|Year : 2020 | Volume
| Issue : 4 | Page : 133-139
Evaluation of Diagnostic Utility of Pentraxin-3 in Acute Coronary Syndrome Patients: A Pilot Study from Tertiary Care Hospital in South India
D Shiva Krishna MD 1, Siraj Ahmed Khan MD 1, M Vijaya Bhaskar MD 1, K S S Sai Baba MD; DNB 1, O Sai Satish MD, DM 2, Iyyapu Krishna Mohan PhD 1
1 Department of Biochemistry, Nizam's Institute of Medical Sciences, Hyderabad, Telangana, India
2 Department of Cardiology, Nizam's Institute of Medical Sciences, Hyderabad, Telangana, India
|Date of Submission||01-May-2020|
|Date of Decision||30-Jul-2020|
|Date of Acceptance||29-Aug-2020|
|Date of Web Publication||09-Feb-2021|
Dr. Iyyapu Krishna Mohan
Department of Biochemsitry, Nizam's Institue of Medical Sciences, Hyderabad, Telangana
Source of Support: None, Conflict of Interest: None
Background: Pentraxin 3 (PTX3), a member of C-reactive protein-like inflammatory protein group, is abundantly expressed in atherosclerotic plaques, as well as in cardiac myocytes. Increased serum PTX3 level has been observed in patients with the acute coronary syndrome (ACS). The diagnostic role of PTX3 in all three types of ACS in the Indian population is limited. This study aimed to investigate whether serum PTX3 can be used as a potential biomarker in the early detection of ACS. Materials and Methods: This is a cross-sectional case-control study comprising of 47 cases and 33 controls. Cases were divided into three groups, out of which 12 patients were of non-ST-segment elevation myocardial infarction (NSTEMI), 23 patients were of ST-segment elevation myocardial infarction (STEMI), and 12 patients were of unstable angina. Patients were recruited within 7 h of post event who are clinically diagnosed as ACS. Lipid parameters were measured on the Roche Cobas c511 analyzer and PTX3 levels were measured by ELISA kit. Results: Serum PTX-3 levels were significantly higher in all three groups of ACS when compared to controls (P < 0.0001). At a cutoff of 4 ng/ml, serum pentraxin-3 showed 97.87% sensitivity and 84.85% specificity in diagnosing ACS cases with a positive predictive value of 90.2% and negative predictive value of 96.6%, and the area under the curve was 0.978. At a cut-off of 3.56 and 6.09 ng/ml, serum PTX-3 has 100% sensitivity and 78.79% specificity and 91.67% sensitivity and 100% specificity in diagnosing NSTEMI and STEMI, respectively. Conclusions: This study demonstrates Pentraxin-3 levels in ACS cases were significantly high and showed as a valuable biomarker for early detection of ACS, particularly within 7 h of postevent. Assessment of pentraxin-3 and Troponin-T together may further improve the early detection of ACS patients.
Keywords: Acute coronary syndrome, creatine kinase-MB, diagnostic biomarker, pentraxin 3, Troponin T
|How to cite this article:|
Krishna D S, Khan SA, Bhaskar M V, Sai Baba K S, Satish O S, Mohan IK. Evaluation of Diagnostic Utility of Pentraxin-3 in Acute Coronary Syndrome Patients: A Pilot Study from Tertiary Care Hospital in South India. J Clin Prev Cardiol 2020;9:133-9
|How to cite this URL:|
Krishna D S, Khan SA, Bhaskar M V, Sai Baba K S, Satish O S, Mohan IK. Evaluation of Diagnostic Utility of Pentraxin-3 in Acute Coronary Syndrome Patients: A Pilot Study from Tertiary Care Hospital in South India. J Clin Prev Cardiol [serial online] 2020 [cited 2022 Jan 26];9:133-9. Available from: https://www.jcpconline.org/text.asp?2020/9/4/133/308973
| Introduction|| |
Acute coronary syndrome (ACS) is a spectrum of clinical symptoms consistent with acute myocardial ischemia and includes unstable angina (UA), non–ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Cardiovascular diseases, particularly coronary heart disease, are epidemic in India. India has the highest burden of ACS in the world. In India, among ACS-related mortality, acute STEMI had male and middle-age predominance with some common risk factors. Although biomarkers for ischemic myocardial damage, such as troponin-T (TnT) and creatine kinase-MB (CK-MB), have been clinically utilized to diagnose ACS, their diagnostic sensitivity and specificity for early detection of ACS remain unclear.
Pentraxin 3 (PTX3), a member of C-reactive protein (CRP)-like inflammatory protein group, is abundantly expressed in atherosclerotic plaques, as well as in cardiac myocytes. PTX3 synthesis is also stimulated in endothelial cells, macrophages, myeloid cells, and dendritic cells by cytokines and endotoxins such as bacterial products, interleukin-1 (IL-1), and tumor necrosis factor. PTX3 is mainly localized in lactoferrin positive-specific granules and is translocated to the surface of late apoptotic neutrophils on stimulation, where it accumulates in blebs and is rapidly released. PTX3 then binds with the high-affinity complement component C1q to initiate the classical pathway of complement activation and facilitate pathogen recognition by macrophages.
PTX3 is a key molecule playing complex regulatory roles at the crossroads of innate immunity, inflammation, tissue repair, and cancer. Vascular endothelial cells are a major source of PTX3 in response to inflammatory signals. Anti-inflammatory and atheroprotective signals, such as high-density lipoproteins (HDL) and IL-10, induce PTX3 expression. This suggests a potential regulatory role of PTX3 in the innate and adaptive immune responses as well as being an anti-atherogenic molecule. An in vivo experimental myocardial infarction (MI) model, PTX3 mRNA expression was upregulated in the left ventricle of wild-type animals, and circulating levels of the protein were increased, with a peak at 24 h. PTX3 is also released from neutrophils in the early phases of AMI in humans. The production of PTX3 by vascular cells in response to inflammatory signals and oxidized- low-density lipoprotein (LDL) and its occurrence in atherosclerotic lesions prompted investigations of PTX3 levels in acute MI (AMI).,
Previous studies have shown that circulating PTX3 levels were significantly elevated in the acute stages of AMI and UA pectoris, which are collectively termed as ACS. PTX3 is involved in a variety of molecular mechanisms leading to vascular damage and its elevated plasma levels represent a significant predictor of frailty in elderly hypertensive patients. Blood vessels produce large amounts of PTX3 during inflammation and the level of circulating PTX3 increases in several pathological conditions affecting the cardiovascular system. PTX3 is increased in circulating blood during the acute stage of ACS. But as a diagnostic test, however, its diagnostic sensitivity and specificity have not yet been compared with lipid parameters. The aim of the present study is to estimate the levels of PTX3 in established cases of ACS and age-matched healthy controls. Furthermore, to correlate PTX3 levels with lipid levels in patients with ACS.
| Materials and Methods|| |
Study design and patient population
This is a cross-sectional case-control study comprising of 47 cases and 33 controls. The study was conducted in the Department of Biochemistry in collaboration with the Department of Cardiology. Cases were recruited from the patients attending Cardiology Department within 7 h of event, clinically diagnosed with ACS as per electrocardiogram, cardiac biomarkers, and other clinical features. Age- and sex-matched healthy controls were recruited in the control group.
Inclusion and exclusion criteria
All the patients who are newly diagnosed with ACS attending our hospital within 7 h postevent were included in the study. Patients with rheumatoid arthritis, chronic kidney disease, vasospastic angina, symptomatic peripheral artery disease and cerebrovascular stroke were excluded from the study. The study was approved by the Institutional Ethics Committee. Written informed consent was obtained from all study participants.
Sample collection and measurement of pentraxin 3
Five milliliter of blood was drawn at the time of admission. The mean time interval from symptom onset to blood collection is 5 h. Blood samples were collected in the plain tube without any anticoagulant. Serum was collected from plain vacutainers by centrifugation at 2000 × g for 10 min at room temperature. Lipid levels were estimated immediately. Part of serum was aliquoted and stored at −40°C for subsequent PTX3 measurement. Lipid Parameters (total cholesterol [TC], LDL-cholesterol [LDL-c], HDL-cholesterol [HDL-C], very-LDL-C, and triglycerides [TG]) were measured immediately on fully automated Cobas c-501 analyzer. PTX3 levels in serum were measured by commercially available RayBio® Human PTX-3 ELISA kit (RayBiotech, Peachtree Corners, Georgia, USA). The detection range of the PTX3 assay is 0.08–20 ng/ml.
The statistical analysis was done by Microsoft Excel, Graph pad prism version 7. The data are expressed as mean ± standard deviation when it is parametric and median (Interquartile ranges) when it is nonparametric. P < 0.05 is considered as significant. One-way ANOVA is done for comparison of groups for normally distributed parameters, and the Kruskal–Wallis test was done for nonnormally distributed parameters. Mann–Whitney U-test and unpaired t-test was performed to test the significance between each ACS group when compared with controls. Pearson's correlation was done to see the association between normally distributed parameters, and spearman's correlation was done for non-normally distributed parameters. Receiver operating characteristic (ROC) curves were plotted to assess the diagnostic potential of PTX-3 in ACS.
| Results|| |
In this study, a total of 47 cases were included, of which 12 patients were of NSTEMI, 23 patients were of STEMI and 12 patients were of UA. 33 age- and sex-matched apparently healthy persons were selected as controls. The mean age group in cases is 52.96 years, while that in controls is 52.88 years. There was no significant difference between age groups (P = 0.97). PTX3 and lipid parameters were measured in both controls and cases for measuring the risk of cardiovascular disease [Table 1]. Cases have significantly higher levels of serum PTX3 (P < 0.0001) when compared to controls. Among the lipid parameters, all parameters except HDL-C, were significantly higher in ACS patients as compared to normal subjects (P < 0.0001). HDL-C is lower in cases when compared to controls, and the difference is significant (P < 0.0001).
PTX3 levels were measured in all three groups of ACS [Table 2]. Serum PTX-3 levels were significantly higher in all three groups of ACS when compared to controls (P < 0.0001). A significant difference in lipid parameters in all three groups of ACS patients as compared to controls (P < 0.0001), except triglyceride levels in the UA group (P = 0.7564). The median of PTX-3 in cases is 8.090 ng/ml, and the median of PTX-3 in controls is 2.030 ng/ml and the difference is significant (P < 0.0001) [Figure 1] and [Table 1]. Median of PTX-3 in Controls, UA, NSTEMI and STEMI groups are 2.03 ng/ml, 5.98 ng/ml 7.63 ng/ml and 9.75 ng/ml, respectively. Median of PTX-3 levels were significantly higher in all 3 groups of ACS patients when compared to controls (P < 0.0001) [Figure 2] and [Table 2].
|Figure 1: Comparison of pentraxin 3 levels in controls and cases. The median of pentraxin 3 in cases is significantly higher than the controls (P < 0.0001)|
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|Figure 2: Comparison of pentraxin 3 levels among different groups of acute coronary syndrome. Median of pentraxin 3 in all 3 groups of acute coronary syndrome is significantly higher when compared to controls|
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|Table 2: Biochemical variables of Controls, non–ST-segment elevation myocardial infarction, ST-segment elevation myocardial infarction, and unstable angina groups|
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To assess the diagnostic performance of PTX3 in all cases of ACS, ROC analysis was done. As shown in [Table 3], at a cutoff of 4 ng/ml, serum PTX3 showed 97.8% sensitivity and 84.85% specificity in diagnosing ACS cases with a positive predictive value of 90.2% and negative predictive value of 96.6%, and the area under curve was 0.978 [Figure 3]. At cutoff of 3.56 ng/ml, serum PTX-3 has 100% sensitivity and 78.7% specificity in diagnosing UA [Figure 4]. At cutoff of 6.09 ng/ml, serum PTX-3 has 91.6% sensitivity and 100% specificity in diagnosing NSTEMI [Figure 5]. In a similar way, at cutoff of 6.09 ng/ml, serum PTX-3 has 95.6% sensitivity and 100% specificity in diagnosing STEMI [Figure 6].
|Figure 3: Receiver operating characteristic curve of serum pentraxin 3 in controls versus cases. At cut-off of 4 ng/ml, serum pentraxin 3 has 97.87% sensitivity and 84.85% specificity in diagnosing acute coronary syndrome|
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|Figure 4: Receiver operating characteristic curve of serum pentraxin 3 in controls versus unstable angina. At cut-off of 3.56 ng/ml, serum pentraxin 3 has 100% sensitivity and 78.79% specificity in diagnosing unstable angina|
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|Figure 5: Receiver operating characteristic curve of serum pentraxin 3 in controls versus non-ST-segment elevation myocardial infarction. At cut-off of 6.09 ng/ml, serum pentraxin 3 has 91.67% sensitivity and 100% specificity in diagnosing non-ST-segment elevation myocardial infarction|
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|Figure 6: Receiver operating characteristic curve of serum pentraxin 3 in controls versus ST-segment elevation myocardial infarction. At cut-off of 6.09 ng/ml, serum pentraxin 3 has 95.65% sensitivity and 100% specificity in diagnosing ST-segment elevation myocardial infarction|
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|Table 3: Diagnostic performance of serum Pentraxin-3 in all 3 groups of acute coronary syndrome|
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| Discussion|| |
ACS is the leading cause of mortality not only in India but also across Asia and rest of the world. Several biomarkers such as creatine kinase, troponin, short pentraxin CRP, and serum amyloid-A protein have been used for early diagnosis and prognosis of AMI. A quick and accurate diagnosis of ACS is essential for guiding treatment and early risk stratification. At present, the diagnosis of ACS requires thorough assessment of the patient's history and findings on physical examination, electrocardiography, radiologic studies, and cardiac biomarker tests. Although biomarkers for ischemic myocardial damage, such as CK, CK-MB, TnT, and troponin-I (TnI), have been clinically utilized to diagnose ACS, their diagnostic sensitivity and specificity for ACS, especially before 7 h of onset, is not very well established. Recently, PTX3 has moved into the focus of research.
In a cohort of 748 patients with MI and ST elevation enrolled in the Lipid Assessment Trial Italian Network, PTX3, CRP, pro b-type natriuretic peptide and TnT were measured within the 1st day from the onset of symptoms. Among all these markers, PTX3 levels >10.73 ng/mL within the 1st day after MI were the only independent predictor of 3-months mortality. Besides being a biomarker of MI reflecting the degree of tissue damage, PTX3 was proposed as a prognostic tool in two large studies aiming to identify predictive factors of CVD: the cardiovascular health study (1583 patients analyzed) and the multi-ethnic study of atherosclerosis (2880 patients). These two studies illustrated a significant relation between PTX3 levels and cardiovascular mortality and all-cause death., PTX3 has been investigated as a possible circulating biomarker in MI, Heart Failure and CA, but the numbers of pathological conditions potentially involving PTX3 as biomarker are larger. The rapid rises in PTX3 plasma levels are compatible with an acute phase response. PTX3 circulating levels were significantly correlated with the severity of disease and mortality and served to monitor the response to therapy. In addition, PTX3 levels rarely correlate with CRP, indicating that the two proteins might have different roles.
PTX3 plasma levels were significantly elevated in patients with arterial inflammation who underwent percutaneous coronary intervention (PCI). A study on 594 patients with stable coronary artery disease (CAD) reported that PTX3 plasma levels were higher 24 h after PCI than before. During the follow-up for major adverse cardiovascular events, patients with higher post-PCI levels of PTX3 had a higher incidence of events. Similarly, in patients with angina who underwent PCI, PTX3 levels resulted to be an independent risk factor associated with troponin increase after PCI. These data suggest that PTX3 could provide a reliable marker for risk stratification in patients undergoing PCI. PTX3 is a multifunctional acute-phase protein involved in plaques' vulnerability. Few previous studies have demonstrated the role of PTX3 in selective cases of either STEMI or UA.
In this study, we have estimated PTX3 levels in all three groups of ACS, i. e., STEMI, NSTEMI, and UA from samples drawn from patients within 7 h of onset of chest pain. The median serum PTX-3 level was significantly higher in all three groups of ACS patients as compared to the control group (P < 0.0001). In the study conducted by Vanitha et al., the mean serum PTX3 of the study group (5.60 ± 2.82) was higher than the control group (1.38 ± 0.52 ng/ml) (P < 0.05), and this rise in serum PTX3 level is mainly due to the neutrophils which undergo activation across the coronary vascular bed in patients with ACS. Neutrophils represent a source of the PTX3 in the blood of patients undergoing AMI, and it was found that intracellular PTX3 is indeed depleted during AMI. This is an acute and transient event, which parallels the early rise in plasma concentration of it within 6–8 h of AMI, and it is proved in previous studies by staining neutrophils with CD15 antibodies. Activation of the neutrophils across the coronary vascular bed, which is the hallmark of ACS is the cause for the elevated concentration of serum PTX3 in STEMI, NSTEMI, and UA. Another study concluded that PTX3 is a sensitive and specific marker when compared with cardiac markers such as neutrophil-activating peptide 2, CTnI within the first 6 h of onset of chest pain.
In our study, we correlated serum PTX-3 levels with TC, TG, HDL-C, LDL, and VLDL in cases. We found that there was no significant correlation between serum PTX-3 and TC. Similar results were also observed by Kume et al. Some patients are on lipid-lowering drugs and that might be the reason for no correlation between PTX-3 levels and lipid parameters. In our study, the PTX-3 level was significantly higher in the NSTEMI group when compared to the control group. Eggers et al. also showed NSTEMI-ACS patients had significantly higher median PTX3 levels as compared to healthy controls (3.8 vs. 1.9 ng/ml; P < 0.001). A similar study was conducted by George et al., who observed that PTX-3 levels were lower in the NSTEMI group of patients as compared to controls (NSTEMI-2.46 [1.71–4.31]) versus (controls 3.99 [1.92–7.2]). The finding in their study is contradictory to our study.
Thus PTX-3 has higher specificity in diagnosing NSTEMI and STEMI compared to UA, whereas PTX-3 has higher sensitivity in diagnosing UA compared to NSTEMI and STEMI, indicating that PTX-3 is a good marker for “ruling in” the diagnosis of NSTEMI and STEMI. This could help in “ruling out” the diagnosis of UA, but this requires further evaluation for confirmation. We also observed that AUC of PTX-3 in the STEMI group (0.995) > NSTEMI group (0.990) > UA group (0.933) showing that PTX-3 is a better marker in diagnosing STEMI compared to NSTEMI and UA. PTX-3 has positive predictive value (PPV) of 100% and negative predictive value (NPV) of 97.1% in diagnosing NSTEMI and STEMI and PPV of 63.2% and NPV of 100% in diagnosing UA.
Limitations of the study
The study population was small. Therefore, the results may not be representative of the population at large. It was a cross-sectional study, and the data were obtained in a single center. Another limitation is the lack of randomization and further follow-up of patients.
| Conclusions|| |
Serum Pentraxin-3 levels in ACS cases were significantly high and showed good sensitivity and AUC in diagnosing ACS. Pentraxin-3 levels are elevated in all three types of ACS patients; thus, pentraxin-3 may be a valuable biomarker for the diagnosis of ACS. In view of higher sensitivity and AUC, Pentraxin-3 has high diagnostic value and edge in early diagnosing of ACS patients. Combined pentraxin-3 and TnT measurements may further improve the diagnostic accuracy in patients with ACS, which can help in minimizing the morbidity and mortality. Further multicentric studies enrolling a larger number of patients with longer duration of follow-up is required to establish the superior diagnostic performance of Pentraxin-3 than troponins in the early detection of ACS patients.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Gupta R, Mohan I, Narula J. Trends in coronary heart disease epidemiology in India. Ann Glob Health 2016;82:307-15.
Singh SS, Paul SK, Pal R, Thatkar PV. Acute coronary syndrome-related mortality audit in a teaching hospital at Port Blair, India. J Family Med Prim Care 2017;6:502-8.
] [Full text]
Collinson PO, Stubbs PJ, Kessler AC, Multicentre Evaluation Of Routine Immunoassay Of Troponin T Study. Multicentre evaluation of the diagnostic value of cardiac troponin T, CK-MB mass, and myoglobin for assessing patients with suspected acute coronary syndromes in routine clinical practice. Heart 2003;89:280-6.
Kimura S, Inagaki H, Haraguchi G, Sugiyama T, Miyazaki T, Hatano Y, et al
. Relationships of elevated systemic pentraxin-3 levels with high-risk coronary plaque components and impaired myocardial perfusion after percutaneous coronary intervention in patients with ST-elevation acute myocardial infarction. Circ J 2014;78:159-69.
Bottazzi B, Bastone A, Doni A, Garlanda C, Valentino S, Deban L, et al
. The long pentraxin PTX3 as a link among innate immunity, inflammation, and female fertility. J Leukoc Biol 2006;79:909-12.
Jaillon S, Peri G, Delneste Y. The humoral pattern recognition receptor PTX3 is stored in neutrophil granules and localizes in extracellular traps. Hum Gene J Exp Med 2007;204:793-804.
Introna M, Alles VV, Castellano M, Picardi G, De Gioia L, Bottazzai B, et al
. Cloning of mouse pt×3, a new member of the pentraxin gene family expressed at extrahepatic sites. Blood 1996;87:1862-72.
Salio M, Chimenti S, De Angelis N, Molla F, Maina V, Nebuloni M, et al
. Cardioprotective function of the long pentraxin PTX3 in acute myocardial infarction. Circulation 2008;117:1055-64.
Halle M, Gabrielsen A, Paulsson-Berne G, Gahm C, Agardh HE, Farnebo F, et al
. Sustained inflammation due to nuclear factor-kappa B activation in irradiated human arteries. J Am Coll Cardiol 2010;55:1227-36.
Maugeri N, Rovere-Querini P, Slavich M, Coppi G, Doni A, Bottazzi B, et al
. Early and transient release of leukocyte pentraxin 3 during acute myocardial infarction. J Immunol 2011;187:970-9.
Altay S, Çakmak HA, Kemaloğlu Öz T, Özpamuk Karadeniz F, Türer A, Erer HB, et al
. Long-term prognostic significance of pentraxin-3 in patients with acute myocardial infarction: 5-year prospective cohort study. Anatol J Cardiol 2017;17:202-9.
Peri G, Introna M, Corradi D, Iacuitti G, Signorini S, Avanzini F, et al
. PTX3, A prototypical long pentraxin, is an early indicator of acute myocardial infarction in humans. Circulation 2000;102:636-41.
Yano Y, Matsuda S, Hatakeyama K, Sato Y, Imamura T, Shimada K, et al
. Plasma Pentraxin 3, but not high-sensitivity C-reactive protein, is a useful inflammatory biomarker for predicting cognitive impairment in elderly hypertensive patients. J Gerontol A Biol Sci Med Sci 2010;65:547-52.
Norata GD, Garlanda C, Catapano AL. The long pentraxin PTX3: A modulator of the immunoinflammatory response in atherosclerosis and cardiovascular diseases. Trends Cardiovasc Med 2010;20:35-40.
Lindahl B, Toss H, Siegbahn A, Venge P, Wallentin L. Markers of myocardial damage and inflammation in relation to long-term mortality in unstable coronary artery disease. FRISC Study Group. Fragmin during Instability in Coronary Artery Disease. N Engl J Med 2000;343:1139-47.
Ross R. Atherosclerosis--an inflammatory disease. N Engl J Med 1999;340:115-26.
Latini R, Maggioni AP, Peri G, Gonzini L, Lucci D, Mocarelli P, et al
. Prognostic significance of the long pentraxin PTX3 in acute myocardial infarction. Circulation 2004;110:2349-54.
Jenny NS, Arnold AM, Kuller LH, Tracy RP, Psaty BM. Associations of pentraxin 3 with cardiovascular disease and all-cause death: The Cardiovascular Health Study. Arterioscler Thromb Vasc Biol 2009;29:594-9.
Jenny NS, Blumenthal RS, Kronmal RA, Rotter JI, Siscovick DS, Psaty BM. Associations of pentraxin 3 with cardiovascular disease: The multiethnic study of atherosclerosis. J Thromb Haemost 2014;12:999-1005.
Garlanda C, Bottazzi B, Magrini E, Inforzato A, Mantovani A. PTX3, a Humoral Pattern Recognition Molecule, in Innate Immunity, Tissue Repair, and Cancer. Physiol Rev 2018;98:623-39.
Alipour-Parsa S, Haybar H, Namazi MH, Safi M, Khaheshi I, Memaryan M, et al
. Evaluation of pentraxin-3 level and its related factors in patients undergoing primary percutaneous coronary intervention. ARYA Atheroscler 2017;13:73-8.
Haibo L, Xiaofang G, Chunming W, Jie Y, Guozhong C, Limei Z, et al
. Prognostic value of plasma pentraxin-3 levels in patients with stable coronary artery disease after drug-eluting stent implantation. Mediators Inflamm 2014;2014:963096:1-7.
Wang Z, Sato A, Akiyama D, Kimura T, Tajiri K, Hoshi T, et al
. Clinical value of plasma pentraxin 3 levels for predicting cardiac troponin elevation after percutaneous coronary intervention. Life Sci 2014;95:40-4.
Soeki T, Niki T, Kusunose K, Bando S, Hirata Y, Tomita N, et al
. Elevated concentrations of pentraxin 3 are associated with coronary plaque vulnerability. J Cardiol 2011;58:151-7.
Vanitha K, Sasivathanam N, Deni NK, Ashok M, Santhi N. Serum pentraxin 3 A novel marker in diagnosing acute coronary syndrome. J Med Sci Health 2016;2:19-24.
Inoue K, Suwa S, Okazaki S, Itoh S, Savchenko AS, Naito M, et al
. Pentraxin 3 released from neutrophils increases plasma levels in patients with acute coronary syndrome. ISRN Vasc Med 2011;2011:6.
Maugeri N, Rovere-Querini P, Evangelista V, Godino C, Demetrio M, Baldini M, et al
. An intense and short-lasting burst of neutrophil activation differentiates early acute myocardial infarction from systemic inflammatory syndromes. PLoS One 2012;7:e39484.
Ustündağ M, Orak M, Güloğlu C, Sayhan MB, Alyan O, Kale E. Comparative diagnostic accuracy of serum levels of neutrophil activating peptide-2 and pentraxin-3 versus troponin-I in acute coronary syndrome. Anadolu Kardiyol Derg 2011;11:588-94.
Kume N, Mitsuoka H, Hayashida K, Tanaka M. Pentraxin 3 as a biomarker for acute coronary syndrome: Comparison with biomarkers for cardiac damage. J Cardiol 2011;58:38-45.
Eggers KM, Armstrong PW, Califf RM, Johnston N, Simoons ML, Venge P, et al
. Clinical and prognostic implications of circulating pentraxin 3 levels in non ST-elevation acute coronary syndrome. Clin Biochem 2013;46:1655-9.
George M, Shanmugam E, Srivatsan V, Vasanth K, Ramraj B, Rajaram M, et al
. Value of pentraxin-3 and galectin-3 in acute coronary syndrome: A short-term prospective cohort study. Ther Adv Cardiovasc Dis 2015;9:275-84.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
[Table 1], [Table 2], [Table 3]