Accuracy of salivary biomarkers in the diagnosis of periodontal status and coronary heart disease.

Inflammatory illnesses, such as periodontitis and atherosclerotic coronary heart disease (ASCHD), trigger the production of pro-inflammatory mediators. The aim of this study was to assess the accuracy of using salivary interleukin-1ß (IL-1ß), interleukin-18 (IL-18), and gasdermin D (GSDMD) in discerning patients with periodontitis with and without ASCHD from healthy individuals, and to assess their correlation with clinical periodontal parameters and low-density lipoprotein (LDL) levels. The study involved 120 participants: 30 were healthy subjects (control group, C), 30 had generalized periodontitis (group P), 30 had ASCHD and clinically healthy periodontium (group AS-C), and 30 had ASCHD and generalized periodontitis (group AS-P). Saliva and blood samples were collected, and periodontal characteristics such as plaque index, bleeding on probing, probing pocket depth, and clinical attachment loss were examined. IL-1ß, IL-18, and GSDMD levels from saliva were determined using ELISA. LDL levels were determined from the blood samples. Groups P, AS-C, and AS-P had higher levels of salivary IL-1ß, IL-18, and GSDMD than group C. The receiver operating characteristic (ROC) curves of all biomarkers showed high diagnostic accuracy, with a significant positive correlation with the clinical parameters and LDL levels. The observed correlations between the studied pro-inflammatory mediators and disease severity suggest that these biomarkers could serve as indicators of disease progression in conditions such as periodontitis and ASCHD.

Jingzhi Guanxin Oral Liquids Attenuate Atherosclerotic Coronary Heart Disease via Modulating Lipid Metabolism and PPAR-Related Targets.

Jingzhi Guanxin Oral Liquids (JZGX), a traditional Chinese medicine formulation prepared from the decoction of five herbs, has been utilized to relieve chest pain with coronary artery disease (CAD). However, the chemical composition and therapeutic mechanisms of JZGX remain obscured. In this research, the potential targets and pathways of JZGX against CAD were anticipated through network pharmacology based on analyzing its chemical constituents using UPLC-Q-TOF-MS/MS. One hundred seven ingredients in JZGX were identified. The 39 active chemicals and 37 key targets were screened, and CAD-related signaling pathways were clustered, mainly associated with lipid metabolism. Subsequently, the atherosclerotic CAD animal model employing 24 weeks of high-fat diet (HFD) ApoE-/- mice was constructed to investigate the JZGX efficacy and underlying mechanisms validating network forecasts. The histological staining examination and cardiovascular biomarker tests confirmed that JZGX reduced plaque formation in the aorta and decreased blood lipids in vivo. It featured anti-inflammatory, anti-thrombotic, and myocardial protective effects. JZGX prevented excessive lipid deposits and inflammation within the liver and exhibited hepatoprotective properties. Serum untargeted metabolomics analysis indicated that JZGX ameliorated metabolic abnormalities in atherosclerotic CAD mice and prompted lipid metabolism, especially linoleic acid. The PPARs and attached critical targets (SREBP1, FASN, PTGS2, and CYP3A), filtered from the networks and connected with lipid metabolism, were dramatically modulated through JZGX administration, as revealed by western blotting. The molecular docking outcomes showed that all 39 active ingredients in JZGX had good binding activity with PPARα and PPARγ. These findings illustrate that JZGX alleviates atherosclerotic CAD progression by remodeling the lipid metabolism and regulating PPAR-related proteins.

PCSK9 induces endothelial cell autophagy by regulating the PI3K/ATK pathway in atherosclerotic coronary heart disease.

OBJECTIVE: Atherosclerosis is a chronic inflammatory disease of the arteries, and its pathogenesis is related to endothelial dysfunction. It has been found that the protein convertase subtilin/kexin9 type (PCSK9) plays an important role in AS, but its specific mechanism is still unclear. METHODS: In this study, we first cultured human umbilical vein endothelial cells (HUVECs) with 50 or 100µg/ml oxidized low-density lipoprotein (ox-LDL) for 24 hours to establish a coronary atherosclerosis cell model. RESULTS: The results showed that ox-LDL induced HUVEC injury and autophagy and upregulated PCSK9 protein expression in HUVECs in a concentration-dependent manner. Silencing PCSK9 expression with siRNA inhibited ox-LDL-induced HUVEC endothelial dysfunction, inhibited the release of inflammatory factors, promoted HUVEC proliferation and inhibited apoptosis. In addition, ox-LDL increased the expression of LC3B-I and LC3B-II and decreased the expression of p62. However, these processes are reversed by sh-PCSK9. In addition, sh-PCSK9 can inhibit PI3K, AKT and mTOR phosphorylation and promote autophagy. CONCLUSION: Taken together, our research shows that silencing PCSK9 inhibits the PI3K/ATK/mTOR pathway to activate ox-LDL-induced autophagy in vascular endothelial cells, alleviating endothelial cell injury and inflammation.

Immune landscape and regulatory mechanisms in human atherosclerotic coronary plaques: Evidence from single-cell and bulk transcriptomics.

Atherosclerosis is a chronic immuno-inflammatory disease, however, the immune landscape and regulatory mechanisms have not been clear. We detected seven principal immune cell clusters with distinct phenotypic and spatial characteristics using single-cell RNA-sequencing of aortic immune cells from patients with acute coronary syndrome and stable angina pectoris. Then we acquired 265 differentially expressed immune-related genes and the high scores were mainly found in T cells and monocytes, which were differentially regulated in atherosclerotic coronary plaques. The CCL signaling pathway was the most relevant pattern in the T cells and CCL5-CCR1 and CCL5-CCR5 ligand-receptor pairs played a vital role in the CCL signaling pathway. Further comparative analysis indicated MCH-I signaling was the most relevant pattern in the T cells and HLA ligand-related ligand-receptor pairs played a vital role. Functional analysis of the single-cell and bulk transcriptomics pointed to multiple pathways, such as antigen presentation and immune response. Nineteen common differentially expressed immune-related genes were found in both immune cells and the human peripheral blood mononuclear cells. Nine common differentially expressed transcription factors were differentially expressed in both T cell and monocyte clusters from the coronary plaques and human peripheral blood mononuclear cells and the network demonstrated that CEBPB might play an essential role in the transcriptional regulation of atherosclerosis as a hub transcription factor. The definition of immune cell diversity and heterogeneity by single-cell level analysis of aortic immune cell subsets not only unveils cell-type-specific pathways and new immune mechanisms but also discovers the functional correlation of immune cells in human atherosclerosis. Our findings provide great promise for the discovery of novel molecular mechanisms and precise therapeutic targets for atherosclerosis.

Superficial Calcified Plates Associated to Plaque Erosions in Acute Coronary Syndromes.

This study investigates the clinical relevance and therapeutic implications of the OCT identification of intracoronary superficial calcified plates (SCPs) in acute coronary syndromes (ACSs). In 70 consecutive ACS patients (pts), we studied the three main underlying ACS mechanisms: plaque erosion (PE), plaque rupture and eruptive calcified nodule (CN). The PE lesions, occurring on an intact fibrous cap overlying a heterogeneous substrate, were identified in 12/70 pts (17.1%). PE on superficial calcified plates (PE-SCP) represented 58.3% of the PE lesions (7/12 pts) and had a 10% overall incidence in the culprit lesions (7/70 pts). PE-SCP lesions occurred mostly on the left anterior descending artery, correlated with white thrombi (85.7%) and had a proximal intraplaque site (71.4%). PE-SCP lesions were treated conservatively, as nonsignificant lesions, in 4/7 pts. Our study emphasizes that the coronary calcium-related ACS risk is not only associated with the spotty calcifications or CN but also with the PE-SCP lesions.

Distinctive Morphological Patterns of Complicated Coronary Plaques in Acute Coronary Syndromes: Insights from an Optical Coherence Tomography Study.

Optical coherence tomography (OCT) is an ideal imaging technique for assessing culprit coronary plaque anatomy. We investigated the morphological features and mechanisms leading to plaque complication in a single-center observational retrospective study on 70 consecutive patients with an established diagnosis of acute coronary syndrome (ACS) who underwent OCT imaging after coronary angiography. Three prominent morphological entities were identified. Type I or intimal discontinuity, which was found to be the most common mechanism leading to ACS and was seen in 35 patients (50%), was associated with thrombus (68.6%; p = 0.001), mostly affected the proximal plaque segment (60%; p = 0.009), and had no distinctive underlying plaque features. Type II, a significant stenosis with vulnerability features (inflammation in 16 patients, 84.2%; thin-cap fibroatheroma (TCFA) in 10 patients, 52.6%) and a strong association with lipid-rich plaques (94.7%; p = 0.002), was observed in 19 patients (27.1%). Type III, a protrusive calcified nodule, which was found to be the dominant morphological pattern in 16 patients (22.9%), was found in longer plaques (20.8 mm vs. 16.8 mm ID vs. 12.4 mm SS; p = 0.04) and correlated well with TCFA (93.8%; p = 0.02) and inflammation (81.3%). These results emphasize the existence of a wide spectrum of coronary morphological patterns related to ACS.

Spontaneous coronary artery dissection: A review of diagnostic methods and management strategies.

Spontaneous coronary artery dissection (SCAD) is a rare non-atherosclerotic cause of acute coronary syndromes defined as non-iatrogenic, non-traumatic separation of the coronary artery wall. The most common profile is a middle-aged woman between 44 and 53 years with few cardiovascular risk factors. SCAD is frequently linked with predisposing factors, such as postpartum, fibromuscular dysplasia or other vasculopathies, connective tissue disease and hormonal therapy, and it is often triggered by intense physical or emotional stress, sympathomimetic drugs, childbirth and activities increasing shear stress of the coronary artery walls. Patients with SCAD usually present at the emergency department with chest discomfort, chest pain, and rapid heartbeat or fluttery. During the last decades, the most common problem of SCAD was the lack of awareness about this condition which has led to significant underdiagnosis and misdiagnosis. However, modern imaging techniques such as optical coherence tomography, intravascular ultrasound, coronary angiography or magnetic resonance imaging have contributed to the early diagnosis of the disease. Treatment of SCAD remains controversial, especially during the last years, where invasive techniques are being used more often and in more emergent cardiac syndromes. Although conservative treatment combining aspirin and beta-blocker remains the recommended strategy in most cases, revascularization could also be suggested as a method of treatment in specific indications, but with a higher risk of complications. The prognosis of SCAD is usually good and long-term mortality seems to be low in these patients. Follow-up should be performed on a regular basis.

Atherosclerotic Coronary Artery Disease in a Younger Adult With Transseptal Anomalous Left Coronary Artery.

We present a case of extensive coronary atherosclerotic disease in a younger patient with an anomalous left coronary artery with transseptal course and show the utility of multimodality evaluation to determine the culprit lesion in patients presenting with this rare association. (Level of Difficulty: Intermediate.).

Design, methods and baseline characteristics of the Beijing Hospital Atherosclerosis Study: a prospective dynamic cohort study.

Background: The atherosclerotic coronary artery disease (CAD) risk assessment based on conventional risk factors have only moderate performance, and residual risks still exist. Thus, we reported here a cohort study that aims to identify and validate the new biosignatures (especially the metabolomics, lifestyle biomarkers and biological age), and elucidate their predictive effect on CAD and subsequent cardiovascular events. Methods: This prospective, single-center, cohort study commenced in March 2017 and seeks to examine patients undergoing coronary angiography (CAG) at the Beijing Hospital. Patients' baseline demographic and medical history data are captured by questionnaires. Blood samples are taken before CAG for clinical laboratory tests and metabolomics analyses. Traditional CAD risk factors are analyzed by routine assays. CAD-related metabolites from different metabolic pathways and lifestyle biomarkers are measured by liquid chromatography-tandem mass spectrometry methods. Biological ages are calculated based on the laboratory and metabolomics data. The enrolled patients attend annual follow-up examinations for 10 years. The primary end points are the composite end points of major adverse cardiovascular events, including death from any cause, non-fatal myocardial infarction, and non-fatal stroke. Quality management and control are carried out through the entire research process, including standardized baseline and follow-up investigation, intra- and inter-run quality controls for laboratory measurements, etc. Results: Baseline data of the enrolled 2,970 patients from 2017 to 2020 were collected and are presented in this article. Among them, there were more males (62.5%) than females, and the patients tended to be old and overweight. The percentages of diagnosed hypertension and diabetes were 67.3% and 35.2%, respectively. A total of 8.5% had a family history of premature CAD. Their lipid profiles were within the normal range, probably due to the use of statins. Conclusions: This study has successfully initiated an investigation into the roles of new biosignatures in predicting CAD among Chinese Han patients undergoing CAG. To the best of our knowledge, this cohort is the first study systematically focusing on the association of lifestyle biomarkers and biological age with CAD risk. Findings from this study will provide biomarkers to discriminate the presence of CAD and to predict subsequent cardiovascular events.

Target and non-target vessel related events at 10 years post percutaneous coronary intervention.

AIMS: To define the incidence of events related to the stented vessel (target vessel related events: TVRE) and events related to non-stented vessels (non-target vessel related events: NTVRE) through to 10-year follow-up in patients post-PCI with newer generation drug eluting stents (DES). METHODS AND RESULTS: The current study is a post-hoc analysis of patient level data from two randomised controlled trials in Germany. Patients older than 18 years with ischemic symptoms or evidence of myocardial ischemia in the presence of ≥ 50% de novo stenosis located in the native coronary vessels were considered eligible. The endpoints of interest were TVRE (a composite of first target vessel myocardial infarction or target vessel revascularization) and NTVRE (a composite of first non-target vessel MI or non-target vessel revascularization) through to 10 years post PCI. We included 4953 patients in this analysis. Through to 10-years post-PCI, TVRE occurred in 1238 of 4953 patients (cumulative incidence: 25.8%) and NTVRE occurred in 1442 of 4953 patients (cumulative incidence: 30.3%). The majority of TVRE and NTVRE were revascularization events. From 0 to 1 years, the cumulative incidence of TVRE was 15.9% and of NTVRE was 12.3%. From 1 to 10 years, the cumulative incidences of TVRE and NTVRE were 11.2% and 22.4%, respectively. CONCLUSION: At 10-year post-PCI with new generation drug eluting stents, events related to remote vessel disease progression account for a higher proportion of events than events related to the stented vessel. TRIAL REGISTRATION: ISAR TEST 4 ClinicalTrials.gov Identifier: NCT00598676. ISAR TEST 5 ClinicalTrials.gov Identifier: NCT00598533.

Optical Coherence Tomography-OCT for Characterization of Non-Atherosclerotic Coronary Lesions in Acute Coronary Syndromes.

Cardiovascular diseases are the main cause of death worldwide, with coronary artery disease being the predominant underlying etiology. The most prevalent coronary lesions are represented by the atherosclerotic plaques, in more than 85% of cases, but there are several other non-atherosclerotic lesions such as spontaneous coronary artery dissection and/or hematoma and spontaneous recanalization of coronary thrombus, which are less common, approximately 5% of cases, but with similar clinical manifestations as well as complications. There are insufficient data regarding the pathological mechanism, true prevalence and optimal treatment of these kind of coronary lesions. Optical coherence tomography (OCT) is an intracoronary imaging technique, developed in order to overcome the diagnostic limitations of a standard coronary angiography and has an extremely high resolution, similar to that of a usual histological evaluation of a biopsy sample, thus, OCT provides a histological-like information, but in a in vivo environment. The aim of this article is to review the current knowledge regarding non-atherosclerotic coronary lesions, with an emphasis on the importance of OCT for optimal identification, characterization of pathogenic mechanisms and optimal treatment selection.

Morphological study of the spectrum of lesions encountered in the heart and coronaries on autopsy.

BACKGROUND AND OBJECTIVES: This research study has been carried out to study the various morphological changes in the heart in medicolegal autopsies and to compile data for the frequency of heart diseases found in autopsy cases. METHODS: The present study comprised 430 medicolegal autopsy cases. Details of the cases were entered in a proforma prepared for the study. The heart was fixed in 10% formalin, and then, opened along the flow of blood. The findings were based on gross and microscopic examinations. RESULTS: Out of 430 adult hearts, 211 (49.0%) cases showed 253 cardiac lesions; 35 (8.1%) cases of coronary atherosclerosis and 196 (45.5%) aortic atherosclerosis were noted; 7 cases of ischemic lesions (1.6%) were identified; 12 (2.7%) cases of hypertrophy; 2 cases of valve calcification; and 1 of cardiomyopathy were noted. CONCLUSION: In the present study, among medicolegal autopsies, atherosclerotic disease was the most frequently encountered lesion followed by hypertrophy. The incidence of atherosclerosis was found to be 47.6%. This study shows the high prevalence of atherosclerosis in the population.

Successful Percutaneous Coronary Intervention in a Patient With aVR ST-Segment Elevation Myocardial Infarction Due to Spontaneous Atherosclerotic Coronary Artery Dissection.

Chest pain is a common clinical symptom that leads to a patient's admission to the emergency department, which may be caused by acute coronary syndrome (ACS). Electrocardiography (ECG) is a useful tool for diagnosis, risk stratification, and treatment response monitoring in clinical practice. The coronary angiography should be done in ACS, which may detect spontaneous atherosclerotic coronary artery dissection (SCAD) that should be followed by urgent revascularization. We present a case of a 55-year-old male with the augmented Vector Right (aVR) ST-segment elevation myocardial infarction due to spontaneous atherosclerotic coronary artery dissection. The patient had a good outcome after we performed early coronary angiography, followed by the percutaneous coronary intervention (PCI).

Obesity and obesity-induced inflammatory disease contribute to atherosclerosis: a review of the pathophysiology and treatment of obesity.

Two billion people worldwide older than 18 years of age, or approximately 30% of the world population, are overweight or obese. In addition, more than 43 million children under the age of 5 are overweight or obese. Among the population in the United States aged 20 and greater, 32.8 percent are overweight and 39.8 percent are obese. Blacks in the United States have the highest age-adjusted prevalence of obesity (49.6%), followed by Hispanics (44.8%), whites (42.2%) and Asians (17.4%). The impact of being overweight or obese on the US economy exceeds $1.7 trillion dollars, which is equivalent to approximately eight percent of the nation's gross domestic product. Obesity causes chronic inflammation that contributes to atherosclerosis and causes >3.4 million deaths/year. The pathophysiologic mechanisms in obesity that contribute to inflammation and atherosclerosis include activation of adipokines/cytokines and increases in aldosterone in the circulation. The adipokines leptin, resistin, IL-6, and monocyte chemoattractant protein activate and chemoattract monocytes/macrophages into adipose tissue that promote visceral adipose and systemic tissue inflammation, oxidative stress, abnormal lipid metabolism, insulin resistance, endothelial dysfunction, and hypercoagulability that contribute to atherosclerosis. In addition in obesity, the adipokines/cytokines IL-1ß, IL-18, and TNF are activated and cause endothelial cell dysfunction and hyperpermeability of vascular endothelial junctions. Increased aldosterone in the circulation not only expands the blood volume but also promotes platelet aggregation, vascular endothelial dysfunction, thrombosis, and fibrosis. In order to reduce obesity and obesity-induced inflammation, therapies including diet, medications, and bariatric surgery are discussed that should be considered in patients with BMIs>35-40 kg/m2 if diet and lifestyle interventions fail to achieve weight loss. In addition, antihypertensive therapy, plasma lipid reduction and glucose lowering therapy should be prescribed in obese patients with hypertension, a 10-year CVD risk >7.5%, or prediabetes or diabetes.

Recurrent spontaneous coronary artery dissection.

Introduction: Spontaneous coronary artery dissection (SCAD) is a cause of non-atherosclerotic acute coronary syndrome and sudden cardiac death that predominantly impacts young and middle-aged women. In addition to the challenges of acute SCAD including arrhythmias, heart failure, and recurrent chest pain, de novo recurrent SCAD occurs in 5-29% of patients. Recurrent SCAD presents both a psychological burden and a significant cardiac risk to patients. Research regarding SCAD recurrence risk has been growing and can guide providers and patients alike.Areas covered: This review provides up-to-date information about many aspects of SCAD with a focus on SCAD recurrence. PubMed articles were reviewed through October 2020, with particular focus on clinical studies and original research. The resulting literature was scrutinized for information on SCAD recurrence. SCAD-associated conditions, genetic data, clinical characteristics, medications, and aspects of post-SCAD care are summarized.Expert Opinion: SCAD recurrence poses a concerning risk for patients with SCAD. Conditions such as hypertension and severe coronary tortuosity may be associated with recurrence. More research is needed to further elucidate risk factors for recurrence and clarify interventions, such as beta blocker therapy, that may reduce recurrence risk.

Development of Novel Artificial Intelligence to Detect the Presence of Clinically Meaningful Coronary Atherosclerotic Stenosis in Major Branch from Coronary Angiography Video.

AIM: The clinically meaningful coronary stenosis is diagnosed by trained interventional cardiologists. Whether artificial intelligence (AI) could detect coronary stenosis from CAG video is unclear. METHODS: The 199 consecutive patients who underwent coronary arteriography (CAG) with chest pain between December 2018 and May 2019 was enrolled. Each patient underwent CAG with multiple view resulting in total numbers of 1,838 videos. A multi-layer 3-dimensional convolution neural network (CNN) was trained as an AI to detect clinically meaningful coronary artery stenosis diagnosed by the expert interventional cardiologist, using data from 146 patients (resulted in 1,359 videos) randomly selected from the entire dataset (training dataset). This training dataset was further split into 109 patients (989 videos) for derivation and 37 patients (370 videos) for validation. The AI developed in derivation cohort was tuned in validation cohort to make final model. RESULTS: The final model was selected as the model with best performance in validation dataset. Then, the predictive accuracy of final model was tested with the remaining 53 patients (479 videos) in test dataset. Our AI model showed a c-statistic of 0.61 in validation dataset and 0.61 in test dataset, respectively. CONCLUSION: An artificial intelligence applied to CAG videos could detect clinically meaningful coronary atherosclerotic stenosis diagnosed by expert cardiologists with modest predictive value. Further studies with improved AI at larger sample size is necessary.

Spontaneous coronary artery dissection, a commonly overlooked etiology of acute coronary syndrome.

Spontaneous coronary artery dissection (SCAD) is a type of non-atherosclerotic coronary artery disease, initially thought to be uncommon but is now being increasingly recognized as a cause of acute coronary syndrome in females. The exact incidence of this remains unknown and most of these cases undergo emergent percutaneous intervention (PCI) due to concern for acute coronary syndrome (ACS). Prior studies have shown that PCI can be detrimental in these cases. It is important to recognize the possibility of SCAD in young female patients so that potentially harmful interventions, such as starting these patients immediately on heparin, use of thrombolytic therapy, and emergent PCI that can lead to worse outcomes, are avoided.

Current state-of-play in spontaneous coronary artery dissection.

For over 80 years, spontaneous coronary artery dissection (SCAD) has been recognised as a cause of myocardial infarction. SCAD is described as a non-iatrogenic, non-atherosclerotic coronary artery dissection, resulting in formation of a false lumen or intramural haematoma in the coronary artery wall that compresses the true lumen, often compromising myocardial blood flow. In early literature, the incidence of SCAD in acute coronary syndrome (ACS) was underestimated. Recent advances in awareness and widespread early angiographic investigation in ACS has led to important shifts in our understanding of the prevalence, predisposing causes, natural history, aetiology, clinical and angiographic features, management, and prognosis of SCAD. It is now well understood that SCAD predominantly affects women and is responsible for around 20% of ACS presentations in females below the age of 60. Despite this, SCAD is still often overlooked and misdiagnosed as atherosclerotic disease. Misdiagnosis is multifactorial; with contributing factors including a low clinical index of suspicion, particularly in young females, a lack of clinician familiarity with angiographic variants, and limitations of angiography. Although increasing evidence suggests that optimal management is distinct from atherosclerotic coronary artery disease, many questions remain unanswered regarding the pathogenesis and optimal treatment of SCAD, heralding prospective research to answer these questions. This review aims to give a current clinical perspective on SCAD and highlight the importance of familiarity and vigilance with this condition when diagnosing and treating ACS.

Potentially critical roles of TNPO1, RAP1B, ZDHHC17, and PPM1B in the progression of coronary atherosclerosis through microarray data analysis.

OBJECTIVE: This study aimed to identify more potentially critical genes associated with atherosclerotic coronary artery disease (CAD). MATERIALS AND METHODS: Gene expression profile of GSE12288 was downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were screened in atherosclerotic CAD samples compared with controls, followed by weighed gene coexpression network analysis (WGCNA) by which the most significant module was identified. Gene coexpression network was constructed based on genes in the most significant module, and functional annotation was also performed. In addition, microRNAs (miRNAs) that were directly associated with CAD were screened from the literature, and the miRNA-target regulatory network was constructed based on genes in the most significant module, followed by Gene Ontology (GO) and pathway enrichment analysis. Furthermore, we used another data set of GSE42148 from the GEO database to perform data validation. RESULTS: WGCNA analysis showed that the turquoise module may have the most important role in atherosclerotic CAD. Genes in this module were involved in translational elongation and intracellular signal transduction. Besides, we identified five confirmed CAD-related miRNAs. TNPO1, RAP1B, and ZDHHC17 could be targeted by four of these miRNAs. Genes such as PPM1B could be regulated by three miRNAs. Moreover, TNPO1 and ZDHHC17 were involved in the GO terms associated with protein localization and transport and the immune system; RAP1B and PPM1B were linked with intracellular signal transduction-related pathways. In addition, PPM1B and ZDHHC17 had accordantly significant expression changes in another data set GSE42148. CONCLUSION: TNPO1, RAP1B, ZDHHC17, and PPM1B may play essential roles in the progression of coronary atherosclerosis.

Lipids and Lipoproteins in Risk Prediction.

Ischemic heart disease remains the leading cause of death worldwide. Low-density lipoprotein cholesterol (LDL-C) has proved to have a causal relationship with atherosclerotic cardiovascular disease. Lowering LDL-C improves outcomes, although some patients continue to have residual risk of cardiovascular disease. Cardiovascular risk prediction calculators are routinely used in to identify patients most at risk. Research into other lipoprotein factors has suggested that they may have advantages over LDL-C and improve the ability to identify those most at risk. Although some technology is not widely available, there is potential for better risk prediction in specific groups.