Early constriction or expansion of the external elastic membrane area determines the late remodeling response and cumulative lumen loss in transplant vasculopathy: an intravascular ultrasound study with 4-year follow-up

Tsutsui, Hiroshi; Schoenhagen, Paul; Ziada, Khaled M.; Crowe, Tim; Klingensmith, Jon D.; Vince, D. Geoffrey; Bott‐Silverman, Corinne; Starling, Randall; Hobbs, Robert E.; Young, James B.; Nissen, Steven E.; Tuzcu, E. Murat

doi:10.1016/s1053-2498(02)01228-7

Cited by 18 publications

(18 citation statements)

References 15 publications

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“…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. 19 The present study is an expansion of the IVUS results from that clinical trial.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the discordant remodeling patterns within the same artery seen in 76% of the arteries is in agreement with previous studies. 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.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

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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“…The atherosclerotic lesions seen in the allografts can be either donor derived lesions or de novo lesions developed after transplantation. Traditional CAD is usually characterized by focal eccentric hypertrophy and formation of fibrofatty plaques with disruption of the elastic lamina [21,25,27]. In contrast, in CAV, histologically the elastic lamina is primarily intact, and narrowing of the vasculature is circumferential rather than eccentric [10,[27][28][29][30][31].…”

Section: Definition and Diagnosismentioning

confidence: 99%

“…Traditional CAD is usually characterized by focal eccentric hypertrophy and formation of fibrofatty plaques with disruption of the elastic lamina [21,25,27]. In contrast, in CAV, histologically the elastic lamina is primarily intact, and narrowing of the vasculature is circumferential rather than eccentric [10,[27][28][29][30][31]. Fibrofatty plaques could be seen in cardiac allografts, however, characteristic lesion of CAV is fibrointimal hyperplasia of the vessel wall leading to insidious narrowing of the vasculature of the allograft [10,[27][28][29][30][31].…”

Section: Definition and Diagnosismentioning

confidence: 99%

“…In contrast, in CAV, histologically the elastic lamina is primarily intact, and narrowing of the vasculature is circumferential rather than eccentric [10,[27][28][29][30][31]. Fibrofatty plaques could be seen in cardiac allografts, however, characteristic lesion of CAV is fibrointimal hyperplasia of the vessel wall leading to insidious narrowing of the vasculature of the allograft [10,[27][28][29][30][31]. While CAD typically takes several years to develop and propagate to clinically significant disease, CAV is rapidly progressive and may become clinically significant in weeks to months [10,32,33].…”

Section: Definition and Diagnosismentioning

confidence: 99%

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Cardiac Allograft Vasculopathy: A Review of Risk Factors and Pathogenesis

Munagala¹,

Phancao²

2018

obm.transplant

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Heart transplant remains the gold standard therapy for patients with end stage heart disease and offers improved survival and quality of life. Significant progress has been achieved in improving one-year mortality after heart transplantation. Nonetheless, longterm graft survival has not changed significantly over the past few decades. Long term survival of heart transplant recipients is limited by chronic rejection, cardiac allograft vasculopathy (CAV), and malignancy. CAV is a major contributor for graft failure and mortality after the first year of in heart transplant recipients. CAV is a proliferative vasculopathy characterized by diffuse myointimal hyperplasia and progressive narrowing of the graft vessels. Both immune dependent and independent factors have been shown to contribute to the pathogenesis of CAV. Understanding these risk factors is essential in developing preventative and therapeutic strategies. Angiography with Intravascular ultrasound has become the key diagnostic tool in the early detection of CAV as well as prognostication. Echocardiographic assessment of allograft function in conjunction with coronary angiographic findings are used in assessing the severity of CAV. Adjustment of immunosuppression and statins remain the initial steps in the management of CAV. Retransplantation is the definitive treatment for severe CAV, however, the paucity of organs along with increased mortality associated with retransplantation makes it a less desirable option. Remarkable progress has been achieved in the understanding of pathogenesis, risk factors for CAV and plaque morphology. Nevertheless, significant knowledge gaps persist in scientific understanding of risk factors, pathogenesis, prevention and treatment of CAV. Further research is warranted to fill these gaps, develop diagnostic modalities to facilitate early detection of CAV, and management strategies to Improve graft tolerance and immune modulation. This review focuses on summarizing the pathogenesis and risk factors for CAV.

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