Association of serum vitamin D levels and TaqIrs731236 among patients with hypertensive coronary heart disease.

The development of cardiovascular diseases (CVD) is influenced through multiple risk factor and hypertension. It may increase the risk of cardiac events, and has a significant impact when combined with other risk factors including low levels of vitamin D and genetic variations like single nucleotide variations (SNV) (TaqIrs731236) in vitamin D receptor (VDR) gene. Blood samples from 500 study participants gathered including 250 hypertensive coronary heart disease patients, 250 age and gender matched healthy controls. To isolate genomic DNA, conventional salting out procedure used followed by amplification of targeted variations through Amplification Refractory Mutation System- Polymerase Chain Reaction (ARMS-PCR) Assay. The amplicon consists of 148 base pairs which was visualized on 2 % agarose gel electrophoresis and confirmed by DNA sequencing. The compared clinical parameters including systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), high density lipoproteins (HDL), low density lipoproteins (LDL), cholesterol, triglycerides found significantly different among patients when compared with controls (P < 0.001). The Vitamin D exhibited insufficient levels at different stages of hypertension which were statistically, found significantly associated among patients with hypertensive coronary heart disease showing compared to controls (P < 0.001). The genotype association SNV (TaqIrs731236) T > C showed significant association with hypertensive coronary heart disease compared to healthy controls (Chi-Square χ2 = 60.75 and P < 0.00001). Further, the odds ratio of allelic association for risk allele (C) showed the strength of association with risk of disease, which increases by 2.02 times(P = 0.01). The results suggest that (TaqIrs731236) T > C as genetic predisposition factor, may contribute to develop the risk of hypertensive coronary heart disease. Hypertension as a risk factor along with insufficient levels of vitamin D and SNV (TaqIrs731236) as genetic variations may have been an important contributor to disease risk of hypertensive coronary heart disease.

Hyperhomocysteinemia as an Independent Risk Factor for Coronary Heart Disease. Comparison with Conventional Risk Factors / Hiper-homocisteinemia como fator de risco independente para doença coronariana: comparação com fatores de risco convencionais

The present study was designed to evaluate the strength of association of raised plasma homocysteine concentration as a risk factor for coronary heart disease independent of conventional risk factor. It was a case control study conducted at Punjab Institute of Cardiology Lahore. A total of 210 subjects aged 25 to 60 years comprising of 105 newly admitted patients of CHD as cases and 105 age and sex matched healthy individuals with no history of CHD as control were recruited for the study. Fasting blood samples were obtained from cases and controls. Plasma homocysteine was analyzed by fluorescence polarization immunoassay (FPIA) method on automated immunoassay analyzer (Abbott IMX). Total cholesterol, triglyceride and HDL cholesterol were analyzed using calorimetric kit methods. The concentration of LDL cholesterol was calculated using Friedewald formula. The patients were also assessed for traditional risk factors such as age, sex, family history of CVD, hypertension, smoking and physical activity, and were compared with control subjects. The collected data was entered in SPSS version 24 for analysis and interpretation.The mean age in controls and experimental groups were 43.00± 8.42 years and 44.72± 8.59 years with statistically same distribution (p- value= 0.144). The mean plasma homocysteine for cases was 22.33± 9.22 µmol/L where as it was 12.59±3.73 µmol/L in control group. Highly significant difference was seen between the mean plasma level of homocysteine in cases and controls (p˂0.001).Simple logistic regression indicates a strong association of coronary heart disease with hyperhomocysteinemia (OR 7.45), which remained significantly associated with coronary heart disease by multivariate logistic regression (OR 7.10, 95%C1 3.12-12.83, p=0.000). The present study concludes that elevated levels of Plasma homocysteine is an independent risk factor [...].

O presente estudo foi desenhado para avaliar a força da associação da concentração elevada de homocisteína no plasma como um fator de risco para doença cardíaca coronária independente do fator de risco convencional. Foi um estudo de caso-controle realizado no Punjab Institute of Cardiology Lahore. Um total de 210 indivíduos com idade entre 25 e 60 anos, compreendendo 105 pacientes recém-admitidos de CHD como casos e 105 indivíduos saudáveis pareados por idade e sexo sem histórico de CHD como controle, foi recrutado para o estudo. Amostras de sangue em jejum foram obtidas de casos e controles. A homocisteína plasmática foi analisada pelo método de imunoensaio de polarização de fluorescência (FPIA) em analisador de imunoensaio automatizado (Abbott IMX). Colesterol total, triglicerídeos e colesterol HDL foram analisados usando métodos de kit calorimétrico. A concentração de colesterol LDL foi calculada pela fórmula de Friedewald. Os pacientes também foram avaliados para fatores de risco tradicionais, como idade, sexo, história familiar de DCV, hipertensão, tabagismo e atividade física, e foram comparados com indivíduos de controle. Os dados coletados foram inseridos no SPSS versão 24 para análise e interpretação. A média de idade nos grupos controles e experimentais foi de 43,00 ± 8,42 anos e 44,72 ± 8,59 anos com distribuição estatisticamente igual (p-valor = 0,144). A homocisteína plasmática média para os casos foi de 22,33 ± 9,22 µmol / L, enquanto no grupo controle foi de 12,59 ± 3,73 µmol / L. Diferença altamente significativa foi observada entre o nível plasmático médio de homocisteína em casos e controles (p ˂ 0,001). A regressão logística simples indica uma forte associação de doença cardíaca coronária com hiper-homocisteinemia (OR 7,45), que permaneceu significativamente associada com doença cardíaca coronária por multivariada regressão logística (OR 7,10, 95% C1 3,12-12,83, p = 0,000). O presente estudo conclui [...].

The prognostic significance of the presence of tenascin-C in patients with stable coronary heart disease.

BACKGROUND: We investigated the prognostic value of tenascin-C in patients with stable coronary heart disease. METHODS: A total of 666 patients were enrolled and followed for 72 months. The primary outcome was a composite of cardiac events. The secondary outcomes were all-cause death, cardiovascular death, acute myocardial infarction (AMI), and heart failure hospitalization. RESULTS: The area under the curve of tenascin-C to discriminate the occurrence of composite cardiac events was 70 % (95 % CI: 64.2 % to 75.8 %), and the corresponding optimal cutoff value was 19.91 ng/ml. A higher concentration of tenascin-C was associated with a greater risk of composite cardiac events (P trend < 0.001). Similar results were observed in all-cause death, AMI, and heart failure hospitalization. CONCLUSION: Tenascin-C was found to be an independent predictor of total cardiovascular events in patients with stable coronary heart disease at 72 months, and also for all-cause death, AMI, and heart failure hospitalization.

Effects of Serum LDL-C, CysC, and D-D in Patients with Coronary Atherosclerotic Heart Disease.

Objective: To investigate the effects of low-density lipoprotein cholesterol (LDL-C) and serum cystatin C (CysC) combined with D-dimer (D-D) on patients with coronary atherosclerotic heart disease (CHD). Methods: 90 patients with CHD who were admitted to our hospital and diagnosed by coronary angiography (CAG) from February 2020 to June 2021 were selected as the study subjects. 90 patients were grouped according to different types and branches of coronary lesions, and 30 patients with outpatient health check-ups at the same period were selected as the control group, and the differences in serum LDL-C, CysC, and D-D levels between the groups were compared. The logistic regression model was built to explore risk factors affecting the occurrence of CHD. Also, receiver operating characteristic (ROC) curves were drawn to analyze the diagnostic value of LDL-C, CysC, and D-D in CHD. Results: In the comparison of LDL-C, CysC, and D-D levels, CHD group > control group (P < 0.05); stable angina (SAP) group > unstable angina (UAP) group > acute myocardial infarction (AMI) group (P < 0.05); three-branch group > two-branch group > single-branch group (P < 0.05). The logistic regression model showed that high expression levels of LDL-C, CysC, and D-D, male gender, and combined hypertension were risk factors for CHD. The area under the curve (AUC) of the combination of LDL-C, CysC, and D-D was 0.868, and the sensitivity and specificity were 88.89% and 73.33%, respectively, which are higher than those in single diagnosis (P < 0.05). Conclusions: LDL-C, CysC, and D-D are highly expressed in CHD samples, and the combination of the three is beneficial to enhance the diagnostic accuracy of clinical CHD.

Circulating Cystatin C Is an Independent Risk Marker for Cardiovascular Outcomes, Development of Renal Impairment, and Long-Term Mortality in Patients With Stable Coronary Heart Disease: The LIPID Study.

Background Elevated plasma cystatin C levels reflect reduced renal function and increased cardiovascular risk. Less is known about whether the increased risk persists long-term or is independent of renal function and other important biomarkers. Methods and Results Cystatin C and other biomarkers were measured at baseline (in 7863 patients) and 1 year later (in 6106 patients) in participants in the LIPID (Long-Term Intervention with Pravastatin in Ischemic Disease) study, who had a previous acute coronary syndrome. Outcomes were ascertained during the study (median follow-up, 6 years) and long-term (median follow-up, 16 years). Glomerular filtration rate (GFR) was estimated using Chronic Kidney Disease Epidemiology Collaboration equations (first GFR-creatinine, then GFR-creatinine-cystatin C). Over 6 years, in fully adjusted multivariable time-to-event models, with respect to the primary end point of coronary heart disease mortality or nonfatal myocardial infarction, for comparison of Quartile 4 versus 1 of baseline cystatin C, the hazard ratio was 1.37 (95% CI, 1.07-1.74; P=0.01), and for major cardiovascular events was 1.47 (95% CI, 1.19-1.82; P<0.001). Over 16 years, the association of baseline cystatin C with coronary heart disease, cardiovascular, and all-cause mortality persisted (each P<0.001) and remained significant after adjustment for estimated GFR-creatinine-cystatin C. Cystatin C also predicted the development of chronic kidney disease for 6 years (odds ratio, 6.61; 95% CI, 4.28-10.20) independently of estimated GFR-creatinine and other risk factors. However, this association was no longer significant after adjustment for estimated GFR-creatinine-cystatin C. Conclusions Cystatin C independently predicted major cardiovascular events, development of chronic kidney disease, and cardiovascular and all-cause mortality. Prediction of long-term mortality was independent of improved estimation of GFR. Registration URL: https://anzctr.org.au; Unique identifier: ACTRN12616000535471.

Pharmacological Inhibition of CETP (Cholesteryl Ester Transfer Protein) Increases HDL (High-Density Lipoprotein) That Contains ApoC3 and Other HDL Subspecies Associated With Higher Risk of Coronary Heart Disease.

OBJECTIVE: Plasma total HDL (high-density lipoprotein) is a heterogeneous mix of many protein-based subspecies whose functions and associations with coronary heart disease vary. We hypothesize that increasing HDL by CETP (cholesteryl ester transfer protein) inhibition failed to reduce cardiovascular disease risk, in part, because it increased dysfunctional subspecies associated with higher risk such as HDL that contains apoC3. Approach and Results: We studied participants in 2 randomized, double-blind, placebo-controlled trials of a CETP inhibitor on a background of atorvastatin treatment: ACCENTUATE (The Addition of Evacetrapib to Atorvastatin Compared to Placebo, High Intensity Atorvastatin, and Atorvastatin With Ezetimibe to Evaluate LDL-C Lowering in Patients With Primary Hyperlipidemia; 130 mg evacetrapib; n=126) and ILLUMINATE (Phase 3 Multi Center, Double Blind, Randomized, Parallel Group Evaluation of the Fixed Combination Torcetrapib/Atorvastatin, Administered Orally, Once Daily [Qd], Compared With Atorvastatin Alone, on the Occurrence of Major Cardiovascular Events in Subjects With Coronary Heart Disease or Risk Equivalents; 60 mg torcetrapib; n=80). We measured the concentration of apoA1 in total plasma and 17 protein-based HDL subspecies at baseline and 3 months. Both CETP inhibitors increased apoA1 in HDL that contains apoC3 the most of all HDL subspecies (median placebo-adjusted percent increase: evacetrapib 99% and torcetrapib 50%). They also increased apoA1 in other HDL subspecies associated with higher coronary heart disease risk such as those involved in inflammation (α-2-macroglobulin and complement C3) or hemostasis (plasminogen), and in HDL that contains both apoE and apoC3, a complex subspecies associated with higher coronary heart disease risk. ApoA1 in HDL that contains apoC1, associated with lower risk, increased 71% and 40%, respectively. Only HDL that contains apoL1 showed no response to either drug. CONCLUSIONS: CETP inhibitors evacetrapib and torcetrapib increase apoA1 in HDL subspecies that contain apoC3 and other HDL subspecies associated with higher risk of coronary heart disease. Subspecies-specific effects shift HDL subspecies concentrations toward a profile associated with higher risk, which may contribute to lack of clinical benefit from raising HDL by pharmaceutical CETP inhibition.

MicroRNA-34a in coronary heart disease: Correlation with disease risk, blood lipid, stenosis degree, inflammatory cytokines, and cell adhesion molecules.

BACKGROUND: MicroRNA-34a (miR-34a) plays an essential role in regulating blood lipid, inflammation, cell adhesion molecules, and atherosclerosis, the latter factors are closely involved in the etiology of coronary heart disease (CHD). However, the clinical value of miR-34a in CHD patients' management is rarely reported. Hence, this study aimed to assess the correlation of miR-34a with disease risk, blood lipid, coronary artery stenosis, inflammatory cytokines, and cell adhesion molecules of CHD. METHODS: A total of 203 CHD patients and 100 controls were recruited in this study, then their plasma samples were collected to detect the miR-34a by reverse transcription quantitative polymerase chain reaction. Furthermore, serum samples from CHD patients were obtained for inflammatory cytokines and cell adhesion molecule measurement by enzyme-linked immunosorbent assay. RESULTS: MiR-34a was elevated in CHD patients compared to controls (p < 0.001) and it disclosed a good diagnostic value of CHD (area under curve: 0.899, 95% confidence interval: 0.865-0.934). Besides, miR-34a positively correlated with triglyceride (p < 0.001), total cholesterol (p = 0.022) and low-density lipoprotein cholesterol (p = 0.004), but not with high-density lipoprotein cholesterol (p = 0.110) in CHD patients. Moreover, miR-34a associated with Gensini score in CHD patients (p < 0.001). As to inflammation-related indexes and cell adhesion molecules, MiR-34a expression was positively linked with C-reactive protein (p < 0.001), tumor necrosis factor alpha (p = 0.005), interleukin (IL)-1ß (p = 0.020), IL-17A (p < 0.001), vascular cell adhesion molecule-1 (p < 0.001), and intercellular adhesion molecule-1 (p = 0.010) in CHD patients, but not with IL-6 (p = 0.118) and IL-10 (p = 0.054). CONCLUSION: MiR-34a might serve as a biomarker in assistance of diagnosis and management of CHD.

LncRNA UCA1, miR-26a, and miR-195 in coronary heart disease patients: Correlation with stenosis degree, cholesterol levels, inflammatory cytokines, and cell adhesion molecules.

BACKGROUND: Long noncoding RNA urothelial cancer-associated 1 (lnc-UCA1) targets microRNA-26a (miR-26a) and microRNA-195 (miR-195) to participate in coronary heart disease (CHD) progression via regulation of vascular smooth muscle cell and microvascular endothelial cell viability and mobility. Therefore, this study set out to further explore the relationship between lnc-UCA1 and miR-26a and miR-195, along with their roles in the management of patients with CHD. METHODS: One hundred and thirty-six CHD patients and 70 age-/gender-matched controls were recruited in this case-control study. Their peripheral blood mononuclear cell samples were collected for lnc-UCA1, miR-26a, and miR-195 measurement. Furthermore, serum samples from CHD patients were obtained for inflammatory cytokines and cell adhesion molecules measurement. The Gensini score was used to evaluate the stenosis severity in CHD patients. RESULTS: Lnc-UCA1 expression tend to be increased, while miR-26a and miR-195 expressions were reduced in patients with CHD compared to that of controls (all p < 0.001). In CHD patients, lnc-UCA1 was negatively correlated with miR-26a (p < 0.001) and miR-195 (p = 0.014). Besides, lnc-UCA1 was positively correlated with Gensini score (p < 0.001), total cholesterol (p = 0.019), low-density lipoprotein cholesterol (p = 0.002), and C-reactive protein (p < 0.001), while miR-26a (p < 0.001) and miR-195 (p = 0.002) were negatively correlated with Gensini score. What's more, lnc-UCA1 was positively correlated with tumor necrosis factor (TNF)-α (p = 0.004), interleukin (IL)-1ß (p = 0.041), vascular cell adhesion molecule-1 (VCAM-1) (p = 0.010), and intercellular adhesion molecule-1 (ICAM-1) (p < 0.001). While miR-26a was negatively correlated with some of the individual inflammatory cytokines and cell adhesion molecules. CONCLUSION: Lnc-UCA1, miR-26a, and miR-195 may serve as potential biomarkers for CHD management.

Analysis of Coronary Artery Lesion Degree and Related Risk Factors in Patients with Coronary Heart Disease Based on Computer-Aided Diagnosis of Coronary Angiography.

A combination of various risk factors results in the development of coronary heart disease. The earlier that one identifies and deals with reversible risk factors for coronary heart disease, the greater the chance of recovery. The main goal of this research is to learn whether risk variables are associated with greater extent of coronary artery disease in people with coronary heart disease. This article selects 290 patients who had had coronary angiography in our hospital from September 2018 to March 2019 using a retrospective research and analytic methodology. Coronary angiography split the patients into two groups: those with coronary heart disease and those without. To determine the correlation between risk factors and a score related to heart disease, computer-aided statistical analysis of data about the differences in those risk factors was performed. The results were analyzed using the Spearman correlation and partial correlation, and the relationship between risk factors and Gensini score was analyzed by multiple linear regression. For the analysis, binary logistic regression was used to calculate the correlation between the risk factors of coronary heart disease and the probability of developing coronary heart disease. The findings concluded that increased age, smoking, elevated hs-CRP, HbA1c, hypertension, diabetes, and hyperuricemia are all contributors to coronary heart disease. Coronary heart disease is an independent risk factor for this condition. Many of the factors that play a role in the long-term development of the severity of coronary artery disease, such as hypertension, diabetes, smoking, elevated hs-CRP, decreased HDL-C, raised LDL-C, and TG, are commonly found in men. hs-CRP is the primary risk factor for the degree of coronary artery stenosis and could contribute to the progression of the condition by playing a major role in creating more stenosis.

Comparison of risk factors for ischemic stroke and coronary events in a population-based cohort.

BACKGROUND: Although coronary events (CE) and ischemic stroke share many risk factors, there are also some important differences. The aim of this paper was to assess the association of risk factors in relation to incident CE and ischemic stroke and to evaluate the heterogeneity in patterns of risk factors between the two outcomes. METHOD: Traditional risk factors and inflammatory markers associated with coronary events and ischemic stroke were measured in the Malmö Diet and Cancer Cohort (MDCS, n = 26 519), where a total of 2270 incident ischemic stroke and 3087 incident CE occurred during a mean follow up time 19 ± 6 years, and in relation to inflammatory markers in the cardiovascular sub-cohort (MDC-CV, n = 4795). Cox regression analysis was used to obtain hazard ratios. A modified Lunn-McNeil competing risk analysis was conducted to assess the significance of any differences in risk profiles of these outcomes. RESULTS: Most cardiovascular risk factors were associated both with incident CE and ischemic stroke. However, current smoking, ApoB, low ApoA1, male sex and education level of ≤ 9 years of schooling were preferentially associated with CE compared to ischemic stroke. Conversely, age showed a stronger association with ischemic stroke than with CE. CONCLUSION: CE and ischemic stroke have broadly similar risk factors profiles. However, there are some important differential associations, as well as substantial differences in the magnitude of the association. These could reflect the distinct biology of atherogenesis in different vascular beds. The difference in the determinants highlights the importance of looking at CE and ischemic stroke, two manifestations of cardiovascular disease, separately.

Associations of serum androgens with coronary heart disease and interaction with age: The Henan Rural Cohort Study.

BACKGROUND AND AIMS: We aimed to investigate the associations of testosterone and androstenedione with coronary heart disease, and the interaction effect of testosterone or androstenedione and age on coronary heart disease. METHODS AND RESULTS: A total of 6178 participants were included in this study. Serum testosterone and androstenedione were detected by liquid chromatography-tandem mass spectrometry. Logistic regression and restricted cubic splines were used to assess the independent effects of testosterone and androstenedione on coronary heart disease. Interactive plots were employed to examine the interaction effects of testosterone or androstenedione with age on coronary heart disease. After adjusting for multiple variables, serum testosterone and androstenedione levels were negatively associated with coronary heart disease in males (tertile 3 vs tertile 1, odd ratio (OR) = 0.56, 95% confidence interval (CI) (0.33, 0.96), and OR = 0.40, 95% CI (0.22, 0.74)). Per 1 unit increase in ln-testosterone and ln-androstenedione was associated with a 24% (OR = 0.76, 95% CI (0.63, 0.91)) and 30% (OR = 0.69, 95% CI (0.55, 0.86)) lower risk of coronary heart disease, respectively. Additionally, the positive association of age with coronary heart disease was attenuated by increasing concentrations of ln-testosterone and ln-androstenedione concentration in males. CONCLUSIONS: The results indicated that serum testosterone and androstenedione were negatively associated with coronary heart disease risk in Chinese rural males. To some extent, this study supports the application of hormone therapy in males with coronary heart disease, which can contribute to reducing the burden of coronary heart disease and related cardiovascular disease.

Validation of lipid-related therapeutic targets for coronary heart disease prevention using human genetics.

Drug target Mendelian randomization (MR) studies use DNA sequence variants in or near a gene encoding a drug target, that alter the target's expression or function, as a tool to anticipate the effect of drug action on the same target. Here we apply MR to prioritize drug targets for their causal relevance for coronary heart disease (CHD). The targets are further prioritized using independent replication, co-localization, protein expression profiles and data from the British National Formulary and clinicaltrials.gov. Out of the 341 drug targets identified through their association with blood lipids (HDL-C, LDL-C and triglycerides), we robustly prioritize 30 targets that might elicit beneficial effects in the prevention or treatment of CHD, including NPC1L1 and PCSK9, the targets of drugs used in CHD prevention. We discuss how this approach can be generalized to other targets, disease biomarkers and endpoints to help prioritize and validate targets during the drug development process.

Low-/high-density lipoprotein cholesterol ratio and carotid plaques in patients with coronary heart disease: a Chinese cohort study.

BACKGROUND: Evidence on the relationship between the low-/high-density lipoprotein cholesterol ratio (LDL-C/HDL-C) and carotid plaques remains limited. This study aimed to examine the association between LDL-C/HDL-C and carotid plaques in participants with coronary heart disease (CHD) and to further explore the extent to which a healthy lifestyle reduces the risk of LDL-C/HDL-C-related carotid plaques. METHODS: This large-scale and multi-centre retrospective study included 9426 CHD patients (aged 35-75 years) between January 1, 2014 and September 30, 2020. The LDL-C/HDL-C values were converted to the following tertiles: lowest (< 2.15), middle (2.15-3), and highest (> 3). Healthy lifestyle-related factors referred to whether or not the participant was a non-smoker and non-drinker. Participants were divided into an unfavourable group (those who did not adhere to healthy lifestyle factors), intermediate (only one unhealthy factor), and favourable (neither of the two unhealthy factors). Logistic regression was used for statistical analyses. RESULTS: Of the 9426 participants, 6989 (74.15%) CHD patients had carotid plaques. After adjustment for confounders, each unit increase in the LDL-C/HDL-C was significantly associated with carotid plaques (OR: 1.61; 95%CI: 1.43-1.84; P <  0.001). Multivariate logistic regression revealed that carotid plaques risk for the highest tertile (> 3) was 1.18 times that of the lowest quartile (< 2.15). Compared with an unfavourable lifestyle, an intermediate or a favourable lifestyle was associated with a significant 30% (OR: 0.70; 95%CI: 0.64-0.78; P <  0.001) or 67% (OR: 0.33; 95%CI: 0.29-0.37; P <  0.001) reduction in carotid plaques risk, respectively, among CHD patients with high LDL-C/HDL-C. There were significantly additive and multiplicative interactions between lifestyle and LDL-C/HDL-C with regards to carotid plaques. CONCLUSION: A high LDL-C/HDL-C is associated with a risk of carotid plaques developing in CHD patients. Adhering to a healthy lifestyle has additive beneficial effects on reducing the risk of carotid plaques, especially in relation to the highest LDL-C/HDL-C.

Low vitamin K status, high sclerostin and mortality risk of stable coronary heart disease patients.

Aim: We explored whether matrix Gla protein (MGP, natural calcification inhibitor) and sclerostin (glycoprotein responsible for osteoblast differentiation) interact in terms of mortality risk in coronary patients. Methods: 945 patients after myocardial infarction and/or coronary revascularization were followed in a prospective study. All-cause death, fatal or nonfatal cardiovascular events and heart failure hospitalizations were registered. Results: Either high desphospho-uncarboxylated MGP (dp-ucMGP) or high sclerostin were independently associated with 5-year all-cause/cardiovascular mortality. However, we observed an additional mortality risk in the coincidence of both factors. Concomitantly high dp-ucMGP (≥884 pmol/l) plus sclerostin (≥589 ng/l) were associated with increased all-cause mortality risk compared with 'normal' concentrations of both factors (HRR 3.71 [95% CI: 2.07-6.62, p < 0.0001]), or if only one biomarker has been increased. A similar pattern was observed for fatal, but not for nonfatal cardiovascular events. Conclusion: Concomitantly high MGP and sclerostin indicate increased mortality risk, which probably reflects their role in cardiovascular calcifications.

Risk Factors Associated with an Increased Risk of Deep Sternal Wound Infections in Patients After Coronary Artery Bypass Grafting and Heart Defect Surgery.

BACKGROUND: Despite improvements over time with regard to morbidity, mortality, and long-term survival, deep sternal wound infection (DSWI) continues to be a major complication after open-heart surgery. This is why it is important to identify possible risk factors for postoperative development of DSWI in patients undergoing coronary artery bypass grafting and valve replacement. The aim of this study was to identify the risk factors for postoperative development of deep sternal wound infection in patients after coronary artery bypass grafting and heart defect surgery at the Department of Thoracic, Cardiac, and Vascular Surgery of the Hospital of Lithuanian University of Health Sciences. METHODS: This retrospective study analyzed 201 patients, who underwent coronary artery bypass grafting and heart defect surgery between January 2017 and December 2018. The case group contained 45 patients, who had to be reoperated because of deep sternal wound infection, and the control group consisted of 156 randomly selected patients. For descriptive statistics, we used means, median values, ranges, standard deviations, and 95% confidence intervals, where appropriate. Categorical data were analyzed using the chi-square or Fisher's exact test. Student T-test and Mann-Whitney used to compare numerical variables. Logistic regression model adjusting for age and gender was used to compare the risk of infection. A P-value of < 0.05 was considered to be statistically significant. SPSS 26.0 was used for calculations. RESULTS: Logistic regression analysis revealed that independent risk factors for sternal wound infection were high BMI (odds ratio [OR] 1.15, CI 1.06-1.24), preoperative CRP (OR 1.08, CI 1.01-1.16), long duration of cardiopulmonary bypass (OR 1.02, CI 1.01-1.03), intraoperative anemia (OR 0.97, CI 0.95-0.99), and postoperative CRP concentration (OR 1.10; CI 1.05-1.16). CONCLUSIONS: Preoperative assessment to identify obese individuals as being at risk and techniques to minimize the duration of surgery and intraoperative blood loss may help reduce postoperative deep sternal wound infections.

CD133+ Stem Cell Therapy Effects on Myocardial Regeneration Through Increased Vascular Endothelial Growth Factor Correlate with Cardiac Magnetic Resonance Imaging Results in Coronary Artery Bypass Graft Surgery Patients with Low Ejection Fraction.

BACKGROUND: Stem cell implantation has become a promising therapy for heart failure due to coronary heart disease (CHD). CD133+ stem cell therapy, together with increases of vascular endothelial growth factor (VEGF) and other growth hormones, can induce myocardial repair. OBJECTIVE: To prove that VEGF plays a role in cardiac regeneration. METHODS: Twenty-six patients with CHD and ejection fractions <35% from Harapan Kita Heart and Vascular Center, Jakarta, Indonesia, from 2016 to 2018 were randomized into 2 groups. The treatment group underwent coronary artery bypass graft (CABG) + CD133+ implantation, and the control group underwent CABG only. Six months later, perfusion and myocardial function were assessed by ejection fraction, wall motion score index (WMSI), ventricular dimensions, and scar size using cardiovascular magnetic resonance imaging. VEGF was assessed with enzyme-linked immunosorbent assay. RESULTS: There was significant improvement in ejection fraction (8.69% ± 9.49% versus 1.43% ± 7.87%, P = .04), WMSI (0.51 ± 0.48 versus -0.01 ± 0.21, P = .003), and scar size (25.46 ± 12.91 versus 27.32  ± 12.92 mm, P = .047) and a significant increase in blood VEGF levels  (61.05 ± 63.01 versus 19.88 ± 33.78 pg/mL, P = .01). Improvements in perfusion defects (13.69 ± 5.03 versus 11.53 ± 5.81 P = .32) and ventricular dimensions (-27.59 ± 84.48 versus -19.08 ± 36.79 mm, P = .06) were not statistically significant. CONCLUSION: CD133+ stem cell implantation improves myocardial function. The increase in VEGF levels is expected to continue improving restoration of myocardial function when myocardial perfusion improvement is still not optimal.

Prevalence of dyslipidemia and gene polymorphisms of ABCB1 and SLCO1B1 in Han, Uygur, Kazak, Hui, Tatar, Kirgiz, and Sibe populations with coronary heart disease in Xinjiang, China.

BACKGROUND: Dyslipidemia is a predisposing factor for coronary heart disease (CHD). High-intensity statin therapy is recommended as secondary prevention. ABCB1 and SLCO1B1 genes influence the efficacy and safety of statins. Xinjiang is a multi-ethnic area; however, little is known about the prevalence of dyslipidemia and gene polymorphisms of ABCB1 and SLCO1B1 in minority groups with CHD. OBJECTIVE: To measure levels of lipid and apolipoprotein and the prevalence of dyslipidemia and gene polymorphisms of ABCB1, SLCO1B1 in Han, Uygur, Kazak, Hui, Tatar, Kirgiz, and Sibe populations with CHD in Xinjiang. METHODS: This descriptive retrospective study compares lipid levels in ethnic groups using Kruskal-Wallis test or analysis of variance. The study compared gene polymorphisms and the prevalence of dyslipidemia among different ethnic groups using the chi-square test. The lipid profiles in plasma were measured before lipid-lowering therapy using commercially available kits. Genotyping of SLCO1B1 and ABCB1 variants was performed using sequencing by hybridization. RESULTS: A total of 2218 patients were successfully screened, including 1044 Han, 828 Uygur, 113 Kazak, 138 Hui, 39 Tatar, 36 Kirgiz, and 20 Sibe patients. The overall mean age was 61.8 ± 10.8 years, and 72.5% of participants were male. Dyslipidemia prevalence in these ethnic groups was 42.1, 49.8, 52.2, 40.6, 48.7, 41.7, and 45.0%, respectively. The prevalence of dyslipidemia, high total cholesterol (TC), high triglycerides (TG), and high low density lipoprotein cholesterol (LDL-C) differed significantly among the groups (P = 0.024; P < 0.001; P < 0.001; P < 0.001, respectively). For the Han group, high LDL-C, high TC, and high TG prevalence differed significantly by gender (P = 0.001, P = 0.022, P = 0.037, respectively). The prevalence of high TC, high TG, and low high density lipoprotein cholesterol (HDL-C) differed significantly by gender in the Uygur group (P = 0.006, P = 0.004, P < 0.001, respectively). The prevalence of high TC in Hui patients significantly differed by gender (P = 0.043). These findings suggest that polymorphisms in ABCB1 and C3435T differ significantly across ethnicities (P < 0.001). CONCLUSIONS: The prevalences of dyslipidemia, high TC, high TG, and high LDL-C in Han, Uygur, Kazak, Hui, Tatar, Kirgiz, and Sibe CHD patients in Xinjiang differed concerning ethnicity. Ethnic, gender, and lifestyle were the key factors that affected the lipid levels of the population. The prevalence of polymorphisms of ABCB1 and C3435T significantly differed across ethnicities. These findings will aid the selection of precision lipid-lowering medications and prevention and treatment of CHD according to ethnicity in Xinjiang.

Polygenic Risk Score to Identify Subclinical Coronary Heart Disease Risk in Young Adults.

BACKGROUND: Polygenic risk scores (PRS) may enhance risk stratification for coronary heart disease among young adults. Whether a coronary heart disease PRS improves prediction beyond modifiable risk factors in this population is not known. METHODS: Genotyped adults aged 18 to 35 years were selected from the CARDIA study (Coronary Artery Risk Development in Young Adults; n=1132) and FOS (Framingham Offspring Study; n=663). Systolic blood pressure, total and HDL (high-density lipoprotein) cholesterol, triglycerides, smoking, and waist circumference or body mass index were measured at the visit 1 exam of each study, and coronary artery calcium, a measure of coronary atherosclerosis, was assessed at year 15 (CARDIA) or year 30 (FOS). A previously validated PRS for coronary heart disease was computed for each subject. The C statistic and integrated discrimination improvement were used to compare improvements in prediction of elevated coronary artery calcium between models containing the PRS, risk factors, or both. RESULTS: There were 62 (5%) and 93 (14%) participants with a coronary artery calcium score >20 (CARDIA) and >300 (FOS), respectively. At these thresholds, the C statistic changes of adding the PRS to a risk factor-based model were 0.015 (0.004-0.028) and 0.020 (0.001-0.039) in CARDIA and FOS, respectively. When adding risk factors to a PRS-based model, the respective changes were 0.070 (0.033-0.109) and 0.051 (0.017-0.079). The integrated discrimination improvement, when adding the PRS to a risk factor model, was 0.027 (-0.006 to 0.054) in CARDIA and 0.039 (0.0005-0.072) in FOS. CONCLUSIONS: Among young adults, a PRS improved model discrimination for coronary atherosclerosis, but improvements were smaller than those associated with modifiable risk factors.

The Role of Galectin-3 and ST2 in Cardiology: A Short Review.

Galectin-3 is a lectin that binds beta-galactosides. It is involved in cardiac remodeling and fibrosis through the activation of macrophages and fibroblasts. ST2 is secreted by myocardial cells due to cardiac overload. These two biomarkers have been traditionally studied in the field of heart failure to guide medical therapy and detect the progression of the disease. Nevertheless, there are novel evidences that connect galectin-3 and ST2 with coronary heart disease and, specifically, with atrial fibrillation. The aim of this article is to concisely review the diagnostic and prognostic role of galectin-3 and ST2 in different cardiac diseases.