Coronary Artery Disease In Population Research Articles

The Neutrophil to Lymphocyte Ratio Modifies Lipoprotein (a)-Related Poor Prognosis in Patients After Percutaneous Coronary Intervention.

Lipoprotein (a) [Lp(a)] could contribute to coronary artery disease (CAD) through proinflammatory effects. The neutrophil to lymphocyte ratio (NLR) is an inflammatory biomarker. We consecutively enrolled 7,922 CAD patients to investigate the synergistic association of Lp(a) and NLR with prognosis in patients undergoing percutaneous coronary intervention (PCI). NLR was calculated as the neutrophil count divided by the lymphocyte count. Cutoff for NLR was a median of 2.07. The threshold value was set at 30mg/dL for Lp(a). The primary endpoint was major adverse cardiac events (MACEs), including all-cause mortality and myocardial infarction. During 2 years follow-up, 111 (1.40%) MACEs occurred. Lp(a) > 30mg/dL was associated with an increased MACE risk in participants with NLR ≥2.07 [adjusted hazard ratio (HR), 1.84; 95% CI, 1.12-3.03], but not in participants with NLR <2.07 (adjusted HR, 0.74; 95% CI, 0.38-1.45) (Pinteraction = 0.021). Subgroup analysis demonstrated that the synergistic association of Lp(a) and NLR with prognosis was more pronounced in female patients (Pinteraction = 0.028). This study suggested that combining Lp(a) and NLR may be useful for risk stratification in CAD population.

Hemodynamic Reactivity to Mental Stress and Cognitive Function in Coronary Artery Disease.

People with coronary artery disease (CAD) are at higher risk of cognitive impairment than those without CAD. Psychological stress is a risk factor for both conditions and assessing the hemodynamic reactivity to mental stress could explain the link between stress and cognitive function. Individuals with stable CAD from two prospective cohort studies were included. All individuals underwent acute mental stress testing, as well as conventional stress testing. Cognitive function was assessed both at baseline and at a 2-year follow-up. The rate-pressure product (RPP) was calculated as the mean systolic blood pressure times the mean heart rate at rest. RPP reactivity was defined as the maximum RPP during standardized mental stress test minus the RPP at rest. After multivariable adjustment, every standard deviation decrease in RPP reactivity with mental stress was associated with slower completion of Trail-A and Trail-B in both cohorts (13% and 11% in cohort 1, and 15% and 16% in cohort 2, respectively, p for all <0.01). After a 2-year follow-up period, every standard deviation decrease in RPP reactivity with mental stress was associated with a 8%, and 9% slower completion of Trail-A and Trail-B, respectively (p for all <0.01). There was no significant association between RPP reactivity with conventional stress testing and any of the cognitive tests. In the CAD population, a blunted hemodynamic response to mental stress is associated with slower visuomotor processing and worse executive function at baseline and with greater decline in these abilities over time.

Feasibility and safety of left bundle branch area pacing for patients with stable coronary artery disease

AimsStable coronary artery disease (CAD) is a prevalent comorbidity among patients requiring pacemaker implantation. This comorbidity may have an impact on the safety and prognosis of traditional right ventricular pacing (RVP). Left bundle branch area pacing (LBBaP) is a new physiological pacing modality. Our aim was to investigate the feasibility and safety of LBBaP in patients with the stable CAD.MethodsThis study included 309 patients with symptomatic bradycardia who underwent LBBaP from September 2017 to October 2021. We included 104 patients with stable CAD (CAD group) and 205 patients without CAD (non-CAD group). Additionally, 153 stable CAD patients underwent RVP, and 64 stable CAD patients underwent His-bundle pacing (HBP) were also enrolled in this study. The safety and prognosis of LBBaP was assessed by comparing pacing parameters, procedure-related complications, and clinical events.ResultsDuring a follow-up period of 17.4 ± 5.3 months, the safety assessment revealed that the overall rates of procedure-related complications were similar between the stable CAD group and the non-CAD group (7.7% vs. 3.9%). Likewise, similar rates of heart failure hospitalization (HFH) (4.8% vs. 3.4%, stable CAD vs. non-CAD) and the primary composite outcome including death due to cardiovascular disease, HFH, or the necessity for upgrading to biventricular pacing (6.7% vs. 3.9%, stable CAD vs. non-CAD), were observed. In stable CAD patients, LBBaP demonstrated lower pacing thresholds and higher R wave amplitudes when compared to HBP. Additionally, LBBaP also had significantly lower occurrences of the primary composite outcome (6.7% vs. 19.6%, P = 0.003) and HFH (4.8% vs. 13.1%, P = 0.031) than RVP in stable CAD patients, particularly among patients with the higher ventricular pacing (VP) burden (&amp;gt;20% and &amp;gt;40%).ConclusionCompared with non-CAD patients, LBBaP was found to be attainable in stable CAD patients and exhibited comparable mid-term safety and prognosis. Furthermore, in the stable CAD population, LBBaP has demonstrated more stable pacing parameters than HBP, and better prognostic outcomes compared to RVP.

Abstract 15377: Traditional Cardiovascular Risk Factors Do Not Fully Explain the Risk of CAD Population in Colombia

Introduction: Major cardiovascular events occur even having reached LDL-C goals. Tolima department has the highest rate of cardiovascular mortality within Colombia. Hypothesis: in patients who underwent percutaneous coronary intervention (PCI) in a healthcare institution in Ibague Colombia, there is an increasing cardiovascular risk regardless of traditional risk factors. Methods: Descriptive, retrospective analysis of a cohort of patients with coronary artery disease (CAD) with PCI between 2020-2023. A multiple logistic regression model was developed, adjusted for predictors of CAD (Figure 1). Data was analyzed through R-4.3.0, JASP0.17.1 and Python3.11. Results: A sample size of 463 patients who underwent PCI was assessed (Table 1). Dyslipidemia was the most prevalent risk factor 43.2%(n=200). Mean LDL-C was 102, mean HDL was 38 and mean triglycerides was 186. The most incident coronary heart disease was NSTEMI 50.5%(n=234). Data was fitted into a logistic regression model accounting for comorbidities, risk factors and lipid profile values. Regression coefficients computed for CAD were around 0.07. Independent variables explain approximately 7 up to 16.1% of the variance observed in the dependent variable (Figure 1). Conclusions: In primary and secondary prevention for CAD, there is a high prevalence of risk factors. Although risk factors impact the outcome, they account for a relatively little variability within the model. Results imply that there are other key factors that contribute to the outcome and may not be measured currently. Further studies must be developed to evaluate markers in residual risk that may have an impact on the prognosis of patients with CAD.

Understanding the Link Between Adult Asthma and Coronary Artery Disease: A Narrative Review.

Asthma is a common pathology worldwide that occurs due to chronic inflammation of the respiratory airways. Persistent pulmonary inflammation leads to low-grade systemic inflammation, influencing blood vessels and triggering coronary artery disease (CAD) events. This review's objectives include discussing the susceptible population for CAD, the mechanism underlying CAD creation in asthma patients, the characteristics of asthma, and the influence of anti-asthmatic medications on CAD development. Adult-onset asthma is strongly linked to CAD and stroke. Future research may shed light on these disparities. Atherosclerosis and asthma are linked through both intrinsic and extrinsic pathways, with inflammation being the intrinsic pathway and hypoxia and tachyarrhythmia being the extrinsic pathways. The most probable mechanisms for increased coronary vasospastic angina (CVsA) incidence in asthmatic patients are vascular smooth muscle cell hypercontraction and endothelial dysfunction. Studies have shown a dose-response relationship between asthma control and myocardial infarction (MI) risk, with uncontrolled asthma at the highest risk. Impairment of ventilatory function is a distinct risk factor for lethal MI and cardiovascular death (CVD). The use of beta-2-agonists and chronic oral glucocorticoid therapy in severe asthmatics has been linked to increasing the risk for CAD. However, some studies have shown that the risk of MI among patients with active asthma is not related to the use of asthma medications. Further research is needed to determine the involvement of adult asthma features and their treatments in the development of CAD.

Elevated urine albumin creatinine ratio increases cardiovascular mortality in coronary artery disease patients with or without type 2 diabetes mellitus: a multicenter retrospective study

BackgroundAlbuminuria has been suggested as an atherosclerotic risk factor among the general population. However, whether this association will be amplified in patients with coronary artery disease (CAD) is unknown. It is also unknown whether diabetes mellitus confounds the association. We aim to analyse the prognosis of elevated urine albumin creatinine ratio (uACR) in the CAD population with or without type 2 diabetes mellitus (T2DM).MethodsThis multi-center registry cohort study included 5,960 patients with CAD. Patients were divided into T2DM and non-T2DM group, and baseline uACR levels were assessed on three grades (low: uACR < 10 mg/g, middle: 10 mg/g ≤ uACR < 30 mg/g, and high: uACR ≥ 30 mg/g). The study endpoints were cardiovascular mortality and all-cause mortality.ResultsDuring the median follow-up of 2.2 [1.2–3.1] years, 310 (5.2%) patients died, of which 236 (4.0%) patients died of cardiovascular disease. CAD patients with elevated uACR had a higher risk of cardiovascular mortality (middle: HR, 2.32; high: HR, 3.22) than those with low uACR, as well as all-cause mortality. Elevated uACR increased nearly 1.5-fold risk of cardiovascular mortality (middle: HR, 2.33; high: HR, 2.34) among patients without T2DM, and increased 1.5- fold to 3- fold risk of cardiovascular mortality in T2DM patients (middle: HR, 2.49; high: HR, 3.98).ConclusionsEven mildly increased uACR could increase the risk of cardiovascular mortality in patients with CAD, especially when combined with T2DM.

Association of hemoglobin glycation index with prognosis of coronary artery disease after percutaneous coronary intervention: A retrospective cohort study.

To analyze the association between hemoglobin glycation index (HGI) and the long-term prognosis of patients with coronary artery disease (CAD) after percutaneous coronary intervention (PCI). Predicted glycated hemoglobin (HbA1c) level was calculated using an established formula and HGI represented the difference between laboratory measured HbA1c and predicted HbA1c. A total of 1780 patients were stratified into three subgroups (HGI < -0.4, -0.4 ≦ HGI < 0.12 and HGI ≧ 0.12). The primary endpoints included all-cause mortality (ACM) and cardiac mortality (CM). The secondary endpoints were major adverse cardiac events (MACEs) and major adverse cardiac and cerebrovascular events (MACCEs). ACM occurred in 54 patients: 22 (3.7) in the low-HGI subgroup, 8 (1.3) in the moderate-HGI subgroup and 24 (4.1) in the high-HGI subgroup (p = .012). After adjusting for the traditional clinical prognostic factors, multivariate Cox regression analysis showed that patients in both the low and high HGI subgroups had significantly increased risk of ACM as compared with patients in the moderate HGI subgroup (hazard ratio [HR] = 4.979, 95% confidence interval [CI]: 1.865-13.297, p = .001 and HR = 2.918, 95% CI: 1.075-7.922, p = .036). However, we did not find significant differences in the incidence of CM, MACEs and MACCEs. HGI can predicts risk for long-term mortality in patients undergoing PCI. This index could be helpful for the effective clinical management of the CAD population.

The Management and Antithrombotic Strategies of Patients with Coronary Artery Disease and High Bleeding Risk.

In this review, we aim to summarize the current understanding of high bleeding risk (HBR) patients in coronary artery disease (CAD) and provide a comprehensive evaluation of the available antithrombotic strategies for both percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) procedures. CAD is a major cause of mortality among cardiovascular diseases, resulting from insufficient blood flow in the coronary artery due to atherosclerosis. Antithrombotic therapy is a crucial component of drug therapy for CAD and multiple studies had been focusing on the optimal antithrombotic strategies of different CAD populations. However, there is no fully harmonized definition of the model of bleeding, and the optimal antithrombotic strategy for such patients at HBR is inconclusive. In this review, we summarize bleeding risk stratification models for CAD patients and discuss the de-escalation of antithrombotic strategies among HBR patients. Furthermore, we realize that for certain subgroups of CAD-HBR patients, more individualized and precise antithrombotic strategy development is needed. So, we highlight special populations, such as CAD patients combined with valvular diseases, with both high ischemia and bleeding risks, and those proceeding surgical treatment, which requires greater research attention. We note that de-escalating therapy for CAD-HBR patients is an emerging trend in managing this population, but the optimal antithrombotic strategies should be re-considered according to the patient's baseline characteristics.

Atrial Fibrillation Recurrence Rate in Different Clinical Groups: Coronary Artery Disease and Age Matter

BACKGROUND: Catheter ablation (CA) is an established method for atrial fibrillation (AF) treatment. Up to 20% of patients with AF develop coronary artery disease (CAD) as a secondary diagnosis. The data on whether the CAD affects the efficacy of AF ablation is contrary, while arterial hypertension is a known risk factor for AF as well as for AF recurrence after the CA.&#x0D; AIM: We conducted this research to assess the AF recurrence rate and its risk factors after the primary catheter AF ablation procedure in the different clinical groups including IdiopathicAF, AF concomitant to arterial hypertension (HTN) and AF concomitant to CAD.&#x0D; MATERIALS AND METHODS: Patients who underwent 451 PVI procedures performed since January 2016 to December 2017 were screened for AH, CAD and other structural heart disease. Among them 153 pts were selected for the subsequent analysis and divided into 3 groups IdiopathicAF, AF + AH, AF + CAD.&#x0D; RESULTS: The presence of CAD (r = 0.313, p 0.001), age (r = 0.224, p = 0.008), CHA2DS2-VASc score (r = 0.279, p = 0.001), history of MI (r = 0.240, p = 0.004), LA size (r = 0.204, p = 0.018) were correlated with the recurrence rate. In the AF + CAD group patients older than 65 years demonstrated dramatically lower AF-free survival rate (37.5%) in comparison to younger CAD population (75%, log-rank p 0.001) as well as to younger and older non-CAD patients.&#x0D; CONCLUSIONS: The presence of CAD should always attract the attention of physicians before considering the AF ablation as an option to treatment. Elderly CAD patients have the lowest ablation efficacy and the best strategy for this group (more extensive primary ablation or conversion to the permanent AF) needs to be studied.

A preliminary study of dobutamine myocardial flow reserve on 99mTc-Sestamibi CZT-SPECT

With improved resolution and sensitivity, the cadmium zinc telluride (CZT) detector measures myocardial blood flow (MBF) and myocardial flow reserve (MFR) via single photon emission computed tomography (SPECT). Recently, many studies have used vasodilator stress to obtain quantitative indexes. However, dobutamine used as a pharmaceutical stress has been rarely used to quantify myocardial perfusion using CZT-SPECT. Our study retrospectively analyzed the blood flow performance of 99mTc-Sestamibi (99mTc -MIBI) CZT-SPECT comparing dobutamine to adenosine. The study aims to explore whether dobutamine stress can be used for the myocardial perfusion quantitative analysis via CZT-SPECT as well as compare dobutamine MBF and MFR to adenosine. It was a retrospective study. A total of 68 patients with suspected or known coronary artery disease (CAD) were consecutively enrolled in this study. Thirty-four patients underwent dobutamine stress 99mTc-MIBI CZT-SPECT. Another thirty-four patients underwent adenosine stress 99mTc-MIBI CZT-SPECT. Patient characteristics, myocardial perfusion imaging (MPI) results, gated-myocardial perfusion imaging (G-MPI) results and quantitative analysis of MBF and MFR were collected. In dobutamine stress group, stress MBF was significantly higher than rest MBF (median [interquartile range], 1.63 [1.46-1.94] vs. 0.89 [0.73-1.06], P < 0.001). In adenosine stress group, similar results were observed (median [interquartile range], 2.01 [1.34-2.20] vs. 0.88 [0.75-1.01], P < 0.001). When comparing the dobutamine and adenosine stress group, global MFR showed significant differences (median [interquartile range], the dobutamine group: 1.88 [1.67-2.38] vs. the adenosine group: 2.19 [1.87-2.64], P = 0.037). MBF and MFR can be measured using dobutamine 99mTc -MIBI CZT-SPECT. In small sample single-center study, there was a difference in MFR produced by adenosine and dobutamine within the suspected or the known CAD population.

Association of an ADRB3 Variant with Coronary Artery Disease Within the Chinese Han Population: Construction of a Predictive Nomogram Model

Objective: Coronary artery disease (CAD) is a the most common type of heart disease, and is associated with the highest mortality rate. The role of the β3-adrenergic receptor gene (ADRB3) in energy homeostasis and lipolysis suggests that it may be associated with obesity, insulin resistance, diabetes, and hypertension. Herein, we sought to examine the relationship between CAD and variants of the ADRB3 gene in individuals with Han and Uygur ethnicities in China. Methods: All 1022 participants were genotyped for two ADRB3 single nucleotide polymorphisms (SNPs; rs1892818 and rs9693898) using real-time polymerase chain reaction (TaqMan). Uygur (259 CAD patients, 161 control group) and Han (308 CAD patients, 294 control group) were included in two case-control studies. We subsequently developed a predictive model using ADRB3 genetic variation and clinical variables to predict risk of CAD. Results: The rs1892818 CT genotype (8.5% vs 3.9%, p = 0.019) and T allele (4.3% vs 1.9%, p = 0.021) were more frequently detected in the control subjects compared to CAD patients of the Han population but not in the Uygur population. The rs9693898 was not associated with CAD in either ethnic population. Logistic regression analysis further demonstrated that carriers of the rs1892818 CT genotype had a lower risk of CAD than did those with the CC genotype (CT vs CC, p = 0.044, odds ratio [OR] = 0.441, 95% confidence interval [CI]: 0.199-0.976). Using this data, we constructed a predictive nomogram model for CAD with an area under the curve (95% CI) of 0.722 (0.682, 0.761). Conclusions: Our results suggest that rs1892818 is associated with CAD in the Han population and that the CT genotype of rs1892818 may serve as a protective factor for CAD in Han individuals. The proposed nomograms can be used for the prediction of CAD in this population.

Measures of insulin resistance as a screening tool for dysglycaemia in patients with coronary artery disease. A report from the EUROASPIRE V population

Abstract Background The optimal screening strategy for dysglycaemia, including type 2 diabetes (T2DM) and impaired glucose tolerance (IGT), in patients with coronary artery disease (CAD) is debated. Purpose We tested the hypothesis that measures of insulin resistance by homeostasis model assessment (HOMA) indexes may constitute accurate screening methods in a CAD population. Methods Insulin, C-peptide, glycated haemoglobin A1c (HbA1c) and an oral glucose tolerance test (OGTT) were centrally assessed in 3534 CAD patients without known dysglycaemia from the EUROASPIRE V survey. Three different HOMA indexes were calculated: HOMA-IR, HOMA2 based on insulin (HOMA2-ins), and HOMA2 based on C-peptide (HOMA2-Cpep). Dysglycaemia was diagnosed based on the two-hour postload glucose (2hPG) value obtained from the OGTT. Information on study participants was obtained by standardised visits. The optimal thresholds of the three HOMA indexes for dysglycaemia diagnosis were obtained by the maximum value of Youden's J statistic on receiver operator characteristics curves. The diagnostic performance of such thresholds was tested for both T2DM (i.e. in reference to a 2hPG value ≥11 mmol/L) and dysglycaemia (i.e. in reference to 2hPG value ≥7.8 mmol/L) and their correlation with several clinical parameters was assessed by Spearman's coefficients. Results The mean age of the patients was 63 years and 25% were women. Fifty-four percent of the patients had central obesity, 18% were current smokers, mean blood pressure was 133/80 mmHg and mean LDL-cholesterol 2.4 mmol/L. The OGTT revealed that 41% were dysglycaemic (IGT = 24% and T2DM = 16%). Mean insulin, C-peptide and HOMA indexes were significantly higher in patients with vs. without newly detected dysglycaemia (all p&amp;lt;0.0001). Sensitivity and specificity of the three HOMA indexes for the diagnosis of dysglycaemia were low and the associations between 2hPG and the other parameters in the total sample were weak, with Spearman correlation coefficients of 0.15 for fasting insulin, 0.19 for C-peptide, 0.24 for HOMA-IR, 0.18 for HOMA2-ins and 0.22 for HOMA2-Cpep. HOMA-IR, HOMA2-ins and C-peptide were strongly correlated with body mass index and waist circumference (Spearman correlation coefficients ranging 0.43–0.47). Conclusion Screening for dysglycaemia in CAD patients by insulin, C-peptide, HOMA-IR, HOMA2-ins and HOMA2-Cpep had insufficient diagnostic performance to detect dysglycaemia with reference to the yield of an OGTT, which should still be prioritized. Further studies are warranted to assess whether measures of insulin resistance might be better markers of unfavourable metabolic derangement beyond dysglycaemia. Funding Acknowledgement Type of funding sources: Private company. Main funding source(s): European Society of CardiologyErling-Perssons Stiftelse

Association of eNOS Glu298Asp polymorphism with cardiometabolic risk and inducible myocardial ischemia in patients with stable coronary artery disease

Abstract Background The endothelial nitric oxide synthase (eNOS) gene deficiency is known to cause insulin resistance, hypertension, hypertriglyceridemia and impaired coronary vasodilating capability in animal models. In the general clinical population, the eNOS gene polymorphism (Glu298Asp, G894T), able to reduce eNOS activity, was associated either with features of the metabolic syndrome or prevalence of coronary artery disease (CAD). Purpose To investigate the possible association of Glu298Asp polymorphism with cardiometabolic risk [insulin resistance, increased triglycerides (TG) and low HDL-cholesterol (HDL-C)], obstructive CAD and inducible myocardial ischemia in stable patients with suspected coronary disease. Methods Six cardiology units enrolled a total of 506 consecutive patients (314 males; mean age 62±9 years) referred for suspected CAD within the BIOGEN-CARE Tuscan Region Italian Study. Among these, 325 patients underwent stress ECG or cardiac imaging to assess the presence of inducible ischemia and 436 patients underwent non invasive computerized tomography or invasive coronary angiography to assess the presence of obstructive CAD (&amp;gt;50% stenosis in at least one major coronary vessel). Blood samples were collected from each patient for genotyping and measurements of lipid and glucose parameters. The TG/HDL-C ratio and the TyG-index [ln(TG × Fasting plasma glucose/2)] were used as synthetic markers of atherogenic dyslipidemia and insulin resistance, main components of the cardiometabolic risk. Results In the whole population, 49.6% of patients were homozygous for the G894allele, 40.9% heterozygotes, and 9.5% homozygous for T894. Myocardial ischemia was documented in 160/325 (49.2%) patients undergoing stress testing and obstructive CAD in 178/436 (40.8%) patients undergoing coronary angiography. Patients carrying the T allele (dominant model TT+GT vs GG) had higher TG/HDL ratio (2.7±1.8 vs 2.5±1.9, P=0.03) (Figure) without differences in other lipid and glucose markers. Independent predictors of obstructive CAD were age, gender, obesity, diabetes and TG/HDL-C ratio but not the the T allele (OR 0.80; CI 0.51–1.25; ns). Independent predictors of inducible ischemia were age, gender, obesity and the T allele (OR 1.91; CI 01.19–3.08; P=0.007). Stratifying the population for both obstructive CAD and ischemia, the T allele was associated with increased risk of ischemia (OR 1.96; CI 1.11–3.44; P=0.02) even after adjustment for the presence of obstructive CAD (OR 3.09; CI 1.85–5.78; P&amp;lt;0.001) (Figure 1). Conclusions In stable patients with suspected CAD, the eNOS Glu298Asp gene polymorphism is an independent risk factor for inducible myocardial ischemia and is significantly associated with the specific cardiometabolic risk expressed by high TG and low HDL-C which independently predicts obstructive CAD. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): “BIOhumoral and GENetic predictors of CARdiac Evolving phenotype in Ischemic Heart Disease (BIOGENCARE-IHD)”; funded by Toscan Region-Programma per la ricerca regionale in materia di Salute 2009

Serum Trimethylamine N-Oxide Levels Correlate with Metabolic Syndrome in Coronary Artery Disease Patients.

Trimethylamine N-oxide (TMAO) is a gut microbial metabolite that affects atherogenesis and glucose dysregulation. The purpose of this study was to look at the link between blood TMAO levels and metabolic syndrome (MetS) in individuals with coronary artery disease (CAD). Blood samples were obtained in fasting status, and serum TMAO level was quantified by high-performance liquid chromatography–mass spectrometry. MetS and its components were defined according to the International Diabetes Federation diagnostic criteria. Of 92 enrolled patients, 51 (55.4%) had MetS. Patients with MetS had a greater proportion of hypertension and diabetes mellitus, higher body weight, waist circumference, body mass index, systolic blood pressure, fasting glucose, triglycerides, blood urea nitrogen, creatinine, C-reactive protein (CRP), insulin level, homeostasis model assessment of insulin resistance, and TMAO level. Multivariable logistic regression models revealed that TMAO level (odds ratio: 1.036, 95% confidence interval: 1.005–1.067, p = 0.023) could be an effective predictor of MetS among the CAD population. In these patients, the log-TMAO level was positively associated with log-CRP (β = 0.274, p = 0.001) and negatively associated with eGFR (β = −0.235, p = 0.022). In conclusion, our study revealed a positive association between serum TMAO level and MetS among patients with CAD.

The U-Shaped Relationship Between Serum Uric Acid and Long-Term All-Cause Mortality in Coronary Artery Disease Patients: A Cohort Study of 33,034 Patients.

BackgroundAssociations between high serum uric acid (SUA) and cardiovascular diseases have been reported. However, few studies have been conducted to explore the relationship between SUA and long-term all-cause mortality in coronary artery disease (CAD) patients. Our study aims to investigate the relationship between SUA and long-term all-cause mortality in patients with CAD.MethodsFrom January 2007 to December 2018, we divided 33,034 patients with CAD admitted in the Guangdong Provincial People's Hospital into five groups (quintile 1: SUA <5.05 mg/dl, quintile 2: 5.05 mg/dl ≤ SUA <5.59 mg/dl, quintile 3:5.59 mg/dl ≤ SUA <6.8 mg/dl, quintile 4, 6.8 mg/dl ≤ SUA <7.93 mg/dl, and quintile 5, SUA ≥7.93 mg/d;). This study used Kaplan–Meier survival analysis to evaluate patient outcomes with different ranges of SUA. Cox proportional hazards regression models and restricted cubic spline were applied to determine the association between serum uric and long-term all-cause mortality.ResultsA total of 33,034 participants were recruited, including 24,780 (75.01%) men and 8,254 (24.99) women in this cohort study. Median follow-up was 4.91 years. We found that SUA is an independent risk factor of long-term all-cause mortality according to the result of Cox proportional hazards models. This study also illustrated an approximate U-shape association between SUA and all-cause mortality when compared with 5.95 mg/lL ≤ SUA <6.8 mg/dl, SUA <5.0 5mg/dl (adjusted hazard ratio (aHR) =1.13, 95% CI: 1.01–1.26, p = 0.03), and SUA ≥8 mg/dL (aHR = 1.18, 95% CI: 1.06-1.32, p = 0.003).ConclusionOur study indicated a U-shaped relationship between SUA and long-term all-cause mortality in patients with CAD. No matter whether SUA is too high or too low, it increased the all-cause mortality in the CAD population, which deserves to be closely monitored.

29 ENDOTHELIN-1 LEVEL IN HYPERTENSIVE SUBJECTS BETWEEN CORONARY ARTERY DISEASE AND HEALTHY POPULATIONS

Background: Hypertension is known as independent factor in correlation with coronary artery disease (CAD) and play important part in atherosclerotic process. In an animal model with hypertension which endothelin-1 play as a vasoconstrictor, there was overexpression of endothelin-1 in the vessel walls. This overexpression suggests a role of endothelin-1 in hypertension patient, especially among CAD. Material and methods: This was a cross-sectional study. A total 226 subjects were analysed, consisted of 127 subjects with CAD and 99 healthy population. The CAD subjects were patients underwent elective coronary angiography with significant CAD lesion. The healthy population were respondents of Sleman-HDSS survey (year 2019). Hypertensive subjects were defined those with history of hypertension from anamnesis. Diabetic subjects were excluded. The endothelin-1 was measured from peripheral serum samples by ELISA method. The comparative analysis was performed with Mann-Whitney test and the correlation was performed with Spearman correlation test. Results: Mean serum endothelin-1 level was 2.1±1.2 pg/mL in hipertensive and 2.6±1.6 pg/mL in normotensive (p=0.063) among CAD subjects. Among healthy population, mean serum endothelin-1 level was 1.7±0.7 pg/mL in hypertensive and 1.8±0.8 pg/mL) in normotensive, (p=0.675). In addition, Spearman correlation between serum endothelin-1 and systolic blood pressure showed correlation coefficient —0.045 (p = 0.543) in CAD subjects and -0.165 (p=0.069) in healthy population which indicated inverse correlation between those parameters in both populations. Conclusion: Serum endothelin-1 level did not differ significantly based on hypertensive status both in CAD and healthy population. There was a tendency toward decreased serum endothelin-1 level in hypertensive subjects.

Circulating serum amyloid A levels but not SAA1 variants predict long-term outcomes of angiographically confirmed coronary artery disease.

Circulating serum amyloid A (SAA) levels are strongly associated with atherosclerotic cardiovascular disease risk and severity. The association between SAA1 genetic variants, SAA levels, inflammatory marker levels, and coronary artery disease (CAD) prognosis has not been fully understood. In total, 2199 Taiwan Biobank (TWB) participants were enrolled for a genome-wide association study (GWAS), and the long-term outcomes in 481 patients with CAD were analyzed. The primary endpoint was all-cause mortality, and the secondary endpoint was the combination of all-cause death, myocardial infarction, stroke, and hospitalization for heart failure. Through GWAS, SAA1 rs11024600 and rs7112278 were independently associated with SAA levels (P = 3.84 × 10-145 and P = 1.05 × 10-29, respectively). SAA levels were positively associated with leukocyte counts and multiple inflammatory marker levels in CAD patients and with body mass index, hemoglobin, high-density lipoprotein cholesterol, and alanine aminotransferase levels in TWB participants. By stepwise linear regression analysis, SAA1 gene variants contributed to 27.53% and 8.07% of the variation of the SAA levels in TWB and CAD populations, respectively, revealing a stronger influence of these two variants in TWB participants compared to CAD patients. Kaplan-Meier survival analysis revealed that SAA levels, but not SAA1 gene variants, were associated with long-term outcomes in patients with CAD. Cox regression analysis also indicated that high circulating SAA levels were an independent predictor of both the primary and secondary endpoints. SAA1 genotypes contributed significantly to SAA levels in the general population and in patients with CAD. Circulating SAA levels but not SAA1 genetic variants could predict long-term outcomes in patients with angiographically confirmed CAD.

Comparison between a genetic risk score and the European SCORE in cardiovascular events prediction in a primary prevention population

Abstract Background The risk for Coronary Artery Disease (CAD) can be estimated using different scores, such as the European SCORE (Systematic Coronary Risk Evaluation) scale or genetic risk score (GRS). The addition of GRS to the European SCORE may increase the precision of predicting MACE (Major Adverse Cardiovascular Events). Purpose This study aims to compare the European SCORE and the multiplicative genetic risk score (mGRS) in predicting MACE. Methods and results The study included 1110 asymptomatic individuals without known CAD from GENEMACOR prospective registry. We defined the primary endpoint of all-cause cardiovascular events. The study population had mean age of 51.6 years, 74.1% male and had risk factors of diabetes (11.6%), dyslipidemia (67.5%), hypertension (48.1%) and smoking (22.9%). Using C-index methodology, mGRS score was superior to SCORE in predicting MACE (mGRS = 0.832 Vs SCORE = 0.615; p=0.014). Conclusions The mGRS score was superior to SCORE in predicting MACE in an asymptomatic and free of CAD population. Genetic information may improve cardiovascular risk stratification in primary prevention. Funding Acknowledgement Type of funding sources: None.

Coronary artery disease and familial hypercholesterolaemia patients' eligibility for PCSK-9 inhibitors: who is to benefit from lower ldl thresholds?

Abstract Purpose High and very high cardiovascular risk patients are usually possible candidates for PCSK-9 inhibitors. Coronary artery disease (CAD) and Familial Hypercholesterolaemia (FH) patients belong to this group by definition, according to 2019 recent dyslipidaemia guidelines. The real contribution of each group to potential eligibility for PCSK-9 is to be investigated. Methods We enrolled 1892 inpatients prospectively for 12 months, diagnosed either with chronic CAD or with acute coronary syndrome (ACS). In order to test eligibility for PCSK-9 inhibitors, three different LDL thresholds were used in our model for very high and high risk groups: 55mg/dl and 70mg/dl, 70mg/dl and 100mg/dl, 100mg/dl and 130mg/dl, as recommended by the 2019 and 2016 ESC/EAS Guidelines for Dyslipidaemia and the National Health Care system, respectively. A proprietary software was developed and eligibility was determined by using patient clinical information and different criteria. Dutch Lipid Clinic Network criteria were used to determine heterozygous FH population. Results The eligible percentage for the three classifications was 18.6%, 7.7% and 1.8%, in the total CAD population respectively. Definite/ probable FH percentages among our population were 4.8%, 3.4%, 1.4%, respectively. Solely CAD eligible population was 13.8%, 4.3% and 0.4% respectively. The increase of the eligible percentages toward more recent guidelines was mostly attributed to the increasing number of coronary patients who become eligible as our criteria become stricter while the percentage of the eligible CAD/FH population only slightly increases. Conclusions FH is a significant cardiovascular risk factor but stricter criteria and LDL thresholds, favour solely CAD patients. Using real-world data and an adjustable model, we provide a realistic estimation of PCSK-9 eligibility among CAD patients. Funding Acknowledgement Type of funding sources: None. Subgroup analysis of eligible population

Genetically determined risk of mood swings and cardiometabolic diseases: mendelian randomization study

Abstract Background Mood swings is believed to associated with increased risk of Cardiometabolic Diseases (CMD). However, the roles of mood swings on CMD are controversial because of the bias of reverse causation and/or confounding in epidemiological studies. Hence, we use a two-sample MR approach to identify the causal association between genetically determined mood swings and CMD. Methods We obtained 33 independent single-nucleotide polymorphisms (SNPs) with genome-wide significant (P&amp;lt;5×10–8) associated with mood swings as instrumental variable in UK Biobank. Summary data of outcomes were extracted from the Coronary Artery Disease Genome-wide Replication and Meta-analysis plus the Coronary Artery Disease Genetics consortium, the Diabetes Genetics Replication and Meta-analysis consortium, the CKDGen consortium, and the International Stroke Genetics Consortium. Results The genetic instrument of 33 SNPs explained 4.8% of the variance in mood swings. Genetically determined mood swings was associated with an increased risk of coronary artery disease (CAD) (odds ratio 3.12, 95% confidence interval 1.92 to 5.08; P=4.32×10–6). However, mood swings had no effect on the other cardiometabolic outcomes. The above estimates were consistent across all three MR methods without significant heterogeneity. Also, there was no evidence of directional pleiotropy for each outcome except for large artery stroke. Conclusions Using MR approaches that are able draw causal inference, our results suggest that interventions aimed at improving mood swings in the population would lead to a reduction risk of CAD, which highlights the importance of mood management in high-risk CAD population. Funding Acknowledgement Type of funding sources: None.