Association between serum lipoprotein-associated phospholipase A2, ischemic modified albumin and acute coronary syndrome: a cross-sectional study

Yang, Fumeng; Ma, Longfei; Zhang, Lili; Wang, Yilian; Zhao, Chenkai; Zhu, Wenjun; Liang, Wei; Liu, Qian

doi:10.1007/s00380-019-01403-3

Cited by 17 publications

(18 citation statements)

References 28 publications

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“…Other therapies targeting inflammation have also been investigated. The phospholipase A2 (PLA2) enzymes are key contributors to lipid metabolism and inflammatory activation and are strongly correlated with plaque burden [ 47 , 79 ]. PLA2 inhibition with varespladib methyl or darapladib showed indistinctive improvements in overall cardiovascular events but rendered patients susceptible to ACS in several large clinical trials [ 19 , 47 ].…”

Section: Therapeutic Approaches Targeting Immune and Inflammation mentioning

confidence: 99%

Immune and Inflammation in Acute Coronary Syndrome: Molecular Mechanisms and Therapeutic Implications

Wang

Liu

Shao

et al. 2020

Journal of Immunology Research

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Acute coronary syndrome (ACS) is a major cause of acute death worldwide. Both innate and adaptive immunity regulate atherosclerosis progression, plaque stability, and thrombus formation. Immune and inflammation dysfunction have been indicated in the pathogenesis of ACS. The imbalance in the proatherogenic and antiatherogenic immune networks promotes the transition of plaques from a stable to unstable state and results in the occurrence of acute coronary events. The residual inflammatory risk (RIR) has received increasing attention in recent years, and lowering RIR has been expected to improve the outcomes of ACS patients. The CANTOS, COLCOT, and LoDoCo trials verified the benefits of reducing cardiovascular events using anti-inflammation therapies; however, most of the other studies focusing on lowering RIR produced negative or contradicting results. Therefore, restoring the balance in autoimmune regulation is essential because proatherogenic and antiatherogenic immunomodulatory effects are equally important in the complex human immune network. In this review, we summarized the recent evidence of the roles of proatherogenic and antiatherogenic immune networks in the pathogenesis of ACS and discussed how immune and inflammation contribute to atherosclerosis progression, plaque instability, and adverse cardiovascular events. We also provide a “from bench to bedside” perspective of a novel and promising personalized strategy in RIR intervention and therapeutic approaches for the treatment of ACS.

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Section: Therapeutic Approaches Targeting Immune and Inflammation mentioning

confidence: 99%

Immune and Inflammation in Acute Coronary Syndrome: Molecular Mechanisms and Therapeutic Implications

Wang

Liu

Shao

et al. 2020

Journal of Immunology Research

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“…Lp‐PLA2 was also reported to be an independent predictor of high thrombus burden in patients with STEMI, 22 and manual thrombus aspiration could effectively reduce Lp‐PLA2 level 27 . Yang et al 20 . reported that the Lp‐PLA2 level provided a staging basis of the degree of risk of patients with STEMI.…”

Section: Discussionmentioning

confidence: 99%

“…The inhibitory of Lp‐PLA2 could be effective for the regulation of atherosclerosis 19 . Yang et al 20 . reported that serum Lp‐PLA2 and ischemia‐modified albumin are predictive of the degree of myocardial ischemia in patients with acute coronary syndrome.…”

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confidence: 99%

The Relationship Between the Level of Serum ESM‐1 and Lp‐PLA2 in Patients With Acute ST‐Segment Elevation Myocardial Infarction

Wei

Zong

Liu

et al. 2020

Clinical Translational Sci

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Acute ST‐segment elevation myocardial infarction (STEMI) is the most lethal coronary heart disease with vascular endothelium dysfunction and inflammation in the disease development process. Endothelial cell‐specific molecule 1 (ESM‐1) and lipoprotein‐associated phospholipase A2 (Lp‐PLA2) are important for the diagnosis and characterization of STEMI. To date, no studies have reported the correlation between ESM‐1 and Lp‐PLA2 levels in patients with STEMI, which may be an important predictor of the fatal disease. To measure the level of serum ESM‐1 and Lp‐PLA2, and to evaluate the relationship and the clinical significance of these two biomarkers in patients with acute STEMI, 37 inpatients with acute STEMI were sequentially enrolled in the research group and 24 study objects with normal coronary artery function were included in the control group. The measurement of the relative parameters was done by enzyme‐linked immunosorbent assay using blood samples taken from the median cubital vein while the inpatients were enrolled. The levels of serum SEM‐1 and Lp‐PLA2 were significantly higher in patients with acute STEMI than in study objects with normal coronary artery function ( P < 0.05). A significant correlation of serum SEM‐1 and Lp‐PLA2 was observed, leading to close linearity ( r 2 = 0.8131, P < 0.0001). In conclusion, the endothelium dysfunction factor ESM‐1 and inflammatory factor Lp‐PLA2 are significantly higher and correlated in patients with acute STEMI. These two factors could be novel and effective biomarkers for acute STEMI diagnosis and evaluation.

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“…Lp‐PLA2 can exert its enzymatic activity to hydrolyze oxidized phospholipids in low‐density lipoproteins and then form lipid pro‐inflammatory substances (such as oxidized free fatty acids and lysolecithin) to produce a variety of atherogenic effects (such as production of cytokines and adhesion factors, endothelial dysfunction, and endothelial cell death) . Therefore, Lp‐PLA2 is considered as a new vascular‐specific inflammatory factor that can be used as an independent risk factor for cardiovascular and cerebrovascular events . The mass and activity of Lp‐PLA2 in blood samples can be easily measured, and we can detect the level of Lp‐PLA2 to predict the long‐term risk of cerebral infarction.…”

Section: Introductionmentioning

confidence: 99%

“…10 Therefore, Lp-PLA2 is considered as a new vascular-specific inflammatory factor that can be used as an independent risk factor for cardiovascular and cerebrovascular events. [11][12][13] The mass and activity of Lp-PLA2 in blood samples can be easily measured, and we can detect the level of Lp-PLA2 to predict the long-term risk of cerebral infarction. Serum amyloid A (SAA) is an acutephase protein, and it exhibits several means that can render it atherogenic.…”

mentioning

confidence: 99%

Evaluation of lipoprotein‐associated phospholipase A2, serum amyloid A, and fibrinogen as diagnostic biomarkers for patients with acute cerebral infarction

Liang

ShiChuan

De-tai

et al. 2019

Clinical Laboratory Analysis

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Objective The aim of this study was to explore the clinical values of combined detection of lipoprotein‐associated phospholipase A2 (Lp‐PLA2), serum amyloid A (SAA), and plasma fibrinogen (FIB) in the diagnosis of acute cerebral infarction (ACI). Methods A case‐control study including 100 hospitalized patients with ACI and 47 healthy controls was carried out. The level of Lp‐PLA2, SAA, and FIB was detected, respectively, and their clinical values were analyzed. Carotid lesions and neurological impairment were also analyzed in each patient. Results The level of Lp‐PLA2, SAA, and FIB in the ACI group was significantly higher than that of the controls, and the three biomarkers showed a significant positive correlation and were considered as risk factors for ACI. The area under the curve (AUC) for Lp‐PLA2, SAA, and FIB was 0.858, 0.743, and 0.672, respectively. When three biomarkers were used in combination, the AUC was 0.879. Compared with the other groups, the levels of three biomarkers in bilateral carotid plaque ACI group were all significantly higher. In addition, the level of Lp‐PLA2 and SAA in ACI patients with severe neurological impairment was also significantly higher than that of the mild‐to‐moderate group. Conclusion Lp‐PLA2 combined with SAA and FIB had a high clinical value for rapid diagnosis and prediction of ACI. These biomarkers were also significantly associated with the formation of bilateral carotid atherosclerotic plaques and the severe neurological impairment in ACI patients.

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Association between serum lipoprotein-associated phospholipase A2, ischemic modified albumin and acute coronary syndrome: a cross-sectional study

Cited by 17 publications

References 28 publications

Immune and Inflammation in Acute Coronary Syndrome: Molecular Mechanisms and Therapeutic Implications

Immune and Inflammation in Acute Coronary Syndrome: Molecular Mechanisms and Therapeutic Implications

The Relationship Between the Level of Serum ESM‐1 and Lp‐PLA2 in Patients With Acute ST‐Segment Elevation Myocardial Infarction

Evaluation of lipoprotein‐associated phospholipase A2, serum amyloid A, and fibrinogen as diagnostic biomarkers for patients with acute cerebral infarction

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