Cardiac allograft vasculopathy pathophysiology: Difference between revisions
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Serial intra-vascular 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. | Serial intra-vascular 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. | 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. | |||
===Pathogenesis=== | ===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. | 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. | Acute phase reactants may be elevated and is thought to be a marker of progression of CAV. | ||
Revision as of 15:14, 27 July 2014
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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.
Pathophysilogy
Pathology
CAV 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.
Serial intra-vascular 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.
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.