Markers of subclinical atherosclerosis in patients with aortic valve sclerosis: A meta-analysis of literature studies

Minno, Matteo Nicola Dario Di; Minno, Alessandro Di; Songia, Paola; Ambrosino, Pasquale; Gripari, Paola; Ravani, A.; Pepi, Mauro; Rubba, P.; Medda, Emanuela; Tremoli, Elena; Baldassarre, Damiano; Poggio, Paolo

doi:10.1016/j.ijcard.2016.08.122

Cited by 26 publications

(19 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As we shown above, reduction in the markers of biological oxidation (oxidized LDL, IOD) in cardiovascular patients treated with GA lycopene translates into increase in tissue oxygenation and flow‐mediated dilation at the end of the observational period. Both parameters are important systemic measures of cardiovascular health (Di Minno et al., ; Schröder, ) which suggests that antioxidant supplementation may have a measurable impact on the outcomes of cardiovascular disease.…”

Section: Discussionmentioning

confidence: 99%

Effect of lycopene supplementation on cardiovascular parameters and markers of inflammation and oxidation in patients with coronary vascular disease

Petyaev

Dovgalevsky

Klochkov

et al. 2018

Food Science & Nutrition

View full text Add to dashboard Cite

Oxidative stress and antioxidant deficiency play a pivotal role in initiation, development, and outcomes of cardiovascular disease. Pharmacokinetic parameters as well as the impact of highly bioavailable lycopene on cardiovascular variables, markers of inflammation and oxidation were investigated during a 30‐day clinical trial in patients with coronary vascular disease. The patients were randomized into two major groups and were supplemented with a single 7 mg daily dose of lycopene ingested either in the form of lactolycopene (68 patients) or in the form of lycosome‐formulated GA lycopene (74 patients). The endpoints included cardiovascular function parameters, serum lipids, and four markers of oxidative stress and inflammation. Ingestion of lycosome‐formulated lycopene increased serum lycopene levels by 2.9‐ and 4.3‐fold, respectively, after 2 and 4 weeks of the trial, whereas supplementation with lactolycopene upregulated serum lycopene by half‐fold only after 4 weeks of ingestion. Lycosome formulation of lycopene resulted by the end of the trial in a threefold reduction in Chlamydia pneumoniae IgG and reduction to the same degree of the inflammatory oxidative damage marker. The decrease in oxidized LDL caused by lycosome‐formulated lycopene was fivefold. Moreover, supplementation with lycosome‐formulated lycopene was accompanied by a significant increase in tissue oxygenation and flow‐mediated dilation by the end of the observational period. In contrast, lactolycopene did not cause any significant changes in the parameters studied. Therefore, enhanced bioavailability of lycopene promotes its antioxidant and anti‐inflammatory functions and endorses a positive effect of lycopene on cardiovascular system.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of lycopene supplementation on cardiovascular parameters and markers of inflammation and oxidation in patients with coronary vascular disease

Petyaev

Dovgalevsky

Klochkov

et al. 2018

Food Science & Nutrition

View full text Add to dashboard Cite

show abstract

“…The prognostic value of MHO in the primary prevention of CVD is the subject of an ongoing debate [4]. Given that the onset of clinical CVD events, following the appearance of metabolic risk factors, requires a long period of time [5], the confirmation of subclinical atherosclerosis, manifested by elevated pulse wave velocity, pulse pressure (PP) or albuminuria [6][7][8][9], may play an important role in the primary prevention of CVD, and may allow better evaluation of the impact of obesity-related factors on the development of overt CVD within a relatively short period.…”

Section: Introductionmentioning

confidence: 99%

Transition of metabolic phenotypes and risk of subclinical atherosclerosis according to BMI: a prospective study

et al. 2020

View full text Add to dashboard Cite

Aims/hypothesis The cardiometabolic risk associated with metabolically healthy obesity (MHO) remains the subject of debate. It is unclear whether MHO is a transient condition that affects subclinical atherosclerosis risk. In this study, we aimed to investigate the association of MHO and its transition over time with incident subclinical atherosclerosis. Methods A prospective study was conducted with 6220 Chinese adults who were free of cardiovascular disease (CVD) at baseline. Obesity was defined as BMI ≥25.0 kg/m 2. Metabolic health was defined as an individual having fewer than two of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (NCEP ATP III) criteria for components of the metabolic syndrome (excluding waist circumference). Subclinical atherosclerosis was measured by brachial-ankle pulse wave velocity, pulse pressure and albuminuria, separately or combined. Participants were cross-classified by BMI categories and by metabolic health status and its transition during follow-up. Inverse probability weighted logistic regression models were used to estimate ORs and 95% CIs for subclinical atherosclerosis. Results The MHO phenotype accounted for 16.3% of the total population and 32.8% of the population with obesity at baseline. Baseline MHO was not significantly associated with incident subclinical atherosclerosis. During a follow-up period of 4.4 years, 46.8% of individuals with MHO developed a metabolically unhealthy status. Those with transient MHO had an increased risk of composite subclinical atherosclerosis compared with those in the metabolically healthy non-obesity reference group (OR 2.52 [95% CI 1.89, 3.36]). A transition from metabolically unhealthy to healthy status was shown to decrease the outcome risk. The relationship between BMI and subclinical atherosclerosis was partly mediated by BP and plasma glucose. Conclusions/interpretation MHO is not a stable condition and transient MHO conferred an increased risk of subclinical atherosclerosis, the early stage of CVD. Hence, individuals may benefit from early behavioural or medical management in order to avoid a deterioration of metabolic status and prevent atherosclerosis and CVD.

show abstract

“…Several clinical studies evidenced an association between AVSc and coronary atherosclerosis with systemic endothelial dysfunction measured by flow-mediated dilation, carotid intima-media thickness and pulse wave velocity [7,30,31]. Indeed, it has been hypothesized that a possible trigger of AVSc is represented by endothelial dysfunction [32].…”

Section: Discussionmentioning

confidence: 99%

“…To date, it is estimated that, in the general population, almost 30% of people over 65 years of age present AVSc with a drastically increased prevalence to develop severe AS, myocardial infarction or stroke [4,5]. Indeed, growing evidence suggests that AVSc is deeply associated with cardiovascular events [6,7]. However, little is known regarding its initial pathogenic mechanisms.…”

Section: Introductionmentioning

confidence: 99%

“…However, little is known regarding its initial pathogenic mechanisms. Recent meta-analyses evaluating subclinical atherosclerosis revealed that AVSc is associated with increased carotid intima-media thickness, carotid plaques, coronary plaques, altered flow-mediated dilation, pulse wave velocity and augmentation index [6,7]. Endothelial dysfunction could represent the initial trigger of aortic leaflet structural deterioration.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Impact of Oxidative Stress and Protein S-Glutathionylation in Aortic Valve Sclerosis Patients with Overt Atherosclerosis

Valerio

Myasoedova

Moschetta

et al. 2019

JCM

Self Cite

View full text Add to dashboard Cite

Aortic valve sclerosis (AVSc) is characterized by non-uniform thickening of the leaflets without hemodynamic changes. Endothelial dysfunction, also caused by dysregulation of glutathione homeostasis expressed as ratio between its reduced (GSH) and its oxidised form (GSSG), could represent one of the pathogenic triggers of AVSc. We prospectively enrolled 58 patients with overt atherosclerosis and requiring coronary artery bypass grafting (CABG). The incidence of AVSc in the studied population was 50%. The two groups (No-AVSc and AVSc) had similar clinical characteristics. Pre-operatively, AVSc group showed significantly lower GSH/GSSG ratio than No-AVSc group (p = 0.02). Asymmetric dimethylarginine (ADMA) concentration was significantly higher in AVSc patients compared to No-AVSc patients (p < 0.0001). Explanted sclerotic aortic valves presented a significantly increased protein glutathionylation (Pr-SSG) than No-AVSc ones (p = 0.01). In vitro, inhibition of glutathione reductase caused β-actin glutathionylation, activation of histone 2AX, upregulation of α2 smooth muscle actin (ACTA2), downregulation of platelet and endothelial cell adhesion molecule 1 (PECAM1) and cadherin 5 (CDH5). In this study, we showed for the first time that the dysregulation of glutathione homeostasis is associated with AVSc. We found that Pr-SSG is increased in AVSc leaflets and it could lead to EndMT via DNA damage. Further studies are warranted to elucidate the causal role of Pr-SSG in aortic valve degeneration.

show abstract

Markers of subclinical atherosclerosis in patients with aortic valve sclerosis: A meta-analysis of literature studies

Cited by 26 publications

References 46 publications

Effect of lycopene supplementation on cardiovascular parameters and markers of inflammation and oxidation in patients with coronary vascular disease

Effect of lycopene supplementation on cardiovascular parameters and markers of inflammation and oxidation in patients with coronary vascular disease

Transition of metabolic phenotypes and risk of subclinical atherosclerosis according to BMI: a prospective study

Impact of Oxidative Stress and Protein S-Glutathionylation in Aortic Valve Sclerosis Patients with Overt Atherosclerosis

Contact Info

Product

Resources

About