scholarly journals Pentraxin 3 Released from Neutrophils Increases Plasma Levels in Patients with Acute Coronary Syndrome

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Kenji Inoue ◽  
Satoru Suwa ◽  
Shinya Okazaki ◽  
Seigo Itoh ◽  
Alexander S. Savchenko ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Mononuclear Cells ◽  
Plaque Rupture ◽  
Pentraxin 3 ◽  
Blood Samples ◽  
Elisa System ◽  
Coronary Syndrome ◽  
Systemic Process ◽  
Rupture Site ◽  
Histological Staining

Background. Our recently developed ELISA system for the detection of human pentraxin 3 (PTX3) in plasma has demonstrated that plasma PTX3 levels are increased in patients with unstable angina pectoris. However, the origin of the PTX3 from the ruptured plaque or a systemic process and which cells release PTX3 remain unclear. Methods. Blood samples were taken using an aspiration catheter from the site of the ruptured plaque and from the aorta during acute coronary interventions in 118 patients with acute coronary syndrome. These samples were analyzed for PTX3, and brain natriuretic peptide (BNP) was used as a control. Aspirated thrombi from patients with acute myocardial infarction (AMI) (n = 32) were examined by histological staining. Results. Plasma PTX3 levels were higher in blood samples taken from the site of plaque rupture compared to samples taken from the aorta (5.61±1.91 ng/mL versus 4.72 ± 5.61 ng/mL, P<0.05). On the other hand, BNP levels, as reference, were not different between the samples (P = 0.45). PTX3-positive neutrophils accounted for 70.4% of cells in harvested thrombi, with the remaining cells consisting of mononuclear cells. Conclusions. Infiltrating neutrophils in thrombi at the plaque rupture site are a diagnostically important source of PTX3 in patients with acute coronary syndrome.

Macrophage infiltrates in coronary plaque erosion portend a worse cardiovascular outcome in patients with acute coronary syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R.A Montone ◽  
V Vetrugno ◽  
M Camilli ◽  
M Russo ◽  
M.G Del Buono ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Vulnerable Plaque ◽  
Cardiac Death ◽  
Cox Regression ◽  
Plaque Rupture ◽  
Culprit Lesion ◽  
Coronary Syndrome ◽  
Fibrous Cap ◽  
Plaque Erosion

Abstract Background Plaque erosion (PE) is responsible for at least one-third of acute coronary syndrome (ACS). Inflammatory activation is considered a key mechanism of plaque instability in patients with plaque rupture through the release of metalloproteinases and the inhibition of collagen synthesis that in turns lead to fibrous cap degradation. However, the clinical relevance of macrophage infiltration has never been investigated in patients with PE. Purpose In our study, we aimed at assessing the presence of optical coherence tomography (OCT)-defined macrophage infiltrates (MØI) at the culprit site in ACS patients with PE, evaluating their clinical and OCT correlates, along with their prognostic value. Methods ACS patients undergoing OCT imaging and presenting PE as culprit lesion were retrospectively selected. Presence of MØI at culprit site and in non-culprit segments along the culprit vessel was assessed. The incidence of major adverse cardiac events (MACEs), defined as the composite of cardiac death, recurrent myocardial infarction and target vessel revascularization (TVR), was assessed [follow-up median (interquartile range, IQR) time 2.5 (2.03–2.58) years]. Results We included 153 patients [median age (IQR) 64 (53–75) years, 99 (64.7%) males]. Fifty-one (33.3%) patients presented PE with MØI and 102 (66.7%) PE without MØI. Patients having PE with MØI compared with PE patients without MØI had more vulnerable plaque features both at culprit site and at non-culprit segments. In particular, culprit lesion analysis demonstrated that patients with PE with MØI had a significantly thinner fibrous cap [median (IQR) 100 (60–120) μm vs. 160 (95–190) μm, p&lt;0.001], higher prevalence of thrombus [41 (80.4%) vs. 64 (62.7%), p=0.028], lipid plaque [39 (76.5%) vs. 50 (49.0%), p&lt;0.001], TCFA [20 (39.2%) vs. 14 (13.7%), p=0.001], and a higher maximum lipid arc [median [IQR] 250.0° (177.5°-290.0°) vs. 190.0° (150.0°-260.0°), p=0.018) at the culprit lesion compared with PE without MØI. MACEs were significantly more frequent in PE with MØI patients compared with PE without MØI [11 (21.6%) vs. 6 (5.9%), p=0.008], mainly driven by a higher risk of cardiac death and TVR. At multivariable Cox regression model, PE with MØI [HR=2.95, 95% CI (1.09–8.02), p=0.034] was an independent predictor of MACEs. Conclusion Our study demonstrates that among ACS patients with PE the presence of MØI at culprit lesion is associated with a more aggressive phenotype of coronary atherosclerosis with more vulnerable plaque features, along with a worse prognosis at a long-term follow-up. These findings are of the utmost importance in the era of precision medicine because clearly show that macrophage infiltrates may identify patients with a higher cardiovascular risk requiring more aggressive secondary prevention therapies and a closer clinical follow-up. Prognosis Funding Acknowledgement Type of funding source: None

scholarly journals Potential relationship between high wall shear stress and plaque rupture that cause acute coronary syndrome: insights from optical coherence tomography based computational fluid dynamic simulation

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Fukuyama ◽  
H Otake ◽  
F Seike ◽  
H Kawamori ◽  
T Toba ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
Shear Stress ◽  
Acute Coronary Syndrome ◽  
Wall Shear Stress ◽  
Plaque Rupture ◽  
Optical Coherence ◽  
Lumen Area ◽  
Segmental Analysis ◽  
Coronary Syndrome ◽  
Fibrous Cap

Abstract Background The direct relationship between plaque rupture (PR) that cause acute coronary syndrome (ACS) and wall shear stress (WSS) remains uncertain. Methods From the Kobe University ACS-OCT registry, one hundred ACS patients whose culprit lesions had PR documented by optical coherence tomography (OCT) were enrolled. Lesion-specific 3D coronary artery models were created using OCT data. Specifically, at the ruptured portion, the tracing of the luminal edge of the residual fibrous cap was smoothly extrapolated to reconstruct the luminal contour before PR. Then, WSS was computed from computational fluid dynamics (CFD) analysis by a single core laboratory. Relationships between WSS and the location of PR were assessed with 1) longitudinal 3-mm segmental analysis and 2) circumferential analysis. In the longitudinal segmental analysis, each culprit lesion was subdivided into five 3-mm segments with respect to the minimum lumen area (MLA) location at the centered segment (Figure. 1). In the circumferential analysis, we measured WSS values at five points from PR site and non-PR site on the cross-sections with PR. Also, each ruptured plaque was categorized into the lateral type PR (L-PR), central type PR (C-PR), and others according to the relation between the site of tearing and the cavity (Figure. 2). Results In the longitudinal 3-mm segmental analysis, the incidences of PR at upstream (UP1 and 2), MLA, and downstream (DN1 and 2) were 45%, 40%, and 15%, respectively. The highest average WSS was located in UP1 in the upstream PR (UP1: 15.5 (10.4–26.3) vs. others: 6.8 (3.3–14.7) Pa, p&lt;0.001) and MLA segment in the MLA PR (MLA: 18.8 (6.0–34.3) vs. others: 6.5 (3.1–11.8) Pa, p&lt;0.001), and the second highest WSS was located at DN1 in the downstream PR (DN1: 5.8 (3.7–11.5) vs. others: 5.5 (3.7–16.5) Pa, p=0.035). In the circumferential analysis, the average WSS at PR site was significantly higher than that of non-PR site (18.7 (7.2–35.1) vs. 13.9 (5.2–30.3) Pa, p&lt;0.001). The incidence of L-PR, C-PR, and others were 51%, 42%, and 7%, respectively. In the L-PR, the peak WSS was most frequently observed in the lateral site (66.7%), whereas that in the C-PR was most frequently observed in the center site (70%) (Figure. 3). In the L-PR, the peak WSS value was significantly lower (44.6 (19.6–65.2) vs. 84.7 (36.6–177.5) Pa, p&lt;0.001), and the thickness of broken fibrous cap was significantly thinner (40 (30–50) vs. 80 (67.5–100) μm, p&lt;0.001), and the lumen area at peak WSS site was significantly larger than those of C-PR (1.5 (1.3–2.0) vs. 1.4 (1.1–1.6) mm2, p=0.008). Multivariate analysis demonstrated that the presence of peak WSS at lateral site, thinner broken fibrous cap thickness, and larger lumen area at peak WSS site were independently associated with the development of the L-PR. Conclusions A combined approach with CFD simulation and morphological plaque evaluation by using OCT might be helpful to predict future ACS events induced by PR. Funding Acknowledgement Type of funding source: None

scholarly journals Clinical Predictors of Culprit Plaque Rupture Assessed on Intravascular Ultrasound in Acute Coronary Syndrome

2010 ◽  
Vol 74 (9) ◽  
pp. 1936-1942 ◽  
Author(s):  
Masaya Kato ◽  
Keigo Dote ◽  
Toru Naganuma ◽  
Shota Sasaki ◽  
Kentaro Ueda ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Intravascular Ultrasound ◽  
Plaque Rupture ◽  
Clinical Predictors ◽  
Coronary Syndrome

scholarly journals Acute Myocardial Infarction In Systemic Mastocytosis: Case Report With Literature Review Of The Role Of Inflammatory Process In Acute Coronary Syndrome

2020 ◽  
Vol 16 ◽  
Author(s):  
Ayman Battisha ◽  
Khalid Sawalha ◽  
Bader Madoukh ◽  
Omar Sheikh ◽  
Karim Doughem ◽  
...  
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Acute Coronary Syndrome ◽  
Plasma Lipids ◽  
Plaque Rupture ◽  
Systemic Mastocytosis ◽  
Cardiac Risk ◽  
Control Group ◽  
Coronary Syndrome

: Systemic Mastocytosis (SM) is a disorder of excessive mast cell infiltration in multiple organ tissues. Atherosclerosis is a major risk factor for developing acute coronary syndrome [1]. In addition to lipid accumulation in the arterial wall, inflammation plays an important role in the pathogenesis of plaque rupture and activating the thrombosis cascade [2]. The Mast cells contribution to plaque destabilization has been well established in multiple animal and human studies [3]. In a recent study, SM has been proven to be associated with a higher incidence of acute coronary syndrome even with lower plasma lipids level [4]. The study showed that 20% of patients with SM had cardiovascular events compared to only 6% in the control group with adjustment to all cardiac risk factors. Here, we present a case of acute myocardial infarction in a patient with SM with limited risk factors other than age.

scholarly journals Association between Serum Magnesium Level with Acute Coronary Syndrome (ACS) in Diabetes Mellitus (DM) Patients

2019 ◽  
Vol 2 (2) ◽  
pp. 96
Author(s):  
Ratih Wulansari ◽  
Soebagijo Adi Soelistijo ◽  
Achmad Lefi
Keyword(s):  
Diabetes Mellitus ◽  
Acute Coronary Syndrome ◽  
Plaque Rupture ◽  
Serum Magnesium ◽  
Demographic Data ◽  
Cardiovascular Complications ◽  
Magnesium Level ◽  
Serum Magnesium Level ◽  
Coronary Syndrome ◽  
Normally Distributed

Introduction: Until now, cardiovascular complications are still the highest cause of death and disability in DM patients. Hypomagnesemia in DM accelerate atherosclerosis and can cause instability and plaque rupture which can lead to acute coronary syndrome.Methods: Design of this study was observational analytic using a "case control" study involved 76 samples of DM patients, consisting of 38 samples with SKA (+) and 38 samples with SKA (-). Subjects of this study were all DM patients in the period July-December 2018 in the Emergency Room (ER) and Outpatient Installation of Endocrine at the RSUD Dr. Soetomo Surabaya, which fulfills the criteria for inclusion and exclusion. Demographic data and clinical characteristics are presented descriptively. If data is normally distributed then an unpaired t test is carried out and if the data is not normally, distributed with Mann Whitney test is performed. The statistical test was stated to be significant if p <0.05. The association between hypomagnesemia and the incidence of ACS a multivariate logistic regression test was performed, the risk number was in the form of odds ratios (OR). Results: This study involved 76 subjects with diabetes mellitus with SKA and non SKA 38 subjects. The mean serum magnesium level in the ACS group was lower than non ACS (1.9 mg / dL vs. 2.1 mg / dL), hypomagnesemia cut-off of <2.08 mg / dL. In this study hypomagnesemia as a risk factor for the incidence of ACS in DM patients with OR 2.8 (CI 1.1-7.6; p = 0.039).Conclusion: Magnesium levels in the ACS group were lower than the non ACS group. Hypomagnesemia Increase The Incidence of Acute Coronary Syndrome in Diabetes Mellitus Patients.

scholarly journals Acute Coronary Syndrome after 17 Years of Bare Metal Stent Implantation: “Very” Very Late Stent Thrombosis

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Raghavendra Rao K ◽  
S. Reddy ◽  
J. R. Kashyap ◽  
K. Vikas ◽  
Hithesh Reddy ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Stent Thrombosis ◽  
Plaque Rupture ◽  
Bare Metal Stents ◽  
Metal Stents ◽  
Bare Metal ◽  
Late Stent Thrombosis ◽  
Very Late Stent Thrombosis ◽  
Mortality And Morbidity ◽  
Coronary Syndrome

Very late stent thrombosis (VLST) is a catastrophic and life-threatening complication after percutaneous coronary intervention which presents as an acute coronary syndrome with significantly high mortality and morbidity. VLST is a rare entity with drug-eluting stents and even rarer with bare metal stents. The exact pathophysiologic mechanism of VLST after BMS implantation is not known although various mechanisms have been proposed. Recently, in-stent neoatherosclerosis with intimal plaque rupture has been proposed as a potential mechanism of VLST after BMS. We report a rare case of VLST occurring 17 years after BMS implantation with angiographic and intravascular imaging evidence which provides insight into the mechanisms of VLST.

scholarly journals Effect of postprandial hyperglycaemia on culprit plaque rupture in diabetic patients with non-ST segment elevation acute coronary syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
G Su ◽  
S.W Zhuang ◽  
T Zhang ◽  
H.X Yang ◽  
W.L Dai ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Hemoglobin A1c ◽  
Plaque Rupture ◽  
Coronary Plaque ◽  
Postprandial Hyperglycemia ◽  
Diabetic Patients ◽  
Funding Source ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
St Segment

Abstract Background Postprandial hyperglycemia was reported to play a key role in established risk factors of coronary artery diseases (CAD) and cardiovascular events. Serum 1,5-anhydroglucitol (1,5-AG) levels are known to be a clinical marker of postprandial hyperglycemia and short-term glycemic excursions. Low serum 1,5-AG levels have been associated with occurrence of CAD; however, the relationship between 1,5-AG levels and coronary plaque rupture has not been fully elucidated. The aim of this study was to evaluate 1,5-AG as a predictor of coronary plaque rupture in diabetic patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS). Methods A total of 132 diabetic patients with NSTE-ACS were included in this study. All patients underwent intravascular ultrasound examination, which revealed 38 patients with plaque rupture and 94 patients without plaque rupture in the culprit lesion. Fasting blood glucose (FBS), hemoglobin A1c (HbA1c) and 1,5-AG levels were measured before coronary angiography. Fasting urinary 8-iso-prostaglandin F2α (8-iso-PGF2α) level was measured and corrected by creatinine clearance. Results Patients with ruptured plaque had significantly lower serum 1,5-AG levels and a tendency of higher hemoglobin A1c levels than patients without ruptured plaque in our study population. In multivariate analysis, low 1,5-AG levels were an independent predictor of plaque rupture (odds ratio 3.3; p=0.006) in diabetic patients with NSTE-ACS, but HbA1c was not. The area under the receiver-operating characteristic curve for 1,5-AG (0.678, p=0.001) to predict plaque rupture was superior to that for HbA1c (0.618, p=0.034). Levels of 1,5-AG were significantly correlated with urinary 8-iso-PGF2α (r=−0.224, p=0.010). Conclusions Postprandial hyperglycaemia appeared to be superior to long-term average blood glucose levels in predicting plaque rupture in culprit lesions, which may be useful to assess the cardiovascular outcomes in diabetic patients. Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): Outstanding Clinical Discipline Project of Shanghai Pudong, Beijing Health Special Foundation

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