scholarly journals Καρδιακοί δείκτες

2013 ◽  
Author(s):  
Κωνσταντίνος Καζάνης

Cardiovascular disease is the primary cause of death in westernizedpopulation. However, a number of cardiovascular fatalities may be preventable if wehave biomarkers upstream from markers of necrosis such as inflammatory cytokines,acute-phase reactants, biomarkers of ischemia and of myocardial stretch, which mayprovide an earlier assessment of overall patient risk. Recently ischemia modifiedalbumin (IMA) has been proposed as a biomarker in clinical conditions related toischemia associated with oxidative stress, such as cardiac ischemia, or persistentperipheral ischemia (chronic kidney disease, systemic sclerosis, hypercholesterolemia,type 2 diabetes). IMA represents the in vivo modification of human serum albuminamino-terminal end by reactive oxygen species (ROS). The N-terminal end (aminoterminal end) of albumin molecule is a binding site for transition metals. As a result ofROS generated by hypoxia, free-radical injury or membrane disruption, the Nterminalof albumin molecule undergoes a decrease in binding capacity in thepresence of ischemia. This alteration can be measured by the albumin cobalt bindingtest (ACB test).Aim: The aim of the present study was to investigate serum levels of IMA, as apotential marker of presence and/or severity of coronary artery disease (CAD) insubjects with documented CAD and without documented CAD in association withmenopause and obesity conditions that are associated with an increase ofcardiovascular risk.Methods and Results: The study included 429 individuals divided into 3 Groups.Group A: consists of 12 hypertensive patients undergoing exercise stress test (EST).IMA, albumin and NT-proBNP kinetics were investigated in 12 hypertensive patientsduring the EST. An hour after stress, IMA and NT-proBNP serum levels weresignificantly higher than baseline suggesting a myocardial ischemic burden and aventricular myocyte stretch respectively. There was not any change of albumin serumlevels an hour after stress. At maximum exercise, there was a decrease of IMA serumlevels as compared to baseline values, attributed probably to the increase of lacticserum levels that generates an analytical interference on ACB test.Group B: consists of 114 patients (88 men and 30 women) aged 43-80 years withdocumented CAD without evidence of acute coronary syndrome (ACS) undergoingcoronary angiography (CA) and 163 controls (131 men and 32 women) of similaraged. Serum IMA levels were measured before CA. Serum levels of high-sensitivityC-reactive protein (hsCRP), cardiac troponin T (cTnT), CK-MB concentration and Nterminalpro brain natriuretic peptide (NT-proBNP), which represent biomarkers ofinflammation, of myocardial ischemia, damage or necrosis as well as serum totalantioxidant status (TAS) were also evaluated. The results indicated that IMA levelswere higher (p<0.001) while TAS was lower (p<0.001) in patients than in controls.IMA and TAS were negatively correlated in all subjects (p<0.001). Among patients,there was no correlation between IMA and the number of diseased vessels (severity ofCAD). Serum levels of hsCRP and NT-proBNP were higher (p<0.001 and p=0.008for NT-proBNP) in patients than in controls. However, although the studied patientswere at high risk of ACS based upon CA documentation, only 8 (7%) of those hadhsCRP levels above the cut-off of 3mg/L, which indicates elevated vascular risk. Inpatients, serum NT-proBNP levels were elevated (above 161 pg/mL) only in thosebelonging to the two upper quartiles of NT-proBNP distribution. The observed cTnTlevels did not suggest myocardial necrosis. Serum IMA determination seems toprovide an index of the presence of CAD before any elevation of cTnT and/or NTproBNP.For CAD diagnosis the best cut-off point for IMA was 101.5 KU/L with asensitivity and a specificity of 87.7% and negative predictive value 83.3%. IMA wasassociated with an increased risk for CAD (OR=1.23, 95% CI: 1.16-1.31; p<0.001).Albumin serum levels, although within the normal range, were decreased in patientsin comparison to controls.Group C: consists of 130 non-smoker postmenopausal women aged 43-80 years, 40with BMI 26-32 kg/m2 (overweight), 60 with BMI 21-25 (non-overweight), and 30with documented CAD and BMI 23-29. Serum IMA, albumin, hsCRP and NTproBNP,glucose and insulin were measured. Homeostasis assessment model score(HOMA) and Quantitative insulin sensitivity index (QUICKI) were co-estimated.Serum IMA levels were significantly elevated in overweight as compared to nonoverweight(p<0.001) women but were similar to those with CAD. hsCRP and NTproBNPdid not differ between overweight and non-overweight while they were lowerin comparison to those with CAD (p<0.001). Glucose, insulin and HOMA wereelevated in overweight compared to non-overweight (p<0.001) while QUICKI waslower (p<0.001). In overweight women, IMA was positively correlated with BMI,hsCRP, insulin, HOMA and negatively with QUICKI. Multivariable regressionanalysis revealed that in postmenopausal women obesity was the strongest significantpredictor (determinant) of circulating IMA levels (p<0.001) contributing, therefore, tothe elevated serum IMA concentration.Conclusions: It is worth pointing out that IMA was measured by the ACB assay and the determinants of the ACB assay mechanism of action include, apart from the proportion of intact N-terminus of serum albumin, serum albumin concentration, thestate of oxidation of cys34 of serum albumin, the plasma pH and the plasmacysteine/cystine ratio encountered with oxidative stress, conditions that are associatedor predispose to atherosclerosis and vascular disease.In conclusion our results suggest that:1. IMA determination may provide earlier information of CAD presence before hsCRP or NT-proBNP elevation, contributing to early assessment of overall patient risk.2. Postmenopausal obesity is associated with elevated serum IMA possibly due to obesity-associated oxidative stress and IMA measurement could provide an assessment of global atherosclerotic burden in postmenopausal women.3. Increased serum IMA levels after EST suggest a large myocardial ischemic burden.Whether that elevation may be useful for predicting the severity of myocardialischemia and/or improve the accuracy of EST remains to be elucidated.IMA measurement might provide alone or in contribution with other serumbiomarkers an earlier assessment of global atherosclerotic burden andcardiovascular risk.

Maturitas ◽  
2011 ◽  
Vol 70 (2) ◽  
pp. 182-187 ◽  
Author(s):  
Konstantinos Kazanis ◽  
Maria Dalamaga ◽  
Eva Kassi ◽  
Charalampos Nounopoulos ◽  
Antonios S. Manolis ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Chwan-Li Shen ◽  
Huanbiao Mo ◽  
Dale M. Dunn ◽  
Bruce A. Watkins

Osteoporosis is a major health problem in postmenopausal women. Herein we evaluated the effects of 12-week tocotrienols (TT) supplementation on serum metabolites in postmenopausal, osteopenic women. Eighty-nine participants (59.7 ± 6.8 yr, BMI 28.7 ± 5.7 kg/m2) were assigned to 3 treatments: placebo (860 mg olive oil/day), 300mg TT (300 mg TT/day), and 600mg TT (600 mg TT/day) for 12 weeks. TT consisted of 90% δ-TT and 10% γ-TT. In this metabolomic study, we evaluated the placebo and 600mgTT at baseline and 12 weeks. As expected, TT and its metabolite levels were higher in the supplemented group after 12 weeks. At baseline, there were no differences in demographic parameters or comprehensive metabolic panels (CMP). Metabolomics analysis of serum samples revealed that 48 biochemicals were higher and 65 were lower in the 600mg TT group at 12 weeks, compared to baseline. The results confirmed higher serum levels of tocotrienols and lysophospholipids, but lower acylcarnitines and catabolites of tryptophan and steroids in subjects given 600mg TT. In summary, 12-week TT supplementation altered many serum metabolite levels in postmenopausal women. The present study supports our previous findings that TT supplementation helps reduce bone loss in postmenopausal osteopenic women by suppressing inflammation and oxidative stress. Furthermore, the body incorporates TT which restructures biomembranes and modifies phospholipid metabolism, a response potentially linked to reduced inflammation and oxidative stress.


2020 ◽  
Vol 21 (1) ◽  
pp. 314
Author(s):  
Arno R. Bourgonje ◽  
Amaal Eman Abdulle ◽  
Areej M. Al-Rawas ◽  
Muna Al-Maqbali ◽  
Mohsin Al-Saleh ◽  
...  

Oxidative stress plays a pivotal role in the pathogenesis of cardiovascular diseases (CVD). Postmenopausal women have an increased risk of developing CVD due to decreased estrogen availability, which is accompanied by increased oxidative stress. Serum free thiols (R-SH) provide a robust and powerful read-out of systemic oxidative stress. In this study, we aimed to establish serum levels of free thiols and explore associations between free thiols and demographic, clinical, and biochemical parameters related to obesity and the risk for developing CVD in both pre- and postmenopausal women. Serum free thiols were measured in a cohort consisting of healthy pre- (n = 223) and postmenopausal (n = 118) Omani women. Postmenopausal women had significantly lower levels of serum free thiols as compared to premenopausal women (762.9 ± 85.3 vs. 780 ± 80.9 μM, age-adjusted p < 0.001). Women′s age was positively associated with serum free thiol levels in premenopausal women (β = 0.36, p = 0.002), whereas an inverse association was observed in postmenopausal women (β = −0.29, p = 0.002). Homocysteine levels were significantly inversely associated with serum free thiol levels in both pre- (β = −0.19, p = 0.005) and postmenopausal (β = −0.20, p = 0.032) women, independent from known cardiovascular risk factors. In this study, we show that postmenopausal women are affected by increased systemic oxidative stress, which independently associates with homocysteine levels.


2019 ◽  
Vol 14 ◽  
pp. 117727191984382 ◽  
Author(s):  
Fawaz Y Azizieh ◽  
Diaa Shehab ◽  
Khaled Al Jarallah ◽  
Renu Gupta ◽  
Raj Raghupathy

Introduction: Receptor activator of nuclear factor κB ligand (RANKL), osteoprotegerin (OPG), and oxidative stress markers are suggested to contribute to bone loss in osteoporosis that occurs in menopause. However, the association between these markers and bone mineral density (BMD) is controversial. The aim of this study was to measure circulatory levels of these parameters in postmenopausal women with normal or low BMD. Methods: The study population included 71 postmenopausal women, of whom 25 had normal BMD, 31 had osteopenia, and 15 had osteoporosis. Serum levels of RANKL, OPG, and 5 oxidative stress markers (catalase, peroxiredoxin 2 [PRX2], superoxide dismutase 1 [SOD1], superoxide dismutase 2 [SOD2], and thioredoxin [TRx1]) were measured using the Multiplex system. Results: As compared with subjects having normal BMD, subjects with low BMD had significantly lower median serum levels of OPG, catalase, SOD2, and PRX2 ( P = .004, .031, .044, and .041 respectively). Although levels of RANKL were not different between the 2 groups, the RANKL/OPG ratio was higher in women with low BMD ( P = .027). Conclusions: These data provide insights into the possible roles of OPG, RANKL, and oxidative stress in the pathogenesis of postmenopausal osteoporosis. However, the lack of association between these markers and BMD indicates that osteoporosis is complex and multivariate.


2020 ◽  
Vol 5 (1) ◽  
pp. e06-e06
Author(s):  
Fatemeh Goli ◽  
Hamid Nasri

Introduction: Hemodialysis (HD) patients have elevated markers of oxidative stress which is contributed to increased mortality. Objectives: The aim of this study was to determine the association of 8-hydroxy-2’-deoxyguanosine (8- OHdG) as a marker of oxidative stress with various demographic and biochemical parameters in HD patients. Patients and Methods: Eighty-five HD patients (58 men and 27 women; mean ± SD of age was 62.8 ± 13.76 years) who were under HD therapy for at least six months and did not have a systemic infection were enrolled in the study. Serum 8-OHDG was measured by ELISA (enzyme-linked immunosorbent assay) method. Additionally levels of vitamin D, magnesium, and intact parathyroid hormone (PTH) were measured with standard kits. Other clinical and biochemical variables were gathered from patients’ files. Results: The result showed no significant correlation between serum levels of 8-OHDG with measured biochemical and demographic parameters. However, in HD patients with diabetes and hypertension (or combined), a significant reverse correlation between serum albumin and 8-OHdG was detected. Conclusion: In the age group under 40 years, we found a positive and significant correlation between albumin and 8-OHdG. This finding requires further investigation to determine relationship between serum 8-OHdG levels and serum albumin types as reduced and oxidized forms.


Biomolecules ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. 261 ◽  
Author(s):  
Gadah Albasher ◽  
Rafa Almeer ◽  
Fatimah O. Al-Otibi ◽  
Noorah Al-Kubaisi ◽  
Ayman M. Mahmoud

Exposure to organophosphorus insecticides causes several health problems to animals and humans. Red beetroot (RBR) is rich in antioxidant ingredients and possesses a promising hepatoprotective activity. This study evaluated the potential of RBR extract to prevent chlorpyrifos (CPF)-induced liver injury, with an emphasis on oxidative stress, inflammation and apoptosis. Rats received 10 mg/kg CPF and were treated with 300 mg/kg RBR extract for 28 days. CPF caused liver injury evidenced by elevated serum levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and bilirubin, along with several histological alterations. Hepatic lipid peroxidation (LPO) and nitric oxide (NO) levels, as well as inducible nitric oxide synthase (iNOS) and pro-inflammatory cytokines were increased in CPF-intoxicated rats. RBR prevented CPF-induced histological alterations, and ameliorated liver function, LPO, NO, iNOS and pro-inflammatory cytokines. RBR boosted glutathione and antioxidant enzymes, and increased Nrf2 expression. In addition, RBR diminished Bax and caspase-3, and increased Bcl-2 expression. In conclusion, RBR prevented CPF-induced liver injury via attenuation of oxidative stress, inflammation and apoptosis. RBR enhanced antioxidant defenses, suggesting that it could be used as a potential therapeutic intervention to minimize CPF hepatotoxicity.


2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Jaroslav Zelenka ◽  
Aleš Dvořák ◽  
Lukáš Alán ◽  
Marie Zadinová ◽  
Martin Haluzík ◽  
...  

Mild constitutive hyperbilirubinemia is associated with a reduced risk of cardiovascular diseases, diabetes, and cancer. Since these pathologies are associated with aging, inflammation, and oxidative stress, we investigated whether hyperbilirubinemia interferes with ROS homeostasis in cell cultures and with inflammation, senescence, and mitochondrial dysfunction in aged rats. Human embryonic kidney cells and rat primary fibroblasts showed a dose-dependent decrease in the ratio of oxidized/reduced glutathione, intracellular H2O2levels, and mitochondrial ROS production, with increasing bilirubin concentrations in the culture media. Compared to their normobilirubinemic siblings, aged hyperbilirubinemic Gunn rats showed significantly smaller amounts of visceral fat, better glucose tolerance, and decreased serum levels of proinflammatory cytokines TNFα, IL-1β, and IL-18. Simultaneously, livers from Gunn rats showed decreased expression of senescence markers and cell cycle inhibitors p21 and p16. Mitochondria from aged Gunn rats showed higher respiration and lower H2O2production compared to controls. In conclusion, we demonstrated that mildly elevated serum bilirubin is generally associated with attenuation of oxidative stress and with better anthropometric parameters, decreased inflammatory status, increased glucose tolerance, fewer signs of cellular senescence, and enhanced mitochondrial function in aged rats.


2018 ◽  
Vol 206 (1-2) ◽  
pp. 62-72 ◽  
Author(s):  
Maha Abu Gazia ◽  
Mohammed Abu El-Magd

This study was conducted to evaluate the potential cardioprotective effect of cardamom (CAR) against myocardial injuries induced by doxorubicin (DOX) in rats through investigation of histological alterations and the associated oxidative stress, apoptosis, inflammation, and angiogenesis. This study included 30 adult male albino rats that were randomized to 3 groups (n = 10/group): group I (control), group II (DOX) rats injected with DOX (2.5 mg/kg body weight [BW] i.p.) every other day for 2 weeks, and group III (CAR+DOX) received CAR extract (200 mg/kg BW) orally for 3 weeks, and 1 week later (starting from the 2nd week) they were injected with DOX (2.5 mg/kg BW i.p.) every other day for 2 weeks. Rats treated with DOX alone exhibited notable myocardial damage (discontinuity and disorganization of cardiac muscle fibers, mononuclear cell infiltration, and apparent increases in collagen fiber deposition) accompanied by loss of function (revealed by elevated serum levels of lactate dehydrogenase, creatine kinase, and cardiac troponin), induction of oxidative stress (indicated by higher levels of nitric oxide and malon­dialdehyde, and lower levels of superoxide dismutase, catalase, and glutathione peroxidase), apoptosis (evidenced by high caspase 3 activity and immunostaining), and inflammation (marked by high cardiac NFκB level). However, administration of CAR not only ameliorated all deleterious effects of DOX but also induced angiogenesis, as indicated by a significant increase in VEGF immunoreactivity. These data indicate that CAR could relieve DOX-induced cardiotoxicity, at least in part, via reductions in oxidative stress, apoptosis, and inflammation and increased tissue regeneration via induction of angiogenesis. Therefore, CAR could be a promising cytoprotective agent against DOX cardiotoxicity.


Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Jong-Won Chung ◽  
Hyun Ah Choi ◽  
Mi Ji Lee ◽  
Joon Hwa Lee ◽  
Moo-Seok Park ◽  
...  

Aims: Endothelial dysfunction and inflammation play a major role in the progression of atherosclerosis. This study aimed to evaluate the differential roles of endothelial dysfunction and inflammation in intracranial atherosclerotic stroke (ICAS). Methods: We prospectively recruited 262 patients with acute cerebral infarcts caused by ICAS and 75 individuals with no history of stroke as controls. Markers of endothelial dysfunction (asymmetric dimethylarginine, ADMA) and inflammation (lipoprotein-associated phospholipase A2, Lp-PLA 2 ) were measured. Acute ischemic lesions were measured in terms of their size, composition, and patterns. Subclinical microangiopathy (degree of leukoaraiosis) and macroangiopathy (presence/number of tandem stenoses) were graded in each patient. Results: Compared to normal controls, serum levels of ADMA (0.69 ± 0.14 vs. 0.47 ± 0.10, P < 0.001) and Lp-PLA 2 (138.1 ± 116.8 vs. 19.0 ± 58.0, P < 0.001) were elevated in patients with ICAS. Although there was a significant correlation between ADMA and Lp-PLA 2 levels in patients with ICAS (r 2 = 0.235, P <0.001), some patients showed high Lp-PLA 2 but low ADMA levels, while others showed high ADMA but low Lp-PLA 2 levels. A high ADMA serum level was associated with a greater prevalence of preclinical microangiopathy and macroangiopathy. Contrastingly, an elevated serum Lp-PLA 2 level was associated with larger ischemic lesions, a greater number of lesions, and a larger cortical pattern. Conclusion: Endothelial dysfunction and inflammation have distinct effects in ICAS patents: endothelial dysfunction is associated with the underlying micro- and macro-atherosclerotic burden, whereas inflammation is associated with acute infarct volume and pattern.


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