Carotid Plaque Echomorphology and Serum Vascular Endothelial Growth Factor Levels

Heliopoulos, Ioannis; Papazoglou, Dimitrios; Piperidou, H.; Vadikolias, Κonstantinos; Maltezos, Efstratios; Artemis, N.

doi:10.1159/000076759

Cited by 10 publications

(5 citation statements)

References 25 publications

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“…The formation of microvessels at the plaque has also been recognized as a contributing factor to destabilization and rupture. Levels of vascular endothelial growth factor (VEGF), were associated with the presence and severity of intracranial (but not extracranial) carotid stenosis 115 and inversely correlated with carotid plaque GSM, 116,117 predicting a higher presence of intraplaque neovessels as reported in histologic studies.…”

Section: Apoe Presence Is High Among Trls Such As Vldl and Idl A Larmentioning

confidence: 96%

Review of serum biomarkers in carotid atherosclerosis

Martinez

Martorell

Riambau

2020

Journal of Vascular Surgery

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Background: Carotid artery atherosclerotic stenosis is a preventable major cause of stroke, but there is still a need for definition of high-risk plaque in asymptomatic patients who might benefit from interventional therapies. Several image markers are recommended to characterize unstable plaques. The measurement of serum biomarkers is a promising method to assist in decision making, but the lack of robust evidence in the carotid environment burdens their potential as a standard of care. The goal of this review was to offer an updated state-of-the-art study of available serum biomarkers with clinical implications, with focus on those that may predict carotid symptom development. Methods: The Cochrane Library and MEDLINE databases were searched (all until September 2018) for studies on carotid plaque and serum biomarkers of atherosclerosis. Nonhuman, basic science, and histology studies were excluded, focusing on clinical studies. Selected abstracts were screened to include the most relevant articles on atherosclerotic plaque presence, progression, instability or symptom development. Results: Some well-established biomarkers for coronary disease are not relevant to carotid atherosclerosis and other inflammatory biomarkers, lipids, interleukins, homocysteine, and adipokines may be useful in quantifying carotid disease-related risk. Some serum biomarkers combined with image features may assist vascular specialists in selecting patients at high risk for stroke and in need of intervention. Conclusions: Prospective studies applying a combination of biomarkers are essential to prove clinical usefulness.

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Section: Apoe Presence Is High Among Trls Such As Vldl and Idl A Larmentioning

confidence: 96%

Review of serum biomarkers in carotid atherosclerosis

Martinez

Martorell

Riambau

2020

Journal of Vascular Surgery

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“…The formation of microvessels at the plaque has also been recognized as a contributing factor to destabilization and rupture. Levels of vascular endothelial growth factor (VEGF), were associated with the presence and severity of intracranial (but not extracranial) carotid stenosis (Yu et al 2017) and inversely correlated with carotid plaque GSM (Heliopoulos et al 2004;Sayed et al 2009), predicting a higher presence of intraplaque neovessels as reported in histologic studies. ii.…”

Section: Haematological and Neovascularization Biomarkersmentioning

confidence: 96%

The cellular biology of atherosclerosis with atherosclerotic lesion classification and biomarkers

Melaku

Dabi

2021

Bull Natl Res Cent

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Background Atherosclerosis is a chronic lipid-driven inflammatory disease with infiltration of low-density lipoprotein and is considered as the pivotal step in plaque formation. The aim of the review is to get into the fine details of pathophysiologic mechanisms responsible for atherosclerosis with atherosclerotic lesion classification. It also provides a summary of current biomarkers other than the traditional risk factors so that new treatment modalities can emerge and reduce the morbidity and mortality associated with atherosclerosis. Main body In the classification of atherosclerosis made by American Heart Association (AHA), AHA Type I lesion is the earliest vascular change described microscopically. AHA Type II lesion is primarily composed of abundant macrophages. AHA Type III lesion is the earliest of progressive lesions, while AHA Type IV lesion consists of an acellular necrotic core. Various biomarkers are implicated in different stages of the pathophysiological mechanism of plaque formation and evolution. C Reactive Protein plays a direct role in promoting the inflammatory component of atherosclerosis. Fibrinogen was demonstrated to be elevated among patients with acute thrombosis. Higher leukocyte count is associated with a greater cardiovascular risk. Cytokines have been implicated in atheroma formation and complications. High rates of protease activated receptor expression are also induced by interleukin-6 secretion in atherosclerotic lesions and areas of vascular tissue injury. Cluster of differentiation 40 receptor and its ligand have been also detected in atherosclerotic plaques. Osteopontin, acidic phosphoprotein, and osteoprotegerin have emerged as novel markers of atherosclerotic plaque composition. There are also overproductions of matrix metalloproteinases in the rupture-prone regions and promote lipid-necrotic core formation in the atherosclerotic plaque. Myeloperoxidase has been proposed as a marker of plaque instability. Oxidized low-density lipoprotein receptor 1 provides a route of entry for oxidized low-density lipoprotein into the endothelium. A human atherosclerotic lesion also expresses lipoprotein-associated phospholipase A2. Short conclusion Atherosclerotic plaques are the battlefield between an unbalanced immune response and lipid accumulation in the intima of arteries. Most of the biomarkers associated with atherosclerosis are indicators of inflammatory response and will also be used for medical purposes.

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“…For VEGF in particular, animal models have shown that even a low dose of VEGF in blood significantly promotes the progress of arteriosclerosis [16,17]. In humans, the severity of arteriosclerosis in the carotid artery correlates with blood VEGF concentrations [18]. Acid FGFs (aFGF/FGF-1), members of the FGF family, relate to the severity of arteriosclerosis, but there is no relation with FGF-2 [18].…”

Section: Safety Issuesmentioning

confidence: 99%

“…In humans, the severity of arteriosclerosis in the carotid artery correlates with blood VEGF concentrations [18]. Acid FGFs (aFGF/FGF-1), members of the FGF family, relate to the severity of arteriosclerosis, but there is no relation with FGF-2 [18]. However, the possibility cannot be excluded that arteriosclerosis progresses by indirect induction of HGF and VEGF in association with overexpression of FGF-2 [19].…”

Section: Safety Issuesmentioning

confidence: 99%

Efficacy and Safety of DVC1-0101 for Intermittent Claudication Secondary to Peripheral Artery Disease: Study Protocol of a Randomized Phase IIb Trial

Tanaka

Matsumoto²,

Morisaki³

et al. 2013

J Clin Trials

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Background: We have developed a new gene transfer vector based on nontransmissible recombinant Sendai virus expressing the human fibroblast growth factor-2 gene (DVC1-0101) to treat peripheral arterial disease. A phase I/IIa open-label four dose-escalations clinical trial for critical limb ischemia was completed. We concluded that DVC1-0101 is safe and well tolerated, and resulted in significant improvement of limb function. We present the protocol of the next phase of our study. Methods: We plan to conduct a phase IIb clinical trial, which will be a randomized, placebo-controlled, parallel design, single-dose blinded and single center clinical trial in Japan. This study will enroll 60 patients diagnosed with PAD with intermittent claudication. Subjects who meet eligibility criteria will be randomized to receive a single dose of either placebo, 5 × 10 9 ciu/limb of DVC1-0101, or 1 × 10 9 ciu/limb of DVC1-0101 administered by direct intramuscular injection. The participation length in this trial for subjects will be approximately 12 months with nine visits. The primary endpoints are to evaluate the efficacy of DVC1-0101 versus placebo on peak walking time, and to evaluate the safety and tolerability of two dosage levels of DVC1-0101. The secondary endpoints are 1) to evaluate the effect of DVC1-0101 on claudication onset time, measured by a treadmill test and quality of life, measured using the Walking Impairment Questionnaire, 2) to determine the effect of DVC1-0101 on qualifying limb hemodynamics, and 3) to explore the pharmacodynamics of DVC1-0101 by evaluating biomarkers. Discussion: The results of this trial will provide insights into the potential of DVC1-0101 for improving walking activities. The results will also help with the design of a possible phase III study.

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Carotid Plaque Echomorphology and Serum Vascular Endothelial Growth Factor Levels

Cited by 10 publications

References 25 publications

Review of serum biomarkers in carotid atherosclerosis

Review of serum biomarkers in carotid atherosclerosis

The cellular biology of atherosclerosis with atherosclerotic lesion classification and biomarkers

Efficacy and Safety of DVC1-0101 for Intermittent Claudication Secondary to Peripheral Artery Disease: Study Protocol of a Randomized Phase IIb Trial

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