Variations of segmental endothelium-dependent and endothelium-independent vasomotor tone after cardiac transplantation (qualitative changes in endothelial function)

Weis, Michael; Peter-Wolfa, Wolf; Mazzilli, Nora; Olbrich, Hans-Georg; C, Schacherer; Wiemer, J.; Burger, Wolfram; Hartmann, Andreas

doi:10.1016/s0002-8703(97)70139-x

Cited by 16 publications

(12 citation statements)

References 27 publications

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“…88 Notably, endothelial function in any one subject may not be diffusely disturbed after cardiac transplantation. 89 The existence of coronary segments with functioning endothelium indicates that the coronary endothelium is not globally impaired in all cardiac transplant recipients and that endothelial function may not be irreversibly damaged. Indeed, Drexler et al have reported that intravenous administration of L-arginine acutely improves endothelial vasodilator function of coronary conduit vessels if given at an early stage of AV.…”

Section: Role Of Endothelium In Cav and Atherosclerosismentioning

confidence: 99%

Allograft Vasculopathy Versus Atherosclerosis

Rahmani¹,

Cruz²,

Granville³

et al. 2006

Circulation Research

297

215

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Abstract-Over the last 4 decades, heart transplantation (HTx) has evolved as a mainstream therapy for heart failure.Approximately half of patients needing HTx have organ failure consequent to atherosclerosis. Despite advances in immunosuppressive drugs, long-term success of HTx is limited by the development of a particular type of coronary atherosclerosis, referred to as cardiac allograft vasculopathy (CAV). Although the exact pathogenesis of CAV remains to be established, there is strong evidence that CAV involves immunologic mechanisms operating in a milieu of nonimmunologic risk factors. The immunologic events constitute the principal initiating stimuli, resulting in endothelial injury and dysfunction, altered endothelial permeability, with consequent myointimal hyperplasia and extracellular matrix synthesis. Lipid accumulation in allograft arteries is prominent, with lipoprotein entrapment in the subendothelial tissue, through interactions with proteoglycans. The apparent endothelial "intactness" in human coronary arteries of the transplanted heart suggest that permeability and function of the endothelial barrier altered. Various insults to the vascular bed result in vascular smooth muscle cell (SMC) activation. Activated SMCs migrate from the media into the intima, proliferate, and elaborate cytokines and extracellular matrix proteins, resulting in luminal narrowing and impaired vascular function. Arteriosclerosis is a broad term that is used to encompass all diseases that lead to arterial hardening, including native atherosclerosis, postangioplasty restenosis, vein bypass graft occlusion, and CAV. These diseases exhibit many similarities; however, they are distinct from one another in numerous ways as well. The present review summarizes the current understanding of the risk factors and the pathophysiological similarities and differences between CAV and atherosclerosis. (Circ Res. 2006;99:801-815.)

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Section: Role Of Endothelium In Cav and Atherosclerosismentioning

confidence: 99%

Allograft Vasculopathy Versus Atherosclerosis

Rahmani¹,

Cruz²,

Granville³

et al. 2006

Circulation Research

297

215

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“…9,15,29 Endothelial function may not be uniformly disturbed after cardiac transplantation. 30 Different vascular remodeling patterns could be observed in the same artery due to variable responses of the local vessel and the interaction of systemic immunologic processes with pre-existing pathology. 29 The randomized trial that formed the basis of this IVUS core laboratory data showed that MMF, an immunosuppressive agent that inhibits cellular proliferation, was more efficacious than Aza in reducing rejection episodes and improving survival among heart transplant recipients.…”

Section: Discussionmentioning

confidence: 99%

Vascular Remodeling 1 Year After Cardiac Transplantation

Tanaka

Chhabra

et al. 2007

The Journal of Heart and Lung Transplantation

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Background:The belief that vascular remodeling and intimal hyperplasia are causes of luminal narrowing in cardiac allograft vasculopathy (CAV) is controversial. This study evaluated the relationship of vascular remodeling and intimal hyperplasia to luminal narrowing 1 year after orthotopic heart transplantation. Methods:Intravascular ultrasound imaging was performed on 190 cardiac transplant recipients at baseline and again 1 year after transplantation as part of a randomized trial of mycophenolate mofetil (MMF) and azathioprine (Aza). Studies 1 year apart were matched at 625 sites. All sites were classified into positive, non-significant and negative remodeling patterns, depending on a change of Ϯ10% in external elastic membrane area. Of the 190 patients, 99 were randomized to receive MMF, and 91 to receive Aza. Results:A total of 625 sites were observed. Of these, 52% had no remodeling, 25%

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“…Endothelial dysfunction of the epicardial arteries can be defined as a paradoxical vasoconstriction of >10% in response to intracoronary injections of acetylcholine and this may be manifested very early status post transplant. Endothelium dependent flow responses declined significantly in a 3 year follow-up study [9][10][11][12]. Homeostatic balance between endothelial vasodilators and vasoconstrictors contributes to adverse changes in vascular structure and reactivity.…”

Section: Endothelial Cell Dysfunction and Molecular Aspects Of Oxidatmentioning

confidence: 99%

Role of Oxidative Stress in Cardiac Allograft Vasculopathy

Nair¹,

Góngora²,

Reynolds³

2013

OJOTS

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Cardiac Allograft Vasculopathy, an accelerated form of arterial occlusive disease, is the major cause of death in the long-term after heart transplantation. Multiple factors influence the initiation and progression of CAV. These include ischemia-reperfusion, dyslipidemia, insulin resistance, and hypertension due to the use of immunosuppressive agents, the direct effects of immunosuppressive agents on endothelial function, and viruses (CMV). Impaired endothelial function reflects abnormalities in the production or activity of several vasoactive substances. Disruption of the nitric oxide synthase (NOS) pathway leads to changes in vascular reactivity, structure, and interaction with circulating blood components. Since endothelium-derived nitric oxide (NO) suppresses vascular cell proliferation and vascular inflammation, a deficit in vascular NO facilitates development of CAV. The link between oxidative stress and CAV largely exists in the balance between free radical superoxide   2 O  generation and NO production. This review focuses on identifying the oxidative stress factors affecting CAV.

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Variations of segmental endothelium-dependent and endothelium-independent vasomotor tone after cardiac transplantation (qualitative changes in endothelial function)

Cited by 16 publications

References 27 publications

Allograft Vasculopathy Versus Atherosclerosis

Allograft Vasculopathy Versus Atherosclerosis

Vascular Remodeling 1 Year After Cardiac Transplantation

Role of Oxidative Stress in Cardiac Allograft Vasculopathy

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