Why the study?
Arterial stiffness and the cardio-ankle vascular index (CAVI) predict adverse cardiovascular outcomes, but their relationship with significant carotid stenosis, cerebrovascular symptoms, and carotid plaque echogenicity remained to be investigated.
Is arterial stiffness, measured by the cardio-ankle vascular index (CAVI), associated with significant carotid atherosclerosis and plaque vulnerability?
Is arterial stiffness, measured by the cardio-ankle vascular index (CAVI), associated with significant carotid atherosclerosis and plaque vulnerability?
Elevated arterial stiffness, as measured by CAVI, is independently associated with significant carotid stenosis, prior cerebrovascular events, and vulnerable plaque characteristics.
CAVI may help stratify carotid stenosis risk; leaves open whether it predicts post-CAS events or warrants routine use.
Arterial stiffness and its valid index, the cardio-ankle vascular index (CAVI), have emerged as predictors of adverse cardiovascular outcomes. We investigated the relationship of the CAVI with significant carotid stenosis (> 50%) and the related cerebrovascular symptoms or carotid plaque echogenicity, assessed by ultrasound gray-scale median (GSM) score, at baseline and after carotid artery stenting (CAS). We prospectively enrolled 113 patients with carotid stenosis (70-99% for asymptomatic and > 50% for symptomatic participants) eligible for CAS. Age- and sex-matched individuals (n = 38) served as controls (CON). Clinical data, CAVI, and biochemical profile were obtained at baseline. Clinical assessment and CAVI measurement were performed 6 months after CAS. Compared with the CON group, the CAS group had a higher incidence of co-morbidities (diabetes, hypertension, and hyperlipidemia), higher CAVI values (9.94 ± 2.14 vs 7.85 ± .97 m/sec, P < .001), but a better lipid profile due to increased prescription of statins. The symptomatic CAS subgroup showed higher CAVI ( P < .001), high-sensitivity C-reactive protein ( P = .048), and osteoprotegerin ( P = .002) levels than the asymptomatic one. In multivariate analysis, CAVI at baseline was independently associated with the presence of significant carotid atherosclerosis (β = .695, P < .001), cerebrovascular events (β = .474, P < .001), and GSM score (β = −.275, P = .042). Raised CAVI values were independently associated with significant carotid stenosis and plaque vulnerability.
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Kadoglou et al. (2022) studied this question.
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