Cardiac allograft vasculopathy pathophysiology: Difference between revisions
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There may also be associated mural thrombi which may lead to acute myocardial infarction. Early clots are platelet rich which may later be replaced by organized thrombus rich in fibrin. Increased platelet activation with expression of surface membrane glycoproteins has been linked to acclerated progression of CAV. | There may also be associated mural thrombi which may lead to acute myocardial infarction. Early clots are platelet rich which may later be replaced by organized thrombus rich in fibrin. Increased platelet activation with expression of surface membrane glycoproteins has been linked to acclerated progression of CAV. | ||
Histologically, the immunological and non-immunological factors cause sub-endothelial inflammation resulting in migration of [[lymphocytes]] ([[T cells]] especially), proliferation of [[smooth muscle cell]]s, formation of lipid laden foam cells and [[fibrosis]]. This further accelerates the process of endothelial dysfunction. The end result is progressive luminal compromise, reduced coronary blood flow and vasodilatory capacity leading to ischemia and chronic ventricular dysfunction. | Histologically, the immunological and non-immunological factors cause sub-endothelial inflammation resulting in migration of [[lymphocytes]] ([[T cells]] especially), proliferation of [[smooth muscle cell]]s, formation of lipid laden foam cells and [[fibrosis]]. This further accelerates the process of endothelial dysfunction. The end result is progressive luminal compromise, reduced coronary blood flow and vasodilatory capacity leading to ischemia and chronic ventricular dysfunction. | ||
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{{Family tree| | | |A01| | | |A01=Immunologic and non-immunologic risk factors}} | |||
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{{Family tree| | | |B01| | | |B01=Persistent enthothelial injury and dysfunction}} | |||
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{{Family tree| | | |C01| | | |C01=Subendothelial accumulation of lymtphocytes, myointimal proliferation, formation of foam cells and fibrosis}} | |||
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{{Family tree| | | |D01| | | |D01=Concentric intimal hyperplasia and luminal narrowing}} | |||
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{{Family tree| | | |E01| | | |E01=Decreased coronary blood flow and reduced vasodilatory capacity}} | |||
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{{Family tree| | | |F01| | | |F01=Myocardial ischemia and ventricular dysfunction}} | |||
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===Pathogenesis=== | ===Pathogenesis=== | ||
Revision as of 17:00, 27 July 2014
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Cardiac allograft vasculopathy Microchapters |
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Differentiating Cardiac allograft vasculopathy from other Diseases |
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Diagnosis |
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Cardiac allograft vasculopathy pathophysiology On the Web |
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Directions to Hospitals Treating Cardiac allograft vasculopathy |
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Risk calculators and risk factors for Cardiac allograft vasculopathy pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
CAV is a fibro-proliferative disorder of the coronary arteries of cardiac allografts. It is characterized by longitudinal concentric intraluminal narrowing secondary to intimal proliferation in epicardial coronary arteries. There is also concentric medial hyperplasia in the myocardial microvasculature. In contrast, epicardial atherosclerotic process is non-circumferential, focal and localized to epicardial vessels.
Pathophysiology
Pathology
Serial intravascular ultrasounds have demonstrated that majority of the intraluminal narrowing occurs in the first year after transplant. In the initial stages, there is expansion of the external elastic lamina and subsequently constriction of this layer leads to intra-luminal narrowing. There may also be associated mural thrombi which may lead to acute myocardial infarction. Early clots are platelet rich which may later be replaced by organized thrombus rich in fibrin. Increased platelet activation with expression of surface membrane glycoproteins has been linked to acclerated progression of CAV.
Histologically, the immunological and non-immunological factors cause sub-endothelial inflammation resulting in migration of lymphocytes (T cells especially), proliferation of smooth muscle cells, formation of lipid laden foam cells and fibrosis. This further accelerates the process of endothelial dysfunction. The end result is progressive luminal compromise, reduced coronary blood flow and vasodilatory capacity leading to ischemia and chronic ventricular dysfunction.
| Immunologic and non-immunologic risk factors | |||||||||||||||||
| Persistent enthothelial injury and dysfunction | |||||||||||||||||
| Subendothelial accumulation of lymtphocytes, myointimal proliferation, formation of foam cells and fibrosis | |||||||||||||||||
| Concentric intimal hyperplasia and luminal narrowing | |||||||||||||||||
| Decreased coronary blood flow and reduced vasodilatory capacity | |||||||||||||||||
| Myocardial ischemia and ventricular dysfunction | |||||||||||||||||
Pathogenesis
The pathogenesis of CAV appears to multifactorial with immunological and non-immunological factors both contributing to the process. Predominant factors include donor specific HLA antibodies, cellular mediated injury, cytomegalovirus infection and hypercholesterolemia. Immunological insult is the most accepted theory owing to the fact that CAV develops in donor arteries only.
Acute phase reactants may be elevated and is thought to be a marker of progression of CAV.
1) HLA mismatch: Studies have reported a higher incidence of CAV in recipients with HLA mismatching. HLA-DR and HLA-A mismatches have been more strongly associated with occurrence of CAV.