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- W2082229834 abstract "Orthotopic heart transplantation (OHT) is a life-saving treatment for end-stage cardiac disease. Short-term results are improving, but long-term survival is limited by an aggressive form of atherosclerotic disease termed transplant coronary artery disease (TxCAD). In patients surviving more than 1 year after transplantation, TxCAD remains the primary cause of death. The disease tends to be a diffuse, panarterial process, with progressive, concentric obliteration of both small and large coronary vessels. The cause is multifactorial, and several risk factors have been implicated. Current evidence shows that histocompatibility mismatch and acute cellular rejection have a role in the development of TxCAD. Also non-immunologic factors such as donor-related factors (age, sex, pre-existing coronary disease, ischemic time), recipient-related factors (age, sex, and obesity), cytomegalovirus infection, hypertension, metabolic derangements (diabetes and increased cholesterol and triglyceride levels), and tobacco use have been associated with TxCAD. Homocysteine (Hcy) has been implicated in the development of TxCAD; however, the evidence to date is largely retrospective (Table I). Hyperhomocysteinemia (HHcy) is almost universal after OHT, and strong evidence links HHcy to vascular dysfunction. This article summarizes the current information available regarding the pathogenesis of the HHcy-induced vascular dysfunction and how these alterations can further explain the association between HHcy and TxCAD." @default.
- W2082229834 created "2016-06-24" @default.
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- W2082229834 date "2003-10-01" @default.
- W2082229834 modified "2023-09-26" @default.
- W2082229834 title "Hyperhomocysteinemia in heart transplantation: from bench to bedside" @default.
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- W2082229834 doi "https://doi.org/10.1016/s1053-2498(02)01153-1" @default.
- W2082229834 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14550816" @default.
- W2082229834 hasPublicationYear "2003" @default.
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