Angina Group Research Articles

Stress-induced coronary spasms: evaluating the role of serum cortisol in variant angina

Abstract Background and purpose Variant angina is a type of angina pectoralis caused by vasospasm, and the patients were recommended to take lifelong medication to suppress spasms. In addition to risk factors, mental stress can be a precipitating factor in vasospasm. We can analyze whether mental stress can affect vasospasm by analyzing the relationship between serum cortisol levels, the major stress hormone, and coronary artery vasospasm. Methods We prospectively enrolled patients who were admitted for coronary angiography from October 2022 to August 2023. We divided them into 2 groups: variant angina and those who had other angiographic findings such as insignificant, stable angina, unstable angina, or non ST segment elevation myocardial infarction. The primary endpoint was the norepinephrine, cortisol, and adrenocorticotropic hormone (ACTH) level at admission, cortisol and ACTH level at Day 1 after admission, and after discharge when visiting the outpatient clinic. We used students' t-tests to examine the differences between groups. Results A total of 196 patients were enrolled, and 23 patients were diagnosed with variant angina. The variant angina group showed significantly higher serum cortisol levels on Day1 than the other diagnosis group (10.1±3.4 µg/dL vs. 8.4±4.1 µg/dL, p-value 0.044). There were no significant differences between baseline norepinephrine, ACTH, cortisol levels, Day 1 ACTH, and serum ACTH, cortisol levels after discharge. However, the serum cortisol levels showed an increased trend than other diagnosis group (baseline cortisol 9.7±3.5 vs. 8.3±4.1, p-value 0.082; after discharge cortisol 9.3±2.7 vs. 8.6±3.6, p-value0.294). Conclusions The variant angina group had a higher level of serum cortisol level than other diagnosis groups. Also, this trend was sustained at baseline and after discharge. Further research with a large cohort is warranted.

Association between lipoprotein-associated phospholipase A2 gene Val279Phe homozygous genotypes and variant angina in Japanese women

Abstract Background The role of the lipoprotein-associated phospholipase A2 gene (PLA2G7) in the pathogenesis of cardiovascular diseases remains controversial. The PLA2G7 gene normally produces a protein called "plasma platelet activating factor-acetylhydrolase"(PAF-AH). Homozygotes of rs76863441, which is PLA2G7 Val279Phe polymorphism, produce none of PAF-AH, and heterozygotes produce less than half of the normal levels. This polymorphism is rare outside of Asia and is particularly common in Japan, where homozygous mutations account for 4% of the population. The association between rs76863441 and risk of myocardial infarction was significant in ethnicity for Japanese population, but not in other countries. Variant angina is a severe case of coronary artery spasm (CSA) and causes an acute myocardial infarction. It is widely accepted that variant angina is more common in Japanese than in other races. Purpose The aim of this study was to examine the possible association between rs76863441 and variant angina. Methods rs76863441 was analyzed by direct sequencing in 62 patients with variant angina (43 men and 19 women with a mean age of 60.0±11.6 years). In all patients, ST segment elevation was recorded on ECG and coronary angiography was performed. Acetylcholine provocation test was performed in 31 patients. We compared genotypes of rs76863441 between variant angina patients and 872 healthy volunteers without a history of heart diseases living in the same area, who participated in the Iwaki Health Promotion Project, which has been conducted by the Hirosaki University School of Medicine since 2005. These volunteers had undergone Japonica Arrays, which is the SNP array for the Japanese population. Results Homozygotes genotype for rs76863441, heterozygotes genotype, and wild genotype were present in 4 (6.5%), 22 (35.5%), and 36 (58.1%) of the variant angina group, respectively, and in 30 (3.4%), 246 (28.2%), and 596 (68.3%) of the control group, respectively. Statistically, there were no significant differences in genotypes between the variant angina group and the control group. Next, males and females were analyzed separately. In males, there were no significant differences in homozygous mutations (1 out of 43 patients (2.3%) in the variant angina group vs. 11 out of 327 patients (3.4%) in the control group, P=1.00). However, in females, there was a significant difference in homozygous mutations (3 out of 19 (15.8%) in the variant angina group vs. 19 out of 545 (3.4%) in the control group, P=0.033). Conclusions These findings indicate that homozygotes of rs76863441, which has PAF-AH deficiency, may be associated with the pathogenesis of variant angina in Japanese women. Further functional analyses of this mutation are of great interest.Genotypes of rs76863441Gender disparities of rs76863441

Differences in clinical characteristics, angina, and quality of life among patients with microvascular vs vasospastic angina and no obstructive coronary artery disease (ANOCA)

Abstract Background In patients with angina and no obstructive coronary disease (ANOCA), the underlying pathophysiology includes microvascular angina (endothelial-dependent and independent coronary microvascular dysfunction (CMD)) and vasospastic angina (microvascular spasm and epicardial spasm) diagnosed with invasive coronary functional angiography (CFA). However, whether there are differences in demographics, clinical characteristics, and outcomes by underlying diagnosis is unknown. We hypothesize that microvascular angina patients will be older and have more cardiovascular risk factors and worse outcomes than the vasospastic angina group. Objective To explore the differences in demographics, risk factors, and outcomes in ANOCA patients with microvascular and vasospastic angina. Methods A prospective registry-based cohort study of consecutive CFA was performed in 156 ANOCA patients between 2020 and 2023 using the Doppler-tipped guide wire method. Patients were classified into microvascular angina, vasospastic angina, and mixed disease. Microvascular angina was defined as endothelial-independent CMD (coronary flow reserve [CFR] < 2.5 in response to adenosine) and/or endothelial-independent CMD (coronary blood flow [CBF] < 50% or no change in vessel diameter in response to 54 mcg intracoronary acetylcholine). Vasospastic angina as microvascular (<90% constriction) and epicardial spasm (>90% constriction) to 108 mcg intracoronary acetylcholine. The mixed disease group included microvascular and vasospastic angina. Validated questionnaires evaluated angina (SAQ-7), functional capacity (DASI), dyspnea severity (UCSD SOB), and perceived stress (PSS) were obtained from patients at office visits prior to undergoing CFA. Results Among 156 ANOCA patients, 114 had microvascular angina, 10 had vasospastic angina, and 32 had mixed disease. The average age was 58.5 (SD 11.2) years. Demographics and prevalence of risk factors, such as hypertension, hyperlipidemia, or diabetes, showed no significant differences among the microvascular, vasospastic, or mixed disease groups. The prevalence of heart failure with preserved ejection fraction (HFpEF) was high across the groups, and outcomes did not differ significantly among them. The SAQ-7 score average ranged from 16.9 to 40.3, consistent with moderate to severe angina, and the DASI score ranged from 32.2 to 34.9, consistent with moderate functional capacity. Dyspnea severity ranged from 30 to 41, consistent with low to moderate severity, and perceived stress ranged from 11.5 to 13, consistent with low to moderate stress among all participants. Conclusion In patients with ANOCA undergoing invasive CFA, demographics, cardiovascular risk factors, and outcomes were similar regardless of underlying diagnosis. We demonstrate a high prevalence of risk factors and HFpEF and evidence of moderate to severe symptoms and functional capacity in ANOCA patients across all diagnoses.Abbreviation explanation for table 1

The correlation between stable angina and inflammatory factors and blood lipids: a case-control study

ObjectiveIn this study, we aimed to compare the levels of inflammatory markers (C-reactive protein, CRP; procalcitonin, PCT) and blood lipids (total cholesterol, TC; triglyceride, TG; high-density lipoprotein cholesterol, HDL-C; low-density lipoprotein cholesterol, LDL-C) between patients with stable angina and control group, and to explore the correlation between these parameters and the severity and prognosis of stable angina.MethodsWe retrospectively selected 113 patients with stable angina and 128 control group from the medical record system, and compared their inflammatory factors and blood lipids. We also assessed the severity of angina using the Canadian Cardiovascular Society (CCS) classification and followed up the patients for 1 year to record any cardiovascular events.ResultsWe found that patients with stable angina had significantly higher levels of CRP, TC, TG, and LDL-C, and lower levels of HDL-C than control group. Moreover, CRP, TC, TG, and LDL-C were positively correlated with the severity of angina, while HDL-C was negatively correlated. During the follow-up period, 37 patients with stable angina experienced cardiovascular events, and they had higher levels of CRP, TC, TG, and LDL-C, and lower levels of HDL-C than those who did not.ConclusionOur study suggests that inflammation and dyslipidemia are closely related to stable angina, and that inflammatory factors and blood lipids can be used as indicators of the severity and prognosis of stable angina.

Morphological Changes of Peri-Coronary Adipose Tissue Together with Elevated NLR in Acute Myocardial Infarction Patients in-Hospital.

Inflammation triggers atherosclerotic plaque rupture, leading to acute myocardial infarction (AMI). Following AMI, peri-coronary adipose tissue (PCAT) undergoes a transition from lipid-rich to hydrophilic characteristics due to vascular inflammation. This study investigates PCAT changes and neutrophil-to-lymphocyte ratio levels during AMI. 60 AMI patients undergoing coronary computed tomography angiography and angiography (Jan 2020-Jun 2022) were studied 60 age, gender, BMI-matched stable angina, and 60 non-coronary artery disease patients were included. Siemens VB20.0 measured PCAT-volume and fat attenuation index (FAI). Neutrophil-to-lymphocyte ratio levels were calculated by peripheral blood tests. The PCAT volume and PCAT-FAI gradually increased across the control, stable angina, and AMI groups, with a corresponding gradual rise in NLR. NLR exhibited weak positive correlation with PCAT-FAI (r=0.35) and PCAT-volume (r=0.24). Multivariable logistic regression identified increased PCAT-volume, PCAT-FAI and neutrophil-to-lymphocyte ratio as possible independent AMI risk factors. No significant PCAT-volume difference was observed between infarct-related artery (IRA) and non-IRA for all three coronary arteries. Only PCAT-FAI around IRA-LAD was higher than non-IRA-LAD (-74.84±6.93 HU vs -79.04±8.68 HU). PCAT-FAI around culprit vessels in AMI was higher than corresponding lesion related vessel in SA. PCAT-volume around narrowed non-IRA in AMI was higher than that of corresponding LRV in SA. PCAT-FAI of narrowed non-IRA-LADs and non-IRA-LCXs in AMI were elevated compared to LADs (-78.46±8.56HU vs -83.13±8.34 HU) and LCXs (-73.83±10.63 HU vs -81.38±7.88 HU) of lesion related vessel in stable angina. We found an association between AMI and inflammation in the coronary perivascular adipose tissue and systemic inflammatory response.

Sex differences in optimal medical therapy following invasive angiography for coronary artery disease

Abstract Funding Acknowledgements Type of funding sources: Other. Main funding source(s): HARP Wellcome Trust PhD Fellowship Grant & NIHR Biomedical Research Centre Introduction Coronary artery disease (CAD) remains the number one cause of death in women worldwide despite advances in treatment (1). Women who experience myocardial infarction (MI) and undergo invasive angiography experience higher morbidity and mortality compared to their male counterparts. Data suggests that this mortality difference may be predominantly in women >55 years (2). Treatment bias may be an important factor. Prognostic benefit of optimal medical therapy (OMT) following MI is well established, however studies and meta-analyses suggest women may be less likely to receive this compared to men e.g (3, 4). Purpose We aimed to establish whether there were sex differences in OMT received following invasive angiography for obstructive CAD at a large cardiac centre. Methods In this single centre retrospective study, we examined OMT received by females and males undergoing invasive angiography in 2019 with proven obstructive CAD, as defined by an angiographic lesion ≥50% of luminal diameter. Discharge medications were extracted from the electronic patient record and entered into a database. Pooled analysis of sex differences and sub-group analysis according to diagnosis (STEMI, NSTEMI, stable angina) and age (≤ 55 years or >55 years) was performed. Multivariate binomial logistic regression was used to adjust for confounders including BMI, diabetes, hypertension, hypercholesterolaemia, previous MI and previous percutaneous coronary intervention. Results 4,346 patients underwent invasive angiography during the study period. 2,358 with obstructive CAD and full medication details available at the present time were included (STEMI: 649 [mean age: 59.7, 20.6 % female], NSTEMI: 439 [mean age 63.4, 22.6% female], Stable angina: 1,270 [mean age 63.7, 22.2% female]). Pooled analysis showed females were less likely to receive aspirin and beta-blockers (OR=0.64, p=0.009, OR=0.66, p=0.001). They also received fewer angiotensin-converting enzyme inhibitors (ACE-I) but more angiotensin receptor blockers (ARB) (OR=0.58, p<0.001, OR=1.45, p=0.009). Subgroup analysis revealed females >55 with STEMI were less likely to receive beta-blockers and high potency antiplatelets compared to males (OR=0.49, p=0.009, OR=0.44, p=0.011). In the NSTEMI group females ≤55 received fewer beta-blockers and statins (OR=0.16, p=0.020, OR=0.004, p=0.045). In the stable angina group females ≤55 were less likely to receive aspirin (OR=0.07, p<0.001). Fewer ACE-I and more ARB in females was predominantly in the stable angina group (OR=0.56, p<0.001, OR= 1.50, p=0.021). Conclusion Women undergoing invasive angiography for obstructive CAD appeared to receive less OMT compared to men across several drug categories, diagnoses and age groups. Future work will be directed at understanding why these differences occurred and the mechanistic consequences of these differences in OMT pharmacology between females and males.

Association of testosterone with myocardial infarction and severity of coronary artery disease among male patients

BackgroundCoronary heart disease (CHD) remains a leading cause of morbidity and mortality, particularly in aging populations. Men typically exhibit higher rates of CHD compared to women, with testosterone levels inversely associated with cardiovascular risk. This study investigates the relationship between testosterone levels and angiographically confirmed CHD, disease severity, and myocardial infarction (MI) among CHD cases. MethodsA cohort of 1724 male patients undergoing diagnostic or interventional coronary angiography was examined. Demographic, clinical, and biochemical data were collected, including serum total testosterone levels. The severity of CHD was assessed using the Gensini score, and MI cases were diagnosed according to World Health Organization criteria. ResultsResults revealed significant differences in testosterone levels among CHD subtypes, particularly between MI and unstable angina/stable angina groups (p < 0.001). Testosterone levels were inversely correlated with CHD severity, as evidenced by the Gensini score (Pearson coefficient = −0.062, P = 0.004). Cross-validation random forest analysis demonstrated the significant contribution of testosterone to CHD severity discrimination (p < 0.05). ConclusionsThere is an association between testosterone and a predisposition to severe CAD indicated by Gensini score and myocardial infarction.

Alterations in the gut mycobiome with coronary artery disease severity

BackgroundCoronary artery disease (CAD) is a prevalent cardiovascular condition, and numerous studies have linked gut bacterial imbalance to CAD. However, the relationship of gut fungi, another essential component of the intestinal microbiota, with CAD remains poorly understood. MethodsIn this cross-sectional study, we analyzed fecal samples from 132 participants, split into 31 healthy controls and 101 CAD patients, further categorized into stable CAD (38), unstable angina (41), and acute myocardial infarction (22) groups. We conducted internal transcribed spacer 1 (ITS1) and 16S sequencing to examine gut fungal and bacterial communities. FindingsBased on ITS1 analyses, Ascomycota and Basidiomycota were the dominant fungal phyla in all the groups. The α diversity of gut mycobiome remained unaltered among the control group and CAD subgroups; however, the structure and composition of the mycobiota differed significantly with the progression of CAD. The abundances of 15 taxa gradually changed with the occurrence and progression of the disease and were significantly correlated with major CAD risk factor indicators. The mycobiome changes were closely linked to gut microbiome dysbiosis in patients with CAD. Furthermore, disease classifiers based on gut fungi effectively identified subgroups with different degrees of CAD. Finally, the FUNGuild analysis further categorized these fungi into distinct ecological guilds. InterpretationIn conclusion, the structure and composition of the gut fungal community differed from healthy controls to various subtypes of CAD, revealing key fungi taxa alterations linked to the onset and progression of CAD. Our study highlights the potential role of gut fungi in CAD and may facilitate the development of novel biomarkers and therapeutic targets for CAD. FundingThis work was supported by the grants from the National Natural Science Foundation of China (No. 82170302, 92168117, 82370432), National clinical key specialty construction project- Cardiovascular Surgery, 2024 Reform and Development Program of Beijing Institute of Respiratory Medicine, the Beijing Natural Science Foundation (No. 7222068); the Reform and Development Program of Beijing Institute of Respiratory Medicine (No. Ggyfz202308); and the Clinical Research Incubation Program of Beijing Chaoyang Hospital Affiliated to Capital Medical University (No. CYFH202209).

Negative association of apelin plasma levels with epicardial fat thickness in patients with stable angina and acute myocardial infarction: A case-control study.

Apelin is one of the endogenous peptides that play a key role in the homeostasis of cardiovascular diseases. The purpose of the current study was to evaluate the correlation between apelin levels and epicardial fat thickness (EFT) in patients with stable angina and acute myocardial infarction (AMI). In a case-control study, 90 patients nominated for angiography were enrolled in the study and divided into three groups: healthy subjects without angiographic findings (Con), stable angina pectoris group (SAP), and acute AMI group. Data collected from all subjects included biochemical, echocardiographic, and angiographical parameters. The Gensini score analyzed the severity of coronary artery disease (CAD). A decrease in adjusted apelin levels was evident in the AMI and SAP groups compared with healthy individuals (for both P < 0.001), especially in the AMI group. In addition, a detectable negative association was identified between apelin and Gensini score (r = -0.288, P = 0.006), Ck-MB (r = -0.300, P = 0.004), EFT (r = -0.300, P = 0.004), and troponin-T (r = -0.288, P = 0.006). Myocardial injury in patients with CAD appears to play a significant role in apelin concentration independent of the role of adipose tissue, which requires further studies.

A Cross-Sectional Study of Acute Coronary Syndrome and Thyroid Profile: Dissecting the Relationship to Improve Patient Care.

Thyroid-releasing hormones are pivotal in regulating cardiovascular (CVS) function and maintaining its hemodynamics and homeostasis. Even a minor alteration in thyroid function has an enormous implication on CVS morbidity and mortality. Moreover, hypothyroidism was found to be a potential menace for coronary artery disease (CAD).The objective of this study was to determine the role of thyroid-releasing hormones in patients suffering from acute coronary syndrome (ACS). Among a cohort of 100 patients suffering with ACS, a complete history and clinical information followed by physical examinationand electrocardiography were recorded. Blood samples were also collected to record the blood sugar levels i.e., fasting blood sugar (FBS), postprandial blood sugar (PPBS), and thyroid profile, including free thyroid stimulating hormone (TSH), free thyroxine (fT4), free triiodothyronine (fT3), and reverse triiodothyronine (rT3). The data was analyzed using SPSS version 26 software (IBM Corp., Armonk, NY, USA). The study identified alterations in the thyroid hormone levelsin 27% of patients suffering from ACS. The prevalence of euthyroid sick syndrome was found to be 59.3%, while subclinical hypothyroidism and subclinical hyperthyroidism were reported among 18.5% and 14.8% of patientsrespectively. Therewas no significant difference found between males and females. The study illustrated a greater occurrence of aberrant thyroid hormone profiles among those aged 40-60 years. The ST-elevated myocardial infarction (STEMI) group had a statistically significant higher prevalence of an aberrant thyroid hormone profile compared to the non-ST-elevated myocardial infarction (NSTEMI) and unstable angina (UA)groups (p=0.02). A total of nine patients died with ACS and all of those had statistically significant low fT3 and TSH values while higher rT3 values (p<0.05). An atypical thyroid status has been found to elevate the likelihood of developing CAD and experiencing CVS mortality. This condition can impact ventricular function and serum cholesterol levelsas well as heart rate and rhythm. Therefore, understanding this relationship could potentially lead to improved treatment strategies for individuals with ACS which will further prevent major CVS complications.

The role of computed tomography angiography in assessing the correlation between properties of coronary atherosclerotic plaque and blood lipids.

Coronary atherosclerotic heart disease (CAHD) is the leading cause of death in developed countries. This study aimed to explore the correlation between the properties of coronary atherosclerotic plaque and blood lipids using computed tomography angiography (CTA). A total of 83 patients with coronary heart disease were included in this study (males: 50; females: 33; average age: [59 ± 8] years old). They were classified into the stable angina group and unstable angina group. Atherosclerotic plaques were classified as fatty plaques (soft plaques), fibrous plaques, and calcified plaques based on the computed tomography (CT) values. SPSS 17.0 statistical software was used to analyze the correlation between the properties of angina and the CT values of atherosclerotic plaques, blood lipids, and plaque properties, and then compared between the stable and unstable angina groups. There were statistically significant differences in plaque properties between the stable and unstable angina groups (P< 0.001). During CTA examination, we found statistically significant differences in the CT density values of atherosclerotic plaques between the stable and unstable angina groups (P< 0.001). There were statistically significant differences between the properties of angina and the level of blood lipids (P< 0.05). Anginal properties negatively correlated with calcified plaques and positively correlated with non-calcified plaques. Calcified plaques negatively correlated with total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG), and positively correlated with high-density lipoprotein cholesterol (HDL-C). Non-calcified plaques negatively correlated with HDL-C and positively correlated with TC, LDL-C, and TG.

Association of GAL-8 promoter methylation levels with coronary plaque inflammation

Background and aimsCoronary heart disease (CHD) is a condition that carries a high risk of mortality and is associated with aging. CHD is characterized by the chronic inflammatory response of the coronary intima. Recent studies have shown that the methylation level of blood mononuclear cell DNA is closely associated with adverse events in CHD, but the roles and mechanisms of DNA methylation in CHD remain elusive. Methods and resultsIn this study, the DNA methylation status within the epigenome of human coronary tissue in the sudden coronary death (SCD) group and control (CON) group of coronary heart disease was analyzed using the Illumina® Infinium Methylation EPIC BeadChip (850 K chip), resulting in the identification of a total of 2553 differentially methylated genes (DMGs). The differentially methylated genes were then subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and significant differential DNA methylation was found. Among the differentially hypomethylated genes were GAL-8, LTF, and RFPL3, while the highly methylated genes were TMEM9B, ANK3, and C6orF48. These genes were mainly enriched in 10 significantly enriched pathways, such as cell adhesion junctions, among which the differentially methylated gene GAL-8 was involved in inflammatory pathway signaling. For functional analysis of GAL-8, we first examined the differences in GAL-8 promoter methylation levels among different subgroups of human coronary tissue in the CON, CHD, and SCD groups using pyrophosphate sequencing. The results revealed reduced GAL-8 promoter methylation levels in the SCD group, while the difference between the CHD and CON groups was not statistically significant (P > 0.05). The reduced GAL-8 promoter methylation level was associated with upregulated GAL-8 expression, which led to increased expression of the inflammatory markers TNF-α, IL-1β, MCP-1, MIP-2, MMP-2, and MMP-9. This enhanced inflammatory response contributed to the accumulation of foam cells, thickening of the intima of human coronary arteries, and increased luminal stenosis, which promoted the occurrence of sudden coronary death. Next, we found that GAL-8 promoter methylation levels in PBMC were consistent with human coronary tissue. The unstable angina group (UAP) had significantly lower GAL-8 promoter methylation levels than stable angina (SAP) and healthy controls (CON) (P < 0.05), and there was a significant correlation between reduced GAL-8 promoter methylation levels and risk factors for coronary heart disease. These findings highlight the association between decreased GAL-8 promoter methylation and the presence of coronary heart disease risk factors. ROC curve analysis suggests that methylation of the GAL 8 promoter region is an independent risk factor for CHD. In conclusion, our study confirmed differential expression of GAL-8, LTF, MUC4D, TMEM9B, MYOM2, and ANK3 genes due to DNA methylation in the SCD group. We also established the consistency of GAL-8 promoter methylation alterations between human coronary tissue and patient peripheral blood monocytes. The decreased methylation level of the GAL-8 promoter may be related to the increased expression of GAL-8 and the coronary risk factors. ConclusionsAccordingly, we hypothesized that reduced levels of GAL-8 promoter methylation may be an independent risk factor for adverse events in coronary heart disease.

Improved heart function and cardiac remodelling following sacubitril/valsartan in acute coronary syndrome with HF.

This study sought to assess the effect of treatment of sacubitril/valsartan (S/V) on improving cardiac function and reversing cardiac remodelling in patients with acute coronary syndrome (ACS) complicated with heart failure with reduced ejection fraction after percutaneous coronary intervention (PCI). We enrolled 275 ACS patients with reduced left ventricular ejection fraction after PCI. The patients were divided into the routine and S/V groups according to the treatment drugs. The symptoms, N-terminal pro-brain natriuretic peptide (NT-proBNP) concentrations, echocardiographic parameters [left ventricular ejection fraction (LVEF), left ventricular mass index (LVMI), left ventricular end-diastolic volume index (LVEDVI), and left ventricular end-systolic volume index (LVESVI)], major adverse cardiac events (MACEs), and adverse reactions were recorded at baseline and 6months after treatment when a clinical follow-up was performed. The S/V group was further divided into prespecified subgroups including unstable angina (UA) group, non-ST-elevation myocardial infarction (NSTEMI) group, and ST-elevation myocardial infarction (STEMI) group according to the type of ACS. We analysed the changes in LVEF, LVMI, LVEDVI, LVESVI, and NT-proBNP in both groups and evaluated the correlation between the changes in the above variables (ΔLVEF, ΔLVMI, ΔLVEDVI, ΔLVESVI, and ΔNT-proBNP). Cox regression model was used to assess the independent risk factors of MACE. Prespecified subgroup analyses were also conducted. Compared with baseline, LVEF increased significantly (P<0.05), NT-proBNP, LVMI, and LVESVI decreased significantly in both groups after 6months (P<0.05), and LVEDVI decreased significantly in the S/V group (P=0.001). In the S/V group, ΔLVEF (t=-2.745, P=0.006), ΔNT-proBNP (P=0.009), ΔLVEDVI (t=4.203, P=0.001), and ΔLVESVI (t=3.907, P=0.001) were significantly improved than those in the routine group. In the S/V group, ΔLVEF was negatively correlated with ΔNT-proBNP (r=-0.244, P=0.004), ΔLVMI (r=-0.190, P=0.028), ΔLVEDVI (r=-0.173, P=0.045), and ΔLVESVI (r=-0.261, P=0.002). In Cox regression model analysis,ΔLVEF {hazard ratio [HR]=0.87 [95% confidence interval (CI) 0.80-0.95], P=0.003}, ΔLVEDVI [HR=1.04 (95% CI 1.01-1.06), P=0.013], and ΔLVESVI [HR=1.04 (95% CI 1.01-1.08), P=0.026] were independent risk factors for MACE. Subgroup analysis showed that ΔLVEF (t=6.290, P=0.001), ΔLVEDVI (t=2.581, P=0.011), and ΔNT-proBNP (P=0.019) in the NSTEMI group were significantly improved than those in the UA group, ΔLVEDVI in the NSTEMI group was significantly better than that in the STEMI group (t=-3.365, P=0.001), and ΔLVEF in the STEMI group was significantly better than that in the UA group (t=-3.928, P=0.001). There was a significant difference in the survival probability without MACE among the three groups in the analysis of the Kaplan-Meier curve (P=0.042). The incidence of MACE in the UA group was significantly higher than that in the NSTEMI group (32.4% vs. 6.3%, P=0.004). The cardiac function is improved and cardiac remodelling is reversed significantly after treatment of S/V in ACS patients with reduced left ventricular ejection fraction after PCI, and the improvement is more obvious than the routine group. There is a significant negative correlation between the change in LVEF and the changes in NT-proBNP, LVMI, LVEDVI, and LVESVI. The increase of LVEF and the decrease of LVEDVI and LVESVI are protective factors to improve the prognosis. Patients with myocardial infarction and reduced left ventricular ejection fraction might benefit more from the initiation of S/V as first-line heart failure treatment after PCI.

Serum circPRDM5 as a novel diagnostic biomarker for acute myocardial infarction

BackgroundCircular RNA (CircRNA) is known to play an important role in cardiovascular diseases, but its use as a biomarker of acute myocardial infarction (AMI) has not been studied. This study explores the feasibility of circPRDM5 as a novel biomarker of AMI. MethodsCircPRDM5 was screened by bioinformatics, the correct circPRDM5 primers were tested by agarose gel electrophoresis (AGE) and Sanger sequencing, and the expression level of serum circPRDM5 was detected by Quantitative Reverse Transcription-Polymerase Chain Reaction.(qRT-PCR), and the diagnostic value of circPRDM5 was analyzed by the receiver operating characteristic (ROC) curve. ResultsThe expression of circPRDM5 in serum of AMI patients was significantly decreased compared with that of healthy control group and angina group (P < 0.001). The area under ROC curve of serum circPRDM5 was 0.862 [95 % CI, 0.814–0.909]. The combined diagnosis of serum circPRDM5, cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB) could improve the sensitivity of diagnosing AMI. The expression level of serum circPRDM5 increased after percutaneous coronary intervention (PCI). ConclusionsCircPRDM5 can be used as a novel biomarker for AMI, and its combination with cTnT and CK-MB can improve diagnostic value.

Homocysteine and Lp-PLA2 levels: Diagnostic value in coronary heart disease.

Coronary heart disease (CHD) is the leading cause of mortality worldwide. Identifying effective diagnostic markers and understanding risk factors is crucial for prevention and management. This study aimed to investigate the levels of homocysteine (Hcy) and lipoprotein-associated phospholipase A2 (Lp-PLA2) in human plasma and their roles in the diagnosis and prognosis of CHD. A retrospective study was conducted on 232 patients with CHD, divided into Acute Myocardial Infarction, unstable angina pectoris, and stable angina pectoris groups, and a control group of 75 healthy adults. Blood samples were analyzed for serum Hcy and Lp-PLA2 levels using the cycling enzyme method and ELISA method, respectively. Statistical analyses were performed to evaluate the risk factors, and diagnostic efficacy was assessed using receiver operating characteristic (ROC) curves. No significant differences in age and sex were observed between the study and control groups, whereas marked disparities in risk factors such as obesity, hypertension, diabetes, and hyperlipidemia were noted. Significant differences in serum Hcy and Lp-PLA2 levels were identified among the CHD subgroups. Univariate and multivariate logistic regression analyses revealed that Hcy, Lp-PLA2, hypertension, and hyperlipidemia were significant risk factors for CHD. The combined diagnostic Area Under the Curve (AUC) for Hcy and Lp-PLA2 was found to be higher than that when using them individually. This study identified the elevation of Hcy and Lp-PLA2 levels as independent risk factors for CHD, and their conjoint analysis significantly enhanced clinical diagnostic efficacy. These findings provide valuable insights for CHD diagnosis, treatment, and prevention, highlighting the importance of these markers in CHD management.

Long-term outcomes of patients with ischemia and no obstructive coronary artery disease (INOCA) - a systematic review and meta-analysis

Abstract Background Myocardial ischemia with no obstructive coronary artery disease (INOCA) is an increasingly recognized syndrome that encompasses coronary vasomotor disorders such as coronary microvascular dysfunction (CMD) and coronary vasospasm. However, the prognosis of patients with INOCA is not well defined. Purpose To perform a systematic review and meta-analysis of previous studies evaluating the long-term prognosis of patients with INOCA stratified by the underlying vasomotor disorder. Methods We searched Medline, Embase, Web of Science, and Cochrane databases combining terms for INOCA and outcomes to identify observational studies evaluating the prognosis of patients with INOCA published between 1984 and 2021. The primary outcomes were composite of all-cause death and MI, and major adverse cardiovascular events (MACE) at annual intervals for up to 5-year follow-up. Meta-analytic averages with 95% confidence intervals (CI) of the incidence of primary outcomes for INOCA, each INOCA endotype, and by method used to determine the diagnosis were calculated using the random effect models. Results We identified a total of 52 studies (19765 patients) meeting eligibility criteria. Of those, 22 included patients with vasospastic angina and 34 with microvascular angina. The rate of all-cause death and MI in the vasospastic angina group was 0.7 (95% CI 0.4-1.0)/100 patient-years [Figure 1] and the rate of MACE was 1.1 (95% CI 0.6-1.9)/100 patient-years [Figure 2]. For patients with microvascular angina the rate of all cause death and MI was 1.2 (95% CI 0.7-1.7)/100 patient-years [Figure 1] and the rate of MACE was 2.8 (95% CI 1.8-4.0)/100 patient-years [Figure 2]. Patients with evidence of microvascular dysfunction by non-invasive (CFR) or invasive (CFR, IMR, TIMI frame count) criteria had 2.7 times higher all-cause death and MI rates than patients whose diagnosis was established solely based on an abnormal exercise or imaging stress test (2.6 (95% CI, 0.8-5.1) vs. 0.7(95% CI, 0.4-1.2)/100 patient-years, p=0.034). Conclusions Overall, patients with INOCA have a low rate of MACE events or death, although there is heterogeneity based on the underlying phenotype. Patients with vasospastic angina have a relatively benign long-term prognosis, whereas patients with microvascular angina have a significantly higher rate of MACE at long-term follow-up. Among patients with microvascular angina, those with objective evidence of abnormal microvascular function (such as reduced CFR) had 2.7 times higher rates of all-cause death and MI.Incidence of all cause death and MIIncidence of MACE

The value of serum lipoprotein-associated phospholipase A2, ischemia-modified albumin, and cystatin C in predicting coronary heart disease risk: a single center retrospective cohort study.

This study aims to explore the value of serum lipoprotein-associated phospholipase A2 (Lp-PLA2), ischemia-modified albumin (IMA), and cystatin C (Cys-C) in predicting the risk of coronary heart disease (CHD). Clinical data from 104 CHD patients admitted to our hospital from January 2020 to December 2022 were analyzed. Of them, 31 patients had stable angina (Group-S), 36 patients were diagnosed with unstable angina (Group-U), and 37 patients had acute myocardial infarction (Group-A). Additionally, clinical data from 35 healthy individuals undergoing physical examination during the same time period were selected as the control group. Levels of blood lipid indicators and serum Lp-PLA2, IMA, and Cys-C levels were compared between the groups. The rates of diabetes, hypertension, and smoking in Group-S, Group-U, and Group-A were significantly higher than those in the control group (p<0.05). Levels of Lp-PLA2, IMA, and Cys-C in Group-S, Group-U, and Group-A were significantly higher than those in the control group (p<0.05). Levels of Lp-PLA2, IMA, and Cys-C in Group-U and Group-A were significantly higher than those in Group-S, and Group-A had the highest value of these indexes (p<0.05). Multivariate logistic regression analysis showed that Lp-PLA2, Cys-C, and IMA were important risk factors for the onset of CHD (p<0.05). Receiver operating characteristic (ROC) curve analysis showed that the area under the curve (AUC) of Lp-PLA2, IMA, and Cys-C predicting the occurrence of CHD was 0.775, 0.835, and 0.735, respectively. The combined prediction of the three factors has an AUC of 0.920, which is higher than the individual prediction. Lp-PLA2, IMA, and Cys-C are closely related to the onset and progression of CHD. These indicators, therefore, can be used in clinical practice to predict and evaluate CHD.

Coronary Heart Disease among Male Patients of Age between 25-39- and 40-70-Years Attending Cardiology Outdoor of BSMMU, Dhaka, Bangladesh

Background: Coronary heart disease (CHD) is a major health concern and the top cause of death in Bangladesh. Similar to other South Asian nations, Bangladeshis are highly susceptible to CHD, with early onset and severe progression. The exact pathophysiology remains unclear, but genetics, metabolic syndrome, and traditional risk factors are significant contributors. Aim of the study: The aim of the study was to compare the risk factors and coronary heart disease severity in male patients between 25-39 and 40-70 years. Methods: This cross-sectional observational study took place in the Cardiology Department of Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh, spanning from September to December 2013. It involved 166 male CHD patients aged 25-70. Group A comprised 83 patients aged 25-39, while Group B consisted of 83 patients aged 40-70, selected purposively. Results: The mean age of all participants was 43.6±10.6 years. In both groups, most patients had stable angina (Group A: 80%, Group B: 78%). Group A had 70% smokers, 34% with hypertension, and 30% with a family history of IHD, overweight/obesity, and impaired fasting glucose (IFG). In contrast, Group B had 48% hypertensive patients, with 45% smokers, 39% IFG, 31% overweight/obesity, 29% diabetes, and 12% family history of IHD. Vessel involvement was evenly distributed in Group A, while in Group B, 46% had triple vessel involvement. Conclusion: Among coronary heart disease patients aged 25-39 years, the smoking rate is higher, while diabetes prevalence is lower compared to the 40-70 year’s age group. Conversely, in the 40-70-year-old patient group, there is a higher incidence of hypertension, double vessel diseases, and triple vessel diseases compared to the younger group.

Role of Neutrophil to Lymphocyte Ratio in Risk Stratifying Patients with Unstable Angina and NSTEMI

Abstract Background A well-known fact about acute myocardial infarction is its association with leukocytosis. The differential analysis of white blood cells gives additional benefit of assessing ACS severity by clinical outcomes. Obtaining peripheral leukocyte count is a cheap and widely available mode. Aim of the Work The aim of the study was to test the value of neutrophil to lymphocyte ratio in risk stratifying patients with acute coronary syndromes and its early outcomes. Patients and Methods A total of 100 patients with UAP and NSTEMI were prospectively evaluated at Ain Shams University Hospital (63% UAP and 37% NSTEMI).The patients were followed for clinical outcomes for 48 hours in-hospital and 1 month after discharge. Results The median (IQR) NLR was 8.4 (5.3 to 9.7) in NSTEMI group versus 1.8 (1.2 to 2.8) in unstable angina group, NLR &amp;gt; 3.9 had a sensitivity of 100%, specificity of 92% as a diagnostic value. All patients were divided into “low risk,” “intermediate risk” and “high risk” groups according to TIMI score. In unstable angina group, the quartiles of NLR in “low risk,” “intermediate risk” and “high risk” groups were 3.01 (2.01, 4.33), 3.39 (2.36, 5.10) and 5.49 (3.44, 9.65). In NSTEMI group, the quartiles of NLR in “low risk,” “intermediate risk” and “high risk” groups were 5.08 (3.07, 8.14), 5.17 (2.98, 9.05) and 6.49 (3.86, 11.68). Meaning that there is positive correlation, as NLR were found to be significantly higher in high risk groups. Conclusion Admission NLR is the strong and independent predictor of cardiovascular outcomes in patients with NSTEMI and UAP. Consequently, given the advantages of NLR, it may be the ideal marker for risk stratification in patients with NSTEMI and UAP. Despite the science of inflammatory biomarkers having been described decades ago, NLR appears to be enjoying a renaissance as a cost-effective biomarker with immediate clinical predictability and prognostication. The ease and rapidity of performing these tests make them an independent, simple, inexpensive and accurate early predictor of high-risk TIMI score patients in ACS. Abbreviations ACS: Acute coronary syndrome; AMI: Acute myocardial infarction; CAD: Coronary artery disease CK: Creatine kinase cTnI: Cardiac troponin I cTnT: Cardiac troponin T; EDTA: Ethylene-diamine-tetra-acetic acid; MI: Myocardial infarction; NLR: Neutrophil-to-lymphocyte ratio; NSTEMI: Non-ST-elevation myocardial infarction; SCD: Sudden cardiac death; STEMI: ST-elevation myocardial infarction; TLC: Total leucocyte count; UA: Unstable angina; UAP: Unstable angina pectoris; VF: Ventricular fibrillation; WBC: White blood cell count

Interleukin-33/sST2: Dynamic assessment in patients with acute coronary syndrome

PurposeInterleukin (IL)-33 and its soluble receptor ST2 (sST2) play a crucial role in the immune response. sST2 has been approved by the Food and Drug Administration as a prognostic biomarker of mortality in chronic heart failure patients, however, the role of IL-33 and sST2 in atherosclerotic cardiovascular disease remains unclear. The aim of this study was to measure serum level of IL-33 and sST2 of patients at the onset of acute coronary syndrome (ACS) and 3 months after primary percutaneous revascularization. Patients and methodsForty patients were divided into ST segment elevation myocardial infarction (STEMI) group, non-ST segment elevation myocardial infarction (NSTEMI) and unstable angina (UA) group. IL-33 and sST2 level were measured with ELISA. Additionally, IL-33 expression in peripheral blood mononuclear cells (PBMCs), was evaluated. ResultsAll ACS patients had a significantly lower level of sST2 3 months after ACS as compared to the baseline (p ​< ​0.039). The STEMI patients had higher serum levels of IL-33 at the moment of ACS as compared to 3 months after the event, with an average decrease of 17.87 ​pg/ml (p ​< ​0.007). Conversely, sST2 serum levels were still high after 3 months following an ACS in STEMI patients. ROC curve demonstrated that increased IL-33 serum level could be STEMI predictor. ConclusionsThe assessment of the baseline and dynamics of changes in IL-33 and sST2 concentrations in patients with ACS may be important for the diagnostic process and may help in understanding of how the immune mechanisms work at the moment of an ACS event.