Arterial Stiffness as an Imaging Biomarker

Laurent, Stéphane; Mousseaux, Élie; Boutouyrie, Pierre

doi:10.1161/hypertensionaha.113.01372

Cited by 24 publications

(11 citation statements)

References 12 publications

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“…For example, the impact of mechanical degeneration may have greatest effect in the more compliant, elastin-rich proximal aorta [11] while endothelial injury may largely impact stiffness in smaller muscular arteries [12]. Risk factors such as diabetes and hypercholesterolemia have been associated with increases in both central and peripheral stiffness [13], but associations between arterial stiffness and cardiovascular outcomes have differed depending on the site of arterial stiffness [14]. This has led to uncertainty over the most appropriate measure of arterial stiffness to apply in clinical practice and research trials.…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular outcome associations among cardiovascular magnetic resonance measures of arterial stiffness: the Dallas heart study

Maroules

Khera²,

Ayers

et al. 2014

Journal of Cardiovascular Magnetic Resonance

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BackgroundCardiovascular magnetic resonance (CMR) has been validated for the noninvasive assessment of total arterial compliance and aortic stiffness, but their associations with cardiovascular outcomes is unknown. The purpose of this study was to evaluate associations of CMR measures of total arterial compliance and two CMR measures of aortic stiffness with respect to future cardiovascular events.MethodsThe study consisted of 2122 Dallas Heart Study participants without cardiovascular disease who underwent CMR at 1.5 Tesla. Aortic stiffness was measured by CMR-derived ascending aortic distensibility and aortic arch pulse wave velocity. Total arterial compliance was calculated by dividing left ventricular stroke volume by pulse pressure. Participants were monitored for cardiovascular death, non-fatal cardiac events, and non-fatal extra-cardiac vascular events over 7.8 ± 1.5 years. Cox proportional hazards regression was used to assess for associations between CMR measures and cardiovascular events.ResultsAge, systolic blood pressure, and resting heart rate were independently associated with changes in ascending aortic distensibility, arch pulse wave velocity, and total arterial compliance (all p < .0001). A total of 153 participants (6.9%) experienced a cardiovascular event. After adjusting for traditional risk factors, total arterial compliance was modestly associated with increased risk for composite events (HR 1.07 per 1SD, p = 0.03) while the association between ascending aortic distensibility and composite events trended towards significance (HR 1.18 per 1SD, p = 0.08). Total arterial compliance and aortic distensibility were independently associated with nonfatal cardiac events (HR 1.11 per 1SD, p = 0.001 and HR 1.45 per 1SD, p = 0.0005, respectively), but not with cardiovascular death or nonfatal extra-cardiac vascular events. Arch pulse wave velocity was independently associated with nonfatal extra-cardiac vascular events (HR 1.18 per 1SD, p = 0.04) but not with cardiovascular death or nonfatal cardiac events.ConclusionsIn a multiethnic population free of cardiovascular disease, CMR measures of arterial stiffness are associated with future cardiovascular events. Total arterial compliance and aortic distensibility may be stronger predictors of nonfatal cardiac events, while pulse wave velocity may be a stronger predictor of nonfatal extra-cardiac vascular events.

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Section: Introductionmentioning

confidence: 99%

Cardiovascular outcome associations among cardiovascular magnetic resonance measures of arterial stiffness: the Dallas heart study

Maroules

Khera²,

Ayers

et al. 2014

Journal of Cardiovascular Magnetic Resonance

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“…Arterial stiffening is a fundamental cause of cardiovascular complications, such as myocardial hypertrophy, myocardial infarction, stroke, renal failure, dementia, and a hallmark of the aging process [22][23][24][25]. This study revealed the roles and signal pathways of salusin-β in VSMCs proliferation, vascular fibrosis and maladaptive vascular remodeling.…”

Section: Discussionmentioning

confidence: 96%

Salusin-β contributes to vascular remodeling associated with hypertension via promoting vascular smooth muscle cell proliferation and vascular fibrosis

Sun

Liu

Zhang

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Vascular smooth muscle cell (VSMC) proliferation and vascular fibrosis are closely linked with hypertension and atherosclerosis. Salusin-β is a bioactive peptide involved in the pathogenesis of atherosclerosis. However, it is still largely undefined whether salusin-β is a potential candidate in the VSMC proliferation and vascular fibrosis. Experiments were carried out in human vascular smooth muscle cells (VSMCs) and in rats with intravenous injection of lentivirus expressing salusin-β. In vitro, salusin-β promoted VSMCs proliferation, which was attenuated by adenylate cyclase inhibitor SQ22536, PKA inhibitor Rp-cAMP, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor AG1478, ERK inhibitor U0126 or cAMP response element binding protein (CREB) inhibitor KG501. It promoted the phosphorylation of ERK1/2, CREB and EGFR, which were abolished by SQ22536 or Rp-cAMP. Furthermore, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor AG1478 diminished the salusin-β-evoked ERK1/2 and CREB phosphorylation. On the other hand, salusin-β increased collagen-I, collagen-III, fibronectin and connective tissue growth factor (CTGF) mRNA and phosphorylation of Smad2/3, which were prevented by ALK5 inhibitor A83-01. In vivo, salusin-β overexpression increased the media thickness, media/lumen ratio coupled with ERK1/2, CREB, EGFR and Smad2/3 phosphorylation, as well as the mRNA of collagen-I, collagen-III, fibronectin, transforming growth factor-β1 (TGF-β1) and CTGF in arteries. Moreover, salusin-β overexpression in rats caused severe hypertension. Intravenous injection of salusin-β dose-relatedly increased blood pressure, but excessive salusin-β decreased blood pressure and heart rate. These results indicate that salusin-β promotes VSMC proliferation via cAMP-PKA-EGFR-CREB/ERK pathway and vascular fibrosis via TGF-β1-Smad pathway. Increased salusin-β contributes to vascular remodeling and hypertension.

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“…Laurent és munkatársai, valamint saját véleményünk alapján is, minden artériás érfalmerevséget mérő műszer, új metodika esetében indokoltnak tartható a követéses, kemény végpontú vizsgálatok elvégzése [19]. Ennek megfelelő-en, a cardiovascularis események előrejelzésére bizonyí-tottan használható készülékek listáját mutatja a 1. táblá-zat, Laurent és munkatársai publikációjából adaptálva, a 2013-as helyzetet rögzítve [19].…”

Section: Az éRfali Merevséget Mérő Különböző Metodikák Problémaköre Aunclassified

Clinical value and measurement of arterial stiffness for the evaluation of cardiovascular risk in the light of novel findings

2015

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A cardiovascularis kockázat pontos becslése a prevenciós és terápiás stratégia egyik sarkalatos kérdése. Bár számos pontrendszer és kockázattáblázat áll rendelkezésre, a becsült és a valós érrendszeri események száma között továbbra is jelentős a különbség. A pontosabb cardiovascularis kockázatbecslés terén nyújt újat és többletet az artériás érfalme-revség mérése. Ennek legfontosabb paramétere az aorta pulzushullám terjedési sebesség. Mint kockázatbecslő metodikai lehetőség, 2007 után ismételten szerepel az Európai Hypertonia Társaság 2013-as évben publikált ajánlásában, bár az amerikai ajánlások egyelőre mellőzik. Összefoglaló közleményükben a szerzők az új módszer klinikai gyakorlatba való bevezetésének fázisait tárgyalják az artériás érfalmerevség vizsgálatával kapcsolatos eddigi ismeretek tükré-ben, valamint kitérnek a módszer metodikai sokszínűségéből adódó, eddig nem teljesen tisztázott kérdésekre is. Orv. Hetil., 2015, 156(6), 211-215. Kulcsszavak: artériás érfalmerevség, cardiovascularis kockázat, szakmai ajánlások Clinical value and measurement of arterial stiffness for the evaluation of cardiovascular risk in the light of novel fi ndingsCardiovascular risk stratifi cation is fundamental for the development of effective prevention and therapeutic strategies. Although there are numerous scores and risk tables available, a difference still exists between the estimated and real number of cardiovascular events. Measurement of arterial stiffness can provide additional information to risk stratifi cation. The most widely accepted parameter of arterial stiffness is aortic pulse wave velocity, which has been included in the guideline of the European Society of Hypertension in 2007 and 2013, although American guidelines still omit it. In this review the authors summarize the evidence with regards to the different steps required for clinical application of arterial stiffness measurement and they also discuss the questions that evolved from the methodological variability of different measurement techniques.

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Arterial Stiffness as an Imaging Biomarker

Cited by 24 publications

References 12 publications

Cardiovascular outcome associations among cardiovascular magnetic resonance measures of arterial stiffness: the Dallas heart study

Cardiovascular outcome associations among cardiovascular magnetic resonance measures of arterial stiffness: the Dallas heart study

Salusin-β contributes to vascular remodeling associated with hypertension via promoting vascular smooth muscle cell proliferation and vascular fibrosis

Clinical value and measurement of arterial stiffness for the evaluation of cardiovascular risk in the light of novel findings

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