scholarly journals Extension of Endocardium-Derived Vessels Generate Coronary Arteries in Neonates

2022 ◽  
Author(s):  
Juan Tang ◽  
Huan Zhu ◽  
Xueying Tian ◽  
Haixiao Wang ◽  
Shaoyan Liu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Molecular Mechanisms ◽  
Gene Knockout ◽  
Lineage Tracing ◽  
Specific Gene ◽  
Genetic Lineage ◽  
Light Sheet Microscopy ◽  
Neonatal Heart

Background: Unraveling how new coronary arteries develop may provide critical information for establishing novel therapeutic approaches to treating ischemic cardiac diseases. There are two distinct coronary vascular populations derived from different origins in the developing heart. Understanding the formation of coronary arteries may provide insights into new ways of promoting coronary artery formation after myocardial infarction. Methods: To understand how intramyocardial coronary arteries are generated to connect these two coronary vascular populations, we combined genetic lineage tracing, light-sheet microscopy, fluorescence micro-optical sectioning tomography, and tissue-specific gene knockout approaches to understand their cellular and molecular mechanisms. Results: We show that a subset of intramyocardial coronary arteries form by angiogenic extension of endocardium-derived vascular tunnels in the neonatal heart. Three-dimensional whole-mount fluorescence imaging showed that these endocardium-derived vascular tunnels or tubes adopt an arterial fate in neonates. Mechanistically, we implicate Mettl3 and Notch signaling in regulating endocardium-derived intramyocardial coronary artery formation. Functionally, these intramyocardial arteries persist into adulthood and play a protective role after myocardial infarction. Conclusions: A subset of intramyocardial coronary arteries form by extension of endocardium-derived vascular tunnels in the neonatal heart.

scholarly journals Perivascular-Derived Mesenchymal Stem Cells

2019 ◽  
Vol 98 (10) ◽  
pp. 1066-1072 ◽  
Author(s):  
V. Yianni ◽  
P.T. Sharpe
Keyword(s):  
Tissue Engineering ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Dental Pulp ◽  
Molecular Mechanisms ◽  
Lineage Tracing ◽  
Specific Gene ◽  
Genetic Lineage ◽  
Differentiation Potential

Cells have been identified in postnatal tissues that, when isolated from multiple mesenchymal compartments, can be stimulated in vitro to give rise to cells that resemble mature mesenchymal phenotypes, such as odontoblasts, osteoblasts, adipocytes, and myoblasts. This has made these adult cells, collectively called mesenchymal stem cells (MSCs), strong candidates for fields such as tissue engineering and regenerative medicine. Based on evidence from in vivo genetic lineage–tracing studies, pericytes have been identified as a source of MSC precursors in vivo in multiple organs, in response to injury or during homeostasis. Questions of intense debate and interest in the field of tissue engineering and regenerative studies include the following: 1) Are all pericytes, irrespective of tissue of isolation, equal in their differentiation potential? 2) What are the mechanisms that regulate the differentiation of MSCs? To gain a better understanding of the latter, recent work has utilized ChIP-seq (chromatin immunoprecipitation followed by sequencing) to reconstruct histone landscapes. This indicated that for dental pulp pericytes, the odontoblast-specific gene Dspp was found in a transcriptionally permissive state, while in bone marrow pericytes, the osteoblast-specific gene Runx2 was primed for expression. RNA sequencing has also been utilized to further characterize the 2 pericyte populations, and results highlighted that dental pulp pericytes are already precommitted to an odontoblast fate based on enrichment analysis indicating overrepresentation of key odontogenic genes. Furthermore, ChIP-seq analysis of the polycomb repressive complex 1 component RING1B indicated that this complex is likely to be involved in inhibiting inappropriate differentiation, as it localized to a number of loci of key transcription factors that are needed for the induction of adipogenesis, chondrogenesis, or myogenesis. In this review, we highlight recent data elucidating molecular mechanisms that indicate that pericytes can be tissue-specific precommitted MSC precursors in vivo and that this precommitment is a major driving force behind MSC differentiation.

Myocardial Infarction in Systemic Lupus Erythematosus – the Sex Specific Risk Profile

2020 ◽  
Vol 26 ◽  
Author(s):  
Marija Vavlukis ◽  
Daniela Pop-Gjorceva ◽  
Lidija Poposka ◽  
Emilija Sandevska ◽  
Sasko Kedev
Keyword(s):  
Myocardial Infarction ◽  
Systemic Lupus Erythematosus ◽  
Cardiovascular Risk ◽  
Coronary Artery ◽  
Young Women ◽  
Lupus Erythematosus ◽  
Molecular Mechanisms ◽  
Clinical Presentation ◽  
Systemic Lupus ◽  
Antiinflammatory Therapy

Background: Accelerated atherosclerosis is widely present in patients with systemic lupus erythematosus. Objective: The aim of this review is to analyze the relationship between systemic lupus erythematosus and cardiovascular diseases, with the emphasis on acute myocardial infarction. Results: Various molecular mechanisms triggered by infection/inflammation are responsible for endothelial dysfunction and development of atherosclerosis at an earlier age. Contributing factor is the cumulative effect of traditional cardiovascular risk factors interaction with disease related characteristics. Myocardial infarction rates are 2- to 10-fold higher compared to the general population. Young women have the highest relative risk, however, men carry at least 3- fold higher risk than women. Coronary involvement varies from normal coronary artery with thrombosis, coronary microartery vasculitis, coronary arteritis, and coronary atherosclerosis. Typical clinical presentation is observed in men and older women, while atypical is more frequent in young women. Treatment is guided by the underlying mechanism, engaging invasive procedures alone, or accompanied with immunosuppressive and/or antiinflammatory therapy. There are significant gender differences in pathophysiology and clinical presentation. However, they receive the same therapeutic treatments. Conclusion: Systemic lupus erythematosus is a major contributor to atherosclerotic and non-atherosclerotic mechanisms involved in the development of myocardial infarction, which should be taken into account during therapeutic treatment. Although Systemic lupus erythematosus per se is a “female” disease, males are at increased cardiovascular risk and worse outcome. Method: We conducted a literature review through PubMed and Cochrane, using key words: SLE, atherosclerosis, atherothrombosis, coronary artery disease, myocardial infarction, prognosis, sex specifics.

scholarly journals Prognostic value of non-invasive coronary artery flow velocity assessment in elderly patients

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
E Kalinina ◽  
A Zagatina ◽  
N Zhuravskaya ◽  
D Shmatov
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Elderly Patients ◽  
Flow Velocity ◽  
Coronary Arteries ◽  
Coronary Flow ◽  
Prognostic Value ◽  
Area Under Curve ◽  
Left Coronary Artery ◽  
Maximal Velocity

Abstract Funding Acknowledgements Type of funding sources: None. Background There is a high prevalence of coronary artery disease (CAD) in the elderly population. However, symptoms of CAD are often non-specific. Dyspnoe, non-anginal pains are among the main symptoms in older patients. Exercise tests are of limited feasibility in these patients, due to neuro-muscular weakness, physical deconditioning, and orthopaedic limitations. Pharmacological tests often are contraindicated in a substantial percentage of elderly patients. Some recent studies indicate using local flow acceleration during routine echocardiography has prognostic potential for coronary artery assessments without stress testing. The aim of the study was to define the prognostic value of coronary artery ultrasound assessment in patients ≥75 years old. Methods This is a prospective cohort study. Patients ≥ 75 years old who underwent routine echocardiography with additional scans for coronary arteries over a period of 24 months were included in the study. The study group consisted of 80 patients aged 75-90 years (56 women; mean age 79 ± 4). Initial exams were performed for other reasons, primarily for arterial hypertension. Fifteen patients had known CAD. Death, non-fatal myocardial infarction (MI), and revascularization were defined as major adverse cardiac events (MACE). All patients were followed up with at a median of 32 months. Results There were 34 patients with high local velocities in the left coronary artery. Eight deaths, two non-fatal myocardial infarctions occurred, and 13 revascularizations were performed. With a ROC analysis, a coronary flow velocity >110 cm/s was the best predictor for risk of death (area under curve 0.84 [95% CI 0.74–0.92]; sensitivity 75%; specificity 88%). Only the maximal velocity in proximal left-sided coronary arteries was independently associated with death (HR 1.03, 95% CI 1.01; 1.05; p < 0.002), or death/MI (HR 1.03, 95% CI 1.01; 1.04; p < 0.0001). The cut-off value of 66 cm/s was a predictor of all MACE (area under curve 0.87 [95% CI 0.77–0.94]; sensitivity 80%; specificity 86%). Any causes of death or MI occurred more frequently in patients with velocities of >66 cm/s (27% vs. 2%; p < 0.002). The rates of MACE were 58.0% vs. 2%; p < 0.0000001, respectively. Conclusion The analysis of coronary flow in the left coronary artery during echocardiography can be used as a predictor of outcomes in elderly patients. Maximal velocities in proximal left-sided coronary arteries is independently associated with further death or myocardial infarction.

Abstract 13804: Clinical Profile and Outcomes of Myocardial Infarction With Non-obstructive Coronary Arteries in Older Adults

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Ara H Rostomian ◽  
Derek Q Phan ◽  
Mingsum Lee ◽  
Ray X Zadegan
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Los Angeles ◽  
Coronary Arteries ◽  
Medical Center ◽  
Invasive Coronary Angiography ◽  
Obstructive Coronary Artery Disease ◽  
Kaiser Permanente ◽  
Artery Disease

Introduction: Myocardial Infarction with non-obstructive coronary artery disease (MINOCA) is found in 5%-6% of patients with acute myocardial infarction (AMI). As such, the diagnosis and management of AMI patients with non-obstructive coronary artery disease (NOCAD) poses a challenge as compared to patients with MI with coronary artery disease (MICAD). Hypothesis: To evaluate the characteristics and outcomes of MINOCA in older patients as compared with MICAD patients, with and without revascularization. Methods: This was a retrospective observational study of patients ≥80 years old who underwent invasive coronary angiography (ICA) for AMI between 2009-2019 at Kaiser Permanente Los Angeles Medical Center. MINOCA was defied as <50% stenosis of coronary arteries on angiography with a troponin level ≥0.05 ng/ml. Patients with MINOCA vs MICAD were compared. Multivariate logistic regression was used to identify independent predictors of MINOCA and Kaplan-Meier survival analysis was used to analyze all-cause mortality between cohorts. Results: A total of 259 patients with MINOCA (mean ± SD age 83.8±2.7 years, 68% female) and 687 patients with MICAD (84.7±3.4 years, 40% female) were analyzed. Younger age (odds ratio [OR]=1.11; 95% confidence interval [CI]=1.05-1.18), female sex (OR=3.14; CI=2.20-4.48), black race (OR=2.53; CI=1.61-3.98), no history of prior stroke (OR=1.56; CI=1.06-2.33), atrial fibrillation or flutter (OR=2.04; CI:1.38-3.02), lower troponin levels (OR=1.08; CI:1.03-1.11), and lower triglyceride levels per 10 mg/dl increments (OR=1.06; CI:1.03-1.11) increased the odds of having MINCOA as compared to MICAD. At median follow-up of 2.4 years, MINOCA was associated with a lower rate of death (44.8% vs 55.2%, p<0.01) compared to un-revascularized MICAD, but no difference (31.3% vs 40.4%, p=0.68) when compared to re-vascularized MICAD. Conclusions: Patients age ≥80 years with MINOCA have fewer traditional risk factors compared to their counterparts with MICAD and fewer deaths compared to un-revascularized MICAD, but similar mortality compared to revascularized MICAD

scholarly journals Myocardial Infarction with Nonobstructive Coronary Artery (MINOCA)

2021 ◽  
Vol 06 (02) ◽  
pp. 115-118
Author(s):  
R. Archana
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Risk Stratification ◽  
Coronary Arteries ◽  
Diagnostic Strategy ◽  
Therapeutic Challenge ◽  
Microvascular Spasm

AbstractMyocardial infarction with nonobstructive coronary arteries (MINOCA) is diagnosed in almost equal to 5 to 6% of patients who present with acute myocardial infarction (AMI). Causes of MINOCA are varied. Appropriate diagnosis and evaluation is important to uncover the correct cause and prescribe specific therapies to treat the underlying cause.Women with evidence of MINOCA are being increasingly recognized. The mechanisms underlying MINOCA, such as coronary microvascular spasm, represent a diagnostic and therapeutic challenge to medical fraternity, as there is neither a uniform nor comprehensive diagnostic strategy for accurate risk stratification, in the present scenario, for these patients.Here, we are reporting a case of MINOCA, which is rare and incompletely evaluated.

scholarly journals Editor’s Choice- Pathophysiology, diagnosis and management of MINOCA: an update

2018 ◽  
Vol 8 (1) ◽  
pp. 54-62 ◽  
Author(s):  
Giancarla Scalone ◽  
Giampaolo Niccoli ◽  
Filippo Crea
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Wall Motion ◽  
Regional Wall Motion ◽  
Left Ventricular ◽  
Regional Wall ◽  
Diagnosis And Management ◽  
Regional Wall Motion Abnormalities ◽  
Wall Motion Abnormalities

Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a syndrome with different causes, characterised by clinical evidence of myocardial infarction with normal or near-normal coronary arteries on angiography. Its prevalence ranges between 5% and 25% of all myocardial infarction. The prognosis is extremely variable, depending on the cause of MINOCA. The key principle in the management of this syndrome is to clarify the underlying individual mechanisms to achieve patient-specific treatments. Clinical history, electrocardiogram, cardiac enzymes, echocardiography, coronary angiography and left ventricular angiography represent the first level diagnostic investigations to identify the causes of MINOCA. Regional wall motion abnormalities at left ventricular angiography limited to a single epicardial coronary artery territory identify an ‘epicardial pattern’whereas regional wall motion abnormalities extended beyond a single epicardial coronary artery territory identify a ‘microvascular pattern’. The most common causes of MINOCA are represented by coronary plaque disease, coronary dissection, coronary artery spasm, coronary microvascular spasm, Takotsubo cardiomyopathy, myocarditis, coronary thromboembolism, other forms of type 2 myocardial infarction and MINOCA of uncertain aetiology. This review aims at summarising the diagnosis and management of MINOCA, according to the underlying physiopathology.

Abstract 129: Chest Pain Characteristics of Myocardial Infarction With Non-Obstructive Coronary Arteries (MINOCA) in Comparison to Myocardial Infarction With Coronary Artery Disease (MI-CAD)

2016 ◽  
Vol 9 (suppl_2) ◽  
Author(s):  
Sivabaskari Pasupathy ◽  
Rosanna Tavella ◽  
Margaret Arstall ◽  
Derek Chew ◽  
Matthew Worthley ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Chest Pain ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Public Hospitals ◽  
Arm Pain ◽  
Retrosternal Pain ◽  
Pain Characteristics ◽  
Artery Disease

Background: Myocardial infarction with non-obstructive coronary arteries (MINOCA) is being increasingly recognized with the frequent use of angiography following Acute Myocardial Infarction (AMI); yet there is little evaluation of these patients in the literature. The current study is a prospective, contemporary analysis of clinical features and chest pain characteristics between patients with MINOCA and Myocardial Infarction with coronary artery disease (MI-CAD). Methods: All consecutive patients undergoing coronary angiography for AMI (as per the Third Universal AMI Definition) in South Australian public hospitals from January 2012 - December 2013 were included. Data was captured by Coronary Angiogram Database of South Australia (CADOSA), a comprehensive registry compatible with the NCDR ® CathPCI ® Registry. The AMI patients were classified as MI-CAD or MINOCA on the basis of the presence or absence of a significant stenosis (≥50%) on angiography. Results: From 3,431 angiography procedures undertaken for AMI, 359 (11%) were classified as MINOCA. MINOCA patients were younger (59 ± 15 vs. 64 ± 13, p <0.01) and more likely to be female (60% vs. 26%, p<0.01), with age adjusted analysis revealing less cardiovascular risk factors in MINOCA compared to MICAD: current smoker (21% vs. 35%, p< 0.01), hypertension (56% vs. 65%, p<0.01), dyslipidaemia (46% vs. 61%, p<0.01), and diabetes (20% vs. 32%, p<0.01). Analysis of presenting chest pain characteristics showed no significant differences between MICAD and MINOCA for the presence of retrosternal pain (81% vs. 82%, p>0.05,) or shoulder pain (27% vs. 26%, p>0.05) respectively, however MINOCA patients were less likely to experience arm pain (33% vs. 40%, p<0.01). In regards to precipitating factors, emotional stress was more common (14% vs. 5%, p<0.001) and exertion related chest pain was less common (27% vs. 40%, p<0.001) in MINOCA patients. Quality of pain for MINOCA and MICAD was similar with the most frequent descriptors being burning (11% vs. 9%, p>0.05), sharp 21% vs. 23%, p>0.05) and tightness (41% vs. 44%, p>0.05). In addition, there were no significant differences observed between groups in relieving factors and duration of chest pain Conclusions: In contemporary cardiology practice, MINOCA presentation is more common than previously appreciated, with younger women frequently implicated. Delineating a MINOCA patient from MICAD on the basis of chest pain characteristics is not feasible.

Abstract 028: Endothelial Nogo-B Controls Sphingolipid de novo Biosynthesis to Impact Coronary Artery Atherosclerosis

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Yi Zhang ◽  
Linda Sasset ◽  
Ren Xu ◽  
Matthew Blake Greenblatt ◽  
Annarita Di Lorenzo
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Vascular Inflammation ◽  
High Cholesterol Diet ◽  
Serine Palmitoyltransferase ◽  
Atherosclerotic Lesions ◽  
Coronary Artery Atherosclerosis ◽  
Artery Disease

Coronary artery disease is a leading cause of myocardial infarction (MI) worldwide. Alterations in sphingolipid levels have been linked to atherosclerosis although specific molecular mechanisms are poorly understood. Recently, we discovered that endothelial Nogo-B, a membrane protein of the ER, regulates vascular functions by inhibiting serine palmitoyltransferase (SPT), the rate-limiting enzyme of the de novo sphingolipid biosynthesis. Mice lacking Nogo-B are resistant to hypertension and heart failure. Here, we employed a novel model of coronary atherosclerotic lesions induced by hypercholesterolemia and hypertension, well-known risk factors for atherosclerosis. To this aim, transverse aortic constriction (TAC) surgery was performed in mice lacking endothelial Nogo-B in ApoE -/- background and ApoE -/- mice as control. ApoE -/- mice developed coronary atherosclerotic lesions within 6 weeks following TAC, (without the need of long-term high-cholesterol diet) and 70% of the mice died of MI at 6-week post-TAC. On the contrary, mice lacking Nogo-B specifically in endothelial cells were markedly resistant to the development of coronary atherosclerotic lesions and MI (20%). Mechanistically, in the absence of endothelial Nogo-B, the biosynthesis of sphingolipids, particularly S1P, is upregulated, protecting the endothelium from hypertension and hypercholesterolemia-triggered vascular inflammation and atherogenesis. This study identifies an important and novel role of endothelial Nogo-B-dependent regulation of sphingolipid de novo biosynthesis in the coronary atherosclerosis, a primary cause of myocardial infarction.

scholarly journals Relationship of a thinned medial layer to the attenuated contractile response in atherosclerotic coronary arteries

2020 ◽  
Vol 318 (1) ◽  
pp. H135-H142
Author(s):  
Takamitsu Nakamura ◽  
Takeo Horikoshi ◽  
Kiyotaka Kugiyama
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Inflection Point ◽  
Contractile Response ◽  
Quadratic Regression ◽  
Previous Myocardial Infarction ◽  
The Relationship ◽  
Medial Area ◽  
Early Atherosclerosis

Coronary arteries with advanced atherosclerosis do not necessarily have greater contractile responses than those with early atherosclerosis. This study aimed to clarify the relationship between thickness of the medial layer and the contractile response to acetylcholine (ACh) in coronary artery using optical coherence tomography (OCT). The OCT and the vasomotor response to ACh in the left anterior descending coronary artery were assessed in 32 patients with previous myocardial infarction. The intimal and medial layer areas were measured by planimetric analysis of the OCT images. The coronary contractile response to ACh had a positive linear relationship with medial area ( r = 0.61, P < 0.001). In contrast, the relationship between the coronary contractile response to ACh and intimal area was described by an inverted U-shaped curve that was fitted to a quadratic regression model ( R2 = 0.35, P = 0.002, y-axis, contraction; x-axis, intimal area). The contractile response increased as the intimal layer thickened up to the inflection point; thereafter, the contractile response declined. The relationship between medial area and intimal area was also described by an inverted U-shaped curve that was fitted to a quadratic regression model ( R2 = 0.41, P < 0.01, y-axis, medial area; x-axis, intimal area). The medial area increased as the intimal area thickened up to the inflection point; thereafter, the medial area thinned. In conclusion, the thinned medial layer was associated with the attenuated contractile response in a coronary artery with greater atherosclerosis. NEW & NOTEWORTHY This is the first clinical study to show the relationship between the contractile response and the thickness of medial smooth muscle layer in coronary artery of patients with previous myocardial infarction using OCT. The contractile response to acetylcholine was attenuated, and medial layer area was thinned in coronary artery with greater atherosclerosis compared with those in coronary artery with mild or moderate atherosclerosis. The coronary contractile response was positively correlated with thickness of the medial layer in coronary arteries with either mild or greater atherosclerosis. Thus, coronary arteries with advanced atherosclerosis do not necessarily have greater contractile responses than those with early atherosclerosis, which could be related to the thinned medial layer.

scholarly journals Serum amyloid A induces endothelial dysfunction in porcine coronary arteries and human coronary artery endothelial cells

2008 ◽  
Vol 295 (6) ◽  
pp. H2399-H2408 ◽  
Author(s):  
Xinwen Wang ◽  
Hong Chai ◽  
Zehao Wang ◽  
Peter H. Lin ◽  
Qizhi Yao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Coronary Arteries ◽  
Molecular Mechanisms ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Dependent Manner ◽  
Amyloid A ◽  
Enos Mrna

The objective of this study was to determine the effects and mechanisms of serum amyloid A (SAA) on coronary endothelial function. Porcine coronary arteries and human coronary arterial endothelial cells (HCAECs) were treated with SAA (0, 1, 10, or 25 μg/ml). Vasomotor reactivity was studied using a myograph tension system. SAA significantly reduced endothelium-dependent vasorelaxation of porcine coronary arteries in response to bradykinin in a concentration-dependent manner. SAA significantly decreased endothelial nitric oxide (NO) synthase (eNOS) mRNA and protein levels as well as NO bioavailability, whereas it increased ROS in both artery rings and HCAECs. In addition, the activities of internal antioxidant enzymes catalase and SOD were decreased in SAA-treated HCAECs. Bio-plex immunoassay analysis showed the activation of JNK, ERK2, and IκB-α after SAA treatment. Consequently, the antioxidants seleno-l-methionine and Mn(III) tetrakis-(4-benzoic acid)porphyrin and specific inhibitors for JNK and ERK1/2 effectively blocked the SAA-induced eNOS mRNA decrease and SAA-induced decrease in endothelium-dependent vasorelaxation in porcine coronary arteries. Thus, SAA at clinically relevant concentrations causes endothelial dysfunction in both porcine coronary arteries and HCAECs through molecular mechanisms involving eNOS downregulation, oxidative stress, and activation of JNK and ERK1/2 as well as NF-κB. These findings suggest that SAA may contribute to the progress of coronary artery disease.

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