Cardiac allograft vasculopathy risk factors: Difference between revisions
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Non-immune risk factors include: | Non-immune risk factors include: | ||
* [[Hyperlipidemia]] | * [[Hyperlipidemia]] | ||
* [[Diabetes mellitus]] | * [[Diabetes mellitus]] | ||
* [[Hypertension]] | * [[Hypertension]] | ||
* [[Smoking]] | * [[Smoking]] | ||
* Older donor age | |||
* Male donor | |||
* Recepient age | * Recepient age | ||
* Recepient gender | * Recepient gender |
Revision as of 19:20, 27 July 2014
Cardiac allograft vasculopathy Microchapters |
Differentiating Cardiac allograft vasculopathy from other Diseases |
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Cardiac allograft vasculopathy risk factors On the Web |
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Risk calculators and risk factors for Cardiac allograft vasculopathy risk factors |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]; Raviteja Guddeti, M.B.B.S. [3]
Overview
Cardiac allograft vasculopathy (CAV) is characterized by concentric intimal proliferation leading to diffuse narrowing of the entire length of the epicardial vessel. Immune mediated processes are thought to be the biggest risk factors driving the process of graft vessel narrowing. However, traditional risk factors for coronary artery disease such as hyperlipidemia, diabetes mellitus, hypertension and smoking have been shown to play a considerable role in the pathogenesis of CAV.
Risk Factors
Few immune mediated risk factors reported include:
- Increased levels of B cell antibodies
- Increased levels of HLA-antibodies
- Acute cellular and humoral mediated rejection
- Sensitization to monoclonal antibody OKT3
- Cytomegalovirus infection
- Elevated soluble interleukin-2 receptor levels
Non-immune risk factors include:
- Hyperlipidemia
- Diabetes mellitus
- Hypertension
- Smoking
- Older donor age
- Male donor
- Recepient age
- Recepient gender
- Obesity
- Pretranplant diagnosis
- Donor ischemic time
LDL and triglycerides as risk factors for CAV have been studied more in depth. LDL oxidation leads to recruitment of macrophages and lymphocytes along with increased expression of HLA antigens and interleukin receptors on T cells. This further accelerates the process of vasculopathy.