Coronary Artery Disease Patients Research Articles

PCSK9 and its relationship with HMGB1, TLR4, and TNFα in non-statin and statin-treated coronary artery disease patients.

Despite statin use in coronary artery disease (CAD), significant risk remains, potentially due to increased proprotein convertase subtilisin/kexin-type 9 (PCSK9) production, which raises LDL-C levels and induces inflammation. The exact relationship between PCSK9, inflammatory markers like TNFα, TLR4, CRP, and HMGB1, and monocyte subsets is poorly understood. This study aimed to explore these relationships in non-statin and statin-taking CAD patients. This case-control study included 91 controls and 91 stable CAD patients, divided into no-statin (NS, n = 25), low-dose statin (LDS, n = 25), and high-dose statin (HDS, n = 41) groups. Serum levels of LDL-C, CRP, PCSK9, TLR4, HMGB1, and TNFα were measured. Monocyte subsets were classified using flow cytometry into classical monocytes (CM), intermediate monocytes (IM), and non-classical monocytes (NCM). CAD patients showed elevated PCSK9, LDL-C, and inflammatory markers compared to controls. Statin groups (LDS, HDS) had lower LDL-C and inflammatory markers but higher PCSK9 than the NS group, with the HDS group showing the lowest LDL-C and inflammatory markers but the highest PCSK9. In the NS group, PCSK9 positively correlated with inflammatory markers (HMGB1, TNFα, TLR4, CRP) and monocyte subsets (IM%, NCM%). In the total statin group (LDS + HDS), PCSK9 negatively correlated with HMGB1, TLR4, and NCM%, for each, respectively, and positively with CM%. Multivariable linear regression showed significant associations between PCSK9 and HMGB1, NCM%, and IM% in the NS group, and HMGB1, NCM%, and TLR4 in the total statin group. In conclusion, we recommend combining PCSK9 inhibitors with statins in high-risk CAD patients. This may enhance statin efficacy, reduce LDL-C, and inhibit the TLR4/NF-кB inflammatory pathway, decreasing atherosclerotic inflammation.

Isovolumic relaxation intraventricular pressure difference predicts elevated left ventricular end-diastolic pressure in patients with coronary artery disease.

Current guideline for evaluating diastolic function requires multiple parameters to identify patients with elevated left ventricular end-diastolic pressure (LVEDP). However, the intermediate result still exists and may cause LVEDP undetermined. Previous studies have shown intraventricular pressure difference (IVPDs) are required for normal LV filling, but the relationship between IVPDs and LVEDP is unknown. In this study, we analyzed the relationship between IVPDs and LVEDP in 54 patients with coronary artery disease (CAD). LVEDP was prospectively measured at the time of coronary intervention and LVEDP > 15 mmHg was considered as elevated LV filling pressure. Simultaneous echocardiographic data was collected prior to the intervention. The relative intraventricular pressure was calculated using the vector flow mapping method. The IVPD was defined as the pressure difference from the apex to the base of LV. From 54 patients presenting with CAD, elevated LVEDP occurred in 30(55.6%). To analyze the changing trend of IVPD with LVEDP, CAD patients were further divided into group I with normal LVEDP (12.7 ± 3.1 mmHg) and group II with elevated LVEDP (26.0 ± 7.2 mmHg). In early diastole, both isovolumic relaxation period and rapid filling period showed decreased IVPD in CAD patients, but only the reduction in isovolumic relaxation period (IVPD-IVR) was statistical different between patients with elevated LVEDP and normal LVEDP (1.03 ± 0.42 mmHg vs. 2.25 ± 1.21 mmHg, p < 0.01). IVPD-IVR had the best correlation with LVEDP (r=-0.499, p < 0.01) among IVPDs. Lower IVPD-IVR was associated with higher risk of elevated LVEDP. Evaluating IVPD-IVR might improve the diagnostic algorithm for predicting elevated LVEDP.

Abstract 4145859: Clonal Hematopoiesis of Indeterminate Potential Increases Mortality Risk in Coronary Artery Disease

Background: Clonal hematopoiesis of indeterminate potential (CHIP) has been associated with an increased incidence of common late-onset diseases including myocardial infarction. Research Question: Here we examined the impact of CHIP on mortality in patients with coronary artery disease (CAD) and further explored potential underlying mechanisms. Methods: CAD patients were examined for CHIP-defining mutations using deep DNA sequencing. Propensity score matching was used to compare CHIP CAD with non-CHIP CAD patients. Survival was analyzed using Kaplan-Meier curves and Cox proportional hazard models. Functional aspects were investigated at the protein and RNA level in cardiovascular relevant human postmortem tissue from the Munich cardIovaScular StudIes biObaNk (MISSION), in CAD patients from an independent cohort and in in-vitro macrophage models. Results: Within 7,933 CAD patients screened by deep-DNA-sequencing with a 13 gene panel, 2,002 carried at least one CHIP defining mutation with a variant allele frequency ≥2%. After 1:1 matching with non-CHIP carriers we revealed a significantly elevated 3-year mortality in the group of CHIP carriers [HR 1.48 (CI 95% 1.23-1.78); p&lt;0.0001)] as well as in carriers of mutations in one out of seven individual genes – ASXL1 , DNMT3A , PPM1D , SF3B1 , SRSF2 , TET2 , and U2AF1 . In human coronary atherosclerotic plaque we visualized CHIP-mutations within leukocytes. Further, within coronary artery plaque of deceased TET2 mutation carriers (n=26 vs. n=13 controls) we identified by proteomic profiling an upregulation of inflammatory and metabolic pathways, including enhanced lipid metabolism. In an independent cohort of CAD patients undergoing coronary bypass surgery, RNA sequencing data from monocyte-derived macrophages revealed in TET2 CHIP carriers associations with CAD complexity. TET2 -mutated macrophages studied in-vitro revealed an increased uptake of low-density lipoprotein (LDL) and oxidized LDL-cholesterol besides a known upregulation of inflammatory pathways. Conclusion: In summary, this study emphasizes CHIP as a significant prognostic factor in CAD patients, associated with increased complexity of CAD and altered gene expression within human coronary artery plaques. Mechanistically, TET2 mutations modify the behavior of CHIP-affected macrophages, leading to heightened inflammation and increased uptake of LDL-cholesterol.

Abstract 4122763: Health Status Outcomes of Antianginal Therapies in Patients After Coronary Revascularization: Insights From the GREAT Disease Registry Study

Background: The impact of antianginal therapies on the health status of coronary artery disease (CAD) patients who have undergone coronary revascularization has not been extensively researched. This study aimed to investigate the effect of nicorandil on the health status in patients after coronary revascularization, measured by the Seattle Angina Questionnaire (SAQ). Methods: We analyzed data from 1,556 patients enrolled in the GREAT Disease Registry Study (Clinicaltrial No. NCT05050773) between September 2021 and May 2022. Changes in SAQ summary score (SAQ-SS) from baseline to 3, 6, 9, and 12 months were assessed. Statistical methods included a linear mixed-effects model and propensity score matching (PSM) for comparative analysis. Results: Among the 1,038 patients receiving revascularization analyzed (22.7% female; mean age [SD], 59.9 [10.2] years), 648 (62.4%) received nicorandil, while 390 (37.6%) did not. In the linear mixed-effects model analysis, statistically significant improvements were observed with nicorandil in SAQ-SS across all time points ( Table 1 ), indicating beneficial effects of nicorandil on health status outcomes after revascularization. Sensitive analysis was conducted using the PSM method. After PSM adjustment, both groups comprised 321 patients each. The change in SAQ-SS from baseline to 12 months was significantly greater in the nicorandil group (19.2 ± 14.06 points) compared to the non-nicorandil group (14.91 ± 12.9 points, p &lt; 0.001). Conclusions: These findings indicated that nicorandil is associated with improved health status outcomes in CAD patients who have undergone coronary revascularization.

Abstract 4135708: Obesity and the risk of cardiac death in coronary artery disease

Background: The prevalence of obesity is increasing worldwide reaching epidemic proportions. Obesity increases the risk of coronary artery disease (CAD), but there is little prospective evidence about the effect of obesity on the risk of cardiac death in CAD patients. Aim: We aimed to investigate the effect of obesity and the risk of cardiac death in a prospective cohort of CAD patients. Methods: We have prospectively enrolled 1,946 patients with CAD (mean age 66.9±8.6, 68% male), with a mean follow-up of 8.7±2.2 years. BMI was measured at baseline and was categorized into 4 groups: 1) BMI 18.5-24.9 kg/m 2 (normal weight, reference group), 2) BMI 25-29.9 kg/m 2 (overweight), 3) BMI 30-34.9 kg/m 2 (class 1 obesity), and 4) BMI &gt;35 kg/m 2 (class 2 obesity). The primary endpoint was cardiac death and secondary endpoints were sudden cardiac death/arrest (SCD/SCA), non-sudden cardiac death, non-cardiac death, and heart failure (HF) hospitalization. Statistical analysis was performed with Cox regression and was adjusted for age, sex, type 2 diabetes, CCS class, kidney function (eGFR), systolic and diastolic blood pressure, LDL, smoking, SYNTAX score, and left ventricle ejection fraction. Results: The prevalence of BMI 18.5-24.9 kg/m 2 was 18.5% (n=359), BMI 25-29.9 kg/m 2 was 47.8% (n=929), BMI 30-34.9 kg/m 2 was 24.0% (n=466), and BMI&gt;35 kg/m 2 was 9.7% (n=189). During the follow-up, cardiac death occurred in 156 subjects, SCD/SCA in 75 subjects, non-sudden cardiac death in 81 subjects, and non-cardiac death in 197 subjects. BMI &gt;35 kg/m 2 was associated with an increased trend of cardiac death (adjusted HR 1.92, 95% CI 0.92-4.01; p=0.08) and an increased risk of non-sudden cardiac death (adjusted HR 4.11, 95% CI 1.58-10.68; p=0.004) and HF hospitalization (adjusted HR 2.83, 95% CI 1.06-7-54; p=0.04), but not with SCD/SCA (adjusted HR 0.79, 95% CI 0.24-2.56; p=0.69) or noncardiac death (adjusted HR 0.85, 95% CI 0.43-1.69; p=0.64). The risk of cardiac death or secondary endpoints was not increased in patients with overweight or class 1 obesity. Conclusions: Class 2 obesity was associated with an increased risk of non-sudden cardiac death and heart failure hospitalization among CAD patients. Obesity may have adverse long-term effects on cardiac function and prognosis among CAD patients, supporting the benefit of optimal weight control therapy.

Abstract 4115015: Hyperpolarized Carbon-13 Metabolic Imaging Detects Changes in Cardiac Mitochondrial Metabolism in Patients Before and After Coronary Artery Bypass Graft Surgery

Background: Coronary Artery Disease (CAD) is a significant global health issue, necessitating improved diagnostic tools for visualizing cardiac energetics. Traditional imaging methods such as PET and dobutamine stress echocardiography do not directly assess mitochondrial metabolism. Hyperpolarized Carbon-13 metabolic magnetic resonance imaging (HP- 13 C MRI) offers a promising non-invasive method for investigating mitochondrial function in CAD. This study utilizes HP- 13 C MRI to detect changes in mitochondrial metabolism in patients undergoing Coronary Artery Bypass Graft (CABG) surgery (Fig.1). Methods: We conducted HP- 13 C MRI examinations on two patients with advanced CAD before and (~4-6 months after CABG surgery and one healthy subject (Fig. 2 A,B). Participating subjects provided informed consent according to a protocol approved by the Institutional Review Board and Protocol Review Committee. Baseline blood samples were analyzed for pyruvate, triglycerides, free fatty acids, and insulin levels. Post-glucose load, patients received an intravenous injection of an IND-approved metabolic probe, [1- 13 C] pyruvic acid, prepared under Good Manufacturing Practice regulations. The HP solution was administered after polarization in a clinical polarizer (SPINlab™, GE Healthcare). Imaging was performed using a GE MR750 MR system with a Helmholtz loop-pair 13 C coil (PulseTeq Limited, UK). Data were reconstructed and analyzed with MATLAB scripts. Results and Discussion: Baseline blood measurements were normal for the healthy subject, but those with advanced CAD showed variable and abnormal values (Fig. 2C). HP- 13 C MRI safely assessed cardiac metabolism in patients with advanced CAD. Patients with advanced CAD exhibited reduced pyruvate metabolism compared to healthy controls, shown by lower myocardial bicarbonate/(bicarbonate+lactate) ratios (Bic/(Bic+Lac)). Following CABG, only Patient 2 showed improved Bic/(Bic+Lac), while Patient 1 did not (Fig. 3A-B). This variability may be influenced by differences in nutrition, hormonal status, medication regimens, or other factors. Changes in % Bic/(Bic+Lac) across different coronary artery segments were observed post-CABG in CAD patients (Fig. 3C). Conclusion: HP- 13 C MRI non-invasively assesses cardiac metabolism in CAD patients, demonstrating the potential to evaluate post-CABG metabolic changes. Our efforts continue to recruit large cohort to understand individual variability.

Weekly Journal Scan: Should we treat obstructive coronary artery disease in patients undergoing transcatheter aortic valve implantation?

Weekly Journal Scan: Should we treat obstructive coronary artery disease in patients undergoing transcatheter aortic valve implantation?

Abstract 4138559: Cystatin C Predicts Cardiovascular Events in Patients With Coronary Artery Disease Both Among Patients With and Among Those Without Type 2 Diabetes

Cystatin C is an established biomarker for renal function, and, given the close association of chronic kidney disease and cardiovascular disease might indicate new-onset or deteriorating cardiovascular disease. However, evidence for cystatin C as a predictor of cardiovascular events is limited and controversial. We therefore aimed at investigating the role of cystatin C as a predictor of future cardiovascular events in a high risk-cohort of patients with established coronary artery disease (CAD). We prospectively recorded cardiovascular events in 1053 patients with angiographically verified CAD over a mean follow-up of 9.5±5.3 years. At baseline, 352 patients had type 2 diabetes mellitus (T2DM) and 701 did not have T2DM. During follow-up, 560 (53.2%) of our patients suffered cardiovascular events. Cystatin C proved to be a strong and independent predictor for cardiovascular events in the total study cohort (standardized adjusted HR 1.22 [1.12-1.33], p&lt;0.001). When T2DM status was taken into account, cystatin C significantly predicted cardiovascular events both in patients with T2DM (HR 1.18 [1.04-1.35], p=0.011) and in non-diabetic patients (HR 1.23 [1.09-1.38], p&lt;0.001). We conclude that cystatin C predicts cardiovascular events in CAD patients both among those with and among those without T2DM.

Abstract 4135746: Assessing Coronary Artery Disease Severity: Leveraging Inflammatory Markers As a Prognostic Indicators

Introduction: Cardiovascular disease continues to be the leading cause of death and a significant cause of morbidity in the United States. In recent years, there has been increased interest in the role of inflammation in predicting and modifying the risk of coronary artery disease. Of the multitude of inflammatory markers studied subsequently, two of the most easily and widely obtained is the neutrophil to lymphocyte ratio (NLR) and the monocyte to lymphocyte ratio (MLR), which can be calculated from a complete blood count with differential. Multiple retrospective studies have demonstrated that the NLR and MLR have been used to diagnose ACS, predict mortality at a year after ACS, and risk stratify patients prior to percutaneous coronary intervention. Research Question: Are the NLR/MLR useful tools in predicting the severity of coronary artery disease (CAD) in patients admitted to a tertiary medical center in Southern Nevada for ACS between 2021 and 2023? Methods: A sample of n=344 patients was used to examine the potential significance of NLR/MLR to diagnose ACS and for predicting CAD severity. Traditional diagnostic test evaluation was used for determining CAD with a ratio of NLR=3.5 + MLR=0.35 (data medians) as the cut-off value. Patient risk group status (1:low risk to 4:high risk) was used as a binary outcome to test NLR/MLR between low and high risk groups using a nonparametric MWW test of medians. Additionally, ROC analysis was used to estimate an optimized cut-off for NLR/MLR as determined by AUC. Results: Results demonstrate for predicting ACS using the median NLR, sensitivity=88.07; specificity=14.88; PPV=52.01; NPV=54.35), LR(+)=1.03 and LR(-)= 0.80, using the median MLR results showed sensitivity=87.28; specificity=14.11; PPV=50.84; NPV=52.17, LR(+)=1.01 and LR(-)= 0.90. Subpopulation analysis demonstrated a statistically significant difference in NLR between “high risk ACS” vs “Low Risk ACS” (p&lt;0.001). Examination of the ROC curve for predicting the high-risk group suggested an optimized cutoff of NLR=3.7; however, AUC was only 0.617, and sensitivity and specificity were not improved compared to using the median NLR. Conclusion: Our findings suggest that an NLR greater than 3.7 may indicate multivessel involvement or proximal/left main disease in CAD patients. However, due to its low specificity and AUC, NLR alone cannot reliably distinguish between single-vessel and multivessel CAD.

Abstract 4135025: Inflammation-related 5-hydroxymethylation signatures as markers for clinical presentations of coronary artery disease

Background: Coronary angiography, an invasive method, remains the gold standard technique for coronary artery disease (CAD) diagnosis in clinical practice. However, due to its invasive nature, it cannot be used for mass population screening. There is an urgent need in the clinical to identify new liquid biopsy molecular markers for screening patients with CAD. Methods: We utilized 5hmC-Seal to generate genome-wide 5hmC profiles in plasma cell-free DNA (cfDNA) from 724 CAD patients. To investigate the correlation between 5hmC modifications and CAD, we separated patients into training and validation cohorts and developed a 5hmC-based logistic regression model from the training cohort to predict CAD patients in the validation cohort. Furthermore, we incorporated an external cohort comprising 167 samples to validate the reliability of our model. Results: We found that the differentially hydroxymethylated genes (DhMGs) in people with the normal coronary artery (NCA), nonfatal stable CAD (sCAD), non-ST-elevation myocardial infarction (NSTEMI), as well as ST-elevation myocardial infarction (STEMI) enriched in neutrophil-mediated inflammatory response pathways, and inflammation-related DhMGs can reflect the progression of atherosclerotic plaque. Furthermore, we used machine learning algorithms to develop a predictive model for predicting the occurrence of myocardial infarction (MI) based on 19 inflammatory markers, and the predictive model could effectively predict MI (NSTEMI and STEMI) (AUC = 0.913). Simultaneously, our model has demonstrated strong performance in external validation. Conclusions: We have identified a novel biomarker, the inflammation-associated 5hmC markers, which can reflect the clinical manifestations of CAD and can effectively predict the occurrence of MI.

Abstract 4122256: Health Status Outcomes of Nicorandil in Patients With Angina Pectoris: A Prospective, Multicenter, Registry-Based Study

Background: Coronary artery disease (CAD) exerts a considerable impact on mortality from cardiovascular disease. Approximately half of patients with CAD initially present with angina pectoris. The GREAT study is designed to establish a large cohort of Chinese patients with angina pectoris and compare the effectiveness of different anti-angina regimens, using the Seattle Angina Questionnaire. Method: The GREAT (reGistRy study of medical thErapy in patients with Angina pecToris) Registry is a multicenter, prospective, observational, cohort study that enrolled 1556 adult CAD patients with angina pectoris from nine hospitals in China. The study included patients currently receiving or eligible to receive oral anti-anginal regimens. The cohort was classified into nicorandil and non-nicorandil groups based on the treatment therapies. The primary outcome was the Seattle Angina Questionnaire summary score (SAQ-SS) changes from baseline to 12 months. The SAQ-SS averages the domains of physical limitation, angina frequency, and quality-of-life scores. Results: From September 2021 to May 2022, a total of 1575 patients were screened, of whom 1556 met the inclusion criteria and were included ( Figure 1 ). Among the patients at the full analysis set (FAS, N=1528), 28.5% were women, and the median age was 61 years. Baseline variables were well balanced after propensity score matching, with both groups containing 450 patients. In the nicorandil group, patients showed a significantly greater increase in mean SAQ-SS score at Month 12 compared to the non-nicorandil group (17.6±14.0 vs 15.1±13.0; difference: 0.19; 95% CI, 0.05-0.32; p=0.003). In addition, patients in the nicorandil versus the non-nicorandil group reported a significantly greater mean improvement in the SAQ-QoL domain (18.9±21.4 vs 16.3±20.4; p=0.042) and SAQ-PL domain (11.7±16.9 vs 10.0±17.0; p=0.001). Over 12 months, a higher proportion of patients in the nicorandil group, compared to the non-nicorandil group, reported substantial improvements in SAQ-SS, with 24.1% experiencing large improvements (20-29 points) and 18.2% reporting very large improvements (≥30 points) versus 20.7% and 12.0%, respectively (p=0.005 across all categories) ( Figure 2 ). Conclusion: This real-world data indicates that nicorandil-based anti-angina regimens are associated with a greater health status outcome improvement compared to those not using nicorandil in CAD patients.

Abstract 4135059: Enhanced Expression of iNOS is Associated with Aortic Valve Stenosis in Patients Undergoing Hemodialysis

Background: Patients undergoing hemodialysis (HD) have a greater prevalence of aortic valve calcification and aortic valve stenosis (AS). High prevalence and rapid progression of AS have been reported in patients undergoing HD. However, the precise mechanism of the relationship between HD treatment and rapid development of AS is still unknown. Several findings suggest a pivotal role for oxidative stress in the progression and acceleration of atherosclerosis in patients undergoing HD. A considerable number of human diseases have an inflammatory component, and a key mediator of immune activation and inflammation is inducible nitric oxide synthase (iNOS). Overexpressed iNOS has been implicated in numerous pathogenetic processes, including coronary plaque destabilization. To elucidate the role of iNOS in the aortic valve of patients with AS, we studied its presence in aortic valve specimens from patients with AS undergoing HD. Methods: We enrolled 32 patients undergoing HD and 42 patients not undergoing HD who had severe AS and underwent AVR. Valve samples were analyzed immunohistochemically with antibodies against macrophages, microvessels, iNOS and 4-hydroxy-2-nonenal (4-HNE), an index of lipid peroxidation. Immunoreactivity was quantified with computer-aided polarimetry. Double immunostaining was also performed to identify cell types that stained positive for iNOS. Results: Quantitative analysis demonstrated that macrophage-, iNOS-, and 4-HNE-positive areas, as well as the number of microvessels, were significantly higher in patients with AS undergoing HD (macrophages, P &lt;0.001; microvessels, P &lt;0.05; 4-HNE, P &lt;0.05; iNOS , P &lt;0.001). iNOS-positive areas were positively correlated with 4-HNE-positive areas (R=0.71, P &lt;0.0001). Double immunostaining for both iNOS and macrophages identified iNOS-positive cells as macrophages. Conclusions: These findings indicate that accumulation of iNOS in macrophages may increase oxidative stress and contribute to the rapid progression of AS in patients undergoing HD.

Abstract 4138739: Insulin Resistance as a Marker of Multivessel Coronary Artery Diseases in Patients With Cardiovascular-Kidney-Metabolic Risk: Inshight From Invasive Coronary Angiography

Background: Cardiovascular-Kidney-Metabolic (CKM) syndrome is the concept of a combined diseases, including diabetes and chronic kidney disease (CKD), to stratify patients at cardiovascular risks. However, whether CKM components and insulin resistance differ in risk for coronary artery disease (CAD) severity is unknown. Purpose: This study aimed to investigate the association of distinct CKM risks and insulin resistance with CAD severity. Methods: In this study, we included 849 patients (74% male, 69±10 years of age) who underwent coronary angiography to assess chronic CAD. We assessed CKM risks using following components: (1) BMI ≥23 kg/m 2 , (2) diabetes, (3) hypertension and dyslipidemia, and (4) CKD. According to the number of CKM risk components, patients were categorized into four groups (Group A as having 0 or 1, Group B as 2, Group C as 3, and Group 4 as 4 risks). Insulin resistance was assessed by HOMA-IR and triglyceride-glucose index (TyG index) calculated as Ln (fasting plasma glucose × triglyceride/2). Coronary artery stenosis was categorized into single-vessel or multi-vessel CAD (MVD) per AHA classification. Gensini score was calculated to assess CAD extent. Logistic regression analysis was performed to determine independent predictors of MVD among CKM risk components. Results: MVD was diagnosed in 26.3% (n = 223) patients (mean Gensini score was 58±40 points). Among the four groups, there were significant differences in age, body mass index, hemoglobin A1c levels, TyG index, HOMA-IR, and Gensini score. Compared with Group A as reference, Group C (odds ratio [OR], 1.58; 95% confidence interval [CI] 1.03–2.42) or Group D (OR, 1.75; 95%CI, 1.06–2.89) but not Group B (OR, 1.09; 95%CI, 0.70–1.71) had higher risk for MVD (Figure). In a logistic regression model adjusting for age, male, smoker, and CRP ≥2 mg/dL, independent predictor of MVD was diabetes (OR, 2.15; 95%CI,1.55–2.99; p &lt; 0.001; model 1 in Table). In addition, when adjusting for age, male, smoker, and CRP ≥2 mg/dL, HOMA-IR&gt;2.5 was an independent predictor of MVD (model 2 in Table). Similarly, TyG index, an alternative marker of insulin resistance, remained as an independent predictor of MVD (model 3 in Table). Conclusions: In chronic CAD patients who underwent coronary angiography, subgroups stratified by the CKM risk components exhibit distinctly different insulin resistance, CAD severity and risk for MVD. Insulin resistance and diabetes were independent risks for MVD in this population.

Abstract 4138555: The ApoB/LDL-C Ratio Predicts Cardiovascular Events in Coronary Artery Disease Patients Independently of Type 2 Diabetes Status

A high ApoB/LDL-C ratio reflects small LDL particle size which like type 2 diabetes (T2DM) is associated with insulin resistance. Whether the ApoB/LDL-C ratio and the presence of T2DM are mutually independent predictors of cardiovascular events is unclear and is addressed in the present study. We enrolled a large high-risk cohort of 1200 patients with coronary artery disease. T2DM was diagnosed according to current ADA guidelines. Prospectively, cardiovascular events were recorded over a mean follow-up period of 10.5±4.9 years. At baseline, the ApoB/LDL-C ratio was significantly higher in patients with T2DM (n=422) than in subjects who did not have T2DM (0.81±0.18 vs. 0.74±0.15 p&lt;0.001). During follow-up, 662 patients suffered cardiovascular events. The Apo B/LDL-C ratio predicted cardiovascular events in univariate analysis (HR=1.11 [1.03-1.20] p= 0.006), and the event rate was higher in patients with than in those without T2DM (62.2% vs. 52.3%; p=0.001). In a multivariate adjusted Cox regression model both the ApoB/LDL-C ratio and T2DM significantly predicted cardiovascular events in a mutually independent manner, with standardized adjusted HRs of 1.11 [1.03-1.20]; p=0.008 and 1.39 [1.18- 1.64]; p&lt;0.001, respectively. We conclude that in subjects with coronary artery disease the ApoB/LDL-C and T2DM are mutually independent predictors of cardiovascular events.

A U-shaped relationship between the atherogenic index of plasma and repeated target vessel revascularization in patients undergoing percutaneous coronary intervention: a retrospective study

BackgroundAtherogenic index of plasma (AIP) has been recognized as a novel and practical marker for the assessment of cardiometabolic risk, but the relevance of AIP as a prognostic biomarker in coronary artery disease (CAD) remains debated. This study investigated the association between AIP and major adverse cardiac and cerebrovascular events (MACCEs) in CAD patients receiving percutaneous coronary intervention (PCI) with drug-eluting stents (DES).MethodsA total of 2,250 patients undergoing PCI with DES were included in this retrospective cohort study. The primary endpoint was MACCEs, encompassing acute myocardial infarction, repeat target vessel revascularization (TVR), stroke, and all-cause mortality. Logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Restricted cubic splines were applied to explore the dose–response associations. And subgroup analysis was conducted to evaluate potential relationship between AIP and MACCEs across different subgroups.ResultsDuring a medium follow-up of 29.8 (25.6–34.0) months, 106 (4.7%) patients experienced TVR. After adjusting for confounders, AIP (per 1 SD increase) was positively associated with TVR (odds ratio [OR] = 1.26, 95% confidence interval [CI] = 1.01–1.58, P = 0.042). In females, there was a significant association (OR = 2.33, 95% CI = 1.40–3.98, P = 0.002), but no significant association was observed in males. There was an interaction between AIP and gender (P = 0.017). Restricted cubic spline analysis depicted a U-shaped relationship between AIP and TVR (Pnonlinear = 0.016), with an elevated risk evident from an AIP of 0.20.ConclusionAIP showed a U-shaped relationship with TVR in PCI patients with DES, particularly pronounced among females. We suggested that the AIP should be used as a plasma marker of key interest for preventing TVR after DES implantation in patients with CAD.

Effectiveness of Coronary Artery Disease Health Education among the patients of Coronary Artery Disease in Tertiary Cardiac Centre

Background and Aims: Secondary prevention of coronary artery disease is vital in preventing the future cardiac events. Inadequate knowledge of the disease is related to non-compliance with the treatment therapy which directly results in disease progression and its complication. The objective of this study is to assess the effectiveness of health education about coronary artery disease among the patients of coronary artery disease in a tertiary cardiac centre. Methods: A quantitative, prospective, interventional research design was designed to collect the data by non-probability convenience sampling method. Patients diagnosed with coronary artery disease and admitted in different wards of Shahid Gangalal National Heart Centre were included. Data was collected from July 2022 to December 2022 in three phases: prior to health education; within 24 hours of health education and after 3 months. A semi structured face to face interview was used to collect data from the patients, which was then filled in the web-based questionnaire and appropriate statistical methods were used for analysis. Results: A total of 167 patients were enrolled during the study period. Only 145 (86.8%) patients completed the 3rd phase of data collection. There was a significant improvement in patients’ overall knowledge (P value; &lt;.01) as well as knowledge regarding medical (P value; &lt;.01), coronary artery disease risk factors (P value; &lt;.01), exercise (P value; &lt;.01), nutrition (P value; &lt;.01) and psychological risk (P value; &lt;.05). There was a significant improvement (P value; &lt;.01) related to behavior related characteristics like smoking, tobacco consumption, alcohol consumption and physical activity. However, correlation between health behaviors and post intervention knowledge showed a non-significant weakly positive relation of knowledge with education (r=.081), whereas there was non-significant weakly negative relation with physical activity (r=-.0126). Conclusion: The educational intervention has significant improvement in level of knowledge and change in behavior pattern among the patients of coronary artery disease. This study demonstrates that targeted health education programs can lead to significant improvements in knowledge and behavior among coronary artery disease patients, potentially reducing hospital readmission rates and promoting better long-term disease management.

Relationship between Myocardial Performance Index (Tei Index) and angiographic severity of coronary artery disease in patients with Acute ST Elevation Myocardial Infarction

Background: Tei index is a Doppler derived measure of combined systolic and diastolic myocardial function and a better predictor of global LV function and outcome in patients with acute STEMI. The objective of this study was to determine the relationship between the myocardial performance index of LV (Tei index) and angiographic severity of coronary artery disease as assessed by SYNTAX score in patients with acute STEMI. Methods: This was a prospective, observational single centered study conducted from March 2022 to November 2022 at Manmohan Cardiothoracic Vascular and Transplant Centre, Institute of Medicine. (MCVTC, IOM). 160 patients with acute STEMI were enrolled. LV Tei index was calculated with the help of 2D and Tissue Doppler imaging, and the lesion severity was categorized with the help of SYNTAX score after the patients underwent coronary angiography. Results: The mean age was 61.23±12.33 years with a male preponderance. 107 (67%) were male with male to female ratio of 2:1. Tei index was significantly higher among the hypertensive (0.74±0.17) and diabetic (0.78±0.18) patients. 64 (40%), 51(31.9%) and 45(28.1%) had Single vessel disease (SVD), Double vessel disease (DVD) and Triple vessel disease (TVD) respectively with the Mean Tei index values 0.57 ± 0.10, 0.76 ± 0.11, and 0.88±0.11 (p&lt;0.05). The Tei index increased when patients were divided into low, mid, and high SYNTAX score groups as 0.58±0.11, 0.61±0.73, 0.88±0.13 respectively, p-value &lt; 0.05). Moreover, the study showed a positive correlation between Tei index and SYNTAX score with increasing severity of coronary artery stenosis. (r=0.654, p-value&lt;0.001). Proximal LAD, LCx and RCA lesions had greater Tei index than the distal lesions. Conclusion: More proximally located LAD, LCx, RCA lesions had higher value of Tei index, as assessed with the SYNTAX score.

Association between triglyceride-glucose index and in-hospital all-cause mortality under different glucose metabolism status among patients with coronary artery disease

BackgroundThis current study aimed to investigate the relationship between the triglyceride-glucose (TyG) index and in-hospital all-cause mortality of coronary artery disease (CAD) in patients with different glucose metabolic statuses.MethodsParticipants were divided into three groups according to tertiles of the TyG index. Glucose metabolic status was classified as normal glucose regulation, pre-diabetes mellitus, and diabetes mellitus (DM). The primary outcome was in hospital all-cause mortality.ResultsWe observed a significant relationship between the TyG index and in-hospital deaths of patients with CAD in this study. After adjusting for multiple factors in the logistic regression model, the TyG index was still an independent risk factor, and the T3 group (OR, 2.311; 95% CI = 1.237–4.317; P = 0.009) was correlated with a 2.311-fold risk compared with the T1 group. In the subgroup analysis of different glucose metabolic status, the T3 group (OR, 1.541; 95% CI: 1.013–2.344; P = 0.043) were associated with a significantly higher risk of in-hospital deaths in CAD patients with DM.ConclusionsAn increased TyG index was correlated with a higher risk of in-hospital all-cause mortality. Our study indicated that TyG index could be a valuable predictor of in-hospital death of CAD patients, especially for individuals with DM.

Elevated Perspectives: Unraveling Cardiovascular Dynamics in High-Altitude Realms.

High-altitude regions pose distinctive challenges for cardiovascular health because of decreased oxygen levels, reduced barometric pressure, and colder temperatures. Approximately 82 million people live above 2400 meters, while over 100 million people visit these heights annually. Individuals ascending rapidly or those with pre-existing cardiovascular conditions are particularly vulnerable to altitude-related illnesses, including Acute Mountain Sickness (AMS) and Chronic Mountain Sickness (CMS). The cardiovascular system struggles to adapt to hypoxic stress, which can lead to arrhythmias, systemic hypertension, and right ventricular failure. Pathophysiologically, high-altitude exposure triggers immediate increases in cardiac output and heart rate, often due to enhanced sympathetic activity. Over time, acclimatisation involves complex changes, such as reduced stroke volume and increased blood volume. The pulmonary vasculature also undergoes significant alterations, including hypoxic pulmonary vasoconstriction and vascular remodelling, contributing to conditions, like pulmonary hypertension and high-altitude pulmonary edema. Genetic adaptations in populations living at high altitudes, such as gene variations linked to hypoxia response, further influence these physiological processes. Regarding cardiovascular disease risk, stable coronary artery disease patients generally do not face significant adverse outcomes at altitudes up to 3500 meters. However, those with unstable angina or recent cardiac interventions should avoid high-altitude exposure to prevent exacerbation. Remarkably, high-altitude living correlates with reduced cardiovascular mortality rates, possibly due to improved air quality and hypoxia-induced adaptations. Additionally, there is a higher incidence of congenital heart disease among children born at high altitudes, highlighting the profound impact of hypoxia on heart development. Understanding these dynamics is crucial for managing risks and improving health outcomes in high-altitude environments.

Diagnostic performance of high and ultra-high-resolution photon counting CT for detection of coronary artery disease in patients evaluated for transcatheter aortic valve implantation.

We assessed the diagnostic performance of both ultra-high-resolution (UHR) and high-resolution (HR) modes of photon-counting detector (PCD)-CT within the confines of standard pre-TAVI CT scans, as well as the performance of UHR mode adjusted specifically for coronary imaging, using quantitative coronary angiography (QCA) as the reference. We included 60 patients undergoing pre-TAVI planning CT scans. Patients were divided into 3 groups: 20 scanned in HR mode, 20 in UHR mode, and 20 in adjusted UHR mode, on a dual-source PCD-CT. The adjusted UHR mode employed a lower tube voltage (90kV vs. 120kV) and a higher image quality level (65 vs. 34) to enhance coronary artery visualization. Patients underwent invasive coronary angiography as part of clinical routine. CCTA and QCA were reviewed to assess CAD presence defined as stenosis ≥ 50% in proximal and middle coronary segments. We included 60 patients (mean age 79 ± 7 years; 39(65%) men). Mean heart rate during scanning was 72 ± 13bpm. Median coronary calcium score was 973[379-2007]. QCA identified significant CAD in 24 patients (40%): 9 patients scanned with HR mode, 10 patients with the UHR mode, and 5 patients with the UHR adjusted mode. Per-patient area under the curves were 0.57 for HR, 0.80 for UHR, and 0.80 for adjusted UHR, with no significant differences between the scan modes, and per-vessel the area under the curves were 0.73 for HR, 0.69 for UHR, and 0.87 for adjusted UHR, with significant differences between UHR and adjusted UHR (p = 0.04). UHR and adjusted UHR modes of dual source PCD-CT show potential for improved sensitivity and negative predictive value for detecting CAD in patients undergoing pre-TAVI scans, however, no statistically significant difference from HR mode was observed.