2006
DOI: 10.1016/j.jacc.2005.10.073
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Coronary Endothelial Vasomotor Function and Vascular Remodeling in Heart Transplant Recipients Randomized for Tacrolimus or Cyclosporine Immunosuppression

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Cited by 55 publications
(36 citation statements)
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“…Cyclosporin A can increase LDL cholesterol levels and induce glucose intolerance, both of which can cause atherosclerosis (20). In addition, cyclosporin A has been shown to be associated with endotheliitis (21), increased circulating levels of endothelin 1, and coronary microvascular dysfunction (22). In the present study, 10 of the SLE patients (53%) were being treated with immunosuppressive drugs (5 with azathioprine and 5 with cyclosporin A) in combination with corticosteroids.…”
Section: Discussionmentioning
confidence: 68%
“…Cyclosporin A can increase LDL cholesterol levels and induce glucose intolerance, both of which can cause atherosclerosis (20). In addition, cyclosporin A has been shown to be associated with endotheliitis (21), increased circulating levels of endothelin 1, and coronary microvascular dysfunction (22). In the present study, 10 of the SLE patients (53%) were being treated with immunosuppressive drugs (5 with azathioprine and 5 with cyclosporin A) in combination with corticosteroids.…”
Section: Discussionmentioning
confidence: 68%
“…In our population, the mean extension of the lesions assessed on IVUS was 14.039 mm, that is, more diffuse lesions than the focal pattern of the lesions associated with atherosclerosis. Studies have suggested that the site in which a concentric atherosclerotic lesion already exists differ from those where lesions associated with CAV occur [21][22][23][24][25][26][27][28] , which does not prevent the existence of both in the same vessel. This could justify the finding of extensive and proximal lesions in our population.…”
Section: Chart 1 -Stanford Classification Of Intracoronary Lesions Asmentioning
confidence: 98%
“…This effect could ultimately increase local cardiac inflammation and consequently facilitate the development of CAV. Although the function and effect of CNI-induced endothelial dysfunction in the pathogenesis of CAV is poorly understood, it has been demonstrated that both CsA and TAC induce vascular oxidative stress, increased endothelin-1 (ET-1) release, and contribute to the dysregulation of endothelial nitric oxide synthase (NOS) in the kidney [44,[62][63][64] . Indeed CNI-induced endothelial dysfunction includes the attenuation of the endothelium to release NO [65] , a physiologically relevant mechanism because decreased NO bioavailability is related to the production of reactive oxygen species (ROS) and thus oxidative stress [65] .…”
Section: Impact Of Immunosuppressive Regimens On Cavmentioning
confidence: 99%