Carotid intima-media thickness as a biomarker of subclinical atherosclerosis

Bauer, Marcus; Caviezel, Seraina; Teynor, Alexandra; Erbel, Raimund; Mahabadi, Amir A.; Schmidt‐Trucksäss, Arno

doi:10.4414/smw.2012.13705

Cited by 108 publications

(116 citation statements)

References 57 publications

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“…Increased carotid IMT and plaque formation are considered as early signs of atherosclerosis [20]. Increased carotid wall thickness has been shown to be a significant predictor of coronary and cerebrovascular diseases [21][22][23].…”

Section: Discussionmentioning

confidence: 99%

Carotid Doppler Ultrasound Evaluation in Patients with Pulsatile Tinnitus

Terzi

Arslanoğlu

Demiray

et al. 2014

Indian J Otolaryngol Head Neck Surg

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A wide range of conditions, including atherosclerosis, may lead to pulsatile tinnitus. The objective of this study was to evaluate the patients with pulsatile tinnitus by means of carotid Doppler ultrasound parameters. Thirty-four patients with pulsatile tinnitus were enrolled in the study. Internal carotid artery intima-media thickness (IMT), blood flow velocities and arterial lumen diameters (LD) were measured and compared with the control group. Mean end diastolic velocity (EDV) (32.29 ± 17.22) and IMT (1.06 ± 0.36) values were significantly higher and mean LD (6.69 ± 1.20) was significantly lower compared to the control group. Peak systolic velocity and EDV values were significantly higher in patients whose IMT were greater than 1 mm. Pulsatile tinnitus may be the first symptom of a severe, life threatening disease. Doppler sonography is a noninvasive, safe and easily applicable diagnostic tool for the evaluation of the vascular structures, in patients with pulsatile tinnitus.

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Section: Discussionmentioning

confidence: 99%

Carotid Doppler Ultrasound Evaluation in Patients with Pulsatile Tinnitus

Terzi

Arslanoğlu

Demiray

et al. 2014

Indian J Otolaryngol Head Neck Surg

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“…[34][35][36] In this study, we used VCAM-1 not as a marker for targeted plaque imaging, but as an inflammation marker in the context of endothelial regeneration after intravascular procedures. The detection of delayed reendothelialization and prolonged endothelial inflammation induced by diet or drug-eluting stents is an acute issue in clinical diagnostics.…”

Section: Discussionmentioning

confidence: 99%

Noninvasive Molecular Ultrasound Monitoring of Vessel Healing After Intravascular Surgical Procedures in a Preclinical Setup

Curaj

Fokong

et al. 2015

ATVB

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Objective— Cardiovascular interventions induce damage to the vessel wall making antithrombotic therapy inevitable until complete endothelial recovery. Without a method to accurately determine the endothelial status, many patients undergo prolonged anticoagulation therapy, denying them any invasive medical procedures, such as surgical operations and dental interventions. Therefore, we aim to introduce molecular ultrasound imaging of the vascular cell adhesion molecule (VCAM)-1 using targeted poly- n -butylcyanoacrylate microbubbles (MB VCAM-1 ) as an easy accessible method to monitor accurately the reendothelialization of vessels. Approach and Results— ApoE −/− mice were fed with an atherogenic diet for 1 and 12 weeks and subsequently, endothelial denudation was performed in the carotid arteries using a guidewire. Molecular ultrasound imaging was performed at different time points after denudation (1, 3, 7, and 14 days). An increased MB VCAM-1 binding after 1 day, a peak after 3 days, and a decrease after 7 days was found. After 12 weeks of diet, MB VCAM-1 binding also peaked after 3 days but remained high until 7 days, indicating a delay in endothelial recovery. Two-photon laser scanning microscopy imaging of double fluorescence staining confirmed the exposure of VCAM-1 on the superficial layer after arterial injury only during the healing phase. After complete reendothelialization, VCAM-1 expression persisted in the subendothelial layer but was not reachable for the MB VCAM-1 anymore. Conclusion— Molecular ultrasound imaging with MB VCAM-1 is promising to assess vascular damage and to monitor endothelial recovery after arterial interventions. Thus, it may become an important diagnostic tool supporting the development of adequate therapeutic strategies to personalize anticoagulant and anti-inflammatory therapy after cardiovascular intervention.

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“…26 cIMT reflects pathological changes in the vessel wall that may result from early atherosclerosis and also from aging of the vessel wall. [22][23][24] High MBL may protect from intimalmedial thickening via its beneficial role in vascular clearup processes and tissue turnover. 7 Importantly, cIMT does not reflect the presence of atherosclerotic plaques.…”

Section: Discussionmentioning

confidence: 99%

“…We investigated their longitudinal associations with biomarker scores that reflect low-grade inflammation and endothelial dysfunction and with cIMT as a marker of subclinical vascular disease. [22][23][24] Furthermore, we determined their associations with incident CVD and incident CVEs over a 7-year follow-up period. Previous studies suggested that the effects of lectin-pathway activation in CVD could be both beneficial and adverse.…”

mentioning

confidence: 99%

Distinct Longitudinal Associations of MBL, MASP-1, MASP-2, MASP-3, and MAp44 With Endothelial Dysfunction and Intima–Media Thickness

Hertle

Arts

Kallen

et al. 2016

ATVB

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12associations with future CVD. When the effect of MBL on complications of established CVD was investigated, low MBL was in fact protective in most studies. [13][14][15] Thus, considerable discrepancy remains in the literature on whether MBL has beneficial or adverse effects in CVD.This reported discrepancy might be explained by a dual role of MBL in different etiologic aspects of CVD. Objective-Previous studies suggested that the lectin-complement pathway plays a complex role in cardiovascular disease (CVD). To date, no prospective human studies have investigated the relationship between the initiating factor of the lectin pathway, that is, mannose-binding lectin (MBL), and low-grade inflammation, endothelial dysfunction, or carotid intima-media thickness (cIMT). Moreover, MBL-associated proteases (MASPs) and MBL-associated proteins (MAps), which mediate downstream complement activation, have not been studied in the development of CVD. Approach and Results-In a prospective cohort (n=574; age 60±7 years; 7-year follow-up), we investigated longitudinal associations of plasma MBL, MASP-1, MASP-2, MASP-3, and MAp44 with biomarker scores that reflect low-grade inflammation and endothelial dysfunction, respectively, and with cIMT. We also investigated their associations with incident CVD (n=73). In adjusted analyses, low-grade inflammation was lowest in the middle tertile (T Middle )

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Carotid intima-media thickness as a biomarker of subclinical atherosclerosis

Cited by 108 publications

References 57 publications

Carotid Doppler Ultrasound Evaluation in Patients with Pulsatile Tinnitus

Carotid Doppler Ultrasound Evaluation in Patients with Pulsatile Tinnitus

Noninvasive Molecular Ultrasound Monitoring of Vessel Healing After Intravascular Surgical Procedures in a Preclinical Setup

Distinct Longitudinal Associations of MBL, MASP-1, MASP-2, MASP-3, and MAp44 With Endothelial Dysfunction and Intima–Media Thickness

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