Evidence of vascular dysfunction in young patients with successfully repaired coarctation of aorta

Brili, Stella; Tousoulis, Dimitris; Antoniades, Charalambos; Aggeli, Constantina; Roubelakis, Apostolos; Papathanasiu, Sotirios; Stefanadis, Christodoulos

doi:10.1016/j.atherosclerosis.2005.01.030

Cited by 109 publications

(92 citation statements)

References 31 publications

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“…lation during reactive hyperemia compared with age-matched control patients (11,12). Atherosclerosis, particularly in coronary artery disease, is associated with endothelial dysfunction as a result of reduced endothelial NO release (17,18,66), and, indeed, high rates of early-onset coronary artery disease are a primary form of morbidity leading to reduced life expectancy in surgically treated CoA.…”

Section: Discussionmentioning

confidence: 99%

“…Untreated CoA provides mechanical stimuli for vascular remodeling in the form of elevated blood pressure (BP) proximal to the coarctation and potentially adverse distributions of wall shear stress (WSS) throughout the thoracic aorta. Normotensive repaired CoA patients have also demonstrated increased carotid intimalmedial thickness and compromised vascular function that appears to persist upon clinical evaluation 12-20 yr after intervention (11,72). The mechanism(s) for this compromised vascular function, possibly involving endothelial function or the expression of smooth muscle (SM) proteins affecting structural and functional properties of the aorta, is not presently known in these postrepair patients.…”

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confidence: 99%

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Altered hemodynamics, endothelial function, and protein expression occur with aortic coarctation and persist after repair

Menon

Eddinger

Wang

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Coarctation of the aorta (CoA) is associated with substantial morbidity despite treatment. Mechanically induced structural and functional vascular changes are implicated; however, their relationship with smooth muscle (SM) phenotypic expression is not fully understood. Using a clinically representative rabbit model of CoA and correction, we quantified mechanical alterations from a 20-mmHg blood pressure (BP) gradient in the thoracic aorta and related the expression of key SM contractile and focal adhesion proteins with remodeling, relaxation, and stiffness. Systolic and mean BP were elevated for CoA rabbits compared with controls leading to remodeling, stiffening, an altered force response, and endothelial dysfunction both proximally and distally. The proximal changes persisted for corrected rabbits despite >12 wk of normal BP (∼4 human years). Computational fluid dynamic simulations revealed reduced wall shear stress (WSS) proximally in CoA compared with control and corrected rabbits. Distally, WSS was markedly increased in CoA rabbits due to a stenotic velocity jet, which has persistent effects as WSS was significantly reduced in corrected rabbits. Immunohistochemistry revealed significantly increased nonmuscle myosin and reduced SM myosin heavy chain expression in the proximal arteries of CoA and corrected rabbits but no differences in SM α-actin, talin, or fibronectin. These findings indicate that CoA can cause alterations in the SM phenotype contributing to structural and functional changes in the proximal arteries that accompany the mechanical stimuli of elevated BP and altered WSS. Importantly, these changes are not reversed upon BP correction and may serve as markers of disease severity, which explains the persistent morbidity observed in CoA patients.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Altered hemodynamics, endothelial function, and protein expression occur with aortic coarctation and persist after repair

Menon

Eddinger

Wang

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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“…[5][6][7] Indeed, it has been shown that normotensive children and young adults who have undergone successful coarctation repair have persistent endothelial dysfunction and impaired arterial reactivity, suggesting the presence of intrinsic vascular abnormalities in this condition. 8,9 Thus, although coarctation of the aorta was regarded initially as a localized abnormality, it is now thought to be a diffuse arteriopathy and part of the spectrum of pathology associated with bicuspid aortic valve disease (Figure 2 and Online Video 2, available online), which can progress to significant valvular stenosis or regurgitation, as well as aortic enlargement and dissection. 10 …”

Section: Diagnosismentioning

confidence: 99%

Resistant Hypertension

Romano

Chacko

Rangarajan

et al. 2015

The American Journal of Medicine

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“…Despite considerably low prevalence of 0.34 per 1000 live births [4], a growing number of adult patients after successful correction of CoAo triggers the need for meticulous follow-up programme [5]. Notwithstanding the relatively early introduction of effective CoAo surgical treatment in 1944 [6] and a further successful implementation of transcatheter approach in 1982 [7], longterm outcome is still compromised on account of the process of arterial remodeling in pre-stenotic vascular bed, associated with arterial stiffness [8][9][10][11] and baroreceptor dysfunction [12]. The resultant markedly increased prevalence of arterial hypertension of 30-50%, regarded as a hallmark of CoAo [13][14], leads to diffuse atherosclerosis [11,[15][16][17] and notably reduced life expectancy [18][19].…”

Section: Introductionmentioning

confidence: 99%

“…Data concerning optimal timing of surgery is inconsistent, with the predominance of reports implying improved long-term outcome in patients operated within the first year after birth [22][23][24]. Nonetheless, even an early intervention does not utterly preclude arterial remodeling, as assessed by ultrasonographic vascular parameters [9][10]21,23]. This phenomenon seems to be unrelated with the occurrence of aortic restenosis [24], hence CoAo may represent a widespread systemic vascular anomaly [13,21].…”

Section: Introductionmentioning

confidence: 99%

Growth differentiation factor 15 and arterial remodeling in adult patients after succesful repair of aortic coarctation (RCD code: IV-5.A.1)

Mizia‐Stec

Wybraniec

Trojnarska

et al. 2013

Journal of Rare Cardiovascular Diseases

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Background: Coarctation of aorta (CoAo) is a congenital heart anomaly associated with high cardiovascular morbidity and mortality attributable to vascular remodeling in adult survivors following surgical management of aortic stenosis. This study sought to adjudicate the significance of novel stress-responsive biomarker, growth differentiation factor 15 (GDF-15), as an indicator of vascular remodeling and its correlation with numerous laboratory and vascular parameters in patients after successful CoAo repair. Methods and results:This research is a case-control study comprising 33 consecutive patients (19 men, 57.58%; mean age 33.9 ±9.3 years; mean age at surgery: 9.1 ±7 years; mean follow-up duration 24.8 ±6.8 years) admitted to outpatient clinic for routine follow-up after repair of CoAo (mainly Dacron patch technique) and matched with 20 healthy controls (10 men, 50%; mean age 34.8 ±9.9 years). Laboratory (GDF-15, high-sensitivity C-reactive protein) and vascular parameters (intima-media thickness, flow-and nitrate-mediated dilation, pulse-wave velocity, central arterial pressure) were assessed. Significant aortic residual gradient was present in 24 (72.7%). The circulating GDF-15 level was lower in CoAo survivors than in control group (539.56 vs. 744.98 pg/ml respectively; p < 0.001). GDF-15 concentration <550 pg/ml successfully differentiated patients after CoA repair (odds ratio [OR] = 9.2; 95%CI: 2.45-34.56, p = 0.0005). There was no difference in GDF-15 level depending on the presence of significant residual gradient (p = 0.19). No significant correlation between GDF-15 and other variables was observed. Conclusions: Low concentration of GDF-15 is characteristic of asymptomatic patients following CoAo repair, however, its clinical significance and relationship with vascular remodeling substantiates further investigation. JRCD 2013; 1 (2): 41-48

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Evidence of vascular dysfunction in young patients with successfully repaired coarctation of aorta

Cited by 109 publications

References 31 publications

Altered hemodynamics, endothelial function, and protein expression occur with aortic coarctation and persist after repair

Altered hemodynamics, endothelial function, and protein expression occur with aortic coarctation and persist after repair

Resistant Hypertension

Growth differentiation factor 15 and arterial remodeling in adult patients after succesful repair of aortic coarctation (RCD code: IV-5.A.1)

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