Endothelium-dependent flow-mediated vasodilation in coronary and brachial arteries in suspected coronary artery disease

Takase, Bonpei; Uehata, Akimi; Ashihara, Takashi; Nagai, Tomoo; Nishioka, Toshihiko; Hamabe, Akira; Satomura, Kimio; Ohsuzu, Fumitaka; Kurita, Akira

doi:10.1016/s0002-9149(98)00702-4

Cited by 399 publications

(270 citation statements)

References 18 publications

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“…FMD renders the endotheliumdependent relaxation of a conduit artery following the post-ischemic increase of blood flow. Brachial artery reactivity, frequently used for non-invasive ultrasonographic assessment of FMD, indicates endotheliumdependent response to increased wall shear stress and when impaired is a marker for endothelial dysfunction and increased cardiovascular risk, correlating with impaired endothelium-dependent relaxation in the coronary arteries (Takase et al 1998;Matsuo et al 2004;Thanyasiri et al 2005). In agreement with previous results (Yavuz et al 2008), the measurement of endothelial-dependent vasodilatation in our old-aged population has evidenced that FMD declines with increasing age (Figs.…”

Section: Resultssupporting

confidence: 91%

Idiopathic deep venous thrombosis and arterial endothelial dysfunction in the elderly

Mazzoccoli

Fontana

Grilli

et al. 2011

AGE

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Arterial and venous thrombosis have always been regarded as different pathologies and epidemiological studies have examined the association between venous thrombosis and indicators of atherosclerosis and/or arterial thromboembolic events. We measured the flow-mediated dilation (FMD), a well-known marker of arterial endothelial dysfunction, in youngmiddle-aged and old-aged patients with and without unprovoked deep venous thrombosis (DVT). The aim of this study was to investigate whether DVT was a significant predictor for impaired FMD, considering all the patients and young-middle-aged (age<65 years) and old-aged (age≥65 years) patients separately. FMD was measured in the brachial artery on a population of 120 subjects with the same atherosclerosis risk factors, 68 male and 52 female, 70 young-middleaged subjects (mean age±SD 49.5±10.5 years) and 50 old-aged subjects (76.2±7.7 years). Patients with DVT showed a significant decrease of FMD compared to patients without DVT (6.8±5.5% vs. 10.9±3.5%, p<0.001). Moreover, old-aged patients showed a significant decrease of FMD compared to the young-middle-aged subjects (7.4±4.1% vs. 9.8± 5.3%, p=0.005). In the whole study population, DVT was strongly associated with FMD (risk factors adjusted β=−4.14, p<0.001). A significant interaction between age and the presence of DVT on predicting FMD was found (p=0.003) suggesting a AGE (2012) differential behavior of DVT as predictor of FMD. In young-middle-aged group, multivariate model confirmed that DVT was the most significant predictor of continuous FMD (β=−6.06, p<0.001). On the contrary, DVT was no more a predictor of FMD in the old age group (β=−0.73, p=0.556). Furthermore, old-aged patients without DVT showed a statistically significant decrease of FMD compared to the youngmiddle-aged subjects without DVT (8.2±2.1% vs. 12.6±2.7%, p<0.001) and old-aged patients with DVT showed a not statistically significant decrease of the FMD compared to the young-middle-aged patients with DVT (6.7±5.3% vs. 6.8±5.7%, p= 0.932). In conclusion, young-middle-aged patients with spontaneous DVT show an impaired FMD, whereas this impairment in old-aged subjects is evident independently from the presence or absence of DVT. Aging per se may be associated with physiologic abnormalities in the systemic arteries and with endothelial dysfunction.34:751-760 DOI 10.1007/s11357-011-9265-

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Section: Resultssupporting

confidence: 91%

Idiopathic deep venous thrombosis and arterial endothelial dysfunction in the elderly

Mazzoccoli

Fontana

Grilli

et al. 2011

AGE

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“…This vasodilatation is mediated by endothelial cell release of nitric oxide (16), and thus FMD is considered to be a measure of endotheliumdependent vasodilatation. FMD results correlate with findings obtained by invasive testing of coronary endothelial function (17) and with the extent and severity of coronary artery disease (CAD) (18). Impaired FMD has been demonstrated in subjects with vascular risk factors such as diabetes mellitus, smoking, hypertension, and hypercholesterolemia (15).…”

mentioning

confidence: 81%

Screening for atherosclerosis in patients with rheumatoid arthritis: Comparison of two in vivo tests of vascular function

Doornum¹,

McColl²,

Jenkins³

et al. 2003

Arthritis & Rheumatism

127

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Objective. Inflammation appears to play a central role in atherosclerosis, and endothelial damage mediated by systemic inflammation may contribute to the increased cardiovascular mortality in rheumatoid arthritis (RA). Brachial artery flow-mediated dilatation (FMD) and pulse wave analysis (PWA) are measures of vascular function. The aim of this study was to determine if FMD and PWA are abnormal in patients with RA.Methods. Twenty-five RA patients and 25 matched healthy controls were studied. All were free of traditional cardiovascular risk factors. FMD was measured in all subjects. PWA was performed in 18 RA patients and 18 controls, with results expressed as large and small artery compliance (C1 and C2). Modified Sharp scores were calculated in 13 RA patients.Results. Results (mean ؎ SD) in RA patients and controls, respectively, were as follows: FMD 107.6 ؎ 4.6% versus 108.5 ؎ 4.1% (P ‫؍‬ 0.49), C1 14.8 ؎ 2.8 ml/mm Hg ؋ 10 versus 17.9 ؎ 3.1 ml/mm Hg ؋ 10 (P ‫؍‬ 0.0033), C2 4.5 ؎ 2.3 ml/mm Hg ؋ 100 versus 7.7 ؎ 3.7 ml/mm Hg ؋ 100 (P ‫؍‬ 0.0039). There was an inverse correlation between C2 and modified Sharp scores in the RA patients (Spearman's rho -0.69, P ‫؍‬ 0.0085).Conclusion. FMD was normal in these RA patients, whereas arterial compliance was markedly reduced. PWA appears to be a more sensitive measure of vascular dysfunction than FMD in RA and may be the preferred surrogate marker of vascular dysfunction in longitudinal studies of RA patients. The inverse correlation between C2 and the modified Sharp score, a measure that reflects disease activity over time, supports the notion that chronic inflammation plays a role in RA-associated atherosclerosis.

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“…This very year, the first non-invasive method to assess endothelial function was published [35] by Celermajer and colleagues. The brachial artery response to shear stress is measured by ultrasound as surrogate for the epicardial coronary arteries, an association later confirmed to be correlated [36]. Flow-mediated dilatation (FMD) is measured sonographically as peak percent dilatation from brachial conduit artery baseline diameter.…”

Section: How Can We Measure Endothelial Function?mentioning

confidence: 98%

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

et al. 2017

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The endothelium has increasingly been recognized as a smart barrier and a key regulator of blood flow in microand macrovascular beds. Endothelial dysfunction marks a stage of atherosclerosis and is an important prognostic marker for cardiovascular disease. Yet, some people who tend to be slim and physically active and with rather low blood pressure show a propensity to respond to certain stimuli such as emotional stress with endothelial-mediated vascular dysregulation (Flammer syndrome). This leads to characteristic vascular symptoms such as cold hands but also a risk for vascularmediated diseases such as normal-tension glaucoma. It is the aim of this review to delineate the differences between Flammer syndrome and its Bcounterpart^endothelial dysfunction in the context of cardiovascular diseases.

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Endothelium-dependent flow-mediated vasodilation in coronary and brachial arteries in suspected coronary artery disease

Cited by 399 publications

References 18 publications

Idiopathic deep venous thrombosis and arterial endothelial dysfunction in the elderly

Idiopathic deep venous thrombosis and arterial endothelial dysfunction in the elderly

Screening for atherosclerosis in patients with rheumatoid arthritis: Comparison of two in vivo tests of vascular function

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

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