Stable Coronary Heart Disease Research Articles

Sample size estimation for stratified cluster randomization trial with survival endpoint.

Cluster randomization trials with survival endpoint are predominantly used in drug development and clinical care research when drug treatments or interventions are delivered at a group level. Unlike conventional cluster randomization design, stratified cluster randomization design is generally considered more effective in reducing the impacts of imbalanced baseline prognostic factors and varying cluster sizes between groups when these stratification factors are adopted in the design. Failure to account for stratification and cluster size variability may lead to underpowered analysis and inaccurate sample size estimation. Apart from the sample size estimation in unstratified cluster randomization trials, there are no development of an explicit sample size formula for survival endpoint when a stratified cluster randomization design is employed. In this article, we present a closed-form sample size formula based on the stratified cluster log-rank statistics for stratified cluster randomization trials with survival endpoint. It provides an integrated solution for sample size estimation that account for cluster size variation, baseline hazard heterogeneity, and the estimated intracluster correlation coefficient based on the preliminary data. Simulation studies show that the proposed formula provides the appropriate sample size for achieving the desired statistical power under various parameter configurations. A real example of a stratified cluster randomization trial in the population with stable coronary heart disease is presented to illustrate our method.

THE VALUE OF HOLTER MONITORING AND THE LEVEL OF SYSTEMIC INFLAMMATION IN PATIENTS WITH STABLE ISCHEMIC HEART DISEASE COMBINED WITH TYPE 2 DIABETES, DEPENDING ON THE NUMBER OF AFFECTED CORONARY ARTERIES

Diabetes mellitus (DM) is one of the significant medical and social problems of modern society, which is due to high morbidity and prevalence, frequent occurrence of chronic micro- and macrovascular complications. Coronary heart disease (CHD) in patients with type 2 diabetes is 2-4 times more common than in people of the same age without diabetes [1]. In the absence of apparent signs of atherosclerosis, the risk of developing coronary artery disease in the next 10 years is 30% [2]. To date, the course and prognosis of this group of patients have not been sufficiently studied, objective clinical and diagnostic criteria for the development of complications of myocardial infarction have not been developed, and the problem of choosing pathogenetically based methods of treatment of CHD in combination with type 2 diabetes remains unresolved [3].The aim of the work was to investigate the informativeness of Holter monitoring (HM), the correlation of HM indicators, C-reactive protein (CRP) and carbohydrate metabolism in patients with stable coronary heart disease (CHD) in combination with type 2 diabetes for the prognosis of the course of this pathology, timely individual treatment and prevention occurrence of endpoints.Material and methods. The study involved 95 patients with coronary heart disease with angina pectoris functional class (FC) III and heart failure (HF FC III with a preserved left ventricular ejection fraction (LVEF); of them, 60 patients had concomitant type 2 DM in the compensation stage.Results. In patients with comorbidity (a combination CHD and type 2 diabetes), episodes of ST depression/elevation, tachycardia, and extrasystoles were more often registered in patients with multivessel lesions of CA (р<0.05), according to HM; the content of CRP in blood serum increased in proportion to the severity of the course of the disease, which depended on the number of affected CA.Conclusions. The nature and severity of the course of CHD correlate with comorbid pathology and the number of CAs affected by atherosclerosis. In the case of multivessel damage, according to the data of clinical, functional and laboratory research, an aggressive progression of cardiac pathology was noted.

Network Motif Detection in the Network of Inflammatory Markers and Depression Symptoms among Patients with Stable Coronary Heart Disease: Insights from the Heart and Soul Study

Background. Network motif analysis is a technique used to explore recurrent and statistically significant subgraphs within a network. Applying a motif analysis to the complex network of inflammation and depression may yield nuanced insight into the specific interaction mechanisms between inflammatory markers and individual depression symptoms, which is our aim. Methods. This cross-sectional study is based on patients with stable coronary heart disease (CHD). A partial correlation network was initially constructed to link inflammatory markers, including C-reactive protein (CRP), Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), individual depression symptoms, and covariates. A network-centric approach searched all possible non-isomorphic subgraph patterns of size k = 4 in the network. Results. Although CRP, IL-6, and TNF-α displayed an insignificant association with specific depression symptoms, the motif analysis revealed various subgraph patterns of interactions between depression symptoms associated with MCP-1. Generally, MCP-1 formed a closed loop with psychomotor problems and sleep disturbances, and this configuration was connected in various forms with other symptoms, particularly cognitive (e.g., feelings of worthlessness, concentration difficulty, and suicidal ideation) and neurovegetative/somatic (e.g., appetite changes and fatigue) symptoms. Moreover, MCP-1 was frequently associated with a closed-loop triangle comprising cognitive and neurovegetative/somatic symptoms but not with mood symptoms (e.g., loss of interest and feelings of sadness). Conclusions. The findings provide insight into how MCP-1 may be involved in the pathology of depression among patients with stable CHD in a more precise manner. This study also proposes future directions for research on depression.

Association of FoxP3<sup>+</sup> T regulatory lymphocytes with epicardial adipose tissue thickness in patients with coronary heart disease

Background. Increase ofthe epicardial adipose tissue (EAT) thickness isassociated with development of inflammation and cardiovascular complications, however, there is no data on the relationship between EAT thickening and the number of immunosuppressive regulatory T lymphocytes.The aim. To study the number of circulating T regulatory lymphocytes and nuclear translocation ofthe FoxP3 transcription factor in patients with stable coronary heart disease (CHD) depending on the epicardial adipose tissue thickness.Materials and methods. We examined 30 patients with chronic stable CHD. The EAT thickness was measured by echocardiography. Patients were divided into groups depending on the presence and absence of EAT thickening above 5 mm (groups 1 and 2, respectively). Imaging flow cytometry was used to determine the number of T regulatory lymphocytes and the level of FoxP3 nuclear translocation. The concentration of cytokines and high sensitivity C-reactive protein (hsCRP) was determined using enzyme-linked immunosorbent assay in blood serum.Results. Anthropometric indicators of obesity and the severity of atherosclerosis were comparable between groups. In group 2, there was an increase in low-density lipoprotein cholesterol concentration (p = 0.043), ratio of low-density lipoprotein cholesterol tohigh-density lipoprotein cholesterol (p = 0.017) and the concentration ofhsCRP (p = 0.044) andIL-1β (p = 0.005), adecrease in the number and relative count of Tregulatory lymphocytes (p = 0.020 andp = 0.026, respectively), aswellas thenumber of cells withFoxP3 nuclear translocation (p = 0.018) compared togroup1. According tomultiple logistic regression, the concentration ofhsCRP, IL-1β and T regulatory lymphocytes relative count in total were the predictors of EAT thickening (accuracy 80 %; sensitivity 75 %; specificity 84,6 %; AUC = 0.89).Conclusions. Thickening of epicardial adipose tissue inpatients withcoronary heart disease is associated with a decrease in the number of T regulatory lymphocytes andFoxP3 nuclear translocation inthem in presence of comparable anthropometric parameters of obesity and the severity of coronary atherosclerosis.

How is inflammation biology truly associated with depression in patients with stable coronary heart disease?: Insights from the heart and Soul study

Depression is known to be associated with inflammation among patients with established coronary heart disease (CHD), but it is unclear whether this is due to individual depression symptoms or to the broader construct of depression. We addressed this gap by using moderated non-linear factor analysis (MNLFA) to determine the extent that inflammation is associated with latent depression and/or individual symptoms in this patient group. We evaluated 1,024 outpatients with stable CHD from the baseline cross-sectional data of the Heart and Soul Study. Depression was assessed using the 9-item Patient Health Questionnaire, while inflammation was evaluated via C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) levels. MNLFA is based on the concept of model parameter moderation with regard to individual characteristics. Using the MNLFA approach, we simultaneously tested for differences in (1) latent depression, (2) individual depression items, and (3) the factor loading of the item on latent depression as a function of inflammatory markers, with and without covariate adjustment. Higher TNF-α levels were associated with both higher levels of a latent depression factor and greater endorsement of an individual symptom (appetite changes). Increased CRP levels were significantly associated with greater appetite changes, lower concentration difficulty, and greater fatigue. Elevated IL-6 levels were only related to greater fatigue, while increased MCP-1 levels were linked to greater sleep disturbance. After adjusting for covariates, some associations became insignificant. Inflammatory markers were not consistent predictors of factor loadings. This study represents the initial step to discussing how inflammation biology is truly related to depression among patients with established CHD.

Post-COVID syndrome: status of carbohydrate metabolism in patients with hypertension and stable ischemic heart disease

Background. Post-COVID syndrome is associated with a wide range of chronic symptoms or conditions. Coronavirus di­sease 2019 (COVID-19) causes metabolic disorders such as hyperglycemia, insulin resistance. Insulin-like growth factor 1 (IGF-1) is associated with an impaired glucose tolerance and a higher risk of developing type 2 diabetes. Currently, the study of molecules regulating carbohydrate metabolism as potential biomarkers of post-COVID syndrome and targets for therapeutic influence is relevant. The purpose of the study was to assess the level of IGF-1 and its relationship with regulation of carbohydrate metabolism, as well as the dynamics of the evaluated indicators under the influence of drug treatment in patients with hypertension and stable coronary heart disease who suffered from COVID-19. Materials and methods. Fifty-five patients who had a mild and moderate COVID-19 were included in the study; their average age was 55.87 [40; 75] years. The results of routine laboratory tests were registered and analyzed. The content of insulin and IGF-1 was assessed by enzyme immunoassay. The HOMA-IR was calculated. Results. In patients with a mode­rate COVID-19 compared to those with a mild one, a significant decrease in the level of IGF-1 (р = 0.008) was found against the background of increased reference values of glucose, insulin, and HOMA-IR (р < 0.01). The influence of the degree of hypertension on the IGF-1 level was revealed (р = 0.004). An inverse relationship between IGF-1 and glucose level was noted (r = –0.28, p = 0.034). The use of meldonium contributed to a significant decrease in glucose and insulin content (p < 0.001), and an increase in IGF-1. Against the background of taking meldonium, the dynamics of the shift towards a decrease in the HOMA-IR was more significant. Conclusions. An inverse relationship was found between IGF-1 and blood glucose, regardless of the level of insulin and HOMA-IR, in patients with hypertension and stable ischemic heart disease in the post-COVID period. Meldonium has been shown to improve carbohydrate metabolism by normalizing insulin levels and redu­cing the phenomena of insulin resistance as a potential drug target. Meldonium improved the clinical course of ischemic heart disease and demonstrated good tolerability and safety.

The Influence of Coronavirus Infection on the Results of Percutaneous Coronary Intervention in Patients with Coronary Artery Disease

Objective — to determine the impact of coronavirus infection incidence on the post-procedural condition of patients after percutaneous coronary intervention (PCI). Materials and methods. This single-centre study was conducted at the «Ukrainian Children’s Cardiac Center, Clinic for Adults» from June 1, 2020, to December 31, 2021. A total of 158 patients participated, of whom 78 had a history of COVID-19 infection and 80 did not, all with stable obstructive coronary artery disease (CAD). All patients underwent PCI, and their long-term outcomes were evaluated within a 6-month period. The study endpoints included repeated myocardial revascularization (defined as narrowing of the stented lumen by more than 70 % in diameter or acute stent thrombosis) and an assessment of CAD progres­sion (formation or progression of atherosclerotic plaques compared to baseline coronary angio­graphy). Results and discussion. The frequency of repeated coronary angio in the first 6 months after PCI due to tension angina or acute coronary syndrome was equal to 10 (12.8 %) patients in the COVID-19 +-group and 3 (3.8 %) cases in the COVID-19 — –group (p < 0.05). According to the study data, patients with coronavirus infection tended to reach endpoints more quickly during the 6-month follow-up, in contrast to patients who did not have the incidence of COVID-19 during the same period. The frequency of repeated PCI within 6 months after the primary PCI in the group of patients with previous PCI was higher — 8 cases out of 78 patients compared to patients in the second group who did not suffer from COVID-19 in the first 6 months after the initial PCI (2 cases out of 80, c2 = 4 .0, p = 0.045). Conclusions. Patients with a mild and moderate course of coronavirus infection and existing stable coronary heart disease with atherosclerotic lesions of the coronary arteries were more likely to undergo repeat PCI within 6 months of the initial PCI. The most common causes of repeat PCI in patients with previous COVID-19 were thrombosis and restenosis of the stent, as well as progression of stenosis at a site other than the location of the previous PCI.

PAR4 Antagonism in Patients With Coronary Artery Disease Receiving Antiplatelet Therapies.

BMS-986141 is a novel potent highly selective antagonist of PAR (protease-activated receptor) type 4. PAR4 antagonism has been demonstrated to reduce thrombus formation in isolation and in combination with factor Xa inhibition in high shear conditions in healthy people. We sought to determine whether PAR4 antagonism had additive antithrombotic effects in patients with coronary artery disease who were receiving antiplatelet therapy. Forty-five patients with stable coronary heart disease and 10 healthy volunteers completed a phase 2a open-label 4-arm single-center study. Patients were allocated to 1 of 3 treatment arms for 7 days: (1) ticagrelor (90 mg BID), (2) aspirin (75 mg QD), or (3) the combination of ticagrelor and aspirin. Agonist-induced platelet aggregation, platelet activation, and ex vivo thrombus formation were measured before and 2 and 24 hours after a single oral 4-mg dose of BMS-986141 on the first study visit day in all participants. BMS-986141 demonstrated highly selective inhibition of PAR4-AP (agonist peptide)-induced platelet aggregation, P-selectin expression, and platelet-monocyte aggregate expression (P≤0.001 for all), which were unaffected by concomitant antiplatelet therapies. PAR4 antagonism reduced ex vivo thrombus area in high shear conditions in healthy volunteers (-21%; P=0.001) and in patients receiving ticagrelor alone (-28%; P=0.001), aspirin alone (-23%; P=0.018), or both in combination (-24%; P≤0.001). Plasma concentration of BMS-986141 correlated with PAR4-AP-induced platelet responses (P≤0.001 for all) and total thrombus area under high shear stress conditions (P≤0.01 for all). PAR4 antagonism has additive antithrombotic effects when used in addition to ticagrelor, aspirin, or their combination, in patients with stable coronary heart disease. URL: https://www.clinicaltrials.gov; Unique identifier: NCT05093790.

Clinical role of triggers and modulation factors of ventricular arrhythmogenesis in stable coronary artery disease

Ventricular arrhythmias are more commonly associated with coronary artery disease. However, ventricular arrhythmogenesis can be initiated by various trigger factors against its background. The substrate of arrhythmias in various nosological forms of stable coronary heart disease is heterogeneous. The patient may have stable exertional angina without severe fibrosis or have a history of myocardial infarction with significant scarring. Therefore the predictive value and prognostic significant of ventricular arrhythmias is not always unambiguous. Thus, for the successful treatment of arrhythmias as a main component of the prevention of sudden cardiac death, an individualized pathogenetic approach is the most important. The purpose of this article is to analyze and clinically interpret the results of studies, publications for 1980-2023, in which the authors describe the etiological, pathophysiological, pathomorphological characteristics of ventricular arrhythmias and their predictive value and prognostic significant for patients with stable coronary artery disease.

White blood cell counts can predict 4-year cardiovascular disease risk in patients with stable coronary heart disease: a prospective cohort study.

The prevalence of cardiovascular disease has increased sharply in the Asian population, and evaluation of the risk of cardiovascular events with stable coronary heart disease remains challenging. The role of white blood cell (WBC) count in assisting clinical decision-making in this setting is still unclear. This study sought to evaluate the prognostic meaning of WBC count among patients with stable coronary heart disease. This study included Asian participants (n = 1,933) from the prospective STABILITY (Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Therapy) trial, which involved 15,828 patients with stable coronary heart disease with 3-5 years of follow-up on optimal secondary preventive treatment. WBC count was measured at baseline. Associations between WBC count and cardiovascular outcomes were evaluated by Cox regression analyses with multivariable adjustments. Hematologic emergencies in patients may introduce potential bias. In the lower WBC count quartiles, patients had lower-risk clinical profiles. Higher WBC counts were associated with greater event probabilities for cardiovascular death, major cardiovascular events, or all-cause death. In Cox regression models, WBC counts were an independent predictor of major adverse cardiovascular events (OR = 2.445, 95% CI 1.427-4.190, P = 0.001) for the primary outcomes. For the secondary outcomes, including the composite of all-cause death, cardiovascular death, myocardial infarction, stroke, and hospitalization for heart failure, WBC counts were significantly predictive of events with similar magnitude (OR = 1.716, 95% CI 1.169-2.521, P = 0.006). In patients with stable coronary heart disease, higher WBC counts were associated with a heightened risk for the primary or secondary outcomes. https://clinicaltrials.gov/; Unique identifier NCT00799903.

СИСТЕМНОЕ ВОСПАЛЕНИЕ У БОЛЬНЫХ СО СТАБИЛЬНОЙ ИШЕМИЧЕСКОЙ БОЛЕЗНЬЮ СЕРДЦА В ПОСТКОВИДНОМ ПЕРИОДЕ В ЗАВИСИМОСТИ ОТ ТЯЖЕСТИ ПЕРЕНЕСЕННОЙ COVID-19

Background. In the post-covid period, systemic inflammation plays an important role in the development of coronary heart disease (CHD) and has a significant impact on the cardiovascular system by improving inflammatory responses, which may lead to progression of atherosclerosis, worsen the condition, and increase the likelihood of complications in patients with stable CHD. Objective. To evaluate clinical and laboratory indices of systemic inflammation in patients with stable coronary heart disease in the post-covid period depending on the severity of COVID-19. Material and methods. An observational descriptive study of two parallel groups including 416 patients with stable CHD who underwent COVID-19 more than 12 weeks ago was conducted. Patients were divided into two groups according to the severity of COVID-19 in the acute period. Group 1 included 203 patients (male 132 (65.3%), female 71 (34.7%)) aged 59.7±6.9 years who had mild SARS-CoV-2 infection; Group 2 included 213 patients (male 132 (62.0%), female 81 (38.0%)) aged 61.1±6.1 years who had moderate COVID-19. Monocyte chemoattractant protein-1 (MCP-1); vascular endothelial growth factor (VEGF); interleukins; interleukins (ILs): IL-1β, IL-4, IL-6, IL-8, IL-10, and IL-18 were determined by PCR. The C3 and C4 components of the complement system were also determined by the immunoturbidimetric method. Statistical calculations were performed in the RStudio software (version 2022.07.2+576, USA) in the R language (version 4.1.3 (2022-03-10), Austria). Results. Uncontrolled hypertension (p<0.001) and grade II obesity (p=0.005) were more frequent in the group of patients with stable CHD who underwent moderate COVID-19. In the same group, type 2 DM (p=0.031), atrial fibrillation (p = 0.029), and grade III angina pectoris (p=0.006) were more frequent, and Simpson's EF was lower (p<0.001) compared to the group of patients with mild SARS-CoV-2 infection. In patients with IBS who underwent COVID-19 of moderate severity, there was a statistically significant increase in the levels of pro-inflammatory cytokines - MCP-1, TNF-α, IL-1β (p<0.01) and the C3 component of the complement system (p=0.048) compared to patients with a mild course of infection in the acute period. In patients with stable coronary heart disease who underwent COVID-19, significant correlations were observed between the studied pro-inflammatory blood markers. Multiple and strongest associations were found for MCP-1, IL-10, IL-1β, IL-2, VEGF and the components of the complement system C3 and C4, which can be used as markers of the unfavorable course of the post-acute period in patients with IBS. Conclusion. Patients with stable CHD who underwent moderate SARS-CoV-2 infection are characterized by a higher incidence of uncontrolled AH, type 2 DM, and atrial fibrillation in the remote period. These patients also have higher levels of pro-inflammatory cytokines MCP-1, TNF-α and IL-1β, which correlate significantly with the severity of the disease and can serve as a predictor of its progression.

Effect of ivabradine on structural and functional changes of myocardium and NT-proBNP levels in patients with stable coronary heart disease after coronary stenting.

Aim: To investigate the effect of ivabradine on the hemodynamics and contractility of the myocardium and the features of NT-pro-BNP production in patients with stable ischemic heart disease after endovascular revascularization of the myocardium depending on the number of affected coronary arteries during 12 months of therapy. Materials and Methods: The object of the study was 120 patients with stable coronary artery disease: angina pectoris of functional class III with heart failure IIA FC III with preserved and moderately reduced ejection fraction of the left ventricle, who underwent coronary artery stenting. The examined patients were randomized according to the number of affected coronary vessels and the method of treatment. Results: Ivabradine in patients with stable ischemic heart disease after 12 months of therapy had a significant beneficial effect on the structural and functional parameters of the myocardium (contributed to the reverse remodeling of the left ventricle), which did not depend on the number of stented coronary arteries (p<0.05). In patients with stented one coronary artery, all structural and functional indicators of the heart after 12 months of treatment reached the values of practically healthy individuals from the control group. The use of ivabradine in patients with stable ischemic heart disease with heart failure with preserved and intermediate ejection fraction of the left ventricle after coronary stenting made it possible to ensure the correction of a number of clinical and pathogenetic links of the disease, which generally contributed to the improvement of metric and volumetric parameters of the heart. Conclusions: Ivabradine made it possible to significantly increase the effectiveness of standard therapy, which was manifested by a faster recovery of the geometry and contractility of the left ventricle. Therefore, the use of ivabradine along with standard therapy was appropriate for such a contingent of patients. The management of patients with stable coronary heart disease should combine adequate (surgical and pharmacological) treatment of the underlying disease, further individual medication correction of symptoms and circulatory disorders inherent in coronary heart disease and heart failure.

Варианты патогенетического лечения аспирининдуцированных гастроэнтеропатий у лиц с хронической ишемической болезнью сердца

Aim: Evaluation of Rebamipide treatment efficiency for aspirin-induced gastroduodenopathy in the patients with stable coronary heart disease (CHD). Design: Randomised controlled study. Materials and methods: In the course of the conducted research 340 CHD patients receiving long-term acetylsalicylic acid therapy in cardioprotective doses were studied. All the patients received complete clinical laboratory examination. For CHD verification there was applied selective method of coronary angiography. Gastroduodenopathy was verified by esophagogastroduodenoscopy. In both cases frequency and structure of the aforesaid events were assessed. For aspirin-induced gastroduodenopathy treatment there were applied either endogenic prostaglandin stimulant Rebamipide in combination with proton pump inhibitor (PPI) Pantoprazole (study group, n = 26) or Pantoprazole only (control group, n = 25). Prior to initiating therapy and on completion all the patients were taken blood samples for evaluation of prostaglandin E2 (PGE2) and proinflammatory cytokines (interleukine-1β Il-1β and interleukine-6 Il-6, TNF-α) levels in blood serum for verification of pathogenetic mechanisms in erosive or ulcer-bearing areas developing in gastrointestinal mucosa in association with long-term aspirin therapy. Соntrol group consisted of 26 CHD patients with no evidence of gastroduodenopathy. Statistical processing of the received data was conducted with the software program “Statistics 10.0”. Results. Aspirin-induced gastroduodenopathy was identified in 51 out of 340 (15,0%) cases. According to esophagogastroduodenoscopy data, erosions of the body and antrum of stomach were prevailing (43,1%) over all the erosive damages. CHD patients before the gastroduodenopathy treatment had significantly lower PGE2 levels in comparison with control group (p &lt; 0,01), while proinflammatory cytokines indices were higher (p &lt; 0,001). On the treatment completion 19 patients in the control group did not show endoscopic evidence of gastroduodenopathy, the laboratory findings tended to normalization. Gastric mucosa condition in the study group stabilized in all the cases, which was confirmed by statistically significant PGE2 level positive alterations (p &lt; 0,001) and also cytokine profile alterations (TNF-α: p &lt; 0,001; Il-1β and Il-6: p &lt; 0,01). Conclusion. The presented study demonstrates clinical features of aspirin-induced gastroduodenopathy development in the CHD patients and proposes possible ways of correction. Key words: aspirin-induced gastroduodenopathy, acetylsalicylic acid, prostaglandin E2, proinflammatory cytokines, rebamipide.

Heart failure biomarkers in revascularized patients with stable coronary heart disease as clinical outcome predictors.

The aim of this study was to investigate serum levels of galectin-3 (Gal-3) and N-terminal pro-brain Natriuretic Peptide (NT-proBNP) in patients with stable obstructive coronary artery disease, as well as their potential to predict clinical outcomes. This was a single-center cross-sectional cohort study. 168 patients were divided into three groups: percutaneous coronary intervention (PCI) group (N 64), coronary artery bypass graft surgery (CABG) group (N 57), and group with no coronary stenosis (N 47). Gal-3 and NT-proBNP levels were measured and the Syntax score (Ss) was calculated. The mean value of Gal-3 was 19.98 ng/ml and 9.51 ng/ml (p < 0.001) in the study group and control group, respectively. Highest value of Gal-3 was found in the group of subjects with three-vessel disease (p < 0.001). The mean value of NT-proBNP in the study group was 401.3 pg/ml, and in the control group 100.3 pg/ml (p = 0.159). The highest value of NT-proBNP was found in the group of subjects with three-vessel disease (p = 0.021). There was a statistically significant association between Gal-3, NT-proBNP and occurrence of adverse cardiovascular event (p = 0.0018; p = 0.0019). Gal-3 and NT-proBNP could be used as an additional tool for diagnosis and severity assessment of stable obstructive coronary artery disease. Furthermore, it could help identify high-risk patients who could experience major adverse cardiovascular events.

Psychological Distress and the Risk of Adverse Cardiovascular Outcomes in Patients With Coronary Heart Disease

BackgroundPsychological distress is a recognized risk factor in patients with coronary heart disease (CHD), but its clinical significance is unclear. ObjectivesThe purpose of this study was to determine if an index of psychological distress is independently associated with adverse outcomes and significantly contributes to risk prediction. MethodsPooled analysis of 2 prospective cohort studies of patients with stable CHD (N = 891). A psychological distress score was constructed using measures of depression, anxiety, anger, perceived stress, and post-traumatic stress disorder, measured at baseline. The study endpoint included cardiovascular death or first or recurrent nonfatal myocardial infarction or hospitalization for heart failure at 5.9 years. ResultsIn both cohorts, first and recurrent events occurred more often among those in the highest tertile of distress score than those in the lowest tertile. After combining the 2 cohorts, compared with the lowest tertile, the hazards ratio for having a distress score in the highest tertile was 2.27 (95% CI: 1.69-3.06), and for the middle tertile, it was 1.52 (95% CI: 1.10-2.08). Adjustment for demographics and clinical risk factors only slightly weakened the associations. When the distress score was added to a traditional clinical risk model, C-statistic, net reclassification index, and integrative discrimination index all significantly improved. ConclusionsAmong patients with CHD, a composite measure of psychological distress was significantly associated with an increased risk of adverse events and significantly improved risk prediction.

INCREASE MIGRATION OF PERIPHERAL BLOOD DERIVED ENDOTHELIAL PROGENITOR CELLS OF STABLE CORONARY ARTERY DISEASE PATIENT WITH ANGIOTENSIN CONVERTING ENZYME INHIBITORS

This research is based on refractory angina pectoris, which remains a problem despite advances in coronary heart disease treatment. Stem cell therapy is still in preclinical research stages to address refractory angina. Endothelial progenitor cells (EPCs) aid in improving endothelium and the growth of new blood vessels. Heart medication has shown to enhance both the quantity and function of EPCs in patients at cardiovascular risk or with heart disease. Previous studies reported that ACE inhibitors (ACEI) have a positive effect on EPCs. Thus, this study analyzes the impact of three different ACE inhibitors on EPC migration in laboratory conditions. Its aim is to ascertain the increase in EPC migration in stable coronary heart disease patients after ACEI administration. The research methodology involves an experimental design with a control group and post-treatment assessment only. Mononuclear cells are isolated from stable coronary heart disease patients' peripheral blood and incubated for 3 days. The EPCs are then divided into captopril, ramipril, lisinopril, and a control group, observed for 48 hours. EPC migration is assessed by counting the cells moving from the upper chamber to the membrane facing the lower chamber using a transwell migration assay after 20 hours, observed with a light microscope and Giemsa staining. Data analysis via ANOVA statistical tests indicates increased EPC migration in the captopril, ramipril, and lisinopril groups compared to the control. Captopril shows the highest effect among the groups, while no significant difference is observed between captopril and lisinopril, as well as between ramipril and lisinopril.

THE EFFECT OF PLATELET-RICH PLASMA ADMINISTRATION ON PROLIFERATION AND DIFFERENTIATION OF ENDOTHELIAL PROGENITOR CELLS IN PATIENTS WITH STABLE CORONARY HEART DISEASE

Endothelial Progenitor Cells (EPCs) are crucial precursors to endothelial cells, playing a key role in regulating blood vessel structure and maintaining homeostasis to protect against inflammation and thrombosis, contributing to stable coronary heart disease (CHD). Growth factors stimulate signal transduction during EPC proliferation and differentiation. Platelet-Rich Plasma (PRP) contains widely recognized growth factors in angiogenesis. Our research aimed to analyze PRP's effects on EPC proliferation and differentiation in stable CHD patients. Using an experimental post-test control group design, mononuclear cells (MNCs) from peripheral blood were cultured with M-199 medium, divided into PRP, Platelet Poor Plasma (PPP), and control groups, and incubated for 14 days. EPC proliferation was quantified with CD34 markers using ANOVA. After 7 days, differentiated cells were counted with von Willebrand Factor (vWF) markers using the Mann-Whitney U test.EPC proliferation significantly increased in the PRP group (1.052 ± 0.16) compared to PPP (0.762 ± 0.19) and the control (0.068 ± 0.05, p=0.000). However, EPC differentiation showed no significant increase in the PRP group compared to PPP (0.00-0.30 vs. 0.00-0.20, p = 0.565) or the control (0.00-0.30 vs. 0.00-0.00, p = 0.064). Additionally, no significant increase in EPC differentiation was observed in the PPP group compared to the control (0.00-0.20 vs. 0.00-0.00, p = 0.144). PRP significantly enhanced EPC proliferation but did not significantly enhance differentiation in the peripheral blood of stable CHD patients compared to PPP and control groups.

Correlation between Mean Platelet Volume and Gensini Score in Patients with Coronary Heart Disease in Different Diabetic States.

To investigate the correlation between mean platelet volume (MPV) levels and Gensini scores in stable coronary heart disease (CHD) patients with or without diabetes. A retrospective analysis was conducted on 2525 patients with stable CHD in Zhongshan Hospital, Fudan University. There were 1274 in the low MPV group and 1251 in the high MPV group, divided by a median MPV level of 10.9 fL. In the total population, 1605 patients were non-diabetic and 920 were diabetic. The severity of coronary artery disease was quantified using the Gensini score. The Gensini score was significantly higher in the high MPV group than in the low MPV group (p < 0.001). MPV levels increased significantly with the number of stenotic (>50%) coronary vessels (p < 0.001). The Spearman analysis showed a positive correlation between MPV and Gensini score (r = 0.189, p < 0.001), which was more significant in the diabetic subgroup (r = 0.232, p < 0.001). Receiver operating characteristic (ROC) curves were employed to assess the predictive value of MPV for high Gensini scores, using the median value of 32 points as the cutoff. MPV levels in the diabetes cohort exhibited a higher predictive value for high Gensini scores (area under the curve: 0.635 [0.614-0.657], p < 0.001). Multivariate linear regression analysis showed that diabetes and MPV were independently associated with Gensini scores. MPV levels in stable CHD patients can predict the severity of coronary artery stenosis. This correlation is more significant in the presence of diabetes.

Chinese expert consensus on the rehabilitation treatment and nursing practice for stable coronary artery disease

Cardiac rehabilitation, with exercise training as the core component, has well-known benefits for stable coronary heart disease. This therapeutic approach is gradually gaining wide application in domestic clinical practice and is currently recommended by major guidelines at home and abroad. In recent years, more progress has been made in the technical specifications and nursing practice of rehabilitation treatment for coronary heart disease. This consensus is written by experts from the Professional Committee of Cardiopulmonary Prevention and Rehabilitation of the Chinese Rehabilitation Medical Association and the Cardiovascular Rehabilitation Committee of the Chinese Medical Association, with a view to further promoting the development of physical therapy and nursing practice for stable coronary heart disease in China.

Trimethyllysine, trimethylamine N-oxide, and long-term risk of stroke: the western norway coronary angiography cohort

Abstract Background Trimethyllysine (TML) is a precursor of the gut-microbiota derived metabolite trimethylamine N-oxide (TMAO), and both biomarkers are associated with adverse cardiovascular outcomes. Whether circulating levels of TML or TMAO predict long-term risk of stroke is uncertain. Purpose To examine prospective associations of plasma TML and TMAO with long-term risk of total and ischemic stroke. Methods By Cox regression analyses, risk-associations were examined among 4132 patients undergoing elective coronary angiography for suspected stable coronary heart disease. Endpoints were obtained from the Cardiovascular Disease in Norway project. Results Median levels of TML and TMAO were 0.67 and 5.7 µmol/L, respectively. Median age was 62 years and 28.1% of the participants were female. During a median follow up of 7.4 years, 240 (5.8%) patients experienced a stroke, of which 193 were ischemic strokes. After multivariable adjustments for cardiovascular risk factors, the hazard ratios (95% confidence intervals) per 1 standard deviation increase in log-transformed plasma TML were 1.05 (0.92-1.19, p=0.49) for total stroke and 0.99 (0.86-1.15, p=0.92) for ischemic stroke. Corresponding risk estimates were 0.99 (0.86-1.13, p=0.83) and 0.95 (0.82-1.12, p=0.55) per 1 standard deviation increase in log-transformed plasma TMAO. Conclusion In this large prospective cohort of patients with suspected coronary heart disease, neither plasma TML nor plasma TMAO predicted long-term (∼7 years) risk of stroke.