High Risk For Coronary Artery Disease Research Articles

PREVALENCE OF ELEVATED LOW DENSITY LIPOPROTEIN CHOLESTEROL (LDL–C) LEVELS IN ADULT PATIENTS WITH COMPLEX CONGENITAL HEART DISEASE

Abstract Background Thanks to advances in both medical care and surgical techniques, survival for adult patients with congenital heart disease (ACHD) has significantly increased over recent years, with about 90% of them now reaching adulthood. However, as CHD patients grow older, their relative risk of developing coronary artery disease (CAD) increases. Elevated low–density lipoprotein cholesterol (LDL–C) levels play a pivotal role in the genesis of CAD in the general population. Limited data exist on the prevalence of hyperlipidemia in the ACHD population. Patients with complex CHD should be considered at increased risk for CAD, mainly related to to the severity of the CHD and aging. For this reason, it could be reasonable to apply targets used for patients at high risk of CAD. Our study aimed at describing the overall prevalence of elevated LDL–C levels in a contemporary cohort of adult patients with complex CHD. Materials and Methods This is a single–centre retrospective study. All adults with complex CHD who attended the outpatient clinic at our tertiary centre from January 2000 to April 2023 were included. Demographic, clinical and laboratory data were obtained in all patients from medical records and our dedicated databases. Results A total of 230 patients with complex CHD were included in the present study (mean age 35±11 years, 124 male, mean follow up of 117±80 months). One hundred forty–three (63%) of them showed biventricular physiology, whereas 86 (37%) patients showed univentricular heart physiology. Eighty patients from our cohort underwent Fontan operation. Twenty patients (9%) showed oxygen saturation at rest lower than 90%. Mean levels of LDL–C was 87±28 mg/dl, with 184 patients (78%) showing LDL–C levels ≥ 55 mg/dl. Conclusion Our study demonstrated that, despite their relatively younger age, elevated LDL–C levels are not uncommon in patients with severe CHD. ACHD patients with complex anatomy, such as patients after Fontan operation, should be considered at increased risk of ischaemic events and treated accordingly. Further research and international collaboration are therefore paramount to understand whether and if these patients should be treated with lower lipid drugs as for the general population.

Classical and Novel Lipid-Lowering Therapies for Diabetic Patients with Established Coronary Artery Disease or High Risk of Coronary Artery Disease-A Narrative Clinical Review.

Diabetic atherosclerosis is a complex process that is characterized by diffuse and unstable lesions increasing 2-4-fold the risk of adverse cardiovascular (CV) events. Diabetic dyslipidemia has a predominant role in coronary artery disease (CAD) and has been the target of classical and emerging pharmaceutical agents with established or promising CV benefits. The aim of the present narrative review was to summarize the effects of classical and novel lipid-lowering pharmaceutical agents on lipid profile and CV outcomes in diabetic patients with established CAD or high risk of CAD. Statins remain the first-line treatment for all diabetic patients since they considerably ameliorate lipid parameters and non-lipid CV risk factors, leading to reduced CV morbidity and mortality. Complementary to statins, ezetimibe exerts lipid-lowering properties with modest but significant reductions in major adverse cardiovascular events (MACEs) and CV mortality. PCSK9 inhibitors considerably reduce LDL-C levels and lower MACEs in diabetic patients. On the other hand, fibrates may confer a very modest decline in MACE incidence, while the CV impact of omega-3 fatty acids is promising but remains questionable. Bempedoic acid and inclisiran have a potential therapeutic role in the management of diabetic dyslipidemia, but this is still not adequately documented. Given the heightened CV risk among individuals with diabetes, more decisive results would be of great importance in the utility of all these drugs.

Cardiac rehabilitation using intensive lifestyle habituation combined with outdoor exercise in an urban forest environment for primary and secondary prevention of coronary artery disease: a feasibility test

Background: We aimed to examine the feasibility of intensive lifestyle habituation with a subsequent home program, including forest-based exercise, as an alternative approach to conventional cardiac rehabilitation for both primary and secondary prevention of coronary artery disease (CAD).Methods: A total of 28 participants were included in a 1-week intensive education program aimed at fostering desirable lifestyle habits in the study: 17 patients who underwent percutaneous coronary intervention and 11 participants at high risk of CAD. Subsequently, they engaged in a self-directed, home-based program that included unstructured exercise in an urban forest. The terrain of the urban forest was analyzed to estimate metabolic equivalent levels and to assess safety and accessibility for patient exercise.Results: Throughout the program, no adverse cardiac events were reported. Additionally, risk factors for CAD—including body composition, blood sugar levels, hemodynamic variables, total cholesterol levels, and cardiorespiratory endurance—showed significant improvement in both groups.Conclusions: Intensive lifestyle habituation and unstructured, self-directed exercise in the forest were as effective and safe as conventional cardiac rehabilitation for patients with CAD. The study demonstrated that an urban forest could serve as a safe exercise environment in both primary and secondary prevention strategies for CAD.

Association of 25-hydroxyvitamin D, lipoprotein-associated phospholipase A2 and asymptomatic coronary artery disease in patients with type 2 diabetes mellitus

AimTo evaluate the relationship of 25-hydroxyvitamin D (25(OH)D), lipoprotein-associated phospholipase A2 (Lp-PLA2), and coronary artery disease (CAD) in type 2 diabetes mellitus (T2DM) patients with no history or symptoms of cardiovascular disease. MethodsThe study identified 66 pairs of T2DM patients with and without CAD using propensity score matching. All subjects performed coronary computed tomography angiography (CCTA). Data on 25(OH)D, Lp-PLA2, and metabolic indexes were collected and analyzed. ResultsCompared to the patients without CAD, the patients with CAD had lower 25(OH)D levels and the rate of vitamin D sufficiency, but higher Lp-PLA2 levels. Meanwhile, subjects in the vitamin D sufficiency group had a lower prevalence of CAD and Lp-PLA2 levels. Furthermore, 25(OH)D was inversely correlated with Lp-PLA2, Gensini score, Leiden score, segment involvement score, and segment stenosis score (P < 0.05). After adjusting for age, gender, blood lipids and blood pressure, 25(OH)D was associated with a decreased risk of CAD (aOR 0.933, 95 %CI 0.887–0.983, P = 0.009), while Lp-PLA2 was associated with an increased risk of CAD (aOR 1.014, 95 %CI 1.005–1.022, P = 0.002). ConclusionsDecreased 25(OH)D and increased Lp-PLA2 could identify patients with a high risk of CAD and are associated with the severity of coronary artery stenosis in T2DM.

Polygenic Risk Score Assessment for Coronary Artery Disease in Asian Indians.

We evaluated the performance of various polygenic risk score (PRS) models derived from European (EU), South Asian (SA), and Punjabi Asian Indians (AI) studies on 13,974 subjects from AI ancestry. While all models successfully predicted Coronary artery disease (CAD) risk, the AI, SA, and EU + AI were superior predictors and more transportable than the EU model; the predictive performance in training and test sets was 18% and 22% higher in AI and EU + AI models, respectively than in EU. Comparing individuals with extreme PRS quartiles, the AI and EU + AI captured individuals with high CAD risk showed 2.6 to 4.6 times higher efficiency than the EU. Interestingly, including the clinical risk score did not significantly change the performance of any genetic model. The enrichment of diversity variants in EU PRS improves risk prediction and transportability. Establishing population-specific normative and risk factors and inclusion into genetic models would refine the risk stratification and improve the clinical utility of CAD PRS.

Abstract MP34: Association of Biological Age Acceleration With Incident Type 2 Diabetes and Coronary Artery Disease

Introduction: Biological age (BA), compared to chronological age, offers a more accurate reflection of aging status and prediction of cardiometabolic disease mortality. Genetics play an important role in the pathogenesis of type 2 diabetes (T2D) and coronary artery disease (CAD). However, the associations of BA acceleration with incident T2D and CAD as well as how the interactions between genetic risk and BA acceleration implicate in the development of these two diseases remain unclear. Hypothesis: We hypothesized that BA acceleration was significantly associated with incident T2D and CAD. We further hypothesized that there were significant interactions between BA acceleration and genetic risk in relation to risk of T2D and CAD. Methods: This prospective cohort study utilized data from the UK Biobank. BA was quantified by KDM-BA and PhenoAge, two composite measures derived from blood chemistry and physical examination data. T2D and CAD were diagnosed using self-reported medical history, medication, and hospital inpatient records. Multivariable Cox proportional hazard models were employed to estimate the associations of BA acceleration with incident T2D and CAD. A polygenic risk score (PRS) for T2D or CAD divided into tertiles was used to assess the interactions between BA acceleration (divided into quartiles) and genetic risk with regards to the development of T2D and CAD. Derived estimates were hazard ratios (HRs) and their 95% confidence intervals (CIs) per one standard deviation increment in each of the two BA measures. Results: This study analyzed 271,855 participants without T2D and 267,293 participants without CAD at baseline. Over a median follow-up time of 14.6 and 14.5 years, 9,562 incident T2D events and 18,509 incident CAD events occurred, respectively. Individuals with greater BA acceleration were at increased risk of T2D (HR for KDM-BA: 1.42, [95% CI: 1.39-1.46]; HR for PhenoAge: 1.23, [95% CI: 1.20-1.25]). Similarly, BA acceleration was significantly associated with a higher risk of CAD (HR for KDM-BA: 1.22, [95% CI: 1.20-1.25]; HR for PhenoAge: 1.12, [95% CI: 1.10-1.14]). People with greater genetic risk and BA acceleration had higher risks of T2D and CAD (P for interaction &lt; 0.002). Compared with participants with the lowest level of PRS and BA acceleration, those with the highest level of PRS and BA acceleration had a higher risk of developing T2D (HR for KDM-BA: 7.03, [95% CI: 6.16-8.02]; HR for PhenoAge: 6.39, [95% CI: 5.38-7.58]) and CAD (HR for KDM-BA: 2.83, [95% CI: 2.62-3.06]; HR for PhenoAge: 2.27, [95% CI: 2.09-2.46]). Conclusions: BA acceleration was significantly associated higher risks of T2D and CAD, especially among individuals with a high genetic predisposition to T2D and CAD.

Alternate day fasting aggravates atherosclerosis through the suppression of hepatic ATF3 in Apoe−/− mice

Abstract Atherosclerosis is the major contributor to cardiovascular mortality worldwide. Alternate day fasting (ADF) has gained growing attention due to its metabolic benefits. However, the effects of ADF on atherosclerotic plaque formation remain inconsistent and controversial in atherosclerotic animal models. The present study was designed to investigate the effects of ADF on atherosclerosis in apolipoprotein E-deficient (Apoe−/−) mice. Eleven-week-old male Apoe−/− mice fed with Western diet (WD) were randomly grouped into ad libitum (AL) group and ADF group, and ADF aggravated both the early and advanced atherosclerotic lesion formation, which might be due to the disturbed cholesterol profiles caused by ADF intervention. ADF significantly altered cholesterol metabolism pathways and down-regulated integrated stress response (ISR) in the liver. The hepatic expression of activating transcription factor 3 (ATF3) was suppressed in mice treated with ADF and hepatocyte-specific overexpression of Aft3 attenuated the effects of ADF on atherosclerotic plaque formation in Apoe−/− mice. Moreover, the expression of ATF3 could be regulated by Krüppel-like factor 6 (KLF6) and both the expressions of ATF3 and KLF6 were regulated by hepatic cellular ISR pathway. In conclusion, ADF aggravates atherosclerosis progression in Apoe−/− mice fed on WD. ADF inhibits the hepatic ISR signaling pathway and decreases the expression of KLF6, subsequently inhibiting ATF3 expression. The suppressed ATF3 expression in the liver mediates the deteriorated effects of ADF on atherosclerosis in Apoe−/− mice. The findings suggest the potentially harmful effects when ADF intervention is applied to the population at high risk of atherosclerosis.

Prevalence of balanced ischemia on positron emission tomography relative perfusion imaging among patients with high-risk coronary artery disease

Prevalence of balanced ischemia on positron emission tomography relative perfusion imaging among patients with high-risk coronary artery disease

Impact of untreated chronic obstructive coronary artery disease on outcomes after transcatheter aortic valve replacement.

In transcatheter aortic valve replacement (TAVR) recipients, the optimal management of concomitant chronic obstructive coronary artery disease (CAD) remains unknown. Some advocate for pre-TAVR percutaneous coronary intervention, while others manage it expectantly. The aim of this study was to assess the impact of varying degrees and extent of untreated chronic obstructive CAD on TAVR and longer-term outcomes. The authors conducted a retrospective cohort study of TAVR recipients from January 2015 to November 2021, separating patients into stable non-obstructive or varying degrees of obstructive CAD. The major outcomes of interest were procedural all-cause mortality and complications, major adverse cardiovascular events, and post-TAVR unplanned coronary revascularization. Of the 1911 patients meeting inclusion, 75%, 6%, 10%, and 9% had non-obstructive, intermediate-risk, high-risk, and extreme-risk CAD, respectively. Procedural complication rates overall were low (death 0.4%, shock 0.1%, extracorporeal membrane oxygenation 0.1%), with no difference across groups. At a median follow-up of 21 months, rates of acute coronary syndrome and unplanned coronary revascularization were 0.7% and 0.5%, respectively, in the non-obstructive population, rising in incidence with increasing severity of CAD (P < .001 for acute coronary syndrome/unplanned coronary revascularization). Multivariable analysis did not yield a significantly greater risk of all-cause mortality or major adverse cardiovascular events across groups. One-year acute coronary syndrome and unplanned coronary revascularization rates in time-to-event analyses were significantly greater in the non-obstructive (98%) vs. obstructive (94%) subsets (Plog-rank< .001). Transcatheter aortic valve replacement can be performed safely in patients with untreated chronic obstructive CAD, without portending higher procedural complication rates and with relatively low rates of unplanned coronary revascularization and acute coronary syndrome at 1 year.

Epidemiology of atherosclerotic cardiovascular disease in polygenic hypercholesterolemia with or without high lipoprotein(a) levels.

Epidemiology of atherosclerotic cardiovascular disease might be different in patients with polygenic hypercholesterolemia plus high levels (≥30 mg/dl) of Lp(a) (H-Lpa) than in those with polygenic hypercholesterolemia alone (H-LDL). We compared the incidence of peripheral artery disease (PAD), coronary artery disease (CAD), and cerebrovascular disease (CVD) in patients with H-Lpa and in those with H-LDL. Retrospective analysis of demographics, risk factors, vascular events, therapy, and lipid profile in outpatient clinical data. Inclusion criteria was adult age, diagnosis of polygenic hypercholesterolemia, and both indication and availability for Lp(a) measurement. Medical records of 258 patients with H-Lpa and 290 H-LDL were reviewed for occurrence of vascular events. The median duration of follow-up was 10 years (IQR 3-16). In spite of a similar reduction of LDL cholesterol, vascular events occurred more frequently, and approximately 7 years earlier (P = 0.024) in patients with H-Lpa than in H-LDL (HR 1.96 1.21-3.17, P = 0.006). The difference was around 10 years for acute events (TIA, Stroke, acute coronary events) and one year for chronic ones (P = 0.023 and 0.525, respectively). Occurrence of acute CAD was higher in H-Lpa men (HR 3.1, 95% CI 1.2-7.9, P = 0.007) while, among women, PAD was observed exclusively in H-Lpa subjects with smoking habits (P = 0.009). Patients with high Lp(a) levels suffer from a larger and earlier burden of the disease compared to those with polygenic hypercholesterolemia alone. These patients are at higher risk of CAD if they are men, and of PAD if they are women.

Coronary Artery Disease Is Related to Methylation Disorders Caused by the c.1286A&gt;C MTHFR Polymorphism and to Low Serum 5-MTHF and Folic Acid Concentrations—Preliminary Results

Background: Single nucleotide polymorphisms in gene encoding is the key enzyme in the folates pathway, methyltetrahydrofolate reductase (MTHFR), which causes methylation disorders associated with coronary artery disease (CAD). We evaluated associations between methylation disorders caused by MTHFR gene polymorphisms and the blood folate concentrations (folic acid, 5-MTHF) in CAD patients. Methods: Study group: 34 patients with CAD confirmed by invasive coronary angiography (ICA). Controls: 14 patients without CAD symptoms or significant coronary artery stenosis, based on ICA or multislice computed tomography (MSCT) with coronary artery calcification (CAC) scoring. Real-time PCR genotyping was assessed using TaqMan™ probes. Folic acid and 5-MTHF concentrations in blood serum were determined using Liquid Chromatography-Mass Spectrometry (LC-MS). Results: The c.[1286A&gt;C];[1286A&gt;C] MTHFR polymorphism occurred significantly more often in (CAD+) patients compared to the (CAD−) cohort and to the selected general European “CEU_GENO_PANEL” population sample. The concentration of 5-MTHF and folic acid in subgroups of CAD+ patients with methylation disorders categorized by genotypes and CAD presence (CAD+) was always lower in CAD+ subgroups compared to non-CAD individuals (CAD−). Conclusions: Further studies on a larger scale are needed to implicate the homozygous c.1286A&gt;C MTHFR variant as CAD genetic marker and the 5-MTHF as CAD biomarker. Identification of high CAD risk using genetic and phenotypic tests can contribute to personalized therapy using an active (methylated) form of folic acid (5-MTHF) in CAD patients with MTHFR polymorphisms.

Haplotype of the Lipoprotein(a) Gene Variants rs10455872 and rs3798220 Is Associated with Parameters of Coagulation, Fibrinolysis, and Inflammation in Patients after Myocardial Infarction and Highly Elevated Lipoprotein(a) Values.

Lipoprotein(a) (Lp(a)) is an independent risk factor for future coronary events. Variants rs10455872 and rs3798220 in the gene encoding Lp(a) are associated with an increased Lp(a) concentration and risk of coronary artery disease. We aimed to determine whether in high-risk coronary artery disease patients these two genetic variants and the kringle IV type 2 (KIV-2) repeats are associated with impairment of inflammatory and hemostatic parameters. Patients after myocardial infarction with elevated Lp(a) levels were included. Blood samples underwent biochemical and genetic analyses. In carriers of the AC haplotype, the concentrations of tumor necrosis factor (TNF)-α (4.46 vs. 3.91 ng/L, p = 0.046) and plasminogen activator inhibitor-1 (PAI-1) (p = 0.026) were significantly higher compared to non-carriers. The number of KIV-2 repeats was significantly associated with the concentration of high-sensitivity C-reactive protein (ρ = 0.251, p = 0.038) and overall fibrinolytic potential (r = -0.253, p = 0.038). In our patients, a direct association between the AC haplotype and both TNF-α and PAI-1 levels was observed. Our study shows that the number of KIV-2 repeats not only affects proatherosclerotic and proinflammatory effects of Lp(a) but is also associated with its antifibrinolytic properties.

Associations of combined polygenic risk score and glycemic status with atrial fibrillation, coronary artery disease and ischemic stroke

BackgroundIt is unknown whether high hemoglobin A1c (HbA1c) is associated with increases in the risk of cardiovascular disease among individuals with elevated genetic susceptibility. We aimed to investigate the association between HbA1c and atrial fibrillation (AF), coronary artery disease (CAD), and ischemic stroke according to the polygenic risk score (PRS).MethodsThe UK Biobank cohort included 502,442 participants aged 40–70 years who were recruited from 22 assessment centers across the United Kingdom from 2006 to 2010. This study included 305,605 unrelated individuals with available PRS and assessed new-onset AF, CAD, and ischemic stroke. The participants were divided into tertiles based on the validated PRS for each outcome. Within each PRS tertiles, the risks of incident events associated with HbA1c levels were investigated and compared with HbA1c < 5.7% and low PRS. Data were analyzed from November 2022 to May 2023.ResultsOf 305,605 individuals, 161,605 (52.9%) were female, and the mean (SD) age was 56.6 (8.1) years. During a median follow-up of 11.9 (interquartile range 11.1–12.6) years, the incidences of AF, CAD, and ischemic stroke were 4.6, 2.9 and 1.1 per 100 person-years, respectively. Compared to individuals with HbA1c < 5.7% and low PRS, individuals with HbA1c ≥ 6.5% and high PRS had a 2.67-times higher risk for AF (hazard ratio [HR], 2.67; 95% confidence interval (CI), 2.43–2.94), 5.71-times higher risk for CAD (HR, 5.71; 95% CI, 5.14–6.33) and 2.94-times higher risk for ischemic stroke (HR, 2.94; 95% CI, 2.47–3.50). In the restricted cubic spline models, while a U-shaped trend was observed between HbA1c and the risk of AF, dose-dependent increases were observed between HbA1c and the risk of CAD and ischemic stroke regardless PRS tertile.ConclusionsOur results suggest that the nature of the dose-dependent relationship between HbA1c levels and cardiovascular disease in individuals with different PRS is outcome-specific. This adds to the evidence that PRS may play a role together with glycemic status in the development of cardiovascular disease.

A risk predictive model for determining the severity of coronary artery lesions in older postmenopausal women with coronary heart disease.

To determine the risk factors affecting the severity of coronary artery disease (CAD) in older postmenopausal women with coronary heart disease (CHD) and to construct a personalized risk predictive model. In this cohort study, clinical records of 527 female patients aged ≥60 with CHD who were hospitalized in the First Affiliated Hospital of the University of Science and Technology of China from March 2018 to February 2019 were analyzed retrospectively. The severity of CAD was determined using the Gensini scores that are based on coronary angiography findings. Patients with Gensini scores ≥40 and <40 were divided into high-risk (n=277) and non-high-risk groups (n=250), respectively. Logistic regression analysis was used to assess independent predictors of CAD severity. The nomogram prediction model of CAD severity was plotted by the R software. The area under the receiver operating characteristic (ROC) and calibration curves were used to evaluate the predictive efficiency of the nomogram model, and the decision curve analysis (DCA) was used to assess the clinical applicability of the nomogram model. Multivariate analysis showed that high-sensitivity C-reactive protein, RBC count, WBC count, BMI, and diabetes mellitus were independent risk factors associated with CAD severity in older menopausal women (P<0.05); the area under the ROC curve of the nomogram constructed based on the independent risk factors was 0.846 (95% CI: 0.756-0.937). The area under the ROC curve after internal validation of the nomogram by the Bootstrap method after resampling 1000 times was 0.840 (95% CI: 0.741-0.923). The calibration curve suggested that the nomogram had an excellent predictive agreement, and the DCA curve indicated that the net benefit of applying the nomogram was significantly higher than that of the "no intervention" and "all intervention" methods when the risk probability of patients with high-risk CAD severity was 0.30-0.81. A personalized risk assessment model was constructed based on the risk factors of severe CAD in older menopausal women with CHD, which had good prediction efficiency based on discrimination, calibration, and clinical applicability evaluation indicators. This model could assist cardiology medical staff in screening older menopausal women with CHD who are at a high risk of severe CAD to implement targeted interventions.

The Systemic Immune-Inflammation Index Predicts In-Hospital Mortality in Patients Who Underwent On-Pump Cardiac Surgery.

Systemic immune-inflammation index (SII), a new inflammatory index calculated using platelet, neutrophil, and lymphocyte counts, has been demonstrated to be an independent risk factor for the identification of high-risk coronary artery disease in patients undergoing percutaneous coronary intervention and cardiovascular surgery with cardiopulmonary bypass (CPB). The relationship between SII and CPB-related mortality rates remains unclear. This research was designed to investigate the use of SII to predict in-hospital mortality in patients undergoing cardiac surgery with CPB. Four hundred eighty patients who underwent a cardiac procedure involving CPB over 3 years, were obtained from the hospital's database. The demographic data, comorbidities, hematological and biochemical profiles, and operative data of the groups were compared. Multiple logistic regression analyses were done to determine independent predictors of mortality. Prognostic factors were assessed by multivariate analysis, and the predictive values of SII, neutrophil-lymphocyte ratio (NLR), and platelet-lymphocyte ratio (PLR) for mortality were compared. A p-value <0.05 was considered significant. Of 480 patients, 78 developed in-hospital mortality after cardiac surgery. SII was an independent predictor of in-hospital mortality (Odds ratio: 1.003, 95% confidence interval: 1.001-1.005, p<0.001). The cut-off value of the SII was >811.93 with 65% sensitivity and 65% specificity (area under the curve: 0.690). The predictive values of SII, PLR, and NLR were close to each other. High preoperative SII scores can be used for early determination of appropriate treatments, which may improve surgical outcomes of cardiac surgery in the future.

O Índice de Imuno Inflamação Sistêmica Prevê Mortalidade Hospitalar em Pacientes Submetidos à Cirurgia Cardíaca com Circulação Extracorpórea

Abstract Background: Systemic immune-inflammation index (SII), a new inflammatory index calculated using platelet, neutrophil, and lymphocyte counts, has been demonstrated to be an independent risk factor for the identification of high-risk coronary artery disease in patients undergoing percutaneous coronary intervention and cardiovascular surgery with cardiopulmonary bypass (CPB). The relationship between SII and CPB-related mortality rates remains unclear. Objective: This research was designed to investigate the use of SII to predict in-hospital mortality in patients undergoing cardiac surgery with CPB. Methods: Four hundred eighty patients who underwent a cardiac procedure involving CPB over 3 years, were obtained from the hospital's database. The demographic data, comorbidities, hematological and biochemical profiles, and operative data of the groups were compared. Multiple logistic regression analyses were done to determine independent predictors of mortality. Prognostic factors were assessed by multivariate analysis, and the predictive values of SII, neutrophil-lymphocyte ratio (NLR), and platelet-lymphocyte ratio (PLR) for mortality were compared. A p-value &lt;0.05 was considered significant. Results: Of 480 patients, 78 developed in-hospital mortality after cardiac surgery. SII was an independent predictor of in-hospital mortality (Odds ratio: 1.003, 95% confidence interval: 1.001-1.005, p&lt;0.001). The cut-off value of the SII was &gt;811.93 with 65% sensitivity and 65% specificity (area under the curve: 0.690). The predictive values of SII, PLR, and NLR were close to each other. Conclusion: High preoperative SII scores can be used for early determination of appropriate treatments, which may improve surgical outcomes of cardiac surgery in the future.

ЗАЛЕЖНІСТЬ ПОКАЗНИКІВ ДИСЛІПОПРОТЕЇДЕМІЇ ВІД МАРКЕРА СИСТЕМНОГО ЗАПАЛЕННЯ С-РЕАКТИВНОГО ПРОТЕЇНУ У ПАЦІЄНТІВ З ХОЗЛ

Aim was to study the correlation between dyslipoproteinemia and systemic inflammation marker C-reactive protein in COPD patients. Materials and methods. Retrospective data analysis of 66 cases of COPD patients aged 40-60 years was conducted. C-reactive protein (CRP) was assessed as a marker of systemic inflammation. We also measured the dyslipoproteinemia markers, such as total cholesterol (TC) and low-density lipoprotein cholesterol (LDLC). Using paired linear regression method there was studied an effect of CRP level on some dyslipoproteinemia indices in COPD patients. Results. The average level of CRP was 11.60 ± 5.54 mg/l, demonstrating the presence of a systemic inflammation in study patients. We revealed a linear correlation between CRP and TC (r = 0,7 ± 4,7). There was even stronger correlation between CRP and LDLC ( r = 0,8 ± 3,5). Conclusion. In patients from this retrospective study, a correlation between the levels of CRP and TC/LDLC as the indicators of high risk of atherosclerosis was found. Therefore, it is possible to assume in COPD patients, it is feasible to screen the level of TC and LDLC for prevention/ early diagnosing of atherosclerosis, which in turn is the leading cause of death worlwide. Key words: chronic inflammation, atherosclerosis, COPD, C-reactive protein, dyslipoproteinemia.

Genetically predicted lifestyle factors, socioeconomic status and risk of coronary artery disease in individuals with diabetes: a Mendelian randomization study.

This study explores the causal links between genetically predicted lifestyle factors, socioeconomic status, and coronary artery disease (CAD) risk in individuals with diabetes using a bidirectional Mendelian-randomization approach. This study explored the potential causal relationships of lifestyle factors and socioeconomic status with the risk of CAD in diabetes patients by a bidirectional, two-sample Mendelian-randomization (MR) analysis. Genetically predicted smoking initiation (p = 0.005, 95% CI: 1.08-1.55) and insomnia (p = 0.001, 95% CI: 1.06-1.29) were associated with a higher risk of CAD in individuals with diabetes, whereas educational attainment (p = 0.0001, 95% CI: 0.47-0.78) was associated with a lower risk of CAD. The lifetime smoking index (p = 0.016, 95% CI: 1.12-3.03) was suggestively associated with a higher risk of CAD, while household income before taxes (p = 0.048, 95% CI: 0.41-1.00) was suggestively associated with a lower risk of CAD. In addition, we observed a suggestive negative association between the genetically predicted risk of CAD and the lifetime smoking index (p = 0.016, 95% CI: 0.98-0.99) and a significant causal relationship between the risk of CAD and household income before taxes (p = 0.006, 95% CI: 0.97-0.99). The results of this study provide evidence that smoking initiation, lifetime smoking index and insomnia are associated with an increased risk of CAD in individuals with diabetes, educational attainment and household income before taxes are associated with a reduced risk of CAD in individuals with diabetes, and the possible role of lifetime smoking index and household income before taxes on the risk of CAD in individuals with diabetes. It provides an opportunity for the prevention and management of CAD in individuals with diabetes.

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.

In vitro and in vivo approaches to assess atherosclerosis following exposure to low-dose mixtures of arsenic and cadmium

Worldwide, millions of people are co-exposed to arsenic and cadmium. Environmental exposure to both metals is linked with a higher risk of atherosclerosis. While studies have characterized the pro-atherosclerotic effects of arsenic and cadmium as single agents, little is known about the potential effects of metal mixtures, particularly at low doses. Here, we used a combination of in vitro and in vivo models to assess the effects of low-dose metals individually and as mixtures on early events and plaque development associated with atherosclerosis. In vitro, we investigated early pro-atherogenic changes in macrophages and endothelial cells with metal treatments. The combined cytotoxic effects of both metals at low concentrations were dose interactive, specifically, synergistic in macrophages, but antagonistic in endothelial cells. Despite this differential behavior across cell types, the mixtures did not initiate early pro-atherogenic events: neither reactive oxygen species generation in macrophages nor adhesion molecule expression on endothelial cells. In vivo, we utilized the well-characterized hyperlipidemic apolipoprotein E knock-out (ApoE−/−) mouse model. Previously, we have shown that low concentrations of arsenic (down to 10 ppb) enhance atherosclerosis in ApoE−/− mice. This model has also been used with cadmium to demonstrate pro-atherogenic effects, although at concentrations above human-relevant exposures. In both sexes, there are some small increases in atherosclerotic lesion size, but very few changes in plaque constituents in the ApoE−/− mouse model. Together, these results suggests that low-dose metal mixtures are not significantly more pro-atherogenic than either metal alone.