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Objective: To explore the effects of Huxin formula (HXF) in curtailing atherosclerosis and its underlying mechanism. Methods: According to random number table method, 24 specific pathogen free male ApoE-/- mice were randomly divided into model group, HXF low-dose (HXF-L) group (8.4 g/kg daily), HXF high-dose (HXF-H) group (16.8 g/kg daily), and pravastatin (8 mg/kg daily) group in Experiment I (n=6 per group). C57BL/6J mice served as the control group (n=6). ApoE-/- mice in HXF-L, HXF-H, pravastatin groups were fed a Western diet and administered continuously by gavage for 12 weeks, while C57BL/6J mice in the control group were fed conventional lab mouse chow for 12 weeks. Further, Tregs were depleted by weekly intraperitoneal injection of purified anti-mouse CD25 antibody (PC61, 250 µg per mouse) for 4 weeks in Experiment II (n=6 per group). Oil Red O and Masson staining were used to evaluate the plaque area and aortic root fibrosis. The CD4+CD25+Foxp3+Treg counts in the lymph nodes and spleen cells were detected using flow cytometric analysis. The transforming growth factor-β1 (TGF-β1), interleukin (IL)-10, and IL-6 serum levels were examined by MILLIPLEX® MAP technology. Quantitative real-time reverse transcription PCR (qRT-PCR) and Western blot were utilized to assess the expression of TGF-β mRNA and protein in the aorta. The expression of CD4+T lymphocytes, macrophages and smooth muscle cells in the aortic root were detected by immunofluorescence staining. Results: HXF reduced plaque area in ApoE-/- mice (P<0.01). HXF increased the Treg counts in the lymph nodes and spleen cells (P<0.05 or P<0.01). Moreover, HXF alleviated inflammatory response via elevating IL-10 and TGF-β 1 serum levels (P<0.05), while decreasing the IL-6 serum levels in ApoE-/- mice (P>0.05). Also, HXF upregulated the expression of TGF-β mRNA and protein in the aorta (P<0.05). Additionally, HXF attenuated CD4+T lymphocytes, macrophages and smooth muscle cells in aortic root plaque (P<0.01). Furthermore, the depletion of Tregs with CD25 antibody (PC61) curtailed the reduction in plaque area and aortic root fibrosis by HXF (P<0.01). Conclusion: HXF relieved atherosclerosis, probably by restraining inflammatory response, reducing inflammatory cell infiltration and attenuating aortic root fibrosis by increasing Treg counts. [ABSTRACT FROM AUTHOR]

Background • In China, there have been instances of sudden cardiac death among university students, with a significant number of students being at risk of cardiovascular diseases. This risk is often attributed to sub-health conditions such as weight gain and obesity, which are triggered by sedentary lifestyles, irregular living habits, and unregulated diets. Therefore, it is crucial to enhance the guidance for participation in physical activities, encouraging students to actively reduce their risk of cardiovascular diseases (CVD). Jogging, characterized by its convenience, simplicity, and low-risk participation, has been widely accepted by university students. This study takes the impact of jogging on the cardiovascular function of university students as a starting point. It aims to explore the content of the changing process suitable for the development of cardiovascular function in university students. The ultimate goal is to promote the healthy development of the cardiovascular system function in university students and improve their adherence to physical activities. Methods • The study recruited 60 university students with no exercise habits through on-campus poster advertisements. These 60 participants were randomly divided into two groups. The students in the experimental group were required to jog no less than three times a week, with each session lasting at least 30 minutes. The organizers of the experiment would remind the students daily in a WeChat group to complete their weekly exercise plan and persist in jogging, promoting the benefits of this activity. During jogging, the students used the Keep mobile application to record their jogging time and heart rate, which they then uploaded to the WeChat group. Follow-ups were conducted with students who did not complete their exercise plan, providing encouragement and guidance to continue participating in the experiment. The study employed a comparative research approach between the experimental group and the control group. Results • According to the experimental protocol, after 12 weeks of jogging intervention, the cardiovascular health indicators of both male and female students in the experimental group showed positive changes. Measurements of cardiac function indicators in the experimental group of boys SPTI, DPTI, ED has decreased, SEVR has increased, the relevant indicators compared with the relevant indicators of the control group (P < .05) is significant; in the experimental group of girls, SPTI, DPTI, SEVR indicators decreased, ED increased, and compared with the relevant indicators of the control group (P < .01) has a very significant significance. Changes in vascular indicators in the experimental and control groups after the experiment, SBP, DBP, PP, CAP decreased in the experimental group, and DBP, CAP in the male and female groups were found to be (P < .01), with highly significant changes; while SBP, PP intergroup comparison (P < .05), with significant changes. Conclusion • Jogging is a good aerobic exercise program characterized by convenient ways of carrying out simple methods and low risk of participation. The benefits of jogging are not only reflected physiologically but also psychologically; it can make participants enhance their self-confidence and make their moods more pleasant. It can also improve sleep quality and maintain a good mental state. Long-term jogging habits can effectively improve endothelial function and heart contraction function, reduce blood pressure effectively prevent atherosclerosis and prevent CVD by reducing the incidence of CVD risk factors. ( [ABSTRACT FROM AUTHOR]

Boldine is a plant-derived bioactive compound that has a beneficial impact on human health. Boldine is an aporphine alkaloid mainly obtained from the leaves and bark of the Chilean Boldo tree (Peumus boldus, Family: Monimiaceae). There are plenty of preclinical evidence supports that boldine exerts its beneficial effects against various diseases. Lumiskin™, a patented and marketed formulation by Revitol Skincare for skin brightening, contains Dicetyl boldine, a boldine derivative. All the available information on the Chilean boldo tree (P. boldus Molina) species was actualized by systematically searching the scientific databases (PubMed, SciFinder, Web of Science, Google Scholar, Scopus and others) and scientific literature. This article covers the recent advances in pharmacokinetic, toxicological, pharmacological/biological activities, and molecular mechanisms of the bioactive compound to understand health benefits of boldine better. Boldine exerts antioxidant, hepatoprotective, anti-atherosclerotic, anti-diabetic, analgesic, antipyretic, anti-inflammatory, anti-epileptic, neuroprotective, nephroprotective, anti-arthritis, anticancer and nootropic effects. Moreover, boldine exhibits its various pharmacological activities by altering antioxidant parameters (MDA, superoxide dismutase, glutathione), peroxynitrite, inflammatory markers apoptotic index, caspase-3, acetyl-cholinesterase, myeloperoxidase, TNF-α (Tumor necrosis factor-α), iNOS, Bcl-2-associated X protein (BAX), ACE-1(Angiotensin-converting enzyme-1), dopamine D2 receptors and nicotinic acetylcholine receptor. Boldine has the potential to modulate a variety of biological networks. Due to its versatile pharmacological effects reported in various experimental animals as well as in randomized clinical trials for the treatment of facial melasma and for treatment of urinary stone lithotripsy in children as a complementary phytotherapy; in the future, this compound might be developed as a novel drug for a different indication [ABSTRACT FROM AUTHOR]

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Background: People with intermediate CVD risk constitute most of the population. Within this group, the proportion of events is lower compared to the high-risk group, but they contribute with the largest absolute number of events. Atherosclerosis is a dynamic process and progression can be slowed or even reversed with medication and lifestyle changes, but adherence to prescribed treatment is crucial. Aim: To investigate the long-term effects of interventions with pictorial risk communication of cardiovascular (CVD) risk on average adherence in a group of statin users. Compare response in adherence over time between men and women after intervention. Methods: Participants on active statin treatment were followed up to 5 years after being randomly assigned to an intervention program aimed at raising CVD risk awareness among participants and their physicians. Merging prescribed medication databases with VIPVIZA study to study adherence over time. A moving average adherence was used to compare groups. Results: Generally, the average adherence to statins among the 512 participants was high. Men had a higher average adherence over time, while women had a sharper increase in adherence in conjuncture with the intervention program. Conclusions: Both men and women were receptive to pictorial information regarding CVD risk, but the intervention effect was more pronounced in women. Sex differences are important when considering risk communication strategies. Periodically repeating the intervention was beneficial for maintaining the intervention effect over time. Trial registration: The VIPVIZA study is registered with ClinicalTrials.gov, May 8, 2013, number NCT01849575. [ABSTRACT FROM AUTHOR]

The World Health Organization (WHO) has launched a new 10-year cardiovascular risk prediction recommendation known as the WHO Cardiovascular Risk Chart 2019 (WHO CRC). However, there is currently no assessment available regarding the relationship between ASCVD classic and occupational profiles to WHO CRC, specifically in occupational settings and in the context of the Indonesian Heart Association's (IHA) adjusted version of the WHO CRC for South-East Asia (WHO CRC-INA). This study aims to fill this gap by examining the relationship between classic (Atherosclerosis Cardiovascular Disease) ASCVD and occupational profiles within the oil and gas industry, specifically the WHO CRC-INA. This study is analytical cross-sectional research data were analyzed using the Chi-square test and logistic regression, with a significance level of P < 0.05. The research using total sampling method amounted to 240 workers from January to May 2022 of Medical Check Up (MCU) in a major oil and gas company. The ASCVD risk measurement instrument uses the final score of the WHO CRC-INA, grouped into low- and medium-high risk. Analysis showed that occupational profiles had a relationship with WHO CRC-INA medium-high risk, as seen in the bivariate analysis for shift work and work type (P = 0.018; OR = 2,045) had a relationship with WHO CRC-INA medium-high risk. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to compare dynamic thiol/disulfide homeostasis and myeloperoxidase (MPO) levels in patients with Gilbert's syndrome (GS) and healthy controls. Background: Thiol/disulfide homeostasis and MPO levels are both associated with increased progression of atherosclerosis. Methods: The study included a total of 130 voluntary participants comprising 65 patients with GS and 65 healthy controls. These patients were selected randomly and dynamic thiol/disulfide homeostasis, MPO, complete blood count results, and biochemistry and lipid parameters were evaluated. Patients with known chronic diseases, medication usage, and acute infections were excluded from the study. Serum total thiol and native thiol levels were measured using the fully automated colorimetric method, while serum MPO levels were measured using the sandwich ELISA method. Results: We found that patients with GS had significantly higher total thiol (352.3±38.6 vs. 317.9±47.9, p<0.001) and native thiol (386.6±42.6 vs. 348.0±51.1, p<0.001) and significantly lower disulfide (15.7±4.0 vs. 17.3±4.0, p=0.022) and MPO (130.7 vs. 166.3, p=0.006). In patients with bilirubin of <1 mg/dL, total thiol and native thiol levels were lower and disulfide, disulfide/native thiol (DNT) and disulfide/total thiol (DTT) ratios, and MPO levels were higher. Patients with bilirubin of <1 mg/dL also had higher total cholesterol. Conclusion: In these patients with GS, the thiol/disulfide balance shifted towards thiols and proinflammatory MPO levels were lower. When bilirubin was <1 mg/dL, disulfide, DNT and DTT ratios, and MPO were higher. Bilirubin levels affected all parameters of thiol/disulfide homeostasis and MPO levels independently of other risk factors. In light of our results, we suggest that mild hyperbilirubinemia in cases of GS has an anti-inflammatory and antioxidant effect and may be protective against atherosclerosis. [ABSTRACT FROM AUTHOR]

• Polycystic ovary syndrome (PCOS) is common worldwide. The syndrome refers to a group of disorders with multiple reproductive, metabolic, and endocrine elements. • PCOS affects women from fetal life throughout their lifespan, often decreasing reproductive ability and quality of life, and increasing other types of morbidity and mortality. It is often undiagnosed and untreated. • Management traditionally focuses on the treatment of hyperandrogenism and oligomenorrhea. Women with PCOS often have dyslipidemia, hypertension, obesity, and metabolic syndrome. Management plans should incorporate diagnosis and management of these factors, if present, because of the strong contribution to risk for atherosclerotic cardiovascular disease. • Understanding that the disease extends throughout life emphasizes the importance of continued screening for and treatment of risk factors to prevent cardiovascular disease throughout a woman's lifespan. • Given the complexities of the syndrome and heterogeneous manifestations, optimal management often requires a multi-disciplinary approach to provide counseling and support for lifestyle modification and addressing the full range of any reproductive, endocrine, and cardiometabolic abnormalities. Polycystic ovary syndrome (PCOS) is a common endocrinopathy worldwide with a heterogeneous clinical presentation including reproductive, metabolic, and endocrine elements. However, the assessment and management of PCOS remains inconsistent, with many women undiagnosed and untreated. We now also understand that the management of PCOS should extend throughout a woman's lifespan as many elements of the syndrome persist after menopause. Management has traditionally focused on the treatment of hyperandrogenism and oligomenorrhea. Women with PCOS often have dyslipidemia, hypertension, obesity, and metabolic syndrome, which may be worsened by the hormonal abnormalities, and are therefore at higher risk for cardiovascular disease morbidity and mortality, a risk that increases after menopause. While treatment with hormonal therapy, in particular combined oral contraceptives, may improve cardiovascular risk factors, management plans should incorporate specific diagnosis and management of these factors, if present, because of the strong contribution to the risk for atherosclerotic cardiovascular disease. Given the complexities of the syndrome, optimal management often requires a multi-disciplinary approach including the lipid and cardiometabolic specialist to provide counseling and support for lifestyle modification along with pharmacologic therapy as indicated to address the full range of any reproductive, endocrine, and cardiometabolic abnormalities. [ABSTRACT FROM AUTHOR]

There is no longer any serious doubt that daily habits and actions profoundly impact on both short- and long-term health and quality of life. An overwhelming body of scientific and medical literature supports this contention. Thousands of studies support the concept that regular physical activity, healthy nutrition and maintaining a healthy body weight, not smoking cigarettes, obtaining healthy sleep, reducing stress and maintaining positive connections with other individuals all profoundly impact on health. The scientific literature the supports the health impact of these daily habits and actions is underscored by its incorporation into virtually every evidence-based clinical guideline in the area of metabolic diseases. Thus, the scientific basis for lifestyle medicine rests on an enormous body of evidence-based literature. The key issue in lifestyle medicine is to provide an overall framework where these studies, which are often spread over scientific literature in multiple disciplines, can be made accessible to the medical community and to the public at large. This is the essence of the field of lifestyle medicine. The academic basis of lifestyle medicine is robust and needs to be emphasized by all practitioners of lifestyle medicine. This is the key to moving this field forward into the future. [ABSTRACT FROM AUTHOR]

BACKGROUND Previous studies have demonstrated the benefits of ideal cardiovascular health (CVH) in reducing cardiovascular risk. However, its role in subclinical atherosclerosis (SA) progression remains unclear. We aim to examine the association of CVH, estimated by the American Heart Association's new Life's Essential 8 (LE8), with the progression of SA. METHODS This prospective cohort study was conducted among 972 asymptomatic Chinese participants and followed up for 5.7 years. The LE8 score (range, 0–100) consisted of blood pressure, lipids, glucose, body mass index, smoking status, diet health, physical activity and sleep health was evaluated in 1998 and 2008–2009. Progression of SA was determined by carotid plaque and coronary artery calcification (CAC) in 2008–2009 and 2013–2014. Log-binomial regression model was used to estimate the association of LE8 score with SA progression. RESULTS Each 10 points increment in LE8 score was associated with 15.2% (RR: 0.848, 95% CI: 0.797–0.902), 17.7% (RR: 0.823, 95% CI: 0.766–0.884) and 12.0% (RR: 0.880, 95% CI: 0.845–0.916) lower risks of carotid plaque, CAC and overall SA progression, respectively. Compared with participants with non-ideal CVH at both visits, the participants with ideal CVH at both visits had 39.1% (RR: 0.609, 95% CI: 0.494–0.752), 41.0% (RR: 0.590, 95% CI: 0.456–0.764) and 29.7% (RR: 0.703, 95% CI: 0.598–0.825) lower risks of carotid plaque, CAC and overall SA progression, respectively. CONCLUSIONS Higher LE8 scores were associated with lower risks of SA progression. Besides, long-term maintenance of optimal CVH was more beneficial to prevent SA progression. [ABSTRACT FROM AUTHOR]

Background: Zinc has been proven to be effective against periodontitis, and also reported to reduce the risk of cardiovascular diseases (CVD). This study aims to explore the regulatory effect of zinc intake on the association between periodontitis and atherosclerotic cardiovascular disease (ASCVD). Methods: This was a cross-sectional study based on the National Health and Nutrition Examination Survey (NHANES). Logistic regression model was used to explore the association between zinc-RDA or periodontitis and 10-year ASCVD risk ≥ 20%, and results were shown as odds ratio (OR) and 95% confidence interval (95% CI). The regulatory effect of zinc intake on the association between periodontitis and 10-year ASCVD risk ≥ 20% was also assessed using logistic regression model. Subgroup analysis was performed based on age, gender, obesity, education level, lipid-lowering therapy, and dental floss. Results: 6,075 patients were finally included for analysis. Zinc intake reaching the recommended level (OR = 0.82, 95%CI: 0.69–0.98) and periodontitis (OR = 2.47, 95%CI: 2.04-3.00) were found to be associated with 0.82-fold and 2.47-fold odds of 10-year ASCVD risk ≥ 20%, respectively. In addition, we found that the odds of 10-year ASCVD risk ≥ 20% was lower in patients with zinc intake reaching the recommended level than those without [OR (95%CI): 2.25 (1.81–2.80) vs. 2.72 (2.05–3.62)]. The similar regulatory effect was found in patients with age ≥ 60 years and < 60 years, in male and female, with or without obesity, in different education levels, with or without lipid lowering therapy, and with or without use of dental floss (all P < 0.05). Conclusions: This study found the regulatory effect of adequate zinc intake on the association between periodontitis and ASCVD, providing guidance for periodontitis patients to decrease the risk of ASCVD. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a significant risk factor for developing cardiovascular disease and a leading cause of death worldwide. The occurrence of atherosclerosis is closely related to factors such as endothelial injury, lipid deposition, immunity, and inflammation. Conventional statins, currently used in atherosclerosis treatment, have numerous adverse side effects that limit their clinical utility, prompting the urgent need to identify safer and more effective therapeutic alternatives. Growing evidence indicates the significant potential of Chinese herbs in atherosclerosis treatment. Herbal monomer components, such as natural flavonoid compounds extracted from herbs like Coptis chinensis and Panax notoginseng, have been utilized for their lipid-lowering and inflammation-inhibiting effects in atherosclerosis treatment. These herbs can be used as single components in treating diseases and with other Chinese medicines to form herbal combinations. This approach targets the disease mechanism in multiple ways, enhancing the therapeutic effects. Thus, this review examines the roles of Chinese herbal medicine monomers and Chinese herbal compounds in inhibiting atherosclerosis, including regulating lipids, improving endothelial function, reducing oxidative stress, regulating inflammation and the immune response, and apoptosis. By highlighting these roles, our study offers new perspectives on atherosclerosis treatment with Chinese herbs and is anticipated to contribute to advancements in related research fields. [ABSTRACT FROM AUTHOR]

The article presents a study which characterized the real-world prescribing patterns of type 2 diabetes medications based on cardiovascular and renal comorbid conditions in the Adult Medicine clinic. Topics discussed include relative contraindications for sodium-glucose cotransporter 2 (SGL2) inhibitors, characteristics of patients included in the study, and primary and secondary outcomes.

Objective: Patients with juvenile‐onset systemic lupus erythematosus (JSLE) have increased atherosclerosis risk. This study investigated novel atherosclerosis progression biomarkers in the Atherosclerosis Prevention in Pediatric Lupus Erythematosus (APPLE) trial, the largest investigator‐led randomized control trial of atorvastatin versus placebo for atherosclerosis progression in JSLE, using carotid intima‐media thickness (CIMT) as the primary outcome. Methods: Unsupervised clustering of baseline CIMT and CIMT progression over 36 months was used to stratify patients with JSLE. Disease characteristics, cardiovascular risk scores, and baseline serum metabolome were investigated in CIMT‐stratified patients. Machine learning techniques were used to identify and validate a serum metabolomic signature of CIMT progression. Results: Baseline CIMT stratified patients with JSLE (N = 151) into three groups with distinct high, intermediate, and low CIMT trajectories irrespective of treatment allocation, despite most patients having low cardiovascular disease risk based on recommended assessment criteria. In the placebo group (n = 60), patients with high versus low CIMT progression had higher total (P = 0.001) and low‐density lipoprotein (LDL) (P = 0.002) cholesterol levels, although within the reference range. Furthermore, a robust baseline metabolomic signature predictive of high CIMT progression was identified in the placebo arm (area under the curve, 80.7%). Patients treated with atorvastatin (n = 61) had reduced LDL cholesterol levels after 36 months, as expected; however, despite this, 36% still had high atherosclerosis progression, which was not predicted by metabolomic biomarkers, suggesting nonlipid drivers of atherosclerosis in JSLE with management implications for this subset of patients. Conclusion: Significant baseline heterogeneity and distinct subclinical atherosclerosis progression trajectories exist in JSLE. Metabolomic signatures can predict atherosclerosis progression in some patients with JSLE with relevance for clinical trial stratification. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases (CVDs) are the leading cause of death and disability worldwide. It is essential to develop novel interventions to prevent/delay CVDs by targeting their fundamental cellular and molecular processes. Melatonin is a small indole molecule acting both as a hormone of the pineal gland and as a local regulator molecule in various tissues. It has multiple features that may contribute to its cardiovascular protection. Moreover, melatonin enters all cells and subcellular compartments and crosses morphophysiological barriers. Additionally, this indoleamine also serves as a safe exogenous therapeutic agent. Increasing evidence has demonstrated the beneficial effects of melatonin in preventing and improving cardiovascular risk factors. Exogenous administration of melatonin, as a result of its antioxidant and anti-inflammatory properties, has been reported to decrease blood pressure, protect against atherosclerosis, attenuate molecular and cellular damage resulting from cardiac ischemia/reperfusion, and improve the prognosis of myocardial infarction and heart failure. This review aims to summarize the beneficial effects of melatonin against these conditions, the possible protective mechanisms of melatonin, and its potential clinical applicability in CVDs. [ABSTRACT FROM AUTHOR]

• Serum VLCFAs and VLC-MUFAs were eluted at 57% after lipoprotein apheresis (LA). • Serum VLCFAs and VLC-MUFAs remained low for 7 days after LA. • LA induces an acute increase in the serum levels of anti-inflammatory BCFAs. • Long-term regular biweekly LA decreased the serum levels of VLC-MUFAs and n3 PUFAs. Lipoprotein apheresis (LA) is an extracorporeal treatment that transiently reduces lipoprotein (a) [Lp(a)] by 60% and leads to an 80–92% reduction in major adverse cardiovascular events. LA has a significant impact on lipid profile in serum of patients with atherosclerotic cardiovascular disease. To investigate the effects of LA on the composition of serum fatty acids (FAs), focusing on those which could have an impact on cardiovascular disease (CVD). This is a prospective study in the First Department of Cardiology of the Medical University of Gdansk, Poland. Serum samples were collected from 28 patients before LA, just after the procedure, and 7 days after LA. Additionally, in a smaller group of patients, the samples were collected after a second tour of LA (2 weeks later), as well as after 1 year from the first procedure. The serum FA profile was analyzed using gas chromatography-mass spectrometry. After the LA procedure, a substantial change in serum FA composition along with low-density lipoprotein cholesterol (LDL-C) and Lp(a) decrease were observed 7 days after procedure, but these parameters returned to the values similar to those before procedure after 14 days. Very long-chain FAs (VLCFAs) and very long-chain monounsaturated FAs (VLC-MUFAs) were eluted at 57% and remained low even 7 days after LA (p=0.027 and p < 0.001, respectively). We also observed an increase in the percentage of total branched-chain FAs (BCFAs) (p=0.004) and anteiso BCFAs (p=0.012) after LA. After 1 year of regular LA, a substantial decrease in serum VLC-MUFAs and n3 polyunsaturated LA (PUFAs) were noted. Decreased VLCFAs and VLC-MUFAs involved in CVD development remained low even 7 days after LA. An acute increase in the levels of anti-inflammatory BCFAs was observed. In turn long-term regular administration of LA substantially decreased VLC-MUFA and n3 PUFA. [Display omitted] [ABSTRACT FROM AUTHOR]

Introduction: Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death and disability worldwide. There is a direct relationship between increasing levels of LDL-C and increased risk of ASCVD. Guidance from the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS) recommends that high-risk ASCVD patients maintain an LDL-C <1.8 mmol/L (70 mg/dL) and very high-risk patients <1.4 mmol/L (55 mg/dL). National data in England reveals that 71% of high-risk secondary prevention patients have an LDL-C >1.8 mmol/L (70 mg/dL). Methodology: An ASCVD risk reduction approach was initiated in a primary care clinic in December 2021. Of those patients who underwent review between December 2021 and July 2023, 102 patients were started on inclisiran treatment in a real-world setting. These patients were retrospectively reviewed to determine the initial effects of using inclisiran after the first dose as part of the patients' ASCVD risk reduction management. Results: After 1 injection of Inclisiran, the patients' mean decrease in LDL-C was 2.00 mmol/L (77.3 mg/dL) after a mean of 87 days. This represented a mean reduction of 61.7% (SD = 19.8) in their LDL-C measurements. The addition of inclisiran resulted in 79.4% of patients achieving an LDL-C target of <1.8 mmol/L (70 mg/dL) and 65.7% of patients attaining an LDL-C of <1.4 mmol/L (55 mg/dL). Conclusion: Healthcare providers working in primary care can achieve recommended LDL-C targets in 4 out of 5 secondary prevention patients after an initial dose of inclisiran as part of their ASCVD risk reduction approach management. [ABSTRACT FROM AUTHOR]

The article presents the discussion on growing global prevalence of obesity and its associated health complications. Topics include emphasizing the need for more comprehensive treatment strategies beyond traditional non-pharmacological interventions; and potential of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) for weight reduction and cardiovascular benefits.

Background: Atherosclerosis (AS) is a fundamental pathological state in various cardiovascular diseases. Geniposide, which is the main active component of Gardenia jasminides, is effective against AS. However, the underlying molecular mechanisms remain unclear. Here, we sought to elucidate them. Methods: The targets of AS and geniposide were collected from online public databases. The potential mechanism of Geniposide in treating AS was predicted by constructing a protein–protein interaction (PPI) network and conducting Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway enrichment analyses. Hub proteins and core pathways were verified by molecular docking and in vivo experiments. Moreover, the effect of geniposide on AS was assessed by measuring the atherosclerotic plaque area in the thoracic aorta of mice. ApoE−/− mice were used to establish AS models and randomly divided into different groups. Two different doses of geniposide were administered to the mice. Hematoxylin and eosin (HE) staining was performed to evaluate the effects of geniposide on AS. Oil Red O and Sirius Red staining were used to evaluate plaque stability. The protein expression of key markers involved in the signalling pathways was examined using western blotting and immunofluorescence. Results: A total of 239 active targets, 3418 AS-related disease targets, and 129 overlapping targets were identified. Hub genes were detected, and molecular docking revealed that geniposide strongly interacted with hub proteins (AKT1, VEGFA, CTNNB1, MMP9, and EGFR). Moreover, 109 signalling pathways, including the Rap1 signalling pathway, were identified using enrichment analysis. The results of in vivo experiments demonstrated that geniposide reduced body weight and blood lipid levels, alleviated the formation of atherosclerotic plaques, enhanced plaque stability, and inhibited inflammation, at least partially, by activating the Rap1/PI3K/Akt signalling pathway in ApoE−/− mice. Conclusion: Geniposide can alleviate AS and enhance the stability of atherosclerotic plaques by regulating the Rap1/PI3K/Akt signalling pathway. [ABSTRACT FROM AUTHOR]

Vitamin K is a lipophilic vitamin, whose absorption, transportation, and distribution are influenced by lipids. The plasma vitamin K level after supplementation is predominantly a lipid-driven effect and independent of existing vitamin K status. However, previous studies examining the efficacy of vitamin K supplementation often overlooked the influence of lipid levels on vitamin K absorption, resulting in inconsistent outcomes. Recent research discovered that impaired transportation of vitamin K2 within uremic high-density lipoproteins (HDL) in individuals with uremia might elucidate the lack of beneficial effects in preventing calcification observed in multiple trials involving menaquinone-7 (MK-7) supplementation among patients with chronic kidney disease. Clinical findings have shown that drugs used to regulate hyperlipidemia interact with the vitamin K antagonist warfarin, because cholesterol and vitamin K share common transport receptors, such as Niemann-Pick C1-like 1 (NPC1L1) and ATP-binding cassette protein G5/G8 (ABCG5/ABCG8), in enterocytes and hepatocytes. Additionally, cholesterol and vitamin K share a common biosynthetic intermediate called geranylgeranyl pyrophosphate (GGPP). It is important to note that statins, which hinder cholesterol synthesis, can also impede vitamin K conversion, ultimately impacting the functionality of vitamin K-dependent proteins. Furthermore, certain studies have indicated that vitamin K supplementation holds potential in managing hyperlipidemia, potentially opening a novel avenue for controlling hyperlipidemia using dietary vitamin K supplements. Therefore, attaining a more comprehensive understanding of the intricate interplay between vitamin K and lipids will yield valuable insights concerning the utilization of vitamin K and lipid regulation. [ABSTRACT FROM AUTHOR]

Objectives The 2022 EULAR recommendations for cardiovascular risk management in patients with rheumatic disorders, including SLE, call for rigorous management of cardiovascular risk factors (CVRF). The impact of CVRF target attainment on atherosclerotic plaque progression hasn't been previously evaluated in prospective ultrasound studies. Methods A total of 115 patients with SLE and 1:1 age and sex-matched healthy controls who had a baseline carotid and femoral ultrasound examination in our cardiovascular research unit were invited for a 7-year follow-up assessment of new plaque development. We aimed to compare the incidence of plaque progression between SLE patients and controls and reveal the extent to which it is affected by the attainment of European Society of Cardiology (ESC) targets for modifiable CVRFs (blood pressure, smoking status, body weight, lipids and physical activity), and disease-related features (disease duration, disease activity, autoantibodies, treatments). Results Eighty-six SLE patients and 42 controls had a 7-year follow-up carotid and femoral plaque examination. New plaque development was observed in 32/86 patients vs 8/42 controls (P  = 0.037). Patients with SLE had a 4-fold higher risk for plaque progression than controls (OR: 4.16, CI: 1.22, 14.19, P  = 0.023), adjusting for potential confounders. Multivariate regression analyses showed a 50% decrease in plaque progression for every modifiable CVRF fulfilling ESC targets (OR: 0.56, CI: 0.34, 0.93, P  = 0.026). Conclusion Patients with SLE develop a rapid progression of atherosclerotic plaques which may be drastically reduced by CVRF target attainment according to ESC guidelines. [ABSTRACT FROM AUTHOR]

Carotid intima-media thickness (CIMT) is a noninvasive marker of atherosclerosis, a typical pathologic process underlying cardiovascular diseases (CVDs). It is essential to explore the relationships between weight loss and the reduction of CIMT. This was an updated systematic review and meta-analysis. A systematic literature search was conducted to collect relevant clinical trials. The pooled results of meta-analyses were assessed by weighted mean difference (WMD) and the corresponding 95 % confidence interval (95% CI). Thirty-three articles involving 2273 participants were collected in this meta-analysis. Among all participants with obesity, the pooled mean of weight loss was −23.26 kg (95% CI: −27.71 to −18.81), and the pooled mean change of CIMT was −0.06 mm (95% CI: −0.08 to −0.04). Compared with Non-surgical interventions, Surgical ones could lead to much higher weight loss (P between groups < 0.001). A more significant CIMT reduction was identified among Surgical intervention patients than among Non-surgical intervention participants (P between groups < 0.001). Effective interventions, especially Surgical interventions, could reduce the weight of patients with obesity, followed by the decline of CIMT, which might further disturb atherosclerosis progression and lower CVD risk. [ABSTRACT FROM AUTHOR]

Background: The glucagon-like peptide-1 (GLP-1) receptor agonist liraglutide (LIRA) is a potential hypoglycemic drug with anti-atherosclerosis (AS) effects. Autophagy in the vascular smooth muscle cells (VSMCs) facilitates AS. However, the role of autophagy in the anti-AS mechanism of LIRA remains unclear. Aims: To examine the role and mechanisms of autophagy in LIRA's improvement of the biological characteristics of VSMCs in high glucose conditions. Study Design: Experimental animal study. Methods: VSMCs isolated from the thoracic aorta of male SD rats were subjected to a high glucose (HG) condition (25 mM) in Dulbecco's Modified Eagle's Medium with or without LIRA, the GLP-1 receptor antagonist exendin9-39 (Exe9-39), a phosphatidylinositol 3-kinase (PI3K) inhibitor (LY294002), and autophagy inhibitors (3-methyladenine [3-MA] and bafilomycin A1 [Baf A1]). Acridine orange staining, western blotting, transmission electron microscopy, and mCherry-GFP-LC3 transfection were performed to evaluate the autophagy flux. Additionally, VSMC migration, calcification, proliferation, and apoptosis in HG conditions were observed. Results: Addition of LIRA alone or in combination with autophagy inhibitors significantly downregulated Beclin, increased the LC3-II/LC3-I ratio, and upregulated p62 in VSMCs in HG conditions. Furthermore, autophagolysosome formation was markedly curbed after treatment with LIRA and/or autophagy inhibitors. Inhibition of autophagy by LIRA and/or the autophagy inhibitors attenuated VSMC phenotype conversion, proliferation, migration, and calcification and promoted VSMC apoptosis in HG conditions. This protective role of LIRA was augmented by LY294002, but inhibited by Exe9-39. Conclusion: LIRA plays a significant role in the improvement of the biological features of VSMCs in HG conditions. [ABSTRACT FROM AUTHOR]

To investigate the effects of rapeseed oil on body composition, blood glucose and lipid metabolism in people with overweight and obesity compared to other cooking oils. We searched eight databases for randomized controlled studies (including randomized crossover trials). The risk of bias for the included studies was assessed using the Cochrane Risk of Bias 2.0 tool. The Grading of Recommendations Assessment Development and Evaluation (GRADE) criteria were used to evaluate the quality of the outcomes. The methodological quality of the included studies was assessed using the Physiotherapy Evidence Database (PEDro) scale. Sensitivity analysis was used to check the stability of the pooled results. Statistical analysis was carried out using Review Manager 5.3 software. As a result, fifteen randomized controlled studies (including six parallel studies and nine crossover studies) were included in this study. Compared to other edible oils, rapeseed oil significantly reduced low density lipoprotein cholesterol (LDL-C) (MD = −0.14 mmol/L, 95% CI: −0.21, −0.08, I2 = 0%, P < 0.0001), apolipoprotein B (ApoB) (MD = −0.03 g/L, 95% CI: −0.05, −0.01, I2 = 0%, P = 0.0003), ApoB/ApoA1 (MD = −0.02, 95% CI: −0.04, −0.00, I2 = 0%, P = 0.02) and insulin (MD = −12.45 pmol/L, 95% CI: −19.61, −5.29, I2 = 37%, P = 0.0007) levels, and increased fasting glucose (MD = 0.16 mmol/L, 95% CI: 0.05, 0.27, I2 = 27%, P = 0.003) levels. However, the differences in body weight and body composition between rapeseed oil and control oils were not significant. In a word, rapeseed oil is effective in reducing LDL-C, ApoB and ApoB/ApoA1 levels in people with overweight and obesity, which is helpful in preventing and reducing the risk of atherosclerosis. PROSPERO registration number: CRD42022333436. [ABSTRACT FROM AUTHOR]

Background: Interplay between gut microbiota and heart, termed "gut-heart" axis, has a crucial role in the pathogenesis of atherosclerosis. Our previous study showed that lycopene possesses anti-inflammatory and anti-atherosclerotic effects, but its link to the gut microbiota is poorly understood. Herein, we surmised that lycopene could regulate the gut microbiota, exert anti-atherosclerotic effect by regulating the "gut-heart" axis. Methods: Male ApoE−/− mice were fed a high-fat diet (HFD) with or without lycopene (0.1% w/w) for 19 weeks. Gut microbiota was analyzed by 16 S rRNA sequencing, the protein levels of zonula occludens-1 (ZO-1), occludin, toll-like receptor 4 (TLR4) and phospho-nuclear factor-κB (NF-κB) p65 were measured by Western blotting, the levels of serum inflammatory factors including monocyte chemotactic protein 1 (MCP-1), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 were assayed using ELISA kits. Also, the concentrations of serum lipopolysaccharide (LPS), D-lactic acid (D-LA) and diamine peroxidase (DAO) were measured through ELISA method. Results: The aortic sinus sections revealed that lycopene supplementation significantly reduced the extent of atherosclerotic lesions and inhibited atherosclerosis development caused by HFD. The analysis of gut microbiota showed that lycopene reduced the ratio of Firmicutes/Bacteroides and increased the relative abundance of Verrucomicrobia, Akkermansia and Alloprevotella, which were related to elevated intestinal barrier function and reduced inflammation. Moreover, lycopene up-regulated the expression of intestinal ZO-1 and occludin and decreased serum LPS, D-LA and DAO levels. In addition, lycopene inhibited the expression of TLR4 and phospho-NF-κB p65 in aortic sinus plaque, serum MCP-1, TNF-α, IL-1β, and IL-6 levels were also lowered by lycopene treatment. Conclusions: Our results indicated the protective effect of lycopene against atherosclerosis induced by HFD and further revealed that its mechanism might be its prebiotic effect on maintaining gut microbiota homeostasis and improving intestinal barrier function, consequently reducing serum LPS-triggered inflammatory response in the heart. [ABSTRACT FROM AUTHOR]

The article discusses outlook for clinical lipidology in the United Kingdom. Topics explored include the introduction of hospital outpatient lipid clinics that offer diagnostic, genetic testing, and therapeutic services, the development of several novel forms of lipid-lowering compounds, and the operations of medical associations that cater to lipidologists in the region such as HEART UK and the British Atherosclerosis Society (BAS).

Context Atherosclerosis is a systemic pro-inflammatory and pro-oxidative disease, accounting for approximately a third of deaths globally. It has been proposed that omega-3s, through their antioxidant and anti-inflammatory properties, mitigate atherosclerotic disease progression. However, due to the systemic pro-inflammatory and pro-oxidative state of atherosclerosis, it is proposed that patients with atherosclerotic disease may have higher omega-3 requirements than the average requirement, due to increased nutrient utilization in anti-inflammatory and anti-oxidant processes. Objective The aim of this review was to determine what dose and duration of omega-3 supplementation is required to reach a therapeutic blood level of omega-3s (eicosapentaenoic acid ≥150 µg/mL or omega-3 index ≥8%) in people with chronic atherosclerotic disease. Data Sources This systematic review comprehensively searched MEDLINE, Emcare, Scopus, and CINAHL using key search terms for atherosclerotic disease, omega-3, supplementation, and blood levels of omega-3s. Data Extraction Two reviewers independently screened 529 randomized controlled trials (RCTs) supplementing omega-3s in patients with chronic atherosclerotic disease. Data Analysis In total, 25 journal articles from 17 original RCTs were included and assessed quantitatively. Supplementation at 1.8 g to 3.4 g per day for a 3-month–6-month duration, and at 4.4 g and above for as little as 1 month–6 months were identified as the most effective dosage ranges for increasing blood levels of omega-3s to therapeutic levels in people with atherosclerotic disease. Conclusions Consideration should be given to routine omega-3 supplementation and to increasing the omega-3 dietary recommendations and upper limits of daily intake to improve clinical outcomes and reduce the risk of cardiac mortality in this population. [ABSTRACT FROM AUTHOR]

Population aging combined with higher susceptibility to cardiovascular diseases in older adults is increasing the incidence of conditions such as atherosclerosis, myocardial infarction, heart failure, myocardial hypertrophy, myocardial fibrosis, arrhythmia, and hypertension. sodium–glucose cotransporter 2 inhibitors (SGLT2i) were originally developed as a novel oral drug for patients with type 2 diabetes mellitus. Unexpectedly, recent studies have shown that, beyond their effect on hyperglycemia, SGLT2i also have a variety of beneficial effects on cardiovascular disease. Experimental models of cardiovascular disease have shown that SGLT2i ameliorate the process of aging-related cardiovascular disease by inhibiting inflammation, reducing oxidative stress, and reversing endothelial dysfunction. In this review, we discuss the role of SGLT2i in aging-related cardiovascular disease and propose the use of SGLT2i to prevent and treat these conditions in older adults. [ABSTRACT FROM AUTHOR]

Personal Health literacy (PHL) is essential in cardiovascular risk management. Hindrances in PHL can lead to poor cardiovascular outcomes. To investigate whether limited PHL is associated with lower likelihoods of i) overall cardiovascular health and ii) individual cardiovascular health components as defined by the American Heart Association's Life Simple (LS7). Multi-Ethnic Study of Atherosclerosis participants (N = 3719; median age[range]: 59[45–84]) completed a PHL questionnaire in 2016–2018. PHL was classified as limited (score ≥10) or adequate (score <10). LS7 components were measured in 2000–2002. Robust Poisson regression was employed to compute prevalence ratios and 95% confidence intervals (PR[95%CI]) of LS7 measures. 14.7% of participants had limited PHL. Limited PHL was associated with lower likelihoods of optimal LS7 (0.69[0.50, 0.95], p =.02) and average LS7 (0.95[0.88, 1.02], p =.15) after adjustment. Limited PHL was significantly associated with a 7% lower likelihood of ideal fasting blood glucose level after adjustment (0.93[0.89, 0.98], p <.01). Limited PHL was modestly associated with suboptimal cardiovascular health and elevated blood glucose, independent of income and education. Health educators and providers should equitably address PHL barriers to improve cardiovascular management and quality of care for patients and communities. [ABSTRACT FROM AUTHOR]

Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death among urban and rural residents in China, and elevated low-density lipoprotein cholesterol (LDL-C) is a risk factor for ASCVD. Considering the increasing burden of ASCVD, lipid management is of the utmost importance. In recent years, research on blood lipids has made breakthroughs around the world, hence a revision of China guidelines for lipid management is imperative, especially since the target lipid levels in the general population vary in respect to the risk of ASCVD. The level of LDL-C, which can be regarded as appropriate in a population without frisk factors, can be considered abnormal in people at high risk of developing ASCVD. As a result, the "Guidelines for the prevention and treatment of dyslipidemia" were adapted into the "China Guidelines for Lipid Management" (henceforth referred to as the new guidelines) by an Experts' committee after careful deliberation. The new guidelines still recommend LDL-C as the primary target for lipid control, with CVD risk stratification to determine its target value. These guidelines recommend that moderate intensity statin therapy in adjunct with a heart-healthy lifestyle, be used as an initial line of treatment, followed by cholesterol absorption inhibitors or/and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, as necessary. The new guidelines provide guidance for lipid management across various age groups, from children to the elderly. The aim of these guidelines is to comprehensively improve the management of lipids and promote the prevention and treatment of ASCVD by guiding clinical practice. [ABSTRACT FROM AUTHOR]

Introduction: Atherosclerosis is a complicated cascade of inflammatory processes, oxidative stress, and apoptosis, making it the most prevalent cardiovascular disease. The onset and progression of cardiovascular diseases are greatly influenced by oxidative stress. Targeting oxidative stress is an effective strategy for treating such diseases. Marrubiin is a bioactive furan labdane diterpenoid acts as a strong antioxidant to protect against oxidative damage. This study aimed to investigate the protective effects of marrubiin against oxidative stress and apoptosis in a cellular model of the vascular system. Methods: Human umbilical vein endothelial cells were treated with varying concentration of marrubiin and its IC50 value was determined. The antioxidant potential of marrubiin was assessed by measuring the intracellular level of glutathione (GSH) using a colorimetric technique. Since apoptosis plays a significant role in the plaque rupture, the study also evaluated the protective effects of marrubiin on the expression of key genes involved in apoptotic pathways. Results: Cells treated with marrubiin showed increased GSH levels compared to cell therapy control cells, indicating marrubiin's ability to counteract the effects of TNF-α's on GSH levels. Furthermore real-time PCR analysis demonstrated that marrubiin upregulated Bcl-xl while downregulating caspase3 and Nox4 in treated cells. These findings suggest that marrubiin protects against apoptosis and oxidative stress. Conclusion: Based on our findings, marrubiin is recommended as a preventive/therapeutic treatment for diseases caused by elevated intracellular reactive oxygen species levels in cardiovascular diseases. [ABSTRACT FROM AUTHOR]

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Background: Cerebrovascular disease (CVD) related to atherosclerosis and Parkinson's disease (PD) are two prevalent neurological disorders. They share common risk factors and frequently occur together. The aim of this study is to investigate the association between atherosclerosis and PD using genetic databases to gain a comprehensive understanding of underlying biological mechanisms. Methods: The gene expression profiles of atherosclerosis (GSE28829 and GSE100927) and PD (GSE7621 and GSE49036) were downloaded from the Gene Expression Omnibus (GEO) database. After identifying the common differentially expressed genes (DEGs) for these two disorders, we constructed proteinprotein interaction (PPI) networks and functional modules, and further identified hub genes using Least Absolute Shrinkage and Selection Operator (LASSO) regression. The diagnostic effectiveness of these hub genes was evaluated using Receiver Operator Characteristic Curve (ROC) analysis. Furthermore, we used single sample gene set enrichment analysis (ssGSEA) to analyze immune cell infiltration and explored the association of the identified hub genes with infiltrating immune cells through Spearman's rank correlation analysis in R software. Results: A total of 50 shared DEGs, with 36 up-regulated and 14 down-regulated genes, were identified through the intersection of DEGs of atherosclerosis and PD. Using LASSO regression, we identified six hub genes, namely C1QB, CD53, LY96, P2RX7, C3, and TNFSF13B, in the lambda.min model, and CD14, C1QB, CD53, P2RX7, C3, and TNFSF13B in the lambda.1se model. ROC analysis confirmed that both models had good diagnostic efficiency for atherosclerosis datasets GSE28829 (lambda.min AUC = 0.99, lambda.1se AUC = 0.986) and GSE100927 (lambda.min AUC = 0.922, lambda.1se AUC = 0.933), as well as for PD datasets GSE7621 (lambda.min AUC = 0.924, lambda.1se AUC = 0.944) and GSE49036 (lambda.min AUC = 0.894, lambda.1se AUC = 0.881). Furthermore, we found that activated B cells, effector memory CD8 + T cells, and macrophages were the shared correlated types of immune cells in both atherosclerosis and PD. Conclusion: This study provided new sights into shared molecular mechanisms between these two disorders. These common hub genes and infiltrating immune cells offer promising clues for further experimental studies to explore the common pathogenesis of these disorders. [ABSTRACT FROM AUTHOR]

Objective: This article describes the importance of identifying inflammation‐inducing conditions in the dental office that are prevalent in the population and have significant systemic health risks for the patient. The role of the dental biofilm will be presented, as will the clinical protocols for treating an unhealthy biofilm. Methods for testing and maintaining a healthy biofilm are also presented. Clinical Considerations: Periodontal disease, dental caries, and periapical infections are inflammation‐inducing diseases that can be identified in the dental office. Additionally, sleep apnea has been linked to chronic systemic inflammation. Dentists can identify risk factors and provide treatments that lower the risk of serious systemic outcomes, such as atherosclerosis, cardiac arrest, and stroke. Conclusions: A thorough dental examination, including a comprehensive periodontal evaluation, can provide important information that can be used to improve or maintain a patient's systemic health. Treatments provided to improve oral health have been shown to improve systemic indicators of cardiovascular health. This is the basis of integrative oral medicine, a collaboration between the medical and dental providers, which can offer patients the best opportunity for improved health outcomes. Clinical Significance: Periodontal disease, caries, periapical infections, and sleep apnea all have negative systemic health consequences for the patient (DiMatteo, Inside Dent, 2017, 13, 30; Nakano, Oral Microbiol Immunol, 2009, 24, 64; El Ouarti, BMC Oral Health, 2021, 21, 124; Lamberg, Steve). Periodontal disease, caries, and root end infections influence the health of the oral biofilm. If the biofilm becomes pathogenic the host inflammatory response can be stimulated, resulting in a cascade of inflammatory processes that damage the supporting structures of the teeth and harm the patient's overall health. A thorough dental exam that includes a comprehensive periodontal evaluation will identify patients with active inflammation or oral conditions that contribute to chronic inflammation. Dentists can integrate this information into treatment strategies that reduce the inflammatory burden and assist in better overall health outcomes. [ABSTRACT FROM AUTHOR]

• Obicetrapib is a selective CETP inhibitor for reducing LDL-C and ASCVD. • Obicetrapib plus ezetimibe on top of high-intensity statin lowers LDL-C by 63%. • Obicetrapib monotherapy and with ezetimibe are both safe and well tolerated. Obicetrapib, a selective cholesteryl ester transfer protein (CETP) inhibitor, reduces low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), lipoprotein particles, and apolipoproteins, when added to high-intensity statin in patients with dyslipidemia. To evaluate the safety and lipid-altering efficacy of obicetrapib plus ezetimibe combination therapy as an adjunct to high-intensity statin therapy. This double-blind, randomized, phase 2 trial administered 10 mg obicetrapib plus 10 mg ezetimibe (n = 40), 10 mg obicetrapib (n = 39), or placebo (n = 40) for 12 weeks to patients with LDL-C >70 mg/dL and triglycerides (TG) <400 mg/dL, on stable high-intensity statin. Endpoints included concentrations of lipids, apolipoproteins, lipoprotein particles, and proprotein convertase subtilisin kexin type 9 (PCSK9), safety, and tolerability. Ninety-seven patients were included in the primary analysis (mean age 62.6 years, 63.9% male, 84.5% white, average body mass index of 30.9 kg/m2). LDL-C decreased from baseline to week 12 by 63.4%, 43.5%, and 6.35% in combination, monotherapy, and placebo groups, respectively (p <0.0001 vs. placebo). LDL-C levels of <100, <70, and <55 mg/dL were achieved by 100%, 93.5%, and 87.1%, respectively, of patients taking the combination. Both active treatments also significantly reduced concentrations of non-HDL-C, apolipoprotein B, and total and small LDL particles. Obicetrapib was well tolerated and no safety issues were identified. The combination of obicetrapib plus ezetimibe significantly lowered atherogenic lipid and lipoprotein parameters, and was safe and well tolerated when administered on top of high-intensity statin to patients with elevated LDL-C. [ABSTRACT FROM AUTHOR]

Familial hypercholesterolaemia (FH) is a frequent genetic disorder characterised by high plasma levels of total and LDL-cholesterol and premature atherosclerosis. If left untreated, affected subjects have a high risk of cardiovascular disease, as they are exposed to very high levels of LDL-cholesterol from birth. Healthy dietary habits and lifestyle are the first treatment option and, if started from childhood, represent a milestone in the prevention of atherosclerotic disease, both as a starting point and in combination with drug therapy. In this work, based on the main consensus documents available so far, we have evaluated the most up-to-date indications of the dietetic-nutritional intervention for the treatment of FH, delving into the peculiar aspects of the diet of the child/adolescent affected by FH. After an analysis of the macro- and micronutrients and the most common dietary patterns currently recommended, we highlighted some practical aspects, some frequent errors and some risks we could fall into when dealing with paediatric nutritional treatment. In conclusion, the dietary intervention for the child/adolescent with FH is a complex task, that should be individualised and tailored taking into account, first of all, the nutritional adequacy for growth and development, but also the multiple aspects linked to the child/adolescent's age, tastes and preferences, the family they belong to, the socio-economic context and the Country they live in. [ABSTRACT FROM AUTHOR]

Background: Apolipoprotein B (Apo B) is an important predictor of the risk of atherosclerotic cardiovascular disease over and above low-density lipoprotein cholesterol (LDL-C), especially in statin-treated patients. Assays of Apo B are not available widely. Objectives: The objective of this study is to derive the Apo B from a lipid profile, using a regression equation and a neural network and compare the results, to compare LDL-C measured by direct assay and a Friedewald equation derived LDL-C in their efficacy to predict Apo B, to determine the effect of lower levels of LDL-C on the prediction models, and to develop an android app "Apo B Calculator" which will calculate the Apo B and also give the predictive accuracy of the result. Methodology: Eight hundred and eighty-five persons were split into a training set and a validation set. Both the regression equation and neural network methods were applied on the training set of 442 patients and the best regression equation and neural network predictive model for Apo B were derived. This was then applied on the validation set of 443 patients to test the R2 of the models. Results: The regression equation Apo B = 25.199 + 0.266 (LDL) + 0.062 (triglycerides level [TGL]) + 0.248 (non-high-density lipoprotein cholesterol) was the best predictor of Apo B when directly measured LDL-C was used. The predictive accuracy of the neural network was lesser than the regression equation (75% vs. 87.4% at 95% confidence interval [CI]). The regression equation for the Friedewald equation derived LDL-C was Apo B = 25.077 + 0.528 friedewald equation (F. LDL) +0.138 (TGL) and was comparable with the neural network (86.4% vs. 85% at 95% CI). The overall efficacy of both the direct assay and Friedewald equation-derived LDL-C were nearly the same (87.4% vs. 86.4% at 95% CI). There was a linear decline in the predictive accuracy of both methods at diminishing LDL-C levels. At lower levels of LDL-C (<70 mg/dl), the accuracy of the Friedewald equation derived LDL-C was a better predictor of Apo B (70% vs. 59.8%). With this data, we developed an android app "Apo B Calculator" which will calculate the Apo B from a directly measured or Friedewald equation derived LDL-C. The app will also mention the predictive accuracy of the results. Conclusions: The regression equation derived from directly measured LDL-C and Friedewald equation derived LDL-C, and the neural network using the Friedewald equation showed near similar efficacy in predicting the Apo B value (87.4%, 86.4%, and 85%). A regression equation using a Friedewald formula is a better predictor of Apo B at LDL-C levels <70 mg/dl. The app "Apo B Calculator" can predict the Apo B from both directly measured and Friedewald equation derived LDL-C and give the predictive accuracy for the method - This will help the clinician to know the Apo B and also the predictive accuracy of such calculated value. [ABSTRACT FROM AUTHOR]

Linoleic acid (LA) has a two-sided effect with regard to serum cholesterol-lowering and pro-inflammation, although whether this fatty acid reduces serum cholesterol and the development of atherosclerosis under high-cholesterol conditions has yet to be ascertained. In this study, we examine the effects of dietary LA on reducing serum cholesterol and atherosclerosis development under high-cholesterol conditions. Male and female apoE-deficient (ApoE-/-) mice were fed AIN-76-based diets containing 10% SFA and 0·04 % cholesterol, 10% LA and 0·04% low cholesterol (LALC), or 10% LA and 0·1% high cholesterol (LAHC) for 9 weeks. The results revealed significant reduction in serum cholesterol levels and aortic lesions with increasing levels of pro-inflammatory biomarkers (urinary isoprostane and aortic MCP-1 mRNA) in male and female LALC groups compared with those in the SFA groups (P < 0·05). Furthermore, whereas there were significant increases in the serum cholesterol levels and aortic lesions (P < 0·05), there was no difference in aortic MCP-1 mRNA levels in male and female LAHC groups compared with those in the LALC groups. A high-dietary intake of cholesterol eliminated the serum cholesterol-lowering activity of LA but had no significant effect on aortic inflammation in either male or female ApoE-/- mice. The inhibitory effect of LA on arteriosclerosis is cancelled by a high-cholesterol diet due to a direct increase in serum cholesterol levels. Accordingly, serum cholesterol levels might represent a more prominent pathogenic factor than aortic inflammation in promoting the development of atherosclerosis. [ABSTRACT FROM AUTHOR]

Simple Summary: Atherosclerosis is a critical cardiovascular disease associated with the use of immune checkpoint inhibitors (ICIs). Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a key orchestrator of atherosclerotic process and it is also involved in cancer progression and immune-resistance. In this context, data from recent meta-analysis and cardiovascular outcome trials associate PCSK9 levels to reduced ICIs-related cancer responsiveness and to high risk of atherosclerotic cardiovascular diseases. This review summarizes the pleiotropic effects of PCSK9 in heart failure, atherosclerosis, and cancer immune recognition, and outlines its ability to represent a new pharmacological target in patients who develop ICIs-related atherosclerosis to reduce cardiovascular mortality and to improve overall survival. Cancer patients treated with immune checkpoint inhibitors (ICIs) are exposed to a high risk of atherosclerosis and cardiometabolic diseases due to systemic inflammatory conditions and immune-related atheroma destabilization. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a key protein involved in metabolism of low-density lipoprotein (LDL) cholesterol. PCSK9 blocking agents are clinically available and involve monoclonal antibodies, and SiRNA reduces LDL levels in high-risk patients and atherosclerotic cardiovascular disease events in multiple patient cohorts. Moreover, PCSK9 induces peripheral immune tolerance (inhibition of cancer cell- immune recognition), reduces cardiac mitochondrial metabolism, and enhances cancer cell survival. The present review summarizes the potential benefits of PCSK9 inhibition through selective blocking antibodies and siRNA in patients with cancer, especially in those treated with ICIs therapies, in order to reduce atherosclerotic cardiovascular events and potentially improve ICIs-related anticancer functions. [ABSTRACT FROM AUTHOR]

Background & Objective: Cardiovascular diseases are the most important causes of death worldwide. Atherosclerosis, as a common form of cardiovascular disease, tends to involve specific areas of the circulatory system. Boron has antiinflammatory and antioxidant properties with potential beneficial effects. In this study, we investigated the effect of Boron on histopathological changes of atherosclerotic plaque and lipid profile in hyperlipidemic rabbits. Materials & Methods: Male rabbits in five groups of control, sham, hyperlipidemia, treatment 1 and treatment 2 were fed on high fat diet (1% cholesterol). Treatment groups received Boron, 4 mg / kg, on the first and 20th days of experiment. Animals’ weights were measured on days 1, 21 and 60. Plasma levels of Cholesterol, LDL, HDL and TG were measured by photometric method. After 60 days, Sudan IV staining method was used for macroscopic study. Hematoxylin-eosin and Masson’s trichrome staining method were performed for quantitative analysis. Results: Animals in the control and sham groups showed no significant change in serum lipid profile with no atherosclerotic plaque in aortic vessels. In the hyperlipidemia group, significant alterations in lipid profile and presence of atheroma plaques were detected. In animals receiving Boron as a protective agent, atheroma plaques were significantly less (p <0.05). This was confirmed by quantitative analysis. Conclusion: Boron ameliorates the development and progression of atherosclerotic plaques. Boron can be used alone or in combination with other drugs as antiatherosclerotic treatment. [ABSTRACT FROM AUTHOR]

BACKGROUND The inflammatory response caused by the NLRP3 is closely related to the formation of myocardial ischemia-reperfusion injury. Costimulatory receptor CD137 and its ligand play a crucial role in regulating the inflammatory immune response in atherosclerosis, which is the fundamental cause of cardiovascular diseases. However, the roles of CD137 signaling in the process of myocardial ischaemia-reperfusion (IR) injury remain unknown. METHODS Genetic ablation was used to determine the functional significance of CD137 in myocardial IR injury. Expression of CD137 was examined by Western-blot, quantitative real-time polymerase chain reaction, and immunohistochemistry in a murine IR model by coronary artery ligation. Even's blue-TTC staining and echocardiography to evaluate the severity of myocardial IR injury. Furthermore, HL-1 cardiomyocytes treated with agonist-CD137 recombinant protein were used to explore the underlying mechanism in CD137 signaling-induced NLRP3 inflammasome activation in response to hypoxia/reoxygenation or LPS/ATP. RESULTS We demonstrated that CD137 knockout significantly improved cardiac function, accompanied by a markedly reduced NLRP3-mediated inflammatory response and IA/AAR which were reversed by mitophagy inhibitor Mdivi-1. Activating CD137 signaling significantly inhibited mitophagy and provoked NLRP3-mediated inflammatory response in H/R-injured or LPS-primed and ATP-stimulated HL-1 cardiomyocytes, the effects of which could be abolished by either anti-CD137 or mitophagy activator FCCP. Besides, mitochondrial ROS was augmented by activating CD137 signaling through the suppression of mitophagy. CONCLUSIONS Our results reveal that activating CD137 signaling aggravates myocardial IR injury by upregulating NLRP3 inflammasome activation via suppressing mitophagy and promoting mtROS generation. [ABSTRACT FROM AUTHOR]

The canonical model of reverse cholesterol transfer (RCT) posits that hepatic uptake of cholesterol ester (CE) by holoparticle uptake of high-density lipoproteins (HDL), and modification of HDL-CE by LCAT play a major role in RCT and atherosclerotic cardiovascular disease (ASCVD) risk. There is currently persuasive evidence that the exchangeability of HDL free cholesterol (FC), particularly its direct transfer to the liver as well as to arterial wall macrophages, may play a major role in atherosclerosis and RCT. Thus, lipoprotein FC mass transfer to and from acceptor/donor particles may be of clinical utility in ASCVD risk assessment. To develop an assay to measure the ability of plasma lipoproteins to either accept or donate FC. We developed two novel cell-free assays to measure exchangeable pools of plasma lipoprotein FC: (i) using acceptor particles formed by coating calcium silicate hydrate (CSH) nanoparticles with excess phospholipid (FC "Pull") and (ii) delivery of additional FC to HDL and other lipoproteins using phospholipid coated donor CSH nanoparticles pre-saturated with FC (FC "Push"). FC mass was measured using the FUJIFILM Wako Free Cholesterol E assay kit™. Lipoproteins were isolated by sequential ultracentrifugation. We optimized the phospholipid mass required to fully coat CSH particles and the excess FC required for FC push, as well as the phospholipid nanoparticle/plasma ratio to allow for lipoprotein FC mass transfer measurement. FC mass transferred from human plasma to acceptor particles varied by sample (≈20-40%, p = <0.0001) and by lipoprotein type (LDL; 70%, HDL; 47%, p=0.0014 and <0.0001 respectively). FC removal was time- and temperature-dependent. The mean FC mass removed from plasma at 37°C and 47°C after 1 hr was 32.23 and 49.37 mg/dL (p= <0.0001, and 0.0065), respectively. Kinetic studies suggest that the FC transfer rate was initially rapid (0-20 min) and decreased thereafter (40-60 min). Similarly, human plasma FC uptake from FC donor particles also varied between samples (≈0-20%, p = <0.0001), and was time- and temperature dependent (after 1 hr at 37°C and 47°C was 14.6 and 42 mg/dL, p=<0.001 and <0.005, respectively). Interestingly, preliminary data suggest that HDL may be the primary acceptor of FC from donor particles. We have developed novel cell-free assays to measure FC mass transfer to and from plasma lipoproteins. The FC push/pull ratio may serve as a useful metric for ASCVD risk. [ABSTRACT FROM AUTHOR]

The prevalence of obesity has been recognized as a major public health issue with rapid increase globally. Obesity triggers other metabolic complications, such as diabetes, dyslipidemia, liver diseases, and cardiovascular diseases. Helianthus tuberosus L. (the Jerusalem artichoke) is an important edible plant that may provide health benefits in treating metabolic diseases. In this study, we investigated potential antiobesity effects of saccharified H. tuberosus L. (SH) and its fermented vinegar (fermented H. tuberosus L. [FH]) in a high-fat diet (HFD)-induced obesity murine model. FH exhibited significantly lower pH, Brix, and total sugar content compared with the SH, along with higher radical-scavenging activity. The body weight and adipose tissue weights were significantly decreased with the administration of SH and FH compared with the HFD group. SH and FH groups significantly attenuated hepatomegaly and lipid accumulation. The increased triglyceride (TG) content in obese mice was remarkably lower in the SH and FH groups. SH and FH alleviated serum dyslipidemia and atherogenic risk. Furthermore, expression of adipogenic genes was significantly downregulated after SH and FH supplementation compared with the HFD group. The TG and total cholesterol (TC) content of serum and adipose tissues significantly decreased by SH and FH administration in comparison with the HFD group. Reduced adiposity with SH and FH administration was confirmed by reduced adipocyte size and weight with inhibition of lipoprotein lipase expression. Our study showed that SH and FH, indeed FH was superior to SH, had antiobesity effects by decreasing adiposity, regulating dyslipidemia in systemic tissues, and inhibiting adipogenic gene expression. [ABSTRACT FROM AUTHOR]

Objective. This study is designed to find out the molecular targets of effective Chinese medicine Ziyin Mingmu pills (ZMPs) in treating age-related macular degeneration (AMD) based on network pharmacology and experimental data. Methods. A comprehensive network pharmacology strategy that consists of three sequential modules (drug-disease target molecular docking, enrichment analysis, and external verification) was carried out to identify potential targets of ZMPs acting on AMD. Results. The active ingredients of ZMPs targeting 66 genes have effects on the process of AMD. GO and KEGG pathway enrichment analyses suggested that response to oxidative stress, regulation of angiogenesis, and lipid and atherosclerosis might serve as the most important signaling pathways in ZMPs for AMD treatment. Combined with the GSE29801 dataset for further analysis, two key genes, EGFR and VEGFA, were identified. Immune infiltration analysis showed that there was a strong association between EGFR and immune cell content. In addition, images were acquired following 24 h in the scratch experiment showed that ZMPs can reduce the percentage of wound healing distance. The Western blot assay found that ZMPs increased the expression of EGFR and decreased the expression of VEGFA. Conclusion. This study sheds light on some mechanisms of ZMP therapy for AMD, particularly the effect of ZMP on the oxidative stress in RPE and cell survival and angiogenesis in AMD. We propound ZMPs as a promising strategy to intervene in the process of AMD. [ABSTRACT FROM AUTHOR]

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) have recently been identified to be closely related to the occurrence and development of atherosclerosis (AS). A growing body of evidence has suggested Chinese medicine takes unique advantages in preventing and treating AS. In this review, the related research progress of AS and LOX-1 has been summarized. And the anti-AS effects of 10 active components of herbal medicine through LOX-1 regulation have been further reviewed. As a potential biomarker and target for intervention in AS, LOX-1 targeted therapy might provide a promising and novel approach to atherosclerotic prevention and treatment. [ABSTRACT FROM AUTHOR]

Background: Atherosclerosis is one of the most important global health hazards and air pollution (AP, PM2.5) has been implicated. In addition to traditional risk factors hyperhomocysteinemia (HC) has been recognized in many parts of China related to risk of stroke. Methods: To evaluate the impact of HC (homocysteine >14µmol/l) and PM2.5 air pollution on atherogenesis in modernizing China, we studied 756 asymptomatic Chinese in China from 1998–2007. PM2.5 exposure, HC, folate, and methylenetetrahydrofolate reductase (MTHFR) C/T genotype were evaluated. Brachial flow-mediated dilation (FMD) and carotid intima-media thickness (IMT) were measured by ultrasound. Locations were categorized as zones 1, 2 and 3, with increasing PM2.5 exposure. Results: HC was higher (19.4±13.1 and 27.1±25.1µmol/l) in high PM2.5-polluted zones 2 and 3 than in zone 1 (9.7±4.5µmol/l, p<0.0015). The top HC tertile was characterized by lower folate and vitamin B12, but a higher proportion of the MTHFR TT genotype, Metabolic Syndrome (MS) and PM2.5 level (p=0.0018). FMD was significantly lower (7.3±2.3%) and carotid IMT thicker (0.63±0.12mm) in the top HC tertile, compared with low HC tertile (8.4±2.5%, p<0.0001; 0.57±0.1mm, p<0.0001 respectively). Similar differences in FMD and IMT were seen in zones 2 and 3, compared with zone 1 (p<0.0001). On multivariate regression, HC was related to male gender (beta=0.106, p=0.021), MTHFR-TT (beta=0.935, p<0.0001), locations (beta=0.230, p<0.0001) and folate-MTHFR interaction (beta=−0.566, p<0.0001). FMD was related to age (beta= −0.221; p<0.0001), male gender (beta= −0.194, p=0.001) PM2.5 and location (beta=−0.285 to −0.303, p<0.0001). Carotid IMT was related to PM2.5 (beta=0.173, p<0.0001), HC (0.122, p=0.006) but not to MTHFR or location, independent of age, gender, MS, and LDL-C. No significant HC-PM2.5 interaction effect on FMD and IMT was observed. Conclusion: HC and PM2.5 pollution but not MTHFR genotype were both related to carotid IMT, independent of other traditional risk factors. This has potential implications in dietary and AP strategies for atherosclerosis prevention in China. [ABSTRACT FROM AUTHOR]

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