Regional heterogeneity within the aorta: Relevance to aneurysm disease

Ruddy, Jean Marie; Jones, Jeffrey A.; Spinale, Francis G.; Ikonomidis, John S.

doi:10.1016/j.jtcvs.2008.06.027

Cited by 138 publications

(117 citation statements)

References 52 publications

(104 reference statements)

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“…(26) More recently, the development of aneurysms in either the thoracic or abdominal region has been similarly attributed to regional specifications such as mechanical, structural, but also possibly embryologic. (27) Our data are thus in line with these reports (23)(24)(25)(26)(27) and provide new evidence regarding the potential role that the origin of vascular cells could play in the development of various vascular diseases.…”

Section: The Adult Aorta Is Developmentally Regionalizedsupporting

confidence: 90%

Pathologic calcification of adult vascular smooth muscle cells differs on their crest or mesodermal embryonic origin

Leroux-Berger¹,

Quéguiner²,

Maciel³

et al. 2011

Journal of Bone and Mineral Research

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Vascular calcifications can occur in the elderly and in patients suffering from various diseases. Interestingly, depending on the pathology, different regions of the arterial system can be affected. Embryonic observations have clearly indicated that vascular smooth muscle cell (VSMC) origin is notably heterogeneous. For instance, in the aorta, VSMCs colonizing the aortic arch region derive from cardiac neural crest cells, whereas those populating the descending aorta derive from the mesoderm. We examined here whether the embryonic origin of aortic VSMCs would correlate with their ability to mineralize. Under hyperphosphatemic conditions that induce vascular calcifications, we performed ex vivo aortic explant cultures as well as in vitro VSMC cultures from wild-type mice. Our data showed that VSMC embryonic origin affects their ability to mineralize. Indeed, the aortic arch media made up of VSMCs of neural crest origin calcifies significantly earlier than the descending aorta composed of VSMCs, which are mesoderm-derived. Similar results were obtained with cultured VSMCs harvested from both aortic regions. We also demonstrated that in a mouse model deficient in matrix Gla protein, a potent calcification inhibitor, developing extensive and spontaneous medial calcifications of the aorta, lesions initiate in the aortic arch. Subsequently, calcifications progress outside the aortic arch region and ultimately spread all over the entire arterial tree, including the descending aorta. Altogether, our results support an unsuspected correlation between VSMCs of embryonic origin and the timing of appearance of calcifications. ß

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Section: The Adult Aorta Is Developmentally Regionalizedsupporting

confidence: 90%

Pathologic calcification of adult vascular smooth muscle cells differs on their crest or mesodermal embryonic origin

Leroux-Berger¹,

Quéguiner²,

Maciel³

et al. 2011

Journal of Bone and Mineral Research

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“…1,2,[17][18][19] It is now widely accepted that the aorta shows major regional heterogeneity between thoracic and abdominal segments. 14,17,18,31,32 This heterogeneity mainly reflects embryologic origin: neural crest for aortic arch and mesoderm for abdominal aorta. Structural and mechanical degradation with severe and progressive atherosclerosis in the abdominal aorta is observed.…”

Section: Discussionmentioning

confidence: 99%

“…Structural and mechanical degradation with severe and progressive atherosclerosis in the abdominal aorta is observed. [31][32][33][34][35][36] Indeed, this heterogeneity is associated with differences in age-related segmental changes of aortic diameters. In general populations, the aging is associated with gradually decreasing slopes (b-coefficients) of diameter-age relationships along the aorta.…”

Section: Discussionmentioning

confidence: 99%

Aortic Aging in ESRD: Structural, Hemodynamic, and Mortality Implications

London

Safar

Pannier

2015

JASN

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Aging incurs aortic stiffening and dilation, but these changes are less pronounced in peripheral arteries, resulting in stiffness and geometry gradients influencing progression of the forward and reflected pressure waves. Because premature arterial aging is observed in ESRD, we determined the respective roles of stiffness and aortic geometry gradients in 73 controls and 156 patients on hemodialysis. We measured aortic pulse wave velocity (PWV) and brachial PWV to evaluate the stiffness gradient [(brachial PWV/aortic PWV) 0.5 ] and ascending aortic and aortic bifurcation diameters to assess aortic taper (ascending aortic diameter/aortic bifurcation diameter). The global reflection coefficient was estimated from characteristic impedance and vascular resistance. Cox proportional hazard models were used to determine mortality risk. The age-associated increase in aortic PWV was higher in patients (P,0.001). In controls, aortic ascending and bifurcation diameters increased with age, with an unchanged aortic taper. In patients on hemodialysis, age did not associate with increased ascending aortic diameter but did associate with increased aortic bifurcation diameter and decreased aortic taper, both of which also associated with abdominal aortic calcifications and smaller global reflection coefficient (P,0.001). In patients, multivariate models revealed all-cause and cardiovascular mortality associated with age, aortic PWV, and aortic bifurcation diameter with high specificity and sensitivity. Using stiffness gradient, aortic taper, or global reflection coefficient in the model produced similar results. Thus, whereas aortic stiffness is a known independent predictor of mortality, these results indicate the importance of also evaluating the aortic geometry in patients on hemodialysis. 27: 183727: -184627: , 201627: . doi: 10.1681 Aging is associated with marked changes in the mechanical and geometric characteristics of the arterial tree. 1 It is characterized by markedly increased aortic stiffness (aortic pulse wave velocity [PWV]), stiffening not observed to the same degree in peripheral muscular arteries. 2 This change reduces the normal centrifugal impedance gradient between central and peripheral artery systems. 2,3 Any change of the impedance gradient generates modifications of partial local wave reflections, which can be considered a continuous phenomenon along the impedance gradient. 3,4 The partial reflections summate to form an apparently unique backward-traveling reflected wave. 5 In the presence of impedance gradient and low aortic PWV, the backward wave returns to the aorta at end systole and early diastole, thereby enhancing late diastolic pressure and coronary perfusion 4 and attenuating the transmission of pulsatile pressure to the microcirculation. 3,6 The central effect of aortic stiffness on impedance J Am Soc Nephrol

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“…Both thoracic aortic (TAA) and abdominal aortic aneurysms (AAA), are also characterized to be silent and asymptomatic diseases and insidious in their progression [1,2]. Despite these common aspects, the two aorta pathologies show a significant heterogeneity in their prevalence, distribution along aorta length, age-at-onset, male:female ratio of disease susceptibility and pathophysiology, as reported in detail in Table 1 [3]. Thus, TAA and AAA are two distinct pathological entities.…”

Section: Introductionmentioning

confidence: 99%

Genetic contribution in sporadic thoracic aortic aneurysm? Emerging evidence of genetic variants related to TLR-4-mediated signaling pathway as risk determinants

Balistreri

2015

Vascular Pharmacology

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Keywords:Sporadic thoracic aortic aneurysms (TAA) and dissections Genetic variants Biomarkers Targets for new personalized therapeutic treatments Sporadic thoracic aortic aneurysms (TAA) and dissections are one of the major causes of morbidity and mortality worldwide, especially in those older than 65 years. The presentation of TAA is varied and often silent. Thus, sporadic TAA detection is often fortuitous, with identification occurring during a routine physical examination or during an unrelated medical evaluation. Once suspected, confirmation by imaging clinical approaches is needed to allow the choose of the unique treatments for TAA, namely the surgery procedures, including elective surgery or endovascular repair before the onset of catastrophic and fatal complications, such as dissection or rupture. At present, there are no biomarkers available to identify TAAs before visible symptoms. However, recent progresses in understanding of molecular and cellular mechanisms involved in the patho-physiology of sporadic TAA are suggesting different molecular pathways and their genetic variants as potential biomarkers, which might be applied into TAA clinical practice in the near future. Here, we report literature evidence on some disease pathways and their genetic variants on TAA susceptibility and compliances, and their translation as promising TAA preventive and prognostic biomarkers and targets for new personalized therapeutic treatments.

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Regional heterogeneity within the aorta: Relevance to aneurysm disease

Cited by 138 publications

References 52 publications

Pathologic calcification of adult vascular smooth muscle cells differs on their crest or mesodermal embryonic origin

Pathologic calcification of adult vascular smooth muscle cells differs on their crest or mesodermal embryonic origin

Aortic Aging in ESRD: Structural, Hemodynamic, and Mortality Implications

Genetic contribution in sporadic thoracic aortic aneurysm? Emerging evidence of genetic variants related to TLR-4-mediated signaling pathway as risk determinants

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