Longitudinal study of vascular remodeling in coronary arteries after heart transplantation

Kobashigawa, Jon A.; Wener, Lianne S.; Johnson, Jessica; Currier, Jesse W.; Yeatman, Lawrence A.; Cassem, J. D.; Tobis, Jonathan M.

doi:10.1016/s1053-2498(00)00100-5

Cited by 54 publications

(39 citation statements)

References 12 publications

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“…4 -6 IVUS imaging quantifies both intimal thickening and changes in external elastic membrane (EEM) area (arterial remodeling) in transplant CAD, and several studies have emphasized that lumen loss is caused not only by intimal thickening but also by changes in EEM area. [7][8][9][10] At present, there are no long-term, systematic follow-up data regarding the relative importance of intimal thickening and EEM area changes in transplant CAD.…”

mentioning

confidence: 99%

Lumen Loss in Transplant Coronary Artery Disease Is a Biphasic Process Involving Early Intimal Thickening and Late Constrictive Remodeling

et al. 2001

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Background-Coronary artery disease is the major cause of late cardiac allograft failure. However, few data exist regarding the natural history of changes in intimal and external elastic membrane (EEM) areas after heart transplantation. Methods and Results-In 38 transplant recipients, serial intravascular ultrasound examinations were performed 3.7Ϯ2.2 weeks after transplantation and annually thereafter for 5 years. In 59 coronary arteries, we compared 135 matched segments among serial studies. In each segment, intravascular ultrasound images were digitized at 1-mm intervals, and mean values of EEM and lumen and intimal areas were analyzed. In the first year after transplantation, the intimal area increased significantly from 1.8Ϯ1.6 to 3.0Ϯ2.1 mm 2 (PϽ0.001). Subsequently, the annual increase in intimal area decreased. EEM area did not change during the first year; however, between years 1 and 3, significant expansion of EEM area occurred (15.4Ϯ4.6 to 17.2Ϯ5.4 mm

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mentioning

confidence: 99%

Lumen Loss in Transplant Coronary Artery Disease Is a Biphasic Process Involving Early Intimal Thickening and Late Constrictive Remodeling

et al. 2001

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“…[21][22][23] This compensatory remodeling is generally inadequate to compensate for the effects of plaque growth in recipients. 12,14 The ability to undergo compensatory vessel enlargement in response to plaque formation is dependent on intact endothelial function. 24 Coronary endothelial dysfunction has been found in the early post-transplantation period before the development of intimal thickening.…”

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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“…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: 95%

“…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%

“…CAV is an accelerated form of coronary vascular disease seen in the heart transplant recipients characterized by neo-intimal hyperplasia and fibrosis of graft vasculature and microvascular occlusion while sparing the recipient's native vasculature [27][28][29][30][31][32][33][34]. Immune mediated factors play a dominant role in the initiation and propagation of CAV [35][36][37].…”

Section: Immunobiology and Pathogenesis Of Coronary Allograft Vasculomentioning

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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Longitudinal study of vascular remodeling in coronary arteries after heart transplantation

Cited by 54 publications

References 12 publications

Lumen Loss in Transplant Coronary Artery Disease Is a Biphasic Process Involving Early Intimal Thickening and Late Constrictive Remodeling

Lumen Loss in Transplant Coronary Artery Disease Is a Biphasic Process Involving Early Intimal Thickening and Late Constrictive Remodeling

Vascular Remodeling 1 Year After Cardiac Transplantation

Cardiac Allograft Vasculopathy: A Review of Risk Factors and Pathogenesis

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