scholarly journals Dynamic Changes in Plasma Urotensin II and its Correlation with Plaque Stability

2020 ◽  
Author(s):  
Chunlin Yin ◽  
Xue Liu ◽  
Hongxia Wang ◽  
Mingcong Yan ◽  
Lijuan Guo ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Vulnerable Plaque ◽  
Gene Transfection ◽  
Dynamic Change ◽  
High Cholesterol Diet ◽  
Atherosclerotic Plaques ◽  
Urotensin Ii ◽  
Plaque Instability ◽  
Coronary Syndrome ◽  
The Stability

Abstract Background: Urotensin II (UII) is involved in the formation of atherosclerosis, but its role in the stability of atherosclerotic plaque is undetermined. The purpose of this study was to observe the dynamic change of plasma UII and analyze its relationship with the stability of atherosclerotic plaques. Methods: The plasma UII concentration in patients with acute coronary syndrome (ACS) was detected. A vulnerable plaque model was established by local transfection of a recombinant P53 adenovirus into plaques of rabbits fed with a high-cholesterol diet and subjected to balloon injury, to evaluate the stability of the atherosclerotic plaques. Results: Our results showed that the level of plasma UII was increased in ACS patients compared with healthy subjects. However, it was significantly decreased in ST-segment elevation myocardial infarction patients (STEMI) and increased again in acute myocardial infarction (AMI) patients that were discharged after three months. UII dynamic change and its correlation with plaques stabilities were further verified in rabbit with atherosclerotic vulnerable plaque. The UII level in rabbits was significantly decreased after P53 gene transfection which can lead to of plaque instability. Conclusions: In conclusion, the level of plasma UII was significantly decreased in ACS with STEMI, which may serve as a reliable biological marker to reflect the progression and stability of atherosclerotic plaques.

Simvastatin Reduces Expression and Activity of Lipoprotein-Associated Phospholipase A2 in the Aorta of Hypercholesterolaemic Atherosclerotic Rabbits

2009 ◽  
Vol 37 (4) ◽  
pp. 1029-1037 ◽  
Author(s):  
Z Qiao ◽  
J Ren ◽  
H Chen
Keyword(s):  
Atherosclerotic Lesion ◽  
Statin Treatment ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Atherosclerotic Plaques ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Local Inflammatory Response ◽  
Plaque Instability ◽  
Significant Difference

Lipoprotein-associated phospholipase A2 (Lp-PLA2) contributes to atherosclerotic plaque instability and subsequent sudden coronary death. Statins are associated with decreased stroke risk and may improve stability of atherosclerotic plaques. The present study investigated the effect of simvastatin on expression of Lp-PLA2 levels in atherosclerotic plaques and on Lp-PLA2 activity in atherosclerotic aortas. Rabbits were a fed chow (control group) or a high-cholesterol diet (atherosclerosis group) for 12 weeks. An additional group on the high-cholesterol diet received simvastatin (5 mg/kg per day) for the last 4 weeks (simvastatin group). Lp-PLA2 activity in plasma and atherosclerotic aortas was significantly higher in the atherosclerosis group than in the control group and, consistent with this, abundant Lp-PLA2 protein was detected in plaques in the atherosclerosis group. Simvastatin significantly reduced Lp-PLA2 activity in plasma and aorta tissue, and reduced Lp-PLA2 protein level in atherosclerotic plaques. Whereas there was no significant difference in total atherosclerotic lesion area between simvastatin and atherosclerosis groups, simvastatin significantly reduced macrophage content, lipid retention and the intima/media ratio but increased the content of smooth muscle cells in atherosclerotic lesions. Thus, statin treatment markedly reduced Lp-PLA2 in both plasma and atherosclerotic plaques. This was associated with attenuation of the local inflammatory response and improved plaque stability.

scholarly journals Matrix Metalloproteinases as Biomarkers of Atherosclerotic Plaque Instability

2020 ◽  
Vol 21 (11) ◽  
pp. 3946 ◽  
Author(s):  
Wioletta Olejarz ◽  
Dominika Łacheta ◽  
Grażyna Kubiak-Tomaszewska
Keyword(s):  
Matrix Metalloproteinases ◽  
Atherosclerotic Plaque ◽  
Atherosclerotic Plaques ◽  
Prognostic Information ◽  
Plaque Instability ◽  
Coronary Syndrome ◽  
Ecm Proteins ◽  
Stable Coronary Heart Disease ◽  
Future Risk ◽  
Traditional Risk Factors

Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases responsible for tissue remodeling and degradation of extracellular matrix (ECM) proteins. MMPs may modulate various cellular and signaling pathways in atherosclerosis responsible for progression and rupture of atherosclerotic plaques. The effect of MMPs polymorphisms and the expression of MMPs in both the atherosclerotic plaque and plasma was shown. They are independent predictors of atherosclerotic plaque instability in stable coronary heart disease (CHD) patients. Increased levels of MMPs in patients with advanced cardiovascular disease (CAD) and acute coronary syndrome (ACS) was associated with future risk of cardiovascular events. These data confirm that MMPs may be biomarkers in plaque instability as they target in potential drug therapies for atherosclerosis. They provide important prognostic information, independent of traditional risk factors, and may turn out to be useful in improving risk stratification.

scholarly journals P977 CT phenotype of high-risk atherosclerotic plaques causing an acute coronary syndrome compared to silent vulnerable plaques

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
R I Hodas ◽  
D Opincariu ◽  
N Rat ◽  
I Rodean ◽  
M Chitu ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
High Risk ◽  
Morphological Characteristics ◽  
Plaque Morphology ◽  
Atherosclerotic Plaques ◽  
Plaque Instability ◽  
Coronary Syndrome ◽  
Atheromatous Plaques ◽  
Group 2 ◽  
Group 1

Abstract Funding Acknowledgements PlaqueImage.- research grant no. 103544/2016, contract number 26/01.09.2016 - Background Previous studies demonstrated that plaque morphology has a crucial role in the development of an acute coronary syndrome (ACS). However, not all vulnerable coronary plaques produce an ACS and the prediction power of various vulnerability features to predict an acute coronary event in a close future, has not been elucidated so far. Objective We aimed to use multi-slice computed tomography angiography (CTA) for assessment of morphological characteristics of culprit lesions producing an ACS in the next several months after CT assessment, in comparison with morphological characteristics of unstable coronary atherosclerotic plaques which did not trigger an ACS. Material and methods We analyzed 40 patients in whom CTA revealed presence of unstable coronary lesions, exhibiting at least one marker of vulnerability: napkin ring sign (NRS), spotty calcium (SC), positive remodeling (PR) or presence of low attenuation plaque (LAP), divided in 2 groups: group 1 - 20 patients who developed an ACS in the next 6 months following CTA examination, and group 2 – 20 patients matched for age, gender and risk factors, who did not present any cardiovascular event 6 month after CTA assessment. Post-processing of multi-slice CTA images was performed in order to assess morphological characteristics and CT-derived markers of atherosclerotic plaque instability. Results Similar mean values of plaque length (17.1 +/- 5.9 mm vs 16.9 +/- 3.4 mm; p = 0.6) and total atheroma volume (188.1 +/- 104.7 mm3vs 186.4 +/- 90.7 mm3; p = 0.8) were obtained for both groups. The mean number of vulnerability markers was 1.6 in group 1 vs 1.2 in group 2 (p = 0.07). However, atherosclerotic lesions in patients from group 1 presented significantly higher values of lipid-rich atheroma (9.8 +/- 10.8 mm3vs 2.6 +/- 1.0 mm3; p = 0.01) and remodeling index (1.14 +/- 0.3 in group 1 vs 0.89 +/- 0.19 in group 2, p = 0.04). At the same time, atheromatous plaques in patients who developed an ACS during the 6-months follow-up showed in a significantly higher proportion LAP (45% in group vs 10% in group 2, p = 0.03) and PR (15%in group 1 versus 5% in group 2, p = 0.04), but not NRS (30% vs 25%, p = ns) or SC (65% vs 40%, p = 0.2). Conclusions Atherosclerotic plaques producing an ACS exhibit a different phenotype than unstable plaques that remain silent. The CTA profile of atheromatous plaques producing an ACS includes the presence of low attenuation, positive remodeling, higher RI and lipid-rich atheroma. Presence of these features in high-risk coronary plaques identifies very high risk patients, who can benefit from adapted therapeutic strategy in order to prevent the development of an ACS.

scholarly journals Early Dynamic Change in High-Sensitivity Cardiac Troponin T in the Investigation of Acute Myocardial Infarction

2011 ◽  
Vol 57 (8) ◽  
pp. 1154-1160 ◽  
Author(s):  
Sally J Aldous ◽  
A Mark Richards ◽  
Louise Cullen ◽  
Martin P Than
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Adverse Events ◽  
Troponin T ◽  
Dynamic Change ◽  
High Sensitivity ◽  
Hazard Ratio ◽  
Diagnostic Sensitivity ◽  
Diagnostic Specificity ◽  
Coronary Syndrome

BACKGROUND The definition of acute myocardial infarction (AMI) requires a rise and/or fall in troponin with 1 or more results ≥99th percentile of the reference range. How much troponin must change has not been specified. We ascertained whether dynamic changes (δ) in high-sensitivity troponin T (hs-TnT) improved diagnostic and prognostic test performance in the emergency department. METHODS We recruited 939 patients with symptoms suggestive of acute coronary syndrome (without ST elevation). hs-cTnT was measured at 0 h and 2 h after presentation. End-points were admission diagnosis of AMI and 1-year adverse events (composite of death, AMI, revascularization). RESULTS Diagnostic specificity of 0–2-h hs-cTnT for AMI (incurred by 200 patients) improved from 79.8% (78.8%–80.5%) by using the 99th percentile alone to 94.2% (92.9%–95.4%) when we also included a δ ≥20%, but diagnostic sensitivity decreased from 94.5% (90.7%–96.9%) to 49.5% (44.6%–53.9%). With the inclusion of those patients with a δ ≥20% when 0–2-h hs-cTnT was <99th percentile, in addition to any with concentrations ≥99th percentile, diagnostic sensitivity increased to 97.5% (94.4%–98.9%). hs-cTnT ≥99th percentile predicted adverse events (incurred by 111 patients), adjusted hazard ratio 1.9 (1.2–2.8), whereas a δ ≥20% did not, hazard ratio 1.1 (0.7–1.7). CONCLUSIONS Diagnostic specificity of hs-cTnT improved with the use of a δ ≥20% in those patients with concentrations ≥99th percentile, but at a cost of a large reduction in sensitivity. Diagnostic sensitivity improved with the use of a δ ≥20% in patients with 0–2-h concentrations <99th percentile. Both approaches may be required for optimum rule-in and rule-out strategies, respectively. The δ criteria seem to be less useful for medium-term risk stratification.

scholarly journals Inflammation as a universal pathogenetic link between injury, repair and regeneration, in acute coronary syndrome. From experiment to clinic

Kardiologiia ◽  
2019 ◽  
Vol 59 (8S) ◽  
pp. 15-23
Author(s):  
V. V. Ryabov ◽  
A. E. Gombozhapova ◽  
Yu. V. Rogovskaya ◽  
M. S. Rebenkova ◽  
Yu. V. Alekseeva ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Coronary Syndrome ◽  
Cardiac Repair ◽  
Atherosclerotic Plaques ◽  
Injury Repair ◽  
Coronary Syndrome ◽  
Anti Inflammatory

Theory of atherogenesis and its complications underwent numerous changes. Today we observe that inflammation is a universal pathogenetic link between various processes such as atherosclerosis, rupture of atherosclerotic plaques and following myocardial infarction, post-infarction cardiac repair and heart failure. This review discusses examples, difficulties, and prospects of implementation of anti-inflammatory therapies in management of acute coronary syndrome and its complications.

scholarly journals Plasma calprotectin was associated with platelet activation and no-reflow phenomenon in acute coronary syndrome

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Nian-Peng Song ◽  
Xiao-Wen Zhen ◽  
Liu-dong Li ◽  
Lin Zhong ◽  
Hua Wang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Coronary Syndrome ◽  
Platelet Activation ◽  
Negative Impact ◽  
Chinese Patients ◽  
Plaque Instability ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
No Reflow ◽  
No Reflow Phenomenon

Abstract Background No-reflow occurs in 3–4% of all percutaneous coronary interventions (PCIs) and has a strong negative impact on clinical outcomes of acute coronary syndrome (ACS). Therefore, the discovery of a biomarker that can early predict the occurrence of no-reflow has great clinical significance. Multiple factors including platelet activation are relevant to no-reflow. Calprotectin is found to be a biomarker of plaque instability and is identified to be a novel diagnostic and prognostic biomarker of cardiovascular diseases. The association of plasma calprotectin with platelet activation and no-reflow phenomenon in ACS is not clear. Methods In this prospective study performed at Yantai Yuhuangding Hospital from 2017 to 2018, a total of 176 Chinese patients with ACS who had undergone PCIs were recruited consecutively, aged from 30 to 88 years. Angiographic no-reflow was defined as thrombolysis in myocardial infarction grade less than 3. Blood samples were collected immediately at admission for the detection of plasma calprotectin and platelet–monocyte aggregates formation. Statistical analysis was performed for the variable’s comparisons between groups and the prediction value of plasma calprotectin for no-reflow. Results The mean age of the 176 included ACS patients were 64(±11) years and acute ST-segment elevation myocardial infarction (STEMI) was present in 41.5% of patients. Twenty-two patients had no-reflow during the PCI procedures and the prevalence was 12.5%. Patients with higher plasma calprotectin had a higher level of platelet–monocyte aggregates (PMA) and a higher prevalence of no-reflow (p < 0.001). The multivariate regression showed that plasma calprotectin and admission hs-cTnI were independently associated with PMA, while plasma calprotectin and serum LDL-c were independent predictors of no-reflow (p < 0.001 and p = 0.017). AUC of calprotectin for predicting no-reflow were 0.898. The cut-off value of plasma calprotectin for no-reflow was 4748.77 ng/mL with a sensitivity of 0.95 and a specificity of 0.77. Conclusion Plasma calprotectin was associated with platelet activation and may act as an early predictive biomarker of no-reflow in patients with acute coronary syndrome.

scholarly journals Plasma calprotectin was associated with platelet activation and no-reflow phenomenon in acute coronary syndrome

2020 ◽  
Author(s):  
Nian-Peng Song ◽  
Xiao-Wen Zhen ◽  
Liu-dong Li ◽  
Lin Zhong ◽  
Hua Wang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Coronary Syndrome ◽  
Platelet Activation ◽  
Negative Impact ◽  
Chinese Patients ◽  
Plaque Instability ◽  
Coronary Syndrome ◽  
No Reflow ◽  
Percutaneous Coronary ◽  
No Reflow Phenomenon

Abstract Background No-reflow occurs in 3–4% of all percutaneous coronary interventions (PCIs) and has a strong negative impact on clinical outcomes of acute coronary syndrome. (ACS). Therefore, the discovery of a biomarker that can early predict the occurrence of no-reflow has great clinical significance. Multiple factors including platelet activation are relevant to no-reflow. Calprotectin is found to be a biomarker of plaque instability and is identified to be a novel diagnostic and prognostic biomarker of cardiovascular diseases. But theThe association of plasma calprotectin with platelet activation and no-reflow phenomenon in acute coronary syndromeACS is not clear. Methods In this prospective study performed at Yantai Yuhuangding Hospital from 2017 to 2018, a total of 176 Chinese patients with acute coronary syndromeACS who had undergone percutaneous coronary interventionsPCIs were recruited consecutively, aged from 30 to 88 years. The coronary angiography and percutaneous coronary intervention procedures were performed and angiographicAngiographic no-reflow was defined as a thrombolysis in myocardial infarction scores grade less than 3. Blood samples were collected immediately at admission for the detection of plasma calprotectin and platelet–monocyte aggregates formation. Statistical analysis was performed for the variable’s comparisons between groups and for the prediction value of plasma calprotectin for no-reflow.Results In this study, we have demonstrated that acute coronary syndromeThe mean age of the 176 included ACS patients were 64(±11) years and acute ST-segment elevation myocardial infarction (STEMI) was present in 41.5 percent of patients. 22 patients had no-reflow during the PCI procedures and the prevalence was 12.5%. Patients with higher plasma calprotectin had an elevateda higher level of platelet activation–monocyte aggregates (PMA) and a higher incidenceprevalence of no-reflow. Plasma (p<0.001). The multivariate regression showed that plasma calprotectin level wasand admission hs-cTnI were independently associated with platelet activation and no-reflow in patients with acute coronary syndrome. Despite that platelet activation biomarker platelet–monocyte aggregate was associated with no-flow, onlyPMA, while plasma calprotectin and serum low density lipoprotein cholesterol acted asLDL-c were independent predictors of no-reflow in patients with acute coronary syndrome.(p<0.001 and p=0.017). AUC of calprotectin for predicting no-reflow were 0.898. The cut-off value of plasma calprotectin for no-reflow was 4748.77 ng/mL with a sensitivity of 0.95 and a specificity of 0.77. Conclusion Plasma calprotectin was associated with platelet activation and may act as an early predictionpredictive biomarker of no-reflow in patients with acute coronary syndrome.

scholarly journals Circulating Biomarkers Reflecting Destabilization Mechanisms of Coronary Artery Plaques: Are We Looking for the Impossible?

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 881
Author(s):  
Marko Kumric ◽  
Josip A. Borovac ◽  
Dinko Martinovic ◽  
Tina Ticinovic Kurir ◽  
Josko Bozic
Keyword(s):  
Coronary Artery ◽  
Vulnerable Plaque ◽  
Cost Effective ◽  
Current Evidence ◽  
Plaque Instability ◽  
Coronary Syndrome ◽  
Non Invasive ◽  
Multiple Biomarkers ◽  
Plaque Destabilization

Despite significant strides to mitigate the complications of acute coronary syndrome (ACS), this clinical entity still represents a major global health burden. It has so far been well-established that most of the plaques leading to ACS are not a result of gradual narrowing of the vessel lumen, but rather a result of sudden disruption of vulnerable atherosclerotic plaques. As most of the developed imaging modalities for vulnerable plaque detection are invasive, multiple biomarkers were proposed to identify their presence. Owing to the pivotal role of lipids and inflammation in the pathophysiology of atherosclerosis, most of the biomarkers originated from one of those processes, whereas recent advancements in molecular sciences shed light on the use of microRNAs. Yet, at present there are no clinically implemented biomarkers or any other method for that matter that could non-invasively, yet reliably, diagnose the vulnerable plaque. Hence, in this review we summarized the available knowledge regarding the pathophysiology of plaque instability, the current evidence on potential biomarkers associated with plaque destabilization and finally, we discussed if search for biomarkers could one day bring us to non-invasive, cost-effective, yet valid way of diagnosing the vulnerable, rupture-prone coronary artery plaques.

scholarly journals Analysis of Predictive Model of Coronary Vulnerable Plaque under Hemodynamic Numerical Simulation

2022 ◽  
Vol 2022 ◽  
pp. 1-10
Author(s):  
Qiang Song ◽  
Mingwei Chen ◽  
Jin Shang ◽  
Zhi Hu ◽  
Hui Cai
Keyword(s):  
Biochemical Markers ◽  
Vulnerable Plaque ◽  
Diagnostic Value ◽  
Plaque Instability ◽  
Coronary Syndrome ◽  
Plaque Area ◽  
Hemodynamic Characteristics ◽  
History Of ◽  
Serum Biochemical ◽  
Auc Value

Objective. Vulnerable plaque is considered to be the cause of most clinical coronary arteries, and linear cytokines are an important factor causing plaque instability. Early prediction of vulnerable plaque is of great significance in the treatment of cardiovascular diseases. Methods. Computational fluid dynamics (CFD) was used to simulate the hemodynamics around plaques, and the serum biochemical markers in 224 patients with low-risk acute coronary syndrome (ACS) were analyzed. Vulnerable plaques were predicted according to the distribution of biochemical markers in serum. Results. CFD can accurately capture the hemodynamic characteristics around the plaque. The patient’s age, history of hyperlipidemia, apolipoprotein B (apoB), adiponectin (ADP), and sE-Selection were risk factors for vulnerable plaque. Area under curve (AUC) values corresponding to the five biochemical markers were 0.601, 0.523, 0.562, 0.519, 0.539, and the AUC value after the combination of the five indicators was 0.826. Conclusion. The combination of multiple biochemical markers to predict vulnerable plaque was of high diagnostic value, and this method was convenient and noninvasive, which was worthy of clinical promotion.

scholarly journals Presence of bacterial DNA in thrombotic material of patients with myocardial infarction

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
P. Piñon-Esteban ◽  
L. Núñez ◽  
R. Moure ◽  
G. M. Marrón-Liñares ◽  
X. Flores-Rios ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Peripheral Blood ◽  
Thrombus Formation ◽  
Coronary Intervention ◽  
Prevotella Intermedia ◽  
Bacterial Dna ◽  
Plaque Instability ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
Viridans Group Streptococci

Abstract Infectious agents have been suggested to be involved in etiopathogenesis of Acute Coronary Syndrome (ACS). However, the relationship between bacterial infection and acute myocardial infarction (AMI) has not yet been completely clarified. The objective of this study is to detect bacterial DNA in thrombotic material of patients with ACS with ST-segment elevation (STEMI) treated with Primary Percutaneous Coronary Intervention (PPCI). We studied 109 consecutive patients with STEMI, who underwent thrombus aspiration and arterial peripheral blood sampling. Testing for bacterial DNA was performed by probe-based real-time Polymerase Chain Reaction (PCR). 12 probes and primers were used for the detection of Aggregatibacteractinomycetemcomitans, Chlamydiapneumoniae, viridans group streptococci, Porphyromonasgingivalis, Fusobacteriumnucleatum, Tannarellaforsythia, Treponemadenticola, Helycobacterpylori, Mycoplasmapneumoniae, Staphylococusaureus,  Prevotella intermedia and Streptococcusmutans. Thus, DNA of four species of bacteria was detected in 10 of the 109 patients studied. The most frequent species was viridans group streptococci (6 patients, 5.5%), followed by Staphylococusaureus (2 patients, 1.8%). Moreover, a patient had DNA of Porphyromonasgingivalis (0.9%); and another patient had DNA of Prevotella intermedia (0.9%). Bacterial DNA was not detected in peripheral blood of any of our patients. In conclusion, DNA of four species of endodontic and periodontal bacteria was detected in thrombotic material of 10 STEMI patients. Bacterial DNA was not detected in the peripheral blood of patients with bacterial DNA in their thrombotic material. Bacteria could be latently present in plaques and might play a role in plaque instability and thrombus formation leading to ACS.

Sign in / Sign up

Export Citation Format

Share Document