Virtual Histology Intravascular Ultrasound Assessment of Cardiac Allograft Vasculopathy From 1 to 20 Years After Heart Transplantation

Hernández, José M. de la Torre; Prada, José Antonio Vázquez de; Burgos, Virginia; Laso, Fermín Sáinz; Valls, Mónica Fernández; Vílchez, Francisco González; Llano, Miguel; Ruano, Javier; Zueco, Javier; Colman, Thierry; Durán, Rafael

doi:10.1016/j.healun.2008.11.915

Cited by 46 publications

(7 citation statements)

References 12 publications

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“…In the heart, TV particularly affects the epicardial and intramyocardial arteries. The vascular lesions increase in area of the necrotic core, calcification, plaque area and burden with progression exhibit migration of SMC into the intima and neointimal thickening which reults in vessel occlusion (3). Renal arteriosclerosis results in inflammatory cell infiltration and a fibrous thickening of the vascular intima due to myofibroblast proliferation (4).…”

Section: Introductionmentioning

confidence: 99%

The link between major histocompatibility complex antibodies and cell proliferation

Valenzuela

Reed

2011

Transplantation Reviews

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Experimental evidence indicates that donor specific antibodies targeting MHC class I and class II molecules can elicit the key features of transplant vasculopathy by acting on the graft vasculature in three ways: directly activating proliferative, pro-survival, and migratory signaling in the target endothelial and smooth muscle cells; increasing expression of mitogenic factors in vascular endothelial cells, creating a potential proliferative autocrine loop; and promoting recruitment of inflammatory cells, which produce mitogenic factors and elicit chronic inflammation, proliferation, and fibrosis. Here we review the experimental literature showing the complement and Fc-independent effects of MHC class I and II antibodies on graft vascular cells which may directly contribute to the proliferative aspect of transplant vasculopathy.

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Section: Introductionmentioning

confidence: 99%

The link between major histocompatibility complex antibodies and cell proliferation

Valenzuela

Reed

2011

Transplantation Reviews

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“…CAC estimates atherosclerotic plaque burden by assessing the calcified portion of coronary plaque; however, it may not detect soft plaque or intimal thickening without calcification. Given the complex pathophysiology of CAV, it is unclear whether CAC score can predict CAV and long-term outcomes [ 34 , 35 ]. It was previously believed that CAC offered no prognostic value because calcification was absent even in severe disease and earlier studies failed to demonstrate any predictive value for CAC in CAV patients [ 36 , 37 , 38 ].…”

Section: Non-invasive Modalitiesmentioning

confidence: 99%

Cardiac Allograft Vasculopathy: Challenges and Advances in Invasive and Non-Invasive Diagnostic Modalities

Kamel,

Scalia,

Badr

et al. 2024

JCDD

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Cardiac allograft vasculopathy (CAV) is a distinct form of coronary artery disease that represents a major cause of death beyond the first year after heart transplantation. The pathophysiology of CAV is still not completely elucidated; it involves progressive circumferential wall thickening of both the epicardial and intramyocardial coronary arteries. Coronary angiography is still considered the gold-standard test for the diagnosis of CAV, and intravascular ultrasound (IVUS) can detect early intimal thickening with improved sensitivity. However, these tests are invasive and are unable to visualize and evaluate coronary microcirculation. Increasing evidence for non-invasive surveillance techniques assessing both epicardial and microvascular components of CAV may help improve early detection. These include computed tomography coronary angiography (CTCA), single-photon emission computed tomography (SPECT), positron emission tomography (PET), and vasodilator stress myocardial contrast echocardiography perfusion imaging. This review summarizes the current state of diagnostic modalities and their utility and prognostic value for CAV and also evaluates emerging tools that may improve the early detection of this complex disease.

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“…Next to individual donor-derived cells, it has been suggested that atherosclerotic plaques in coronary vessels of the donor, pre-existing in the transplanted heart, influence the outcome of CAV in the recipient [ 84 ]. The atherosclerotic lesions make the intima and the endothelium of the donor coronary arteries more vulnerable for the development of fibrotic lesions during CAV [ 12 ].…”

Section: Cardiac Allograft Vasculopathy: Fibrosismentioning

confidence: 99%

Cardiac Allograft Vasculopathy: A Donor or Recipient Induced Pathology?

Hoogen

Huibers

Sluijter

et al. 2015

J. of Cardiovasc. Trans. Res.

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Cardiac allograft vasculopathy (CAV) is one of the main causes of late-stage heart failure after heart transplantation. CAV is characterized by concentric luminal narrowing of the coronary arteries, but the exact pathogenesis of CAV is still not unraveled. Many researchers show evidence of an allogeneic immune response of the recipient, whereas others show contrasting results in which donor-derived cells induce an immune response against the graft. In addition, fibrosis of the neo-intima can be induced by recipient-derived circulating cells or donor-derived cells. In this review, both donor and recipient sides of the story are described to obtain better insight in the pathogenesis of CAV. Dual outcomes were found regarding the contribution of donor and recipient cells in the initiation of the immune response and the development of fibrosis during CAV. Future research could focus more on the potential synergistic interaction of donor and recipient cells leading to CAV.

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Virtual Histology Intravascular Ultrasound Assessment of Cardiac Allograft Vasculopathy From 1 to 20 Years After Heart Transplantation

Cited by 46 publications

References 12 publications

The link between major histocompatibility complex antibodies and cell proliferation

The link between major histocompatibility complex antibodies and cell proliferation

Cardiac Allograft Vasculopathy: Challenges and Advances in Invasive and Non-Invasive Diagnostic Modalities

Cardiac Allograft Vasculopathy: A Donor or Recipient Induced Pathology?

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