Onset Of Coronary Artery Disease Research Articles

Association between pre-treatment with statin and its inhibitory effect on the onset of coronary artery disease at the time of coronary computed tomography angiography: a new look at an old medication.

Coronary artery stenosis is often advanced by the time coronary computed tomography angiography (CCTA). Statins are the most important anti-lipidemic medication for improving the prognosis of coronary artery disease (CAD) patients. Although lipid-lowering therapy using statins appears to have been established as a method for preventing CAD, there remains the problem that CAD cannot be completely suppressed. In this study, we investigated whether pre-treatment with statin could significantly inhibit the onset of CAD when patients received CCTA for screening of CAD. The subjects were 1164 patients who underwent CCTA as screening for CAD. CAD was diagnosed when 50% or more coronary stenosis was present in the coronary arteries. Patient backgrounds were investigated by age, gender, body mass index, coronary risk factors [family history of cardiovascular diseases, smoking history, hypertension (HTN), diabetes mellitus (DM), dyslipidemia, chronic kidney disease (CKD) or metabolic sydrome] and medications. Patients were classified into two groups according to the presence or absence of statin pre-administration during CCTA [statin (-) group (n = 804) and (+) group (n = 360)]. Compared with the statin (-) group, the statin (+) group was significantly older and had higher rates of family history, HTN, and DM. The statin (+) group had a significantly higher % CAD than the statin (-) group. Serum levels of low-density lipoprotein cholesterol (LDL-C) were significantly lower in the statin (+) group than in the statin (-) group. There was no significant difference in either high-density lipoprotein cholesterol levels or triglyceride levels between the two groups. Age, male gender, HTN, DM and pre-treatment with statin were all associated with CAD (+) in all patients. In addition, factors that contributed to CAD (+) in the statin (-) group were age, male gender, and DM, and factors that contributed to CAD (+) in the statin (+) group were age, smoking, HTN and % maximum dose of statin. At the time of CCTA, the statin (+) group had a high rate of CAD and coronary artery stenosis progressed despite a reduction of LDL-C levels. To prevent the onset of CAD, in addition to strict control of other coronary risk factors (HTN etc.), further LDL cholesterol-lowering therapy may be necessary.

Impacts of ABCG2 loss of function variant (p. Gln141Lys, c.421 C > A, rs2231142) on lipid levels and statin efficiency: a systematic review and meta-analysis

BackgroundThe latest evidence indicates that ATP-binding cassette superfamily G member 2 (ABCG2) is critical in regulating lipid metabolism and mediating statin or cholesterol efflux. This study investigates whether the function variant loss within ABCG2 (rs2231142) impacts lipid levels and statin efficiency.MethodsPubMed, Cochrane Library, Central, CINAHL, and ClinicalTrials.gov were searched until November 18, 2023.ResultsFifteen studies (34,150 individuals) were included in the analysis. The A allele [Glu141Lys amino acid substitution was formed by a transversion from cytosine (C) to adenine (A)] of rs2231142 was linked to lower levels of high-density lipoprotein cholesterol (HDL-C), and higher levels of low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC). In addition, the A allele of rs2231142 substantially increased the lipid-lowering efficiency of rosuvastatin in Asian individuals with dyslipidemia. Subgroup analysis indicated that the impacts of rs2231142 on lipid levels and statin response were primarily in Asian individuals.ConclusionsThe ABCG2 rs2231142 loss of function variant significantly impacts lipid levels and statin efficiency. Preventive use of rosuvastatin may prevent the onset of coronary artery disease (CAD) in Asian individuals with dyslipidemia.

Food and Cardiovascular Disease: What to Eat and What Not to Eat

In 2019, the Global Burden of Disease study revealed alarming statistics regarding cardiovascular disease (CVD) in Pakistan. The estimated age-standardized incidence and death rates were 918.18 and 357.88 per 100,000 respectively, surpassing global averages.1 Notably, Pakistan faces unique challenges with a high prevalence of Rheumatic heart disease and early onset coronary artery disease.1
 The World Health Organization's 2021 factsheet underscores four pivotal modifiable behavioral risk factors for CVD and stroke: unhealthy diet, physical inactivity, tobacco use, and harmful alcohol consumption. These behaviors manifest in individuals as elevated blood pressure, glucose, lipids, and adverse body mass index, exacerbating cardiovascular risk.2 In Pakistan, the consumption of unhealthy foods and excessive calories significantly contributes to adverse cardiometabolic profiles, including obesity and dyslipidemia.2
 Recent research, such as that by Daruish Mozaffain et al. in "Food is Medicine," advocates for food-based interventions tailored to individual health conditions, ranging from medically tailored meals to nutritional and culinary education.3 However, Pakistani patients with CVD face challenges due to the lack of localized guidelines, educational resources, and accessible nutritionists. Shah et al.'s review underscores the importance of providing clear and culturally relevant dietary guidance for the local population.4
 Addressing these challenges requires the development of high-quality, culturally sensitive educational materials. These resources should be readily understandable, pictorial, and integrated into both inpatient and outpatient care. Local experts, including dietitians and researchers, can play a crucial role in creating tailored educational content. Figures 1 exemplify the efforts of these experts to provide practical guidance to the Pakistani population.4
 In conclusion, there is an urgent need for comprehensive, easy-to-understand patient education resources catering to the unique nutritional needs of Pakistani individuals with cardiovascular disease. By addressing these gaps, we can empower patients to make informed dietary choices and improve cardiovascular outcomes.
 References
 
 Samad Z, Hanif B. Cardiovascular Diseases in Pakistan: Imagining a Postpandemic, Postconflict Future. Circulation. 2023;147(17):1261-3.
 Liaquat A, Javed Q. Current trends of cardiovascular risk determinants in Pakistan. Cureus. 2018;10(10):e3409.
 Mozaffarian D, Aspry KE, Garfield K, Kris-Etherton P, Seligman H, Velarde GP, et al. “Food Is Medicine” Strategies for Nutrition Security and Cardiometabolic Health Equity: JACC State-of-the-Art Review. J Am Coll Cardiol. 2024;83(8):843-64.
 Shah SU, Waseem T, Afridi T, Shah MI. Nutritional Needs for Cardiovascular Health in Pakistani Population. Pak Heart J. 2022;55(2):101-13.
 American Heart Association. Lifestyle Changes for Heart Failure. Accessed on March 30, 2024. Available at: https://www.heart.org/en/health-topics/heart-failure/treatment-options-for-heart-failure/lifestyle-changes-for-heart-failure
 American Diabetes Association. What superstar foods are good for diabetes? Accessed on March 30, 2024. Available at: https://diabetes.org/food-nutrition/food-and-blood-sugar/diabetes-superstar-foods
 American Heart Association. The American Heart Association Diet and Lifestyle Recommendations. Accessed on March 30, 2024. Available at: https://www.heart.org/en/healthy-living/healthy-eating/eat-smart/nutrition-basics/aha-diet-and-lifestyle-recommendations
 American Heart Association. Managing Blood Pressure with a Heart-Healthy Diet. Accessed on March 30, 2024. Available at: https://www.heart.org/en/health-topics/high-blood-pressure/changes-you-can-make-to-manage-high-blood-pressure/managing-blood-pressure-with-a-heart-healthy-diet

Association of air pollution exposure and increased coronary artery disease risk: the modifying effect of genetic susceptibility

BackgroundBoth genetic factors and air pollution are risk factors for coronary artery disease (CAD), but their combined effects on CAD are uncertain. The study aimed to comprehensively investigate their separate, combined and interaction effects on the onset of CAD.MethodsWe utilized data from the UK Biobank with a recruitment of 487,507 participants who were free of CAD at baseline from 2006 to 2010. We explored the separate, combined effect or interaction association among genetic factors, air pollution and CAD with the polygenic risk score (PRS) and Cox proportional hazard models.ResultsThe hazard ratios (HRs) [95% confidence interval (CI)] of CAD for 10-µg/m3 increases in PM2.5, NO2 and NOx concentrations were 1.25 (1.09, 1.44), 1.03 (1.01, 1.05) and 1.01 (1.00, 1.02), respectively. Participants with high PRS and air pollution exposure had a higher risk of CAD than those with the low genetic risk and low air pollution exposure, and the HRs (95% CI) of CAD in the PM2.5, PM10, NO2 and NOx high joint exposure groups were 1.56 (1.48, 1.64), 1.55(1.48, 1.63), 1.57 (1.49, 1.65), and 1.57 (1.49, 1.65), respectively. Air pollution and genetic factors exerted significant additive effects on the development of CAD (relative excess risk due to the interaction [RERI]: 0.12 (0.05, 0.19) for PM2.5, 0.17 (0.10, 0.24) for PM10, 0.14 (0.07, 0.21) for NO2, and 0.17 (0.10, 0.24) for NOx; attributable proportion due to the interaction [AP]: 0.09 (0.04, 0.14) for PM2.5, 0.12 (0.07, 0.18) for PM10, 0.11 (0.06, 0.16) for NO2, and 0.13 (0.08, 0.18) for NOx).ConclusionExposure to air pollution was significantly related to an increased CAD risk, which could be further strengthened by CAD gene susceptibility. Additionally, there were positive additive interactions between genetic factors and air pollution on the onset of CAD. This can provide a more comprehensive, precise and individualized scientific basis for the risk assessment, prevention and control of CAD.

Diagnosis of Coronary Artery Disease using Adult Data from Blood Tests and Electrocardiograms

Objective:
 Many modifiable risk factors affect the onset of coronary artery disease (CAD), a condition that is extremely common throughout the globe. Predictive models created using machine learning (ML) algorithms may help physicians identify CAD earlier and may lead to better results. The goal of this project was to use ML algorithms to predict CAD in patients.
 
 Methods:
 The gathered dataset of UCI heart disease was used in this study to evaluate a variety of machine learning methods to predict CAD. Just the most crucial aspects of the hypothesis testing method were kept. Support vector machines (SVM) were used in a comparative analysis employing a variety of assessment measures.
 
 Results:
 All machine learning methods achieved accuracy levels of at least 80%, with the SVM algorithm obtaining accuracy levels of at least 90%. Predictive ML models had high diagnostic relevance in CAD, as seen by the SVM model's high recall (0.9), which is was the highest of all the models.
 
 Conclusion:
 The findings of the current study demonstrated that, independent of the measures used to evaluate machine learning models, feature selection has a significant impact on performance. Finding the most useful features is thus crucial. SVM was chosen as the top model based on the features we considered.

Machine Learning in Cardiovascular Risk Prediction and Precision Preventive Approaches.

In this review, we sought to provide an overview of ML and focus on the contemporary applications of ML in cardiovascular risk prediction and precision preventive approaches. We end the review by highlighting the limitations of ML while projecting on the potential of ML in assimilating these multifaceted aspects of CAD in order to improve patient-level outcomes and further population health. Coronary artery disease (CAD) is estimated to affect 20.5 million adults across the USA, while also impacting a significant burden at the socio-economic level. While the knowledge of the mechanistic pathways that govern the onset and progression of clinical CAD has improved over the past decade, contemporary patient-level risk models lag in accuracy and utility. Recently, there has been renewed interest in combining advanced analytic techniques that utilize artificial intelligence (AI) with a big data approach in order to improve risk prediction within the realm of CAD. By virtue of being able to combine diverse amounts of multidimensional horizontal data, machine learning has been employed to build models for improved risk prediction and personalized patient care approaches. The use of ML-based algorithms has been used to leverage individualized patient-specific data and the associated metabolic/genomic profile to improve CAD risk assessment. While the tool can be visualized to shift the paradigm toward a patient-specific care, it is crucial to acknowledge and address several challenges inherent to ML and its integration into healthcare before it can be significantly incorporated in the daily clinical practice.

Risk factor burden in familial hypercholesterolaemia with early onset coronary artery disease

Abstract Background Familial hypercholesterolaemia (FH) is considered a causal risk factor for premature coronary artery disease (CAD) with a priority placed on identifying index cases and their relatives for preventative interventions. However recent population sequencing studies have identified that not all FH mutation carriers develop CAD. We hypothesised that a significant burden of traditional risk factors is required in addition to genetic risk to develop CAD. Methods We interrogated the clinical registry of patients attending the CVD risk and Lipids clinic at St Bartholomew’s Hospital in London which serves a large multi-ethnic population. Patients were prioritized for genetic testing based on Simon Broome and Dutch Lipid criteria. A second cohort of patients from the clinic consisted of premature CAD patients without phenotypic FH. CAD was defined as > 50% stenosis in an epicardial vessel by invasive or non-invasive imaging. Results We identified 40 patients with genetically confirmed FH and CAD (FH+/CAD+) and 116 people with FH and without CAD (FH+/CAD-). Of 10 traditional risk factors evaluated, prevalence of each was higher in FH +/CAD+ compared to FH+/CAD- patients. Collectively, FH+/ CAD+ patients had a median number of risk factors of 5(4,6) compared to 4(3,5) for FH+/CAD- patients, (P<0.001). In non-FH patients, risk factors burden was higher in those with CAD (FH-/CAD+), compared to those without CAD: 5(4,6) V. 4(3,5) risk factors, respectively(P<0.001). Importantly, in patients who developed CAD, the traditional risk factor burden was greater in FH- patients than that of FH+ patients whereas, the genetic risk burden was greater in FH+ patients (Figure-1). The mean age of onset of CAD in both FH+ and FH- patients was comparable: 43± 10 V. 43± 12years. Patients with FH+/CAD+ were older (53± 11 V 49± 13 years, P=0.276) but had an earlier onset of CAD, when risk burden was greater (43± 8 years if ≥ 5 risk factors v 49± 15 years if < 5 risk factors, P=0.192). Conclusion In a selected population from a large specialist lipid clinic, we demonstrate that traditional risk factor burden is additive to genetic risk for the development and age of onset of CAD, supporting a disease liability threshold model in FH.Figure-1.Risk Burden in FH with CAD

The gut microbiota and coronary artery calcification in Japanese men

The gut microbiota differs between patients with coronary artery disease (CAD) and healthy controls; however, it currently remains unclear whether these differences exist prior to the onset of CAD. We herein investigated the gut microbiota associated with subclinical coronary artery calcification (CAC) in a Japanese population. A total of 663 Japanese men were enrolled in this cross-sectional study. Computed tomography and gut microbiology tests were performed, and CAC scores were calculated using the Agatston method. Participants were categorized into four groups based on their CAC scores: CAC = 0, 0 <CAC ≤100, 100 <CAC, and with a CAD history. The bacterial 16S ribosomal RNA gene was amplified, and DNA sequencing was conducted on a MiSeq System. QIIME2 and LEfSe were used to analyze the gut microbiota, and the results obtained were compared among the four CAC categories. The mean age of participants was 68.4 years (46-83 years). The numbers of participants in CAC = 0, 0 <CAC ≤100, 100 <CAC, and with a CAD history were 219, 200, 193, and 51, respectively. The medians of the Firmicutes to Bacteroidota ratio were 1.50, 1.52, 1.67, and 1.80 for each CAC category (P = 0.020). One standard deviation higher phylum Firmicutes, class Bacilli, and order Lactobacillales were associated with a 1.3- to 1.4-fold higher risk of CAD. These taxa were also associated with a higher CAC score category. The family Streptococcaceae and genus Streptococcus showed a higher risk of CAD. The order Enterobacterales and family Enterobacteriaceae correlated with CAC scores. The genus Blautia showed a preventive direction for CAD, but did not correlate with CAC scores. The gut microbiota significantly differed from the phylum to genus level in a manner that was dependent on CAC scores, even before the onset of CAD.

Risk Factor Burden in Familial Hypercholesterolaemia With Early Onset Coronary Artery Disease

Risk Factor Burden in Familial Hypercholesterolaemia With Early Onset Coronary Artery Disease

Smooth muscle α-actin missense variant promotes atherosclerosis through modulation of intracellular cholesterol in smooth muscle cells.

The variant p.Arg149Cys in ACTA2, which encodes smooth muscle cell (SMC)-specific α-actin, predisposes to thoracic aortic disease and early onset coronary artery disease in individuals without cardiovascular risk factors. This study investigated how this variant drives increased atherosclerosis. Apoe-/- mice with and without the variant were fed a high-fat diet for 12 weeks, followed by evaluation of atherosclerotic plaque formation and single-cell transcriptomics analysis. SMCs explanted from Acta2R149C/+ and wildtype (WT) ascending aortas were used to investigate atherosclerosis-associated SMC phenotypic modulation. Hyperlipidemic Acta2R149C/+Apoe-/- mice have a 2.5-fold increase in atherosclerotic plaque burden compared to Apoe-/- mice with no differences in serum lipid levels. At the cellular level, misfolding of the R149C α-actin activates heat shock factor 1, which increases endogenous cholesterol biosynthesis and intracellular cholesterol levels through increased HMG-CoA reductase (HMG-CoAR) expression and activity. The increased cellular cholesterol in Acta2R149C/+ SMCs induces endoplasmic reticulum stress and activates PERK-ATF4-KLF4 signaling to drive atherosclerosis-associated phenotypic modulation in the absence of exogenous cholesterol, while WT cells require higher levels of exogenous cholesterol to drive phenotypic modulation. Treatment with the HMG-CoAR inhibitor pravastatin successfully reverses the increased atherosclerotic plaque burden in Acta2R149C/+Apoe-/- mice. These data establish a novel mechanism by which a pathogenic missense variant in a smooth muscle-specific contractile protein predisposes to atherosclerosis in individuals without hypercholesterolemia or other risk factors. The results emphasize the role of increased intracellular cholesterol levels in driving SMC phenotypic modulation and atherosclerotic plaque burden.

Widespread Aneurysms Secondary to Myosin Light-Chain Kinase Gene Mutation Leading to Multifocal Right Hemispheric Stroke (P3-5.001)

<h3>Objective:</h3> Familiarize providers with the presence of the Myosin Light-Chain Kinase (MYLK) and the possible vascular manifestations in individuals carrying this autosomal dominant gene mutation. <h3>Background:</h3> Myosin Light-Chain Kinase is a ubiquitously expressed kinase involved in the physiological contraction of smooth muscle cells within hollow organs. Variations in the Myosin Light-Chain Kinase (MYLK) gene lead to decrease in phosphorylation of 20kDa regulatory light-chain leading to a reduction in smooth muscle contractile function. MYLK gene mutations have been associated with autosomal dominant thoracic aortic aneurysms and dissections, however there are limited studies mentioning the involvement of other vascular structures containing these dysfunctional smooth muscle cells. In this report, we present a case of a 43-year-old individual who presented to the hospital for quadrantanopia, hearing loss and headache who was subsequently found to have an acute stroke of multiple foci involving the right ACA and MCA territories. Past medical history was significant for hemochromatosis, early onset coronary artery disease in self and close family members. Etiology workup revealed a right internal carotid artery aneurysm measuring 10cm. Complains of abdominal pain led to imaging revealing focal dissection of the abdominal aorta, a right common iliac artery 2.3cm aneurysm as well as a proximal celiac artery 1.7cm aneurysm. On outpatient genetic testing, the patient was found to be a carrier of the MYLK (p.Val509Met) gene mutation; variance was of unclear significance, however familial thoracic aneurysms/dissections have been reported in the Clinical Variance Database. The patient has since been managed with dual anti-platelet therapy and was instructed to follow closely with neurological and vascular surgery for close monitoring. <h3>Design/Methods:</h3> NA <h3>Results:</h3> NA <h3>Conclusions:</h3> This case highlights the MYLK gene mutation and its possible relationship with widespread malformations in the carotid, celiac, and mesenteric vasculature to familiarize practitioners with manifestations and clinical sequelae of individuals affected with this gene. <b>Disclosure:</b> Dr. Hamzoian has nothing to disclose. Dr. Abdelmasih has nothing to disclose. Dr. Ditamo has nothing to disclose. Dr. Kahila has nothing to disclose.

Increased level of plasma Cyclophilin A in early diabetic population suggesting it as a reliable pro inflammatory biomarker of coronary artery disease in diabetic patients

Abstract Funding Acknowledgements Type of funding sources: Other. Main funding source(s): Institute of Cardiovascular disease, Madras Medical Mission Background Type 2 Diabetes (DM) is a pro-inflammatory state in the pathogenesis of Atherosclerosis with the presence of many active proteins, of which CyclophilinA (CypA) has been shown to have a positive correlation with the presence and severity of vascular diseases. As Cyp A is proven to be secreted in varying levels from cells, in response to inflammatory stimuli, viz., hypoxia, infection, and oxidative stress, it is found ideal, to study it further as one of a reliable pro-inflammatory biomarker responsible for the progression of Coronary Artery Disease (CAD) in early DM. Purpose A prospective cross-sectional study was conducted to quantify CypA in the early phase of DM before the onset of CAD, in comparison to non-diabetic volunteers and to review it as one of the pro-inflammatory biomarkers of CAD, in association with hsCRP and other proven biomarkers (Insulin, Lipid profile, HBA1C, and Glucose). Methods The study subject comprised 299 patients with DM and 50 healthy volunteers. History of duration of DM and other co-morbidities was obtained. A comprehensive clinical examination and non-invasive evaluation of atherosclerotic vascular disease were done to rule out CAD. CypA was analyzed by ELISA kit in serum. P-value of &amp;lt;0.05 was considered statistically significant. Results The average age group of study population is 51­ with an SD of 9.4(Male 206; Female 143). The observed range of CypA in our study is 50–1974 ng/ml, which is much higher than the values obtained in other studies (2–200 ng/ml). An increased level of CYP A is seen in DM than control group with a significant P Value of &amp;lt;0.001 [DM - Mean 462.5 ; Median of 328 ng/ml; Control group(Non diabetic) - Mean 273 ; Median 190 ng/ml]. CypA value in early diabetics (&amp;lt;5 years) is higher than patients with &amp;gt;5 years of DM (one-way ANOVA). Review of hsCRP shows statistically different levels between DM and the control group (p=0.012). Scatter plots of CypA and hsCRP concentration showed values within 500 ng/ml of CypA distributed in the mid to average risk category of hsCRP (&amp;lt;1–3 mg/l). The probability of proposing CypA as a pro-inflammatory biomarker compared to hsCRP in DM is reviewed by the ROC curve (AUC 0.684 with a sensitivity of 80% and specificity of 50%). Increased CypA and hsCRP are observed in females than males (CypA: p=0.04 and hsCRP: p&amp;lt;0.001). No significant difference is observed between the two groups in other variables (Insulin (P=0.69), Cholesterol (P= 0.33), TGL (P=0.77), HDL (P=0.17), LDL (P=0.06). Conclusion In our study CypA level is increased in the early stage of DM when compared with non-Diabetes. The range obtained is higher than the previous study values. CypA value of &amp;lt;500 ng/ml is observed to be related to CAD when reviewed along with the hsCRP cardiac risk stratification range. The scope of CypA as a reliable pro-inflammatory biomarker of CAD in early DM is more promising and its edge over hsCRP as an early biomarker is to be reviewed further.

Immune-related potential biomarkers and therapeutic targets in coronary artery disease.

Coronary artery disease (CAD) is a complex illness with unknown pathophysiology. Peripheral biomarkers are a non-invasive method required to track the onset and progression of CAD and have unbeatable benefits in terms of early identification, prognostic assessment, and categorization of the diagnosis. This study aimed to identify and validate the diagnostic and therapeutic potential of differentially expressed immune-related genes (DE-IRGs) in CAD, which will aid in improving our knowledge on the etiology of CAD and in forming genetic predictions. First, we searched coronary heart disease in the Gene Expression Omnibus (GEO) database and identified GSE20680 (CAD = 87, Normal = 52) as the trial set and GSE20681 (CAD = 99, Normal = 99) as the validation set. Functional enrichment analysis using protein-protein interactions (PPIs), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) was carried out on the identified differentially expressed genes. Optimal feature genes (OFGs) were generated using the support vector machine recursive feature elimination algorithm and the least absolute shrinkage and selection operator (LASSO) algorithm. Furthermore, immune infiltration in CAD patients and healthy controls was compared using CIBERSORT, and the relationship between immune cells and OFGs was examined. In addition, we constructed potential targeted drugs for this model through the Drug-Gene Interaction database (DGIdb) database. Finally, we verify the expression of S100A8-dominated OFGs in the GSE20681 dataset to confirm the universality of our study. We identified the ten best OFGs for CAD from the DE-IRGs. Functional enrichment analysis showed that these marker genes are crucial for receptor-ligand activity, signaling receptor activator activity, and positive control of the response to stimuli from the outside world. Additionally, CIBERSORT revealed that S100A8 could be connected to alterations in the immune microenvironment in CAD patients. Furthermore, with the help of DGIdb and Cytoscape, a total of 64 medicines that target five marker genes were subsequently discovered. Finally, we verified the expression of the OFGs genes in the GSE20681 dataset between CAD patients and normal patients and found that there was also a significant difference in the expression of S100A8. We created a 10-gene immune-related prognostic model for CAD and confirmed its validity. The model can identify potential biomarkers for CAD prediction and more accurately gauge the progression of the disease.

Prévalence et caractéristiques de la dysfonction érectile chez les patients coronariens à l'Institut de cardiologie d'Abidjan en Côte d'Ivoire

IntroductionErectile dysfunction (ED) represents an independent and/or predictive risk factor for coronary heart disease according to many studies. The aim of our study is to determine the prevalence and risk factors associated with erectile dysfunction in coronary patients confirmed by coronary angiography. Material and methodWe conducted a descriptive and analytical cross-sectional study. A total of 60 patients were included with proven atheromatous coronary lesions after coronary angiography. The study period was from June 1, 2020 to February 29, 2021. After assessment of erectile status based on the short version of the International Index of Erectile Function (IIEF-5). Measures of association were adjusted odds ratios and odd ratios with their confidence intervals. Multivariate analysis was conducted using logistic regression. Only patients with erectile insufficiency underwent penile pharmocodoppler. ResultsThe mean age was 56 ± 8.4 years with extremes of 28 and 65 years. Erectile status was classified according to the IIEF-5 score as follows: severe ED (32%), moderate (13%), mild (15%) and normal erectile function (40%). The time to onset of ED was> 2 years in 69.4% of cases before the onset of coronary artery disease with a mean time of 2.37 years ± 1.29.In 20% of the cases, the patients were already on treatment before the erectile disorder, 65% undergoing treatment after the erectile disorder and 15% had no undergoing treatment. The main factors associated with ED were: high blood pressure (OR = 7; p = 0.0007), dyslipidemia (OR = 4.86; p = 0.004), diabetes (OR = 3.8; p = 0.02), obesity (OR = 4, 45; p = 0.02) as well as beta blockers (OR = 5.3; p = 0.004), calcium channel blockers (OR = 4.5; p = 0.004) and angiotensin-converting enzyme inhibitors (OR = 4.3; p = 0.008). The vascular cause clearly dominates (95%) of which 61% arterial mechanism, 17% mixed and 17% venous mechanism. The factor associated with a decrease PSVpi was the diabetes (OR = 28; p = 0.01). In multivariate analysis, no factor was statistically associated with ED or decrease in PSVpi. ConclusionIsolated ED appears as an early marker of generalized endothelial dysfunction. Hence the advantage of systematic screening, especially in subjects at risk of cardiovascular disease.

Complementary role of evinacumab in combination with lipoprotein apheresis in patients with homozygous familial hypercholesterolemia.

Patients with homozygous familial hypercholesterolemia (FH) have severe hypercholesterolemia from birth and if untreated may experience very early onset of coronary artery disease in childhood or young adulthood with an aggressive course resulting in early death. Early initiation of aggressive low-density lipoprotein cholesterol (LDL-C) lowering is the mainstay of treatment, which requires the use of a multidrug treatment regimen, often in combination with lipoprotein apheresis, but LDL-C goal achievement is frequently unattainable due to the severity of baseline hypercholesterolemia and hyporesponsiveness to many LDL-C-lowering medications. Evinacumab, a monoclonal antibody that sequesters angiopoietin-like 3 protein and lowers LDL-C by an average of 49% in patients with homozygous FH, was approved by the Food and Drug Administration in February 2021 and is a major advance in treatment of these high-risk patients. In this report, we describe the complementary role of evinacumab in combination with lipoprotein apheresis in two patients with homozygous FH.

Polymorphism rs7079 in miR-31/-584 Binding Site in Angiotensinogen Gene Associates with Earlier Onset of Coronary Artery Disease in Central European Population.

Angiotensinogen (AGT) represents a key component of the renin-angiotensin-aldosterone system (RAAS). Polymorphisms in the 3' untranslated region (3'UTR) of the AGT gene may alter miRNA binding and cause disbalance in the RAAS. Within this study, we evaluated the possible association of AGT +11525C/A (rs7079) with the clinical characteristics of patients with coronary artery diseases (CAD). Selective coronarography was performed in 652 consecutive CAD patients. Clinical characteristics of the patients, together with peripheral blood samples for DNA isolation, were collected. The genotyping of rs7079 polymorphism was performed with TaqMan® SNP Genotyping Assays. We observed that patients with the CC genotype were referred for coronarography at a younger age compared to those with the AA+CA genotypes (CC vs. AA+CA: 59.1 ± 9.64 vs. 60.91 ± 9.5 (years), p = 0.045). Moreover, according to the logistic regression model, patients with the CC genotype presented more often with restenosis than those with the CA genotype (p = 0.0081). In conclusion, CC homozygotes for rs7079 present with CAD symptoms at a younger age compared with those with the AA+CA genotype, and they are more prone to present with restenosis compared with heterozygotes.

The Morphology of Coronary Artery Disease in South Asians vs White Caucasians and Its Implications.

South Asians (SAs) experience a higher prevalence and earlier onset of coronary artery disease and have worse outcomes compared with White Caucasians (WCs) following invasive revascularisation procedures, a mainstay of coronary artery disease (CAD) management. We sought to review the differences in the CAD pattern and risk factors between SA and WC patients and to discuss their potential impact on the development of coronary disease, acute coronary syndrome, and revascularisation outcomes. SAs have a more diffuse pattern with multivessel involvement compared with WCs. However, less is known about other morphologic characteristics, such as calcification of atherosclerotic plaque and coronary diameter in SA populations. Despite a similar coronary calcification burden, higher noncalcified plaque composition, elevated thrombosis, and inflammatory markers likely contribute to the disease pattern. Although the current evidence on the role of coronary vessel size remains inconsistent, smaller diameters in SAs could play a potential role in the higher disease prevalence. This is especially important given the impact of coronary artery diameter on revascularisation outcomes. In conclusion, SAs have a unique CAD risk profile composed of traditional and novel risk factors. Our findings highlight the need for additional awareness of health professionals of this specific risk profile and potential therapeutic targets, as well as the need for further research in this vulnerable population.

ОСОБЕННОСТИ КЛИНИЧЕСКОГО ТЕЧЕНИЯ ИНФАРКТА МИОКАРДА, ОСЛОЖНЕННОГО ОСТРОЙ ЗАДЕРЖКОЙ МОЧИ, У МУЖЧИН МОЛОДОГО И СРЕДНЕГО ВОЗРАСТА

Abstract. Relevance. Acute urinary retention (AUR) in myocardial infarction (MI) negatively affects the course and prognosis of the disease. Aim. To evaluate the MI clinical course of AUR development during the acute and subacute periods of disease in men under 60 years old to improve prevention and outcomes. Materials and methods. The study included men aged 19-60 years with type I myocardial in-farction. Patients were divided into two age-comparable groups: I - study group, with ACR - 22 patients; II - control, without urination disorders - 644 patients. A comparative analysis of the features of the medical history and clinical course in the selected groups were performed. Pear-son's Chi-square method was used to analyze the risks of ACR development. Results of the study. The study group differed from the control group in a higher frequency of cardiac arrhythmias and conduction disorders at the onset of coronary artery disease (I: 61.9; II: 24.9%; p = 0.0007), higher incidence of multiple MI complications (100 and 44.0%; ; respectively; p &lt; 0.0001), severe and extremely severe condition of patients (59.0 and 19.6%; p &lt; 0.0001). Asystole (absolute risk: 42.1%; relative: 18.0; p &lt; 0.0001), hydrothorax (41.7%; 15.9; p &lt; 0.0001), the patient’s severe condition in the first hours of illness (30%; 36.5; p &lt; 0.0001), and onset of CHD with heart rhythm and conduction disturbances (7.7%; 4.6; p = 0.0001) were the most significant ACR predictors. Conclusion. Patients with ACR are characterized by a more severe MI course. Combinations of listed above factors indicate an increased risk of development this complication. It is advisable to use them for predictive modeling and the formation of risk groups for timely prevention.

Does MicroRNA Profile Differ in Early Onset Coronary Artery Disease?

MicroRNAs have been explored as potential biomarkers for many pathological processes including coronary artery disease. In this study, we aimed to compare the circulating levels of selected atherosclerosis-associated miRNAs in patients with a history of early-onset coronary artery disease with that of age- and sex-matched healthy controls and older patients with late-onset coronary artery disease. Study population consisted of 30 patients with early onset coronary artery disease, 31 age- and sex-matched healthy controls, and 30 patients with late-onset coronary artery disease. Plasma levels of 13 microRNAs (endothelial cell-related miR-126, -92a/b; vascular smooth muscle cell-related miR-145; inflammation-related miR-16, -21, -125b, -146a/b, -147b, -150, -155; lipometabolism-related miR-27b, -122, -370) were evaluated by using real-time polymerase chain reaction. In patients with early onset coronary artery disease, plasma expressions of the lipometabolism-related miR-27b, miR-122; inflammation-related miR-125b, miR-146a/b, miR-147b, miR-150, miR-155; and VSMC-related miR-145 were significantly downregulated and endothelial cell-related miR-126 was significantly upregulated compared to age- and sexmatched healthy controls. Circulating microRNA profile of patients with early onset coronary artery disease was also different from that of older patients with late-onset coronary artery disease. Plasma levels of miR-21, miR-27b, miR-122, miR-125b, miR-146b, miR-147b, and miR-155 were lower and plasma levels of miR-16 and miR-92a were higher in patients with early onset coronary artery disease compared to older patients with late-onset coronary artery disease. MicroRNAs are promising biomarkers for early onset coronary artery disease.

Effect of Adiponectin Variant on Lipid Profile and Plasma Adiponectin Levels: A Multicenter Systematic Review and Meta-Analysis.

Background Adiponectin is a recognized antiatherogenic molecule; this study was aimed at clarifying the effects of adiponectin variants on lipid and adiponectin levels. Methods By searching PubMed and Cochrane databases for studies published before March 31, 2022, a total of 86,610 individuals were included in the analysis. Results Variants of rs2241766 and rs266729 were associated with decreased adiponectin and high-density lipoprotein cholesterol (HDL-C), as well as increased triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels. In contrast, the rs1501299 variant was correlated with increased adiponectin and HDL-C, as well as decreased TG, TC, and LDL-C levels. Subgroup analysis indicated that the significant effect of the rs2241766 and rs266729 variants on lipid profile was predominant in Chinese, while the significant effect of the rs1501299 variant on lipid profile was primarily in Caucasians. Moreover, a stronger effect of the rs2241766 and rs1501299 variants on LDL-C levels was observed in males, while a considerable effect of the rs266729 variant on LDL-C levels was observed in children. Conclusions The present study indicated that Chinese with the rs2241766 and rs266729 variants were at high risk of dyslipidemia, atherosclerosis, or coronary artery disease (CAD). Males with the rs2241766 variant were at high risk of CAD. Children with the rs266729 variant had a high risk to develop dyslipidemia, atherosclerosis, and even early onset of CAD in the future. These findings are beneficial to clinical physicians to choose different management strategies for cardiovascular disease (CVD) prevention.