implantation. All patients received aspirin (100 mg) and ticlopidine (200 mg) daily until angioscopy. We defined 2 grades of neointimal coverage as follows: insufficient coverage including no or partial neointimal coverage of stent struts, and sufficient coverage. The possible promoters of neointimal formation that were evaluated in this study were the condition of coronary artery disease (stable angina or acute coronary syndrome); angioscopic markers, including visible thrombus and plaque color (white or yellow); serum markers, including low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, fasting blood glucose, hemoglobin A(1c), high-sensitive C-reactive protein, and fibrinogen; blood pressure and smoking; intervention markers, including stent size and length and intravascular ultrasound measurements; and medication, including statins, anticoagulants, angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers, calcium antagonists, and β-blockers. RESULTS: Univariate analysis revealed that high-sensitive C-reactive protein, plaque color, and the condition of coronary artery disease were significantly correlated with the grade of neointimal coverage. Multivariate analysis using these 3 parameters revealed that only acute coronary syndrome (vulnerable disease) significantly promoted neointimal coverage. CONCLUSION: Vulnerable disease may promote neointimal coverage after SES implantation. 2010 Mosby, Inc. All rights reserved.
BACKGROUND: Neointimal formation can protect against thrombosis after sirolimus-eluting stent (SES) implantation; however, promoters of neointimal formation are unknown. METHODS: Six-month follow-up angioscopy was performed in 141 consecutive patients with SES implantation. All patients received aspirin (100 mg) and ticlopidine (200 mg) daily until angioscopy. We defined 2 grades of neointimal coverage as follows: insufficient coverage including no or partial neointimal coverage of stent struts, and sufficient coverage. The possible promoters of neointimal formation that were evaluated in this study were the condition of coronary artery disease (stable angina or acute coronary syndrome); angioscopic markers, including visible thrombus and plaque color (white or yellow); serum markers, including low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, fasting blood glucose, hemoglobin A(1c), high-sensitive C-reactive protein, and fibrinogen; blood pressure and smoking; intervention markers, including stent size and length and intravascular ultrasound measurements; and medication, including statins, anticoagulants, angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers, calcium antagonists, and β-blockers. RESULTS: Univariate analysis revealed that high-sensitive C-reactive protein, plaque color, and the condition of coronary artery disease were significantly correlated with the grade of neointimal coverage. Multivariate analysis using these 3 parameters revealed that only acute coronary syndrome (vulnerable disease) significantly promoted neointimal coverage. CONCLUSION: Vulnerable disease may promote neointimal coverage after SES implantation. 2010 Mosby, Inc. All rights reserved.