A Systematic Histopathologic Evaluation of Type-A Aortic Dissections Implies a Uniform Multiple-Hit Causation

Grewal, Nimrat; Velders, Bart J.J.; Groot, Adriana C. Gittenberger‐de; Poelmann, Robert E.; Klautz, Robert J.M.; Brakel, Thomas J. van; Lindeman, J.

doi:10.3390/jcdd8020012

Cited by 19 publications

(11 citation statements)

References 23 publications

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“…Although several risk factors have been described predisposing individuals for this lethal condition, the exact pathogenesis has not yet been identified ( 18 ). Roughly, the development of an aortic dissection requires three main pathological conditions, being mechanical wall stress, a susceptible intimal layer and medial degeneration ( 12 , 19 ). Our previous study had shown that medial pathology in type A aortic dissections is comparable with thoracic aneurysms in patients with a tricuspid aortic valve with smooth muscle cell nuclei loss, mucoid extracellular matrix accumulation and elastic fiber fragmentation and loss ( 12 ).…”

Section: Discussionmentioning

confidence: 99%

“…Roughly, the development of an aortic dissection requires three main pathological conditions, being mechanical wall stress, a susceptible intimal layer and medial degeneration ( 12 , 19 ). Our previous study had shown that medial pathology in type A aortic dissections is comparable with thoracic aneurysms in patients with a tricuspid aortic valve with smooth muscle cell nuclei loss, mucoid extracellular matrix accumulation and elastic fiber fragmentation and loss ( 12 ). The intimal layer was, however, significantly thinner as compared to the tricuspid thoracic aortopathy patients, resembling the intima in patients with Marfan syndrome and a bicuspid aortic valve ( 20 , 21 ).…”

Section: Discussionmentioning

confidence: 99%

“…Less is, however, known about the role of atherosclerosis in patients with a type A aortic dissection. Recently we concluded that patients with a type A aortic dissection also demonstrate a significantly thinner intimal layer, even in the absence of a genetic syndrome or a bicuspid aortic valve ( 12 ). Considering the overlap in pathogenetic mechanisms between BAV, MFS, and type A aortic dissections it is particularly interesting to study the presence of atherosclerosis in aortic dissections.…”

Section: Introductionmentioning

confidence: 99%

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Are acute type A aortic dissections atherosclerotic?

Grewal

Dolmaci²,

Jansen³

et al. 2023

Front. Cardiovasc. Med.

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BackgroundType A aortic dissections (TAAD) are devastating aortic complications. Patients with Marfan syndrome, a bicuspid aortic valve or a thoracic aortic aneurysm have an increased risk to develop a TAAD. These predisposing conditions are characterized by a histologically thin intimal layer and hardly any atherosclerosis. Little is known about the susceptibility for atherosclerosis in patients with a type A aortic dissection.ObjectiveWe aim to systematically describe atherosclerotic lesions in TAAD patients.Materials and methodsA total of 51 patients with a TAAD (mean age 62.5 ± 10.8 years, 49% females) and 17 control patients (mean age 63 ± 5.5 years, 53% females) were included in this study. Cardiovascular risk factors were assessed clinically. All sections were stained with Movat pentachrome and hematoxylin eosin. Plaque morphology was classified according to the modified AHA classification scheme proposed by Virmani et al.ResultsIn the TAAD group thirty-seven percent were overweight (BMI > 25). Diabetes and peripheral arterial disease were not present in any of the patients. Fifty-nine percent of the patients had a history of hypertension. The intima in TAAD patients was significantly thinner as compared to the control group (mean thickness 143 ± 126.5 μm versus 193 ± 132 μm, p < 0.023). Seven TAAD patients had a normal intima without any form of adaptive or pathological thickening. Twenty-three TAAD patients demonstrated adaptive intimal thickening. Fourteen had an intimal xanthoma, also known as fatty streaks. A minority of 7 TAAD patients had progressive atherosclerotic lesions, 4 of which demonstrated pathological intimal thickening, 3 patients showed early fibroatheroma, late fibroatheroma and thin cap fibroatheroma. In the control group the majority of the patients exhibited progressive atherosclerotic lesions: three pathologic intimal thickening, two early fibroatheroma, six late fibroatheroma, one healed rupture and two fibrotic calcified plaque.DiscussionThis study shows that TAAD patients hardly exhibit any form of progressive atherosclerosis. The majority of TAAD patients showcase non-progressive intimal lesions, whereas the control group mostly demonstrated progressive intimal atherosclerotic lesions. Findings are independent of age, sex, or the presence of (a history of) hypertension.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Are acute type A aortic dissections atherosclerotic?

Grewal

Dolmaci²,

Jansen³

et al. 2023

Front. Cardiovasc. Med.

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“…In specimens from patients with chronic aortic dilatation, the tenascin-C content in media was considerably lower and distributed more homogeneously around aortic media, whereas in healthy patients, tenascin-C was absent from the aortic specimens (71). Further, several histological studies have shown that dissection occurs most commonly in the outer third of the media layer in the area vascularized by the vasa vasorum network (72,73). In contrast, in patients with connective tissue disorder, the dissection is located closer to the aortic lumen in the middle third of aortic media (72).…”

Section: Dynamic Continuum Of Aortic Diseasementioning

confidence: 99%

Synthesis of multidimensional pathophysiological process leading to type A aortic dissection: a narrative review

Uimonen¹

2021

J Thorac Dis

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Objective: This review aims to synthesize the existing knowledge on the etiological process leading to type A aortic dissection (TAAD) and to clarify the relationship between mechanical, biochemical, and histopathological processes behind the aortic disease. Background: Extensive research has previously identified several risk factors for TAAD as well as pathological mechanisms leading to TAAD. However, due to the complexity of the pathological process and limited knowledge on the relationships between distinct pathomechanisms leading to TAAD, the ability to identify the patients at high risk for TAAD has been poor. Methods: PubMed (National Library of Medicine) database was searched for suitable literature. The most relevant articles focusing on anatomy, histopathology, physiology, and mechanics of ascending aorta and aortic diseases were reviewed. Conclusions: Pathophysiology of the TAAD is related to biochemical and histological as well as mechanical and hemodynamic alterations leading to a degeneration of the aortic wall via inflammatory response. The degradative mechanisms of aortic wall structures and the mechanical forces, to which the wall is predisposed, are interrelated and influence one another. The relativity between the factors influencing aortic wall strength and healing capacity, and factors influencing mechanical stress on the aortic wall suggest that the risk of TAAD is not a linear but rather a dynamic phenomenon. Accounting for the dynamical property of the aortic disease in assessing the need for preventive surgical aortic reconstruction may provide a wider perspective in identifying patients at risk of TAAD and in planning preventive medical therapies.

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“…An aortic dissection is a serious condition in which the inner layer of the aorta tears, blood surges through the tear, causing the inner and middle layers of the aorta to separate (dissect). 1 Based on their location and extent, an aortic dissection is classified as Stanford type-A aortic dissections (TAAD) (dissections involving the aortic root and/or ascending aorta, which can propagate to the aortic arch and further into the descending aorta), and type-B dissections (dissections that do not involve the ascending aorta). 2 …”

Section: Introductionmentioning

confidence: 99%