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

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.

2020 ◽  
Author(s):  
Chunlin Yin ◽  
Xue Liu ◽  
Hongxia Wang ◽  
Mingcong Yan ◽  
Lijuan Guo ◽  
...  

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.


2015 ◽  
pp. 229-245
Author(s):  
J. FRANEKOVÁ ◽  
J. KETTNER ◽  
Z. KUBÍČEK ◽  
A. JABOR

C-reactive protein (CRP) is a marker of arterial inflammation while lipoprotein-associated phospholipase A2 (Lp-PLA2) is related to plaque instability. The aim of this study was to evaluate the correlation between the risk of unstable plaque presenting as acute coronary syndrome (ACS) and Lp-PLA2, and to assess the influence of statins on interpretation of Lp-PLA2. A total of 362 consecutive patients presenting to the emergency department (ED) with acute chest pain suggestive of ACS were evaluated by cardiologists as STEMI, NSTEMI, or unstable angina, and non-ACS. Serum biomarkers measured on admission: troponin I, C-reactive protein (Abbott), and Lp-PLA2 (DiaDexus). Four groups were defined according to the final diagnosis and history of statin medication: ACS/statin−; ACS/statin+; non-ACS/statin−; non-ACS/statin+. Lp-PLA2 was highest in ACS/statin− group; statins decreased Lp-PLA2 both in ACS and non-ACS of about 20 %. Lp-PLA2 was higher in ACS patients in comparison with non-ACS patients group without respect to statin therapy (p<0.001). Lp-PLA2 predicted worse outcome (in terms of acute coronary syndrome) effectively in patients up to 62 years; limited prediction was found in older patients. C-reactive protein (CRP) failed to discriminate four groups of patients. Statin therapy and age should be taken into consideration while interpreting Lp-PLA2 concentrations and lower cut-off values should be used for statin-treated persons.


2004 ◽  
Vol 23 (3) ◽  
pp. 201-211 ◽  
Author(s):  
Mauro Panteghini

This article reviews the current contribution of the determination of biochemical markers to clinical cardiology and discusses some important developments in this field. Biochemical markers play a pivotal role in the diagnosis and management of patients with acute coronary syndrome (ACS), as witnessed by the incorporation of cardiac troponins into new international guidelines for patients with ACS and in the redefinition of myocardial infarction. Despite the success of cardiac troponins, there is still a need for development of early markers that can reliably rule out ACS from the emergency room at presentation and detect myocardial ischemia also in the absence of irreversible myocyte injury. Under investigation are two classes of indicators: markers of early injury/ischemia and markers of coronary plaque instability and disruption. Finally, with the characterization of the cardiac natriuretic peptides, Laboratory Medicine is also assuming part in the assessment of cardiac function.


Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 881
Author(s):  
Marko Kumric ◽  
Josip A. Borovac ◽  
Dinko Martinovic ◽  
Tina Ticinovic Kurir ◽  
Josko Bozic

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.


Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2133
Author(s):  
Francisco O. Cortés-Ibañez ◽  
Sunil Belur Nagaraj ◽  
Ludo Cornelissen ◽  
Gerjan J. Navis ◽  
Bert van der Vegt ◽  
...  

Cancer incidence is rising, and accurate prediction of incident cancers could be relevant to understanding and reducing cancer incidence. The aim of this study was to develop machine learning (ML) models that could predict an incident diagnosis of cancer. Participants without any history of cancer within the Lifelines population-based cohort were followed for a median of 7 years. Data were available for 116,188 cancer-free participants and 4232 incident cancer cases. At baseline, socioeconomic, lifestyle, and clinical variables were assessed. The main outcome was an incident cancer during follow-up (excluding skin cancer), based on linkage with the national pathology registry. The performance of three ML algorithms was evaluated using supervised binary classification to identify incident cancers among participants. Elastic net regularization and Gini index were used for variables selection. An overall area under the receiver operator curve (AUC) <0.75 was obtained, the highest AUC value was for prostate cancer (random forest AUC = 0.82 (95% CI 0.77–0.87), logistic regression AUC = 0.81 (95% CI 0.76–0.86), and support vector machines AUC = 0.83 (95% CI 0.78–0.88), respectively); age was the most important predictor in these models. Linear and non-linear ML algorithms including socioeconomic, lifestyle, and clinical variables produced a moderate predictive performance of incident cancers in the Lifelines cohort.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R.A Montone ◽  
V Vetrugno ◽  
M Camilli ◽  
M Russo ◽  
M.G Del Buono ◽  
...  

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


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Kimura ◽  
K Hara ◽  
M Ohmori ◽  
R Tateishi ◽  
T Kaneda ◽  
...  

Abstract Background Many vulnerable plaques would progress without clinical events and might result in healed plaques (HPs). Histopathological or intracoronary image assessment of HPs has been reported. However, the morphological characteristics of HPs remain unclear yet. Purpose We sought to assess the healed vulnerable plaque components in patients with coronary artery lesions using optical coherence tomography (OCT) and coronary angioscopy (CAS). Methods We enrolled 47 patients with 50 native coronary artery lesions with angiographical severe stenosis (&gt;90% diameter-stenosis) and without severe calcification (36 lesions with stable angina pectoris (SAP) and 14 acute coronary syndrome (ACS)) undergoing pre-intervention OCT and CAS. HPs was defined as layered phenotype on OCT. Lesion morphologies and plaque characteristics in lesions with HPs were assessed using OCT and CAS images. Results HPs were observed in 27 lesions (54.0%) and their prevalence were similar among each clinical status (SAP 52.8%, ACS 57.1%, p=1.00). Lesions with HPs had higher prevalence of OCT-macrophage (88.0% vs. 52.0%, p=0.01), CAS-red thrombus (88.8% vs. 52.2%, p=0.004) and CAS-low grade-yellow plaque (grade 1) (55.6% vs. 21.7%, p=0.02) than those without. SAP lesions with HPs had higher prevalence of CAS-yellow plaque (35.3% vs. 5.9%, p=0.09) and OCT-thin-cap fibroatheroma (42.1% vs. 5.9%, p=0.04) than SAP without HPs. ACS lesions with HPs had less CAS-red thrombus (0.0% vs. 50.0%, p=0.03) and OCT-plaque rupture (12.5% vs. 66.7%, p=0.04) than ACS without HPs. Multivariate logistic regression analysis revealed that OCT-macrophages (odds ratio (OR): 6.65, 95%-confidence intervals: 1.07–41.5, p=0.043), CAS-red thrombus (OR 8.77, 95% CI 1.33–57.8, p=0.02), and low grade-yellow plaque (OR 13.05, 95% CI 1.97–86.5, p=0.008) were independently related with the existence of HPs lesions. Combination of these 3 factors showed a high predictive value of OCT-HPs lesions (90.9%). Conclusions HPs lesions showed the lower lesion vulnerability than common ACS lesions but had more intraplaque inflammatory condition compared with common SAP lesions. Combined CAS and OCT examination might be useful to clarify the plaque components of HPs lesions in vivo, leading to help us understand the clinical significance of HPs. Funding Acknowledgement Type of funding source: None


PEDIATRICS ◽  
1952 ◽  
Vol 10 (3) ◽  
pp. 311-318
Author(s):  
WILLIAM J. WATERS ◽  
SEYMOUR S. KALTER ◽  
JOHN T. PRIOR

The clinical, laboratory and pathologic findings of a series of cases of cat scratch syndrome have been reviewed. In spite of a variable clinical course, certain features associated with a selected group of laboratory tests appear to be constant enough to be of diagnostic value. A history of contact with a cat and/or scratch which is usually associated with a peripheral skin lesion, lack of lymphangitis, presence of regional lymphadenopathy with tenderness to palpation are the most constant clinical findings. Fever, so frequently emphasized as a characteristic clinical sign, may be extremely variable in type and duration or entirely absent. A skin test with cat scratch antigen has been positive in all cases. Lacking this antigen, a negative Frei skin test in conjunction with a positive complement fixation test (Lygranum C. F.) is suggestive evidence for the diagnosis. With positive evidence from the above data, biopsy of an affected gland with its relatively nonspecific pathologic picture is not considered essential for the establishment of the diagnosis of cat scratch syndrome.


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