scholarly journals The Relationship between Coenzyme Q10, Oxidative Stress, and Antioxidant Enzymes Activities and Coronary Artery Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Bor-Jen Lee ◽  
Yi-Chin Lin ◽  
Yi-Chia Huang ◽  
Ya-Wen Ko ◽  
Simon Hsia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Antioxidant Enzymes ◽  
Coronary Artery ◽  
Coenzyme Q10 ◽  
Control Group ◽  
Enzymes Activities ◽  
Antioxidant Enzymes Activities ◽  
Artery Disease ◽  
The Relationship

A higher oxidative stress may contribute to the pathogenesis of coronary artery disease (CAD). The purpose of this study was to investigate the relationship between coenzyme Q10 concentration and lipid peroxidation, antioxidant enzymes activities and the risk of CAD. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery were assigned to the case group (n=51). The control group (n=102) comprised healthy individuals with normal blood biochemical values. The plasma coenzyme Q10, malondialdehyde (MDA) and antioxidant enzymes activities (catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx)) were measured. Subjects with CAD had significant lower plasma coenzyme Q10, CAT and GPx activities and higher MDA and SOD levels compared to those of the control group. The plasma coenzyme Q10 was positively correlated with CAT and GPx activities and negatively correlated with MDA and SOD. However, the correlations were not significant after adjusting for the potential confounders of CAD with the exception of SOD. A higher level of plasma coenzyme Q10 (≥0.52 μmol/L) was significantly associated with reducing the risk of CAD. Our results support the potential cardioprotective impact of coenzyme Q10.

scholarly journals The Association between theLPAGene Polymorphism and Coronary Artery Disease in Chinese Han Population

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Zi-Kai Song ◽  
Hai-Di Wu ◽  
Hong-Yan Cao ◽  
Ling Qin
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chinese Han Population ◽  
Control Group ◽  
Case Group ◽  
Chinese Han ◽  
Han Population ◽  
Increased Risk ◽  
Artery Disease ◽  
The Relationship

Lp(a) has been well known as an independent risk factor for coronary artery disease (CAD). TheLPAgene, as it encodes apo(a) of the Lp(a) lipoprotein particle, was associated with increased risk of CAD. The purpose of this study was to analyze the relationship between the polymorphisms ofLPAgene and CAD in Chinese Han population. Five SNPs (rs1367211, rs3127596, rs6415085, rs9347438, and rs9364559) in theLPAgene were genotyped using Sequenom MassARRAY time-of-flight mass spectrometer (TOF) in 560 CAD patients as case group and 531 non-CAD subjects as control group. The numbers of these two groups were from Chinese Han ancestry. The results showed that allele (P=0.046) and genotype (P=0.026) of rs9364559 in theLPAgene was associated with CAD. The frequency of rs9364559 minor allele (G) in case group was obviously higher than that in control group. Results of haplotype analysis showed that 4 haplotypes which contained rs9364559-G were associated with increased risk of CAD in this population. This study explored rs9364559 in theLPAgene may be associated with the pathogenesis of CAD; and the risk of CAD might be higher in the population carrying 4 haplotypes of different blocks in theLPAgene.

Serum Selenium and Glutathione Peroxidase Concentrations in Iranian Patients with Angiography-Defined Coronary Artery Disease

Angiology ◽  
2008 ◽  
Vol 60 (2) ◽  
pp. 186-191 ◽  
Author(s):  
Parizadeh Seyyed Mohammad Reza ◽  
Mohsen Moohebati ◽  
Fahimeh Ghafoori ◽  
Majid Ghayour-Mobarhan ◽  
Seyyed Mohammad Reza Kazemi-Bajestani ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Glutathione Peroxidase ◽  
Fasting Blood Glucose ◽  
Mean Value ◽  
Control Group ◽  
Serum Selenium ◽  
Artery Disease ◽  
The Relationship ◽  
Iranian Patients

This study investigated the relationship between serum selenium (Se) and glutathione peroxidase (GPx) levels and the presence of coronary artery disease (CAD) among Iranian patients. Three groups were compared: patients undergoing angiography with angiographically defined CAD, individuals with a normal angiogram, and apparently healthy controls with no evidence of overt CAD. Anthropometric measurements, blood pressure, fasting blood glucose and lipid profiles, serum Se and GPx measurements, and angiographic assessment were carried out using standard protocols. Mean serum Se concentrations were not significantly different between patients with and without CAD and the control group. The mean value of serum GPx in the control group was significantly higher than in patients with or without CAD. Selenium status did not differentiate between patients with and without CAD, which may be related to the fact that angiography is not a very sensitive index of global atherosclerosis, and it is possible that patients who were CAD negative by angiogram still have significant disease. It may also be that Se is not a good marker of CAD.

Inverse Correlation Between Plasma Beta-Carotene and Interleukin-6 in Patients with Advanced Coronary Artery Disease

2010 ◽  
Vol 80 (6) ◽  
pp. 369-377 ◽  
Author(s):  
Vladimíra Muzáková ◽  
Roman Kand’ár ◽  
Milan Meloun ◽  
Jirí Skalický ◽  
Karel Královec ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Interleukin 6 ◽  
Inverse Correlation ◽  
Beta Carotene ◽  
Alpha Tocopherol ◽  
Control Group ◽  
Artery Disease ◽  
Advanced Coronary Artery Disease

The interrelationships between plasma beta-carotene, alpha-tocopherol, and the level of systemic inflammation and oxidative stress were investigated in patients with advanced coronary artery disease (CAD). Plasma beta-carotene, alpha-tocopherol, malondialdehyde, free radicals, interleukin-6, high sensitive C-reactive protein levels, and other risk factors of CAD were determined in a group of patients with advanced CAD [significant stenosis according to coronarographic examination (n = 91) and a control group of examined patients with coronary arteries with no stenosis (n = 49)]. Between-group differences in continuous variables were analyzed with the Hotelling T2-test (software NCSS2000), analyses of correlation matrix with the software STATISTICA. Advanced CAD coincided with significantly lower plasma concentrations of high-density lipoprotein (HDL)-cholesterol and beta-carotene as well as with elevated levels of all inflammatory markers, but only with mild increase of oxidative stress. Beta-carotene significantly inversely correlated with interleukin-6. This inverse correlation could suggest potential protective effect of beta-carotene on atherosclerosis due to the inhibition of inflammatory processes.

scholarly journals Correlations between Oxidative DNA Damage, Oxidative Stress and Coenzyme Q10 in Patients with Coronary Artery Disease

2012 ◽  
Vol 9 (8) ◽  
pp. 621-626 ◽  
Author(s):  
Yüksel KAYA ◽  
Ayşegül ÇEBİ ◽  
Nihat SÖYLEMEZ ◽  
Halit DEMİR ◽  
Hamit Hakan ALP ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Dna Damage ◽  
Coronary Artery ◽  
Coenzyme Q10 ◽  
Oxidative Dna Damage ◽  
Artery Disease

scholarly journals A Study of Effects of Addition of Coenzyme Q 10 to High Dose Statins in Patients of Coronary Artery Disease with Special Reference to Oxidative Balance

2017 ◽  
Vol 02 (01) ◽  
pp. 006-013
Author(s):  
Malleswara Dangeti ◽  
Siva Katkam ◽  
Raghu Galla ◽  
Ravi Kiran ◽  
Indrani Garre
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Statin Therapy ◽  
Coenzyme Q10 ◽  
Coenzyme Q ◽  
High Dose ◽  
Plasma Glutathione ◽  
Artery Disease ◽  
Plasma Malondialdehyde

AbstractBackground: Oxidative stress is one of the most potent inductors of endothelial dysfunction and is involved at all stages of atherosclerotic plaque evolution. Statins are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and are potent inhibitors of cholesterol biosynthesis. In clinical trials, statins are beneficial in the primary and secondary prevention of coronary heart disease. Statins also possess direct free radical scavenging activity. However, the prooxidant effect of statins has also been reported as statins block the mevalonate pathway and the synthesis coenzyme Q10. This Additional Coenzyme Q10 depletion by statins in patients with coronary artery disease (CAD) may be a critical issue as it may reduce absolute benefits of statins.Objectives: The purpose of this study was to investigate the effects of high dose statins on plasma Malondialdehyde (MDA) levels and plasma glutathione levels in CAD patients who underwent recent PCI and to study whether addition of coenzyme Q10 (100 mg/d) has any additional effect on plasma Malondialdehyde (MDA) levels and plasma glutathione levels in patients already receiving high dose statin therapy.Methods: Twenty-one consecutive patients who underwent percutaneous transluminal coronary angioplasty (PTCA) in Department of Cardiology at our institute were studied. The cases (n = 21) were given high dose statins for first 1 week and then coenzyme Q10 (100 md /day) is added for next 1 week. Plasma Malondialdehyde(MDA) levels and plasma glutathione levels were analyzed at the time of admission before giving statins and at the end of 1 week of statin therapy and again after 1 week of Co-Q therapy.Results: Our results indicate that a relation exists between high plasma Malondialdehyde (MDA) levels and low plasma glutathione levels with coronary artery disease. High dose statins decrease MDA levels and increase plasma glutathione levels, even though they decrease coenzyme q levels in the body. It was also shown that addition of Coenzyme Q10 at 100 mg/d enhances plasma glutathione levels and decreases plasma MDA level still further in patients who have CAD, already receiving high dose statin therapy.Conclusions: Addition of Coenzyme Q10 at 100 mg/d has an additive effect with high dose statins in decreasing oxidative stress. Particularly in light of the excellent tolerance and affordability of this natural physiological compound, supplemental Coenzyme Q10 may emerge as an attractive option in future, and merits evaluation in additional large studies.

scholarly journals Association of Mitral Annulus Calcification with High-Sensitivity C-Reactive Protein, Which Is a Marker of Inflammation

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Ertuğrul Kurtoğlu ◽  
Hasan Korkmaz ◽  
Erdal Aktürk ◽  
Mücahid Yılmaz ◽  
Yakup Altaş ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Systemic Inflammation ◽  
High Sensitivity ◽  
Control Group ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Hs Crp ◽  
Artery Disease ◽  
The Relationship

Objectives. There are limited clinical data revealing the relationship between mitral annular calcification (MAC) and systemic inflammation. The goal of the present study was to compare high-sensitivity C-reactive protein (hs-CRP) levels in patients with and without MAC and investigate the relationship between MAC and hs-CRP.Methods. One hundred patients with MAC who underwent transthoracic echocardiography (TTE) and 100 age-matched controls without MAC who underwent TTE were included in our study. Hs-CRP levels were compared between groups.Results. Prevalence of female gender, hypertension, and coronary artery disease were significantly higher in the MAC group than in the control group (64% versus 45%,P=0.007, 42% versus 28%,P=0.03and 37% versus 18%,P=0.003, resp.). On multivariate analysis, age, gender, and coronary artery disease were the only independent predictors of MAC. The levels of hs-CRP were higher in the MAC group than in the control group (2.02±0.35versus1.43±0.47 mg/dl,P<0.001). This increase in hs-CRP levels in the MAC group persisted in patients without hypertension, coronary artery disease, and in male patients when compared to the control group.Conclusions. Our study demonstrated that hs-CRP, which is a sensitive marker of systemic inflammation, increased in patients with MAC.

scholarly journals The relationship between lipoprotein(a) and coronary artery disease, as well as its variable nature following myocardial infarction

2011 ◽  
Vol 34 (1) ◽  
pp. 14 ◽  
Author(s):  
Ender Ornek ◽  
Sani Murat ◽  
Mustafa Duran ◽  
Murat Turfan ◽  
Alparslan Kurtul ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Angina Pectoris ◽  
Control Group ◽  
Clinical Form ◽  
Variable Nature ◽  
Acute Mi ◽  
Artery Disease ◽  
The Relationship

Purpose: The present study aimed to investigate the relationship between the severity of coronary artery disease (CAD) and level of Lipoprotein (LP)(a). Methods: The study included 52 CAD patients and a control group consisting of 38 individuals. The patients were classified into three groups based on the clinical form of CAD (stable angina pectoris, SAP, unstable angina pectoris,UAP, and myocardial infarction,MI), and were further divided into three groups based on CAD severity (1-, 2- and 3-vessel). Serum Lp(a) levels were monitored 4, 8, and 24 h, 10 and 30 days following acute MI in 18 patients. Results: Based on regression analysis, Lp(a) was not correlated with other lipoproteins or with risk factors of CAD, such as body mass index, smoking, family history, diabetes, age, gender, and hypertension (r = 0.08-0.22). 72% of the patients in the CAD group and 24% of the control group had an Lp(a) level > 30 mg dL–1 (P = 0.004), and Lp(a) levels were higher in 3-vessel patients than in 2-vessel and 1-vessel CAD patients (86% vs. 68%, P = 0.02 and 86% vs. 62%, P=0.01, respectively). Serum Lp(a) levels were higher in the UAP and MI groups than in the SAP group (48 ± 44.7 mg dL–1, 49 ± 36.1 mg dL–1 and 31.2 ± 22.3 mg dL–1 , respectively,P=0.02). Lp(a) levels increased after acute MI, and reached peak levels 10 days post-MI (41% increase, P=0.001) and remained considerably elevated (18%) 30 days post-MI (P=0.01). Conclusion: Serum Lp(a) was higher in the UAP and MI patients in comparison with the SAP patients, and was higher in 3-vessel CAD in comparison with 1- and 2-vessel CAD patients.

Sign in / Sign up

Export Citation Format

Share Document