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Cardiovascular diseases (CVD) are major causes of death worldwide. Recently, new roles for intestinal microbiota in pathology and treatment of CVD have been proposed. Butyrate, a bacterial metabolite, is synthesized in the gut and performs most of its functions in there. However, researchers have discovered that butyrate could enter to portal vein and interact with various organs. Butyrate exhibits a broad range of pharmacological activities, including microbiome modulator, anti-inflammatory, anti-obesity, metabolic pathways regulator, anti-angiogenesis, and antioxidant. In this article we review evidence supporting a potentially therapeutic role for butyrate in CVD and the mechanisms and pathways involved in the cardio-protective effects of butyrate from the gut and circulation to the nervous system. In summary, although butyrate exhibits a wide variety of biological activities in different pathways including energy homeostasis, glucose and lipid metabolism, inflammation, oxidative stress, neural signaling, and epigenetic modulation in experimental settings, it remains unclear whether these findings are clinically relevant and whether the molecular pathways are activated by butyrate in humans.

Myocardial ischaemia–reperfusion (IR) injury poses a severe threat to cardiac health, particularly in the ageing population, where susceptibility to such damage is significantly heightened owing to age‐related declines in mitochondrial function, thus highlighting mitochondria as crucial targets for innovative therapies. The aim of this study was to investigate the combined modality therapy involving mitochondrial transplantation and the mitochondrial boosters mitoquinone and melatonin to address myocardial IR injury in aged rats. A total of 54 male Wistar rats, aged 22–24 months, were randomly divided into groups that either received IR injury or not, and were subjected to various treatments, both individually and in combination. Myocardial IR injury was induced by temporarily blocking and reopening the left anterior descending coronary artery. Mitoquinone was given intraperitoneally for 14 days prior to ischaemia, while melatonin and isolated mitochondria were administered intraperitoneally and intramyocardially, respectively, at the onset of reperfusion. Finally, we evaluated changes in haemodynamic indices, creatine kinase‐MB levels, mitochondrial function endpoints and the expression of mitochondrial biogenesis genes, including sirtuin 1 (SIRT‐1), peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC‐1α) and nuclear respiratory factor 2 (NRF‐2). The triple therapy enhanced myocardial function, decreased creatine kinase‐MB levels and improved mitochondrial function along with the expression of mitochondrial biogenesis genes in aged IR rats. This combined approach elicited significant cardioprotection in comparison to single or dual therapies. The triple therapy provided substantial cardioprotection in aged rat hearts by improving mitochondrial function and biogenesis through enhanced SIRT‐1/PGC‐1α/NRF‐2 profiles, suggesting a promising strategy for mitigating IR injury in elderly patients. What is the central question of this study? Can combined therapy with mitochondrial transplantation, mitoquinone and melatonin effectively reduce myocardial ischaemia–reperfusion injury in aged rats? What is the main finding and its importance? The triple therapy significantly improved myocardial function, reduced creatine kinase‐MB levels and enhanced mitochondrial function and biogenesis by modulating the sirtuin 1, peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha and nuclear respiratory factor 2 profiles, thereby providing substantial cardioprotection. This approach represents a promising therapeutic strategy for mitigating ischaemia–reperfusion injury, particularly in elderly patients who are at higher risk of cardiac damage.

The effects of hyperglycemia on the prognosis of MI patients remain uncertain. This investigation evaluates the prognostic significance of hyperglycemia upon hospital admission in patients with ST-Elevation Myocardial Infarction and assesses how diabetes mellitus (DM) affects its prognostic relevance. This cross-sectional study examined data from 334 patients diagnosed with ST-segment elevation acute coronary syndrome, obtained from the Persian Cardiovascular Disease Registry. The study assessed hospital and one-year mortality as primary outcomes. Furthermore, cut-off points for blood glucose level on admission were determined and the predictive value of these cut-off values was analyzed using logistic regression analysis. In-hospital and one-year mortality rates were 22.1% and 26% for diabetic patients, and 20.2% and 24.1% for non-diabetic patients, with no substantial discrepancy between the groups ( P  = 0.607, P  = 0.401). ROC curve analysis determined the admission blood glucose cut-off for predicting hospital mortality at 214 mg/dl in patients with diabetes (AUC = 0.66) and 148 mg/dl in patients without diabetes (AUC = 0.71). Blood glucose values was an independent factors related to in-hospital mortality, with odds ratios of 3.78 (95% CI 1.33–10.68, P  = 0.012) for diabetics and 3.07 (95% CI 1.25–7.51, P  = 0.014) for non-diabetics. Additionally, heightened admission glucose was correlated with greater mortality in one year in patients affected with MI irrespective of diabetes status. Blood glucose levels at admission independently predicted increased risk of mortality both during hospitalization and at one-year follow-up in patients with MI, with a notable effect on non-diabetic patients.

A 54-year-old woman presented with fatigue, intermittent hemorrhoidal bleeding, and spoon-shaped nails. Iron-deficiency anemia and koilonychia were diagnosed.

This study aimed at modelling the underlying predictor of ASCVD through the Bayesian network (BN). Data for the AZAR Cohort Study, which evaluated 500 healthcare providers in Iran, was collected through examinations, and blood samples. Two BNs were used to explore a suitable causal model for analysing the underlying predictor of ASCVD; Bayesian search through an algorithmic approach and knowledge-based BNs. Results showed significant differences in ASCVD risk factors across background variables’ levels. The diagnostic indices showed better performance for the knowledge-based BN (Area under ROC curve (AUC) = 0.78, Accuracy = 76.6, Sensitivity = 62.5, Negative predictive value (NPV) = 96.0, Negative Likelihood Ratio (LR−) = 0.48) compared to Bayesian search (AUC = 0.76, Accuracy = 72.4, Sensitivity = 17.5, NPV = 93.2, LR− = 0.83). In addition, we decided on knowledge-based BN because of the interpretability of the relationships. Based on this BN, being male (conditional probability = 63.7), age over 45 (36.3), overweight (51.5), Mets (23.8), diabetes (8.3), smoking (10.6), hypertension (12.1), high T-C (28.5), high LDL-C (23.9), FBS (12.1), and TG (25.9) levels were associated with higher ASCVD risk. Low and normal HDL-C levels also had higher ASCVD risk (35.3 and 37.4), while high HDL-C levels had lower risk (27.3). In conclusion, BN demonstrated that ASCVD was significantly associated with certain risk factors including being older and overweight male, having a history of Mets, diabetes, hypertension, having high levels of T-C, LDL-C, FBS, and TG, but Low and normal HDL-C and being a smoker. The study may provide valuable insights for developing effective prevention strategies for ASCVD in Iran.

Purpose: Lethal ventricular arrhythmias are a significant clinical concern following reperfusion therapies in elderly patients with myocardial infarction. The combination of multi-target therapies to achieve optimal anti-arrhythmogenesis and improve the chances of successful translation for patient benefit has prompted considerable interest. This study examined the anti-arrhythmic effect of nicotinamide mononucleotide (NMN)/ubiquinol combination treatment following myocardial ischemia/reperfusion (IR) injury in aged rats, with an emphasis on the role of oxidative stress and nitric oxide (NO). Methods: Male Wistar rats (n=30, 22-24 months old, 400-450 g) were randomized into five groups with or without IR and/or NMN and ubiquinol, either alone or in combination. NMN (100 mg/kg/48 hours) was administered intraperitoneally for 28 days before IR, and ubiquinol (30 mg/kg) was injected intravenously at early reperfusion. Electrocardiographic signals were recorded during the ischemia and the first 30 minutes of reperfusion. Two hours after reperfusion, myocardial hemodynamic and LDH release were measured, and the left ventricle samples were obtained to evaluate oxidative stress markers and NO levels. Results: NMN/ubiquinol combination treatment significantly minimized the occurrence and severity of IR-induced arrhythmias, improved myocardial function, and reduced LDH release (P<0.05). It also decreased MDA content, increased superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) activities, and enhanced NO formation (P<0.05). This combined treatment showed greater efficacy than the single treatments. Conclusion: This study revealed the anti-arrhythmic effect of NMN/ubiquinol combination treatment in IR-treated aged rats, which may be associated with reduced oxidative stress and increased NO formation. This combinational approach deserves more investigation due to its potential to confer better anti-arrhythmic effect during aging.

The Mediterranean diet (Med-Diet) is widely recognized for its protective effect in cardiovascular diseases (CVDs), less is known about the associations between health and adherence to the Prime Diet Quality Score (PDQS). This study investigates the relationship between adherence to the Med-Diet and PDQS with the risk of premature coronary artery disease (PCAD) in an Iranian population. A total of 3287 participants were included in this multicenter case-control study across various ethnic groups in Iran, categorized into PCAD cases ( n  = 2106) and controls ( n  = 1181). PCAD cases were defined as individuals with at least one coronary artery exhibiting ≥ 75% stenosis or a left main coronary artery with ≥ 50% stenosis, while controls had normal coronary arteries. Dietary intake was assessed using a semi-quantitative food frequency questionnaire (FFQ), previously validated for accuracy in the Iranian population Adherence to the Med-Diet was assessed using a standardized scoring system, awarding one point for higher consumption of beneficial food groups (such as vegetables, whole grains, legumes, fish, nuts, and a high monounsaturated-to-saturated fat ratio) and one point for lower consumption of less favorable foods (such as red and processed meats). The total score ranged from 0 to 9, with higher scores indicating greater adherence to the Med-Diet. The PDQS, a dietary quality index, evaluated adherence across 14 healthy and 7 unhealthy food groups, with higher scores reflecting better diet quality. Logistic regression models were employed to examine the association between dietary scores and PCAD risk. Participants with higher adherence to both the Med-Diet and PDQS had significantly lower odds of PCAD (OR = 0.30, 95% CI: 0.22, 0.40; P for trend < 0.001 for PDQS), with a stronger association observed for the Med-Diet (OR = 0.08, 95% CI: 0.06, 0.10; P for trend < 0.001). Additionally, higher adherence to the Med-Diet (OR = 0.04, 95% CI 0.03, 0.05) and PDQS (OR = 0.21, 95% CI: 0.17, 0.26) was inversely associated with PCAD severity in the fully adjusted model. This study showed a protective association of the Med-Diet and PDQS with reduced risk of PCAD in the Iranian population.

Contrast‐induced nephropathy (CIN) is a serious complication that occurs subsequent to the administration of contrast media for therapeutic angiographic interventions. As of present, no effective therapy exists to prevent its occurrence. This single‐center double‐blind randomized controlled trial aimed to evaluate the effect of edaravone, an antioxidant, in a group of high‐risk patients undergoing coronary angiography. Ninety eligible patients with chronic kidney disease Stages 3–4 were randomly assigned to either the control group (n = 45) or the intervention group (n = 45). In the intervention group, one dosage of edaravone (60 mg) in 1 L of normal saline was infused via a peripheral vein 1 h prior to femoral artery‐directed coronary angiography. Patients in the control group received an equal amount of infusion in their last hour before angiography. Both groups received intravenous hydration with 0.9% sodium 1 mL/kg/h starting 12 h before and continuing for 24 h after angiography. The primary outcome measure was the onset of CIN, defined as a 25% increase in serum creatinine levels 120 h after administration of contrast media. The occurrence of CIN was observed in 5.5% (n = 5) of the studied population: 2.2% of patients in the intervention group (n = 1) and 8.9% of controls (n = 4). However, this difference was not statistically significant. Administration of a single dosage of edaravone 1 h prior to infusion of contrast media led to a reduction in the incidence of CIN. Further investigations, employing larger sample sizes, are warranted to gain a comprehensive understanding of its efficacy. CONSORT diagram. The eligibility assessment of enrolled participants in the study.

Studies have shown that sulforaphane (SFN) has potent anti-inflammatory and free radical scavenging effects on obesity and associated disorder such as diabetes, polycystic ovary syndrome, and metabolic syndrome. fractalkine (CX3CL1) and its receptor, CX3CR1, play an important role in muscle metabolism by improving insulin-sensitizing effects. Here, in this study we examined the SFN effect on CX3CL1 and its receptor, CX3CR1, in C2C12 myotubes in palmitic acid (PA)-induced oxidative stress and inflammation. The results showed that PA (750 μM) evoked lipotoxicity as a reduction in cell viability, increased IL-6 and TNF-α expression, and enhanced reactive oxygen species (ROS). However, SFN pretreatment attenuated the levels of, IL-6 and TNF-α in C2C12 myotubes exposure to PA. Moreover, SFN pretreatment up-regulated nuclear factor erythroid related factor 2 (Nrf2) /heme oxygenase-1(HO-1) pathway protein in C2C12 cells as indicated by a decrease in ROS levels. Interestingly, PA also caused an increase in CX3CL1 and CX3CR1 expression that SFN abrogated it. We also found the protective effect of SFN agonist PA-induced lipotoxicity with promotes in UCP3 gene expression in C2C12 cells. Collectively, these findings suggest that SFN hampers the PA-induced inflammation in C2C12 cells by modulation of the Nrf2/HO-1 pathway and CX3CL1/CX3CR1 axis and may propose a new therapeutic approach to protect against obesity-associated disorders in skeletal muscle cells.

Many studies have investigated the relationship between coffee and diabetes. Evaluation of the current evidence on the effect of coffee intake on diabetes is critical. Therefore, we aimed to investigate the potential association between green coffee extract (GCE) and fasting blood glucose (FBG), insulin and homeostatic model assessment of insulin resistance (HOMA-IR) by pooling together the results from clinical trials. PubMed, Scopus and Google Scholar were searched for experimental studies which have been published up to December 2018. Randomized controlled trials (RCTs) that investigated the effect of GCE supplementation on FBG, insulin and HOMA-IR in adults were included for final analysis. A total of six articles were included in the meta-analysis. Results revealed that GCE supplementation reduced FBG level (SMD: −0.32, 95% CI − 0.59 to − 0.05, P = 0.02) but had no effect on insulin levels (SMD: −0.22, 95% CI −0.53 to 0.09, P = 0.159). Although analysis showed that GCE supplementation cannot change the HOMA-IR status (SMD: −0.30, 95% CI −0.73 to 0.13, P = 0.172), after stratified studies by GCE dosage (< 400 mg/day versus > 400 mg/day) there was a significant decrease in HOMA-IR status in a dose greater than 400 mg. These findings suggest that GCE intake might be associated with FBG improvement.