Long-Term Outcomes of Heart Transplantation Recipients With Transplant Coronary Artery Disease Who Develop In-Stent Restenosis After Percutaneous Coronary Intervention

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• 作者：Michael S. Lee ; MD^a ; ^{mslee@mednet.ucla.edu} ; Richard K. Cheng ; MD^a ; David E. Kandzari ; MD^b ; Ajay J. Kirtane ; MD ; SM^c
• 刊名：The American Journal of Cardiology
• 出版年：2012
• 期刊代码：5_00029149
• 类别：med
• 出版时间：15 June, 2012
• 卷：109
• 期：12
• 页码：1729-1732
• 文件大小：488 K

摘要

This retrospective study assessed long-term clinical outcomes of patients with orthotopic heart transplantation (OHT) and transplant coronary artery disease (TCAD) who developed in-stent restenosis (ISR) after percutaneous coronary intervention (PCI). TCAD is a major cause of morbidity and mortality after the first year after OHT. Description of outcomes in patients with ISR after revascularization for TCAD is limited. One hundred five patients underwent PCI with bare-metal stents or drug-eluting stents at the UCLA Medical Center from 1995 throughout 2009, of whom 83 patients (79.0%) underwent repeat angiography for clinical symptoms or surveillance. The primary end point was the composite of death, myocardial infarction, or repeat OHT. ISR occurred in 26 patients (31.3%) who underwent follow-up angiography. Initial treatment strategies for the 26 patients with ISR were target vessel revascularization in 19 (73.1%), repeat OHT in 3 (11.5%), and medical therapy in only 4 (15.4%). At 7 years freedom from the primary end point was lower in patients with ISR compared to patients without ISR (27.9%vs 63.2%, p = 0.006, log-rank test) primarily driven by a lower survival rate in patients with ISR (38.5%vs 84.2%, p <0.001, log-rank test). Although numerically smaller in patients with ISR, there were no statistically significant differences in freedom from myocardial infarction (80.8%vs 91.2%, log-rank p = 0.18) and freedom from repeat OHT (73.1%vs 84%, p = 0.22, long-rank test). In conclusion, patients with OHT who develop ISR after PCI have poor long-term prognosis. Improvements in prevention and treatment of TCAD such as increased pharmacotherapy are needed.