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The Gut Microbiota (Microbiome) in Cardiovascular Disease and Its Therapeutic Regulation.
Rahman, MM, Islam, F, -Or-Rashid, MH, Mamun, AA, Rahaman, MS, Islam, MM, Meem, AFK, Sutradhar, PR, Mitra, S, Mimi, AA, et al
Frontiers in cellular and infection microbiology. 2022;12:903570
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Cardiovascular disease (CVD) accounts for 31% of all-cause mortality worldwide. Irregularities in the composition of intestinal microbial composition, genetic factors, nutrition, metabolic irregularities, and smoking are among the potential causes of CVD. Intestinal permeability and translocation of endotoxins and bacterial metabolites to systemic circulation may trigger an immune response and inflammation, which may increase the risk of CVD. Synthesis of bacterial metabolites such as trimethylamine N-oxide (TMAO) by choline-inducing gut bacteria and reduced consumption of dietary TMAO precursors may elevate the CVD risk. This review explores the latest research on the role of gut microbiota in the development of atherosclerosis and CVD, as well as potential strategies to prevent CVD by targeting TMAO-producing gut bacteria. Elevated levels of TMAO in the bloodstream can lead to the buildup of cholesterol and ultimately result in atherosclerosis. However, consuming probiotics and fibre-rich foods can help regulate gut bacteria, reduce inflammation, and improve lipid profiles, all of which contribute to better cardiovascular health. More future robust studies are required to examine the mechanistic insights and confirm whether TMAO can serve as a biomarker for preventing CVD through the therapeutic modulation of intestinal bacteria.
Abstract
In the last two decades, considerable interest has been shown in understanding the development of the gut microbiota and its internal and external effects on the intestine, as well as the risk factors for cardiovascular diseases (CVDs) such as metabolic syndrome. The intestinal microbiota plays a pivotal role in human health and disease. Recent studies revealed that the gut microbiota can affect the host body. CVDs are a leading cause of morbidity and mortality, and patients favor death over chronic kidney disease. For the function of gut microbiota in the host, molecules have to penetrate the intestinal epithelium or the surface cells of the host. Gut microbiota can utilize trimethylamine, N-oxide, short-chain fatty acids, and primary and secondary bile acid pathways. By affecting these living cells, the gut microbiota can cause heart failure, atherosclerosis, hypertension, myocardial fibrosis, myocardial infarction, and coronary artery disease. Previous studies of the gut microbiota and its relation to stroke pathogenesis and its consequences can provide new therapeutic prospects. This review highlights the interplay between the microbiota and its metabolites and addresses related interventions for the treatment of CVDs.
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Evidence for the Benefits of Melatonin in Cardiovascular Disease.
Tobeiha, M, Jafari, A, Fadaei, S, Mirazimi, SMA, Dashti, F, Amiri, A, Khan, H, Asemi, Z, Reiter, RJ, Hamblin, MR, et al
Frontiers in cardiovascular medicine. 2022;9:888319
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Cardiovascular disease (CVD) encompasses a group of disorders involving blood vessels or the heart. The beneficial effects of melatonin [hormone] in treating various human diseases have been broadly investigated. Melatonin is an indoleamine-derived molecule, which is synthesised at night. The aim of this review was to point out therapeutic potentials of melatonin in the treatment of CVDs with an emphasis on the molecular mechanisms of action. This review shows that: - nearly all the studies have reported positive effects of melatonin on cardiovascular physiology, and the prevention of damage to the myocardium after heart attack, reperfusion injury, or sepsis. - melatonin can help blood pressure and heart arrhythmia. - some clinical trials indicated that the utilization of melatonin in CVDs is associated with more inconsistencies regarding its cardioprotective effects. Authors conclude that further preclinical and clinical studies are required to better delineate the cardiovascular benefits of melatonin.
Abstract
The pineal gland is a neuroendocrine gland which produces melatonin, a neuroendocrine hormone with critical physiological roles in the circadian rhythm and sleep-wake cycle. Melatonin has been shown to possess anti-oxidant activity and neuroprotective properties. Numerous studies have shown that melatonin has significant functions in cardiovascular disease, and may have anti-aging properties. The ability of melatonin to decrease primary hypertension needs to be more extensively evaluated. Melatonin has shown significant benefits in reducing cardiac pathology, and preventing the death of cardiac muscle in response to ischemia-reperfusion in rodent species. Moreover, melatonin may also prevent the hypertrophy of the heart muscle under some circumstances, which in turn would lessen the development of heart failure. Several currently used conventional drugs show cardiotoxicity as an adverse effect. Recent rodent studies have shown that melatonin acts as an anti-oxidant and is effective in suppressing heart damage mediated by pharmacologic drugs. Therefore, melatonin has been shown to have cardioprotective activity in multiple animal and human studies. Herein, we summarize the most established benefits of melatonin in the cardiovascular system with a focus on the molecular mechanisms of action.
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Psoriasis and cardiovascular disease risk in European and East Asian populations: evidence from meta-analysis and Mendelian randomization analysis.
Zhang, L, Wang, Y, Qiu, L, Wu, J
BMC medicine. 2022;20(1):421
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Psoriasis constitutes a chronic, inflammatory skin disease with an immune-genetic basis that has been linked to numerous diseases, including metabolic syndrome, cancer, as well as cardiovascular disease (CVD). The aim of this study was to determine if the relationship of psoriasis with CV events (CVE) risk is congruent with causal associations. This study is a report employing a meta-analysis of observational studies and a two-sample mendelian randomised trial (MR). Results from the meta-analysis show that psoriasis was remarkably associated with a higher risk of incident coronary artery disease (CAD) and myocardial infarction (MI) and was not associated with heart failure risk. Furthermore, the MR approach showed that psoriasis was linked with a higher risk of CAD in both European and East Asian populations. Additionally, psoriasis was also causally linked to an elevated risk of MI in European population. Authors conclude that their findings indicate a causal association of psoriasis with CAD and MI. However, further studies are needed to establish the mechanisms of the causal relationship of psoriasis with CAD and MI.
Abstract
BACKGROUND Psoriasis has been linked to cardiovascular disease (CVD), including coronary artery disease (CAD), myocardial infarction (MI), and heart failure (HF). However, available studies regarding this relationship have shown inconsistent results. Therefore, in this report, we performed a comprehensive review of the literature to assess the effects of psoriasis on risk of these CVDs. METHODS A search of literature until 24 December 2021 was done in PubMed, the Cochrane Library, Web of Science, Google Scholar, and Embase. Within European and East Asian populations, meta-analyses of observational studies assessing correlations between psoriasis and various CVD risk factors were conducted. Mendelian randomization (MR) was then employed to assess the causative impact of genetic pre-disposition for psoriasis on these CVD risk factors. RESULTS The results of the meta-analyses indicated that, in both the European and East Asian populations, psoriasis was significantly linked to an elevated risk in the incidence of CAD (RR = 1.51, 95% confidence interval (CI): 1.04-2.18, p = 0.028 and RR = 1.91, 95% CI: 1.62-2.25, p < 0.001) and MI (RR = 1.23, 95% CI: 1.04-1.46, p = 0.017 and RR = 2.17, 95% CI: 1.44-3.28, p < 0.001). A positive genetic relationship of psoriasis with CAD was found in European individuals (IVW OR1.03; 95% CI: 1.01-1.06, p = 0.005) and in East Asian individuals (IVW OR1.18; 95% CI: 1.03-1.32, p = 0.031). We also established that psoriasis was causally linked with an elevated risk of MI (IVW OR1.05; 95% CI: 1.01-1.09, p = 0.026) in the European population as determined using an MR approach. Moreover, our MR results were congruent with the null findings from the meta-analysis assessing associations of psoriasis with HF risk. CONCLUSIONS This research work provides preliminary evidence that psoriasis and CVD have a common genetic origin and that targeted psoriasis treatment might improve cardiovascular outcomes. These results not only increase our knowledge of the genetic underpinnings linking a comorbidity of psoriasis with CVD but also suggests a novel approach for CVD prevention.
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Anti-inflammatory effects of resveratrol in patients with cardiovascular disease: A systematic review and meta-analysis of randomized controlled trials.
Teimouri, M, Homayouni-Tabrizi, M, Rajabian, A, Amiri, H, Hosseini, H
Complementary therapies in medicine. 2022;70:102863
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Cardiovascular diseases (CVDs) include various heart or/and blood vessel disorders, such as cerebrovascular disease, congenital heart disease, and coronary artery disease. It is well shown that prolonged or chronic inflammation plays a key role in the pathogenesis of several disorders, especially CVDs. Resveratrol has recently been considered a choice for preventing and treating inflammatory conditions. The aim of this study was to evaluate the impact of resveratrol on serum/plasma concentration of specific inflammatory markers - tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and c-reactive protein (CRP) - in patients with CVDs. This study is a systematic review and meta-analysis of six randomised controlled studies with a total of 415 participants. Results show that resveratrol significantly decreases CRP and TNF-α concentration; however, it did not significantly affect the serum concentration of IL-6 in patients with CVDs. Authors conclude that there is a potential preventive effect of resveratrol supplementation on inflammatory conditions in CVD patients. However, larger randomised clinical trials are needed to further investigate and explore the effects of resveratrol supplementations.
Abstract
BACKGROUND Chronic inflammation is one of the most important factors involved in the development and progression of cardiovascular disease (CVDs). Accumulating evidence has described the effect of resveratrol, a natural polyphenolic compound, on biomarkers of inflammation among patients with CVDs; however, findings are controversial. Here we performed a systematic review and meta-analysis of randomized controlled trials to evaluate the effect of resveratrol supplements on TNF-α, IL-6, and CRP levels in CVDs patients. METHODS Online research was conducted in the following database: MEDLINE, EMBASE, Cochrane Library, Web of Science databases, and Scopus. This systematic review and meta-analysis were conducted to investigate the effects of resveratrol supplements on inflammatory biomarkers among patients with CVDs. The meta-analysis was performed using Comprehensive Meta-Analysis (CMA) V3 software. RESULTS Six RCTs met the inclusion criteria and were selected for the current meta-analysis. Our results demonstrated that resveratrol significantly decreases serum levels of CRP (MD = -0.63, 95 % CI: -0.1.13, -0.12; p = 0.01), and TNF-α (MD = -0.55, 95 % CI: -1.04, -0.06; p = 0.02), however, resveratrol had not significant effect on serum concentration of IL-6 (MD = -0.12, 95 % CI: -0.52, 0.27; p = 0.53), in patients with CVDs. CONCLUSION Our results suggest that resveratrol can be used as a potential treatment in patients with CVD by reducing inflammatory conditions.
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Effect of Flaxseed (Linum usitatissimum L.) Supplementation on Vascular Endothelial Cell Morphology and Function in Patients with Dyslipidaemia-A Preliminary Observation.
Kanikowska, D, Malińska, A, Mickiewicz, A, Zawada, A, Rutkowski, R, Pawlaczyk, K, Sato, M, Bręborowicz, A, Witowski, J, Korybalska, K
Nutrients. 2022;14(14)
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Flaxseed appears to be a valuable source of polyunsaturated fatty acids, phytosterols and fibre, which lower lipids and have anti-atherogenic activity. The aim of this study was to determine the effects of 10 weeks of supplementation with the flaxseed (28g/day) on endothelial cells function, serum lipids and proinflammatory mediators in patients with mild and severe dyslipidaemia. This study is a prospective study of two groups of patients. The first group (n=14) was composed of lean (n=6), and obese (n=8) outpatients receiving therapy of lipoprotein apheresis (once every two weeks) for severe hyperlipidaemia. The second group was composed of 11 obese outpatients with dyslipidaemia receiving a diet at home. In both groups, flaxseed was given blindly. Results show that patients diagnosed with dyslipidaemia who took 28g daily of flaxseed showed a significant reduction in serum lipids but exhibited a slight beneficial effect on endothelial cells. However, it only shows that flaxseed might have the potential ability to improve endothelial function but, in obese patients, it does not have the potency to reverse endothelial ultrastructural changes observed in electron microscopy. Authors conclude that flaxseed supplementation produced consistent lipid-lowering effects and can modulate VEGF (endothelial cell marker) concentration depending on the severity of dyslipidaemia.
Abstract
CONTEXT Flaxseed has a characteristic fatty acids composition and unique phytonutrient profile that may have health-promoting properties. OBJECTIVE This study aimed to determine the effects of 10 weeks of supplementation with the flaxseed (28 g/day) on endothelial cells (EC) function, serum lipids and proinflammatory mediators in patients with mild and severe dyslipidaemia. MATERIALS AND METHODS Eleven lean patients with severe dyslipidaemia treated with apheresis (group 1; 10 weeks treated in four phases: (i) ordinary diet, (ii) ordinary diet + flaxseed, (iii) ordinary diet (wash out), (iv) ordinary diet + placebo) and eleven obese patients with mild dyslipidaemia-not treated with apheresis (group 2; 10 weeks treated in two phases: (i) ordinary diet, (ii) low fat diet + flaxseed). Flaxseed was given blindly. Serum was collected at the end of each phase of the study. ECs were exposed in vitro to the medium supplemented with pooled serum taken from patients from both groups to detect their morphological changes using light and electron microscopy. ECs proliferation was also measured at the end of each study phase. RESULTS Serum vascular endothelial growth factor was decreased after flaxseed supplementation but only in group 1. ECs proliferation was increased after flaxseed supplementation only in obese patients. ECs exposed to medium supplemented with obese patients' serum revealed the following cellular abnormalities: accumulation of lipid droplets, changes of rough endoplasmic reticulum and mitochondria, and flaxseed did not reverse observed changes. At the same time, flaxseed supplementation decreases total cholesterol in both tested groups, low-density lipoprotein cholesterol in group 1 and triglycerides in group 2. CONCLUSIONS Our findings support the potential role of flaxseed in treating dyslipidaemia but indicate only a slight impact on endothelial cell function.
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Effect of Omega-3 Dosage on Cardiovascular Outcomes: An Updated Meta-Analysis and Meta-Regression of Interventional Trials.
Bernasconi, AA, Wiest, MM, Lavie, CJ, Milani, RV, Laukkanen, JA
Mayo Clinic proceedings. 2021;96(2):304-313
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There is mixed evidence to support the use of omega-3 fatty acids for the prevention and treatment of cardiovascular disease. Animal studies have shown promising results, but randomised control trials are inconsistent, possibly due to differing doses used, or differences in the subject’s omega-3 levels at the start of the trial. This meta-analysis of 40 studies with over 135,000 subjects aimed to determine whether omega-3 supplementation reduces heart disease risk and whether dosage has a role. The results showed that omega-3 supplementation reduced the risk of heart attacks, death from heart attacks and deaths due to heart disease, and the higher the dose, the greater the protection. The majority of studies were on individuals who had already had a heart attack or who had suffered from a related condition. It was concluded that supplementation with omega-3 is effective in preventing heart disease and heart attacks and the protective effect increases with dosage. This study could be used by healthcare professionals to prevent further heart disease and heart attacks in individuals who have already suffered from one of these conditions.
Abstract
OBJECTIVES To quantify the effect of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids on cardiovascular disease (CVD) prevention and the effect of dosage. METHODS This study is designed as a random effects meta-analysis and meta-regression of randomized control trials with EPA/DHA supplementation. This is an update and expanded analysis of a previously published meta-analysis which covers all randomized control trials with EPA/DHA interventions and cardiovascular outcomes published before August 2019. The outcomes included are myocardial infarction (MI), coronary heart disease (CHD) events, CVD events (a composite of MI, angina, stroke, heart failure, peripheral arterial disease, sudden death, and non-scheduled cardiovascular surgical interventions), CHD mortality and fatal MI. The strength of evidence was assessed using the Grading of Recommendations Assessment, Development, and Evaluation framework. RESULTS A total of 40 studies with a combined 135,267 participants were included. Supplementation was associated with reduced risk of MI (relative risk [RR], 0.87; 95% CI, 0.80 to 0.96), high certainty number needed to treat (NNT) of 272; CHD events (RR, 0.90; 95% CI, 0.84 to 0.97), high certainty NNT of 192; fatal MI (RR, 0.65; 95% CI, 0.46 to 0.91]), moderate certainty NNT = 128; and CHD mortality (RR, 0.91; 95% CI, 0.85 to 0.98), low certainty NNT = 431, but not CVD events (RR, 0.95; 95% CI, 0.90 to 1.00). The effect is dose dependent for CVD events and MI. CONCLUSION Cardiovascular disease remains the leading cause of death worldwide. Supplementation with EPA and DHA is an effective lifestyle strategy for CVD prevention, and the protective effect probably increases with dosage.
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Interaction Between Type 2 Diabetes Prevention Strategies and Genetic Determinants of Coronary Artery Disease on Cardiometabolic Risk Factors.
Merino, J, Jablonski, KA, Mercader, JM, Kahn, SE, Chen, L, Harden, M, Delahanty, LM, Araneta, MRG, Walford, GA, Jacobs, SBR, et al
Diabetes. 2020;69(1):112-120
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Individual risk of Coronary Artery Disease (CAD) and type 2 diabetes reflects the interplay between lifestyle behaviours acting on a backdrop of genetic predisposition. The aim of this study was to examine whether type 2 diabetes prevention strategies, either an intensive lifestyle intervention (ILS) or metformin treatment (MET), modify the association between CAD genetic risk and cardiometabolic risk factors (CRFs) in participants at high risk of type 2 diabetes. The study is a randomised controlled trial were participants were randomly allocated to one of the three groups; ILS (n = 1,079), MET (850 mg twice daily [n = 1,073]), or placebo (n = 1,082). Results indicate that there weren’t major significant differences in baseline characteristics, except for lower high-density lipoprotein and higher triglyceride in the placebo individuals compared with individuals assigned to MET or ILS. In fact, either an ILS or MET has a beneficial effect on 1-year change in different CRFs. Authors conclude that type 2 diabetes–preventive strategies for individuals at high risk of type 2 diabetes provide beneficial effects on CRFs regardless of CAD genetic risk profile.
Abstract
Coronary artery disease (CAD) is more frequent among individuals with dysglycemia. Preventive interventions for diabetes can improve cardiometabolic risk factors (CRFs), but it is unclear whether the benefits on CRFs are similar for individuals at different genetic risk for CAD. We built a 201-variant polygenic risk score (PRS) for CAD and tested for interaction with diabetes prevention strategies on 1-year changes in CRFs in 2,658 Diabetes Prevention Program (DPP) participants. We also examined whether separate lifestyle behaviors interact with PRS and affect changes in CRFs in each intervention group. Participants in both the lifestyle and metformin interventions had greater improvement in the majority of recognized CRFs compared with placebo (P < 0.001) irrespective of CAD genetic risk (P interaction > 0.05). We detected nominal significant interactions between PRS and dietary quality and physical activity on 1-year change in BMI, fasting glucose, triglycerides, and HDL cholesterol in individuals randomized to metformin or placebo, but none of them achieved the multiple-testing correction for significance. This study confirms that diabetes preventive interventions improve CRFs regardless of CAD genetic risk and delivers hypothesis-generating data on the varying benefit of increasing physical activity and improving diet on intermediate cardiovascular risk factors depending on individual CAD genetic risk profile.
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Comorbid Chronic Diseases are Strongly Correlated with Disease Severity among COVID-19 Patients: A Systematic Review and Meta-Analysis.
Liu, H, Chen, S, Liu, M, Nie, H, Lu, H
Aging and disease. 2020;11(3):668-678
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Symptomatic COVID-19 infection is accompanied by a cluster of flu-like symptoms and life-threatening severe illnesses including acute respiratory distress syndrome, acute kidney injury, myocarditis, and organ failure. The aim of this study was to provide a systematic evaluation and detailed estimate on the prevalence and effects of pre-existing chronic conditions in COVID-19 patients. This study is a systemic review and meta-analysis of 24 studies (with a total of 10948 COVID-19 patients) for qualitative and quantitative synthesis. Results show that: - male participants were more susceptible to COVID-19. - both sexes exhibited clinical presentations similar in symptomatology. - diabetes and coronary artery disease/cardiovascular disease were prevalent in 10.0% and 8.0% of the patients, respectively. - pre-existing chronic diseases were strongly correlated with the increased disease severity and increased admittance to ICU. Authors conclude that patients with pre-existing chronic diseases may have a higher risk for developing severe COVID-19 and should be given close attention.
Abstract
Coronavirus disease 2019 (COVID-19) has resulted in considerable morbidity and mortality worldwide since December 2019. In order to explore the effects of comorbid chronic diseases on clinical outcomes of COVID-19, a search was conducted in PubMed, Ovid MEDLINE, EMBASE, CDC, and NIH databases to April 25, 2020. A total of 24 peer-reviewed articles, including 10948 COVID-19 cases were selected. We found diabetes was present in 10.0%, coronary artery disease/cardiovascular disease (CAD/CVD) was in 8.0%, and hypertension was in 20.0%, which were much higher than that of chronic pulmonary disease (3.0%). Specifically, preexisting chronic conditions are strongly correlated with disease severity [Odds ratio (OR) 3.50, 95% CI 1.78 to 6.90], and being admitted to intensive care unit (ICU) (OR 3.36, 95% CI 1.67 to 6.76); in addition, compared to COVID-19 patients with no preexisting chronic diseases, COVID-19 patients who present with either diabetes, hypertension, CAD/CVD, or chronic pulmonary disease have a higher risk of developing severe disease, with an OR of 2.61 (95% CI 1.93 to 3.52), 2.84 (95% CI 2.22 to 3.63), 4.18 (95% CI 2.87 to 6.09) and 3.83 (95% CI 2.15 to 6.80), respectively. Surprisingly, we found no correlation between chronic conditions and increased risk of mortality (OR 2.09, 95% CI 0.26 to16.67). Taken together, cardio-metabolic diseases, such as diabetes, hypertension and CAD/CVD were more common than chronic pulmonary disease in COVID-19 patients, however, each comorbid disease was correlated with increased disease severity. After active treatment, increased risk of mortality in patients with preexisting chronic diseases may reduce.
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The effects of coenzyme Q10 supplementation on biomarkers of inflammation and oxidative stress in among coronary artery disease: a systematic review and meta-analysis of randomized controlled trials.
Jorat, MV, Tabrizi, R, Kolahdooz, F, Akbari, M, Salami, M, Heydari, ST, Asemi, Z
Inflammopharmacology. 2019;27(2):233-248
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Cardiovascular disease is the leading cause of death worldwide. Systemic inflammation and oxidative stress significantly contribute to the narrowing of the blood supply to the heart leading to coronary artery disease (CAD). Increased levels of several markers of inflammation, such as C-reactive protein (CRP), tumour necrosis factor-α (TNF- α), and interleukin-6 (IL-6), appear to be indicative of heart attack risk. Coenzyme Q10 (CoQ10) is a naturally occurring nutrient made in the body but can also be found in some foods or taken via supplements. It is an antioxidant that protects cell membranes and mitochondria against oxidative damage and also does so in the heart by preventing endothelial damage and the associated narrowing of blood vessels. Several trials investigated the effects of CoQ10 on inflammation and oxidative stress, with some noteworthy results and yet also some conflicting evidence. Hence this systematic review and meta-analysis aimed to shed some light on the controversial findings regarding coenzyme Q10 (CoQ10) supplementation on biomarkers of inflammation and oxidative stress amongst patients with CAD. The authors included 13 clinical randomised controlled trials, amounting to 364 cardiac patients in the intervention groups. The treatment duration ranged from 4 to 48 weeks, and the dosage of CoQ10 varied between 60 to 300 mg/day. In conclusion, the meta-analysis showed that CoQ10 supplementation increased antioxidant markers of superoxide dismutase (SOD) and catalase (CAT), and decreased the oxidative stress marker malondialdehyde (MDA) and its derivative forms. There was no consistent effect on inflammatory markers of CRP, TNF-α, IL-6 or the levels of the antioxidant glutathione peroxidase. The discrepancies amongst the different studies may be a result of the divergent study designs, different population characteristics, the dosage of CoQ10 used and the duration of intervention.
Abstract
OBJECTIVE Systemic inflammation and oxidative stress significantly contribute in developing coronary artery disease (CAD). This systematic review and meta-analysis was aimed to determine the effects of coenzyme Q10 (CoQ10) supplementation on biomarkers of inflammation and oxidative stress among patients with CAD. METHODS The electronic databases including MEDLINE, EMBASE, Scopus, Web of Science, and Cochrane Library databases were systematically searched until Oct 2018. The quality assessment and heterogeneity of the selected randomized clinical Trials (RCTs) were examined using the Cochrane Collaboration risk of bias tool, and Q and I2 tests, respectively. Given the presence of heterogeneity, random-effects model or fixed-effect model were used to pool standardized mean differences (SMDs) as summary effect sizes. RESULTS A total of 13 clinical RCTs of 912 potential citations were found to be eligible for the current meta-analysis. The pooled findings for biomarkers of inflammation and oxidative stress demonstrated that CoQ10 supplementation significantly increased superoxide dismutase (SOD) (SMD 2.63; 95% CI, 1.17, 4.09, P < 0.001; I2 = 94.5%) and catalase (CAT) levels (SMD 1.00; 95% CI, 0.57, 1.43, P < 0.001; I2 = 24.5%), and significantly reduced malondialdehyde (MDA) (SMD - 4.29; 95% CI - 6.72, - 1.86, P = 0.001; I2 = 97.6%) and diene levels (SMD - 2.40; 95% CI - 3.11, - 1.68, P < 0.001; I2 = 72.6%). We did not observe any significant effect of CoQ10 supplementation on C-reactive protein (CRP) (SMD - 0.62; 95% CI - 1.31, 0.08, P = 0.08; I2 = 87.9%), tumor necrosis factor alpha (TNF-α) (SMD 0.22; 95% CI - 1.07, 1.51, P = 0.73; I2 = 89.7%), interleukin-6 (IL-6) (SMD - 1.63; 95% CI - 3.43, 0.17, P = 0.07; I2 = 95.2%), and glutathione peroxidase (GPx) levels (SMD 0.14; 95% CI - 0.77, 1.04, P = 0.76; I2 = 78.7%). CONCLUSIONS Overall, this meta-analysis demonstrated CoQ10 supplementation increased SOD and CAT, and decreased MDA and diene levels, but did not affect CRP, TNF-α, IL-6, and GPx levels among patients with CAD.
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Comparison of the Effects of Fasting Glucose, Hemoglobin A1c, and Triglyceride-Glucose Index on Cardiovascular Events in Type 2 Diabetes Mellitus.
Su, WY, Chen, SC, Huang, YT, Huang, JC, Wu, PY, Hsu, WH, Lee, MY
Nutrients. 2019;11(11)
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Cardiovascular disease generally refers to the narrowing or blockage of the arteries of the heart, which can lead to a heart attack or stroke and is the major cause of death in individuals with type 2 diabetes. Identifying individuals with type 2 diabetes who are at high risk of developing cardiovascular disease could ensure better management of these patients. This retrospective observational study of 3524 individuals with type 2 diabetes aimed to investigate if the amount of sugar found in the blood over the last few months, known as haemaglobin A1c (HbA1c) can predict cardiovascular disease in individuals with type 2 diabetes. In addition, the study looked at the triglyceride-glucose (TyG) index and its relationship to cardiovascular disease outcomes. The results showed that several factors were associated with cardiovascular disease, however of main note was that the TyG index and the amount of sugar in the blood following a fast were associated with increased cardiovascular events in individuals with type 2 diabetes, but HbA1c was not. It was concluded that TyG and the blood sugar level could be used to allow early identification and management of type 2 diabetics to prevent cardiovascular events. Clinicians could use this study to justify the use of measuring the TyG index and blood sugar levels as a predictor for cardiovascular events to ensure that patients are managed not only for type 2 diabetes but also to reduce their risk of cardiovascular events in the future.
Abstract
The triglyceride-glucose (TyG) index has been correlated with insulin resistance. We aim to investigate the role of the TyG index on cardiovascular (CV) events in type 2 diabetes mellitus and compare the roles of fasting glucose, hemoglobin A1c, and the TyG index in predicting CV events. This retrospective study enrolled 3524 patients with type 2 diabetes from the Kaohsiung Medical University Research Database in 2009 in this longitudinal study and followed them until 2015. The TyG index was calculated as log (fasting triglyceride level (mg/dL) × fasting glucose level (mg/dL)/2). CV events included myocardial infarction, unstable angina, stroke, hospitalization for coronary artery disease, peripheral artery disease, and CV-related death. The association between variables and CV events was assessed using a multivariable stepwise Cox proportional hazard analysis. Two hundred and fifteen CV events (6.1%) were recorded during a follow-up period of 5.93 years. The multivariable stepwise analysis showed that high fasting glucose (HR, 1.007; p < 0.001) and a high TyG index (HR, 1.521; p = 0.004) but not hemoglobin A1c or triglycerides were associated with a higher rate of CV events. Adding fasting glucose and the TyG index to the basic model improved the predictive ability of progression to a CV event (p < 0.001 and p = 0.018, respectively), over that of hemoglobin A1c (p = 0.084) and triglyceride (p = 0.221). Fasting glucose and the TyG index are useful parameters and stronger predictive factors than hemoglobin A1c and triglyceride for CV events and may offer an additional prognostic benefit in patients with type 2 diabetes.