scholarly journals Detection and Optimization of Cardiac Markers Based on High Sensitivity C-Reactive Protein

2020 ◽  
Vol 9 (1) ◽  
pp. 9
Author(s):  
Dai Chen

Cardiac markers play an important role in prognosis and follow-up treatment. Therefore, it is of great practical significance to study the detection methods of high-sensitivity C-reactive protein cardiac markers. The purpose of this paper is to study the optimal method for the detection of cardiac markers of high-sensitivity C-reactive protein. In this paper, the significance of cardiac markers and high-sensitivity C-reactive protein and the relationship between them and myocardial infarction were first described. The BCA method for the purification and identification of C-reactive protein was studied, and then the determination and optimization of high-sensitivity C-reactive protein and high-sensitivity C-reactive protein in healthy people were further understood. To explore the application of serum high sensitive C-reactive protein in the detection of cardiac markers in 50 patients with acute myocardial infarction and 50 healthy people. The results showed that the experimental group was (21.57 ± 1.50), (37.62 ± 1.66), (529.20 ± 5.72), (95.79 ± 6.24) ng / ml, the control group was (0.90 ± 1.10), (1.71 ± 0.14), (35.25 ± 4.21), (0.99 ± 0.71) ng / ml, and the difference between the two groups was statistically significant (P < 0.05).

Angiology ◽  
2016 ◽  
Vol 68 (4) ◽  
pp. 354-359 ◽  
Author(s):  
Chong-Rong Qiu ◽  
Qiang Fu ◽  
Jian Sui ◽  
Qian Zhang ◽  
Peng Wei ◽  
...  

Endothelial dysfunction is involved in the process of acute myocardial infarction (AMI), that is, the endothelial cell–specific molecule 1 (ESM-1; endocan) is a novel endothelial dysfunction marker. However, the relationship between patients with AMI and serum ESM-1 levels is not very clear. Patients with AMI (n = 216) and a control group (n = 60) without AMI were included in the study. High-sensitivity C-reactive protein (hsCRP) was measured, and the severity of AMI was assessed by a modified Gensini stenosis scoring system. Serum ESM-1 levels were significantly higher in the AMI group ( P < .05). High-sensitivity C-reactive protein levels were also significantly higher in the AMI group ( P < .05). In patients with AMI, serum ESM-1 levels were not significantly correlated with hsCRP levels. There was no significant correlation between serum ESM-1 level and Gensini score. Our findings suggest that serum ESM-1 levels may be a novel biomarker of endothelial dysfunction in patients with AMI.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Toshiyuki Takahashi ◽  
Toshihisa Anzai ◽  
Hidehiro Kaneko ◽  
Atsushi Anzai ◽  
Yoshinori Mano ◽  
...  

We have previously reported that elevated serum C-reactive protein (CRP) level after acute myocardial infarction (MI) is associated with adverse outcomes including cardiac rupture, left ventricular (LV) remodeling and cardiac death. Recent experimental studies have shown that CRP per se has some biological properties including proinflammatory and proapoptotic effects, suggesting a pathogenetic role of CRP in the remodeling process after MI. We tested the hypothesis that increased CRP expression would exacerbate adverse LV remodeling after MI through some deleterious effects of CRP. Transgenic mice with human CRP expression (CRP-Tg) and their nontransgenic littermates (Control) underwent proximal ligation of the left coronary artery. Despite increased serum CRP level and cardiac CRP expression in CRP-Tg mice, there was no difference in phenotype between CRP-Tg and control mice before MI. Mortality at five weeks after MI was not different between groups (CRP-Tg: 49%, n=35; Control: 38%, n=40, P =0.28). Five weeks after MI, echocardiography showed that CRP-Tg mice had more LV dilation (LVEDD, CRP-Tg: 5.8 ± 0.1 mm, n=14; Control: 5.2 ± 0.1 mm, n=17, P =0.002) and worse LV function (EF, CRP-Tg: 13 ± 2%, n=14; Control: 19 ± 1%, n=17, P =0.01). Hemodynamic studies indicated that LV +dP/dt (CRP-Tg: 2,947 ± 480 mmHg/s, n=9; Control: 3,788 ± 656 mmHg/s, n=10, P =0.02) and -dP/dt (CRP-Tg: −2,230 ± 48 mmHg/s, n=9; Control: −2,890 ± 161 mmHg/s, n=10, P =0.003) were lower in the CRP-Tg group than in the Control group, although infarct size was comparable. Histological evaluation at one week after MI showed a higher rate of apoptosis in the border zone of infarcted hearts from CRP-Tg mice (CRP-Tg: 1,434 ± 322 per 10 5 nuclei; Control: 596 ± 112 per 10 5 nuclei, n=6 for each, P =0.03). Quantitative RT-PCR showed that angiotensin II type 1a receptor and interleukin-6 were upregulated in viable LV samples from CRP-Tg mice compared with controls. Increased CRP expression exacerbates LV dysfunction and remodeling after MI, associated with increased apoptotic rates, increased angiotensin II receptor expression and exaggerated inflammatory response.


Cardiology ◽  
2018 ◽  
Vol 141 (2) ◽  
pp. 88-97 ◽  
Author(s):  
Yan Gao ◽  
Yan Qiu ◽  
Jihua Wu ◽  
Wei Diao ◽  
Haibo Zhang ◽  
...  

Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a promising target for lowering plasma low-density lipoprotein cholesterol and preventing cardiovascular (CV) disease. Whether plasma PCSK9 measured during the acute phase predicts recurrent CV events in patients with acute myocardial infarction (AMI) remains unresolved. Methods and Results: Plasma PCSK9 levels were measured in 1,646 patients with AMI from the China PEACE-Prospective AMI Study at the acute phase. Additionally, 248 patients were resampled and measured at 1 month post-AMI. Associations of acute-phase PCSK9 tertiles with clinical characteristics and recurrent CV events within 1 year were assessed. Female gender (OR 1.94, 95% CI 1.24–3.03), premature coronary heart disease (CHD; OR 2.12, 95% CI 1.37–3.26), higher high-sensitivity C-reactive protein (OR 1.67, 95% CI 1.44–1.95), and higher triglycerides (OR 1.46, 95% CI 1.03–2.09) were associated with higher baseline PCSK9. Plasma PCSK9 levels in the highest tertile (versus lowest) did not have an increased risk of 1-year recurrent CV events in the AMI cohort (HR 0.78, 95% CI 0.52–1.16) or any subgroup. There was also no association between percentage changes in PCSK9 over the first month and 1-year recurrent events, although there was a trend of differences between patients in the upper versus lower tertiles. Conclusion: Plasma PCSK9 levels measured during the acute phase were associated with high-sensitivity C-reactive protein, triglycerides, premature CHD, and gender in patients with AMI but did not predict recurrent CV events within 1 year. Dynamic changes in PCSK9 suggested a trend yet no significance value in predicting recurrent CV events.


2021 ◽  
Vol 10 ◽  
pp. e1512
Author(s):  
Parichehr Alizadeh ◽  
Ehsan Bahramali ◽  
Arvin Hedayati ◽  
Azizallah Dehghan

Background: The natural history of acute myocardial infarction (AMI) as the most prevalent public health issue in Iran has changed with the introduction of novel therapeutic strategies that have reduced its mortality significantly. Major depressive disorder (MDD) is a prevalent and disabling psychiatric disorder and frequently co-exist with AMI. There are proposed pathophysiological links between the two diseases among which inflammation is the most important. With more patients surviving a myocardial infarction (MI) event, post-MI depression has become an important determinant of disability and mortality. Materials and Methods: In this study we defined a 1-month post-MI depressive scale of 200 patients using Beck’s inventory questionnaire II and measured serum high Sensitivity C-Reactive Protein (hs-CRP) and carotid intima-media thickness (CIMT) to look for the association between inflammatory state and atherosclerosis in different depression score categories. Results: Minimum and maximum Beck scores were 1 and 43, respectively with a mean of 13±8. The mean CIMT was 0.77±0.26 mm. Serum hs-CRP level was measured with a mean of 1.51±1.6 mg/L. According to BDI-II scores, 44.2% of patients 1-month post-MI suffered from more than mild depression. Being affected was not correlated with either the level of hs-CRP or CIMT. Nearly 44 percent of patients suffered more than mild depression. There was a negative association between serum hs-CRP level and CIMT as a measure of atherosclerosis in groups of depressed versus non-depressed patients. This may indicate that the extent of atherosclerosis is not correlated with the inflammatory state after MI in depressed versus non-depressed patients. Conclusions: The results of this study indicate that the extent of atherosclerosis is not correlated with the inflammatory state after MI in depressed versus non-depressed patients. Nonetheless, the prognostic indications of increased hs-CRP and depression after AMI remains to be investigated further. [GMJ.2021;10:e1512]


2017 ◽  
Vol 23 (1) ◽  
Author(s):  
Wael Rumaneh

Arterial hypertension is an independent predictor of acute myocardial infarction. Nowadays, plasma level of high-sensitive C-reactive protein is a marker of cardiovascular risk. The objective of the research was to evaluate plasma level of high-sensitive C-reactive protein in patients with acute myocardial infarction and arterial hypertension depending on myocardial remodeling type. Materials and methods. 130 patients with myocardial infarction (63 individuals with concomitant arterial hypertension and 67 individuals without it) were observed. Transthoracic echocardiogram was used. To evaluate plasma level of high-sensitive C-reactive protein the ELISA method was applied. Results. Plasma level of high-sensitive C-reactive protein in patients with acute myocardial infarction increased by 5.11 times compared to the control group: (10.67 [5.43; 12.89]) mg/l and (2.09 [1.40; 4.60]) mg/l, respectively (p<0.001). In myocardial infarction and arterial hypertension, this parameter increased by 6.57 times (to (13.73 [7.05; 15.17]) mg/l) (p<0.001), and by 1.27 times (p<0.05) as compared to patients without arterial hypertension. No differences in plasma level of high-sensitive C-reactive protein were detected in patients with different types of left ventricular remodeling.Conclusions. Acute myocardial infarction caused by high plasma level of high-sensitive C-reactive protein is severer in co-existent arterial hypertension. There are no differences in blood levels of high-sensitive C-reactive protein depending on the type of left ventricular remodeling.


2020 ◽  
Vol 19 (3) ◽  
pp. 2316
Author(s):  
O. V. Khlynova ◽  
E. A. Shishkina ◽  
N. I. Abgaryan

Aim. To study the association of cytokine status with coronary atherosclerosis severity in patients with myocardial infarction (MI).Material and methods. Between 11.2018 and 07.2019, 92 patients hospitalized with MI in Perm Clinical Cardiology Dispensary were included in the study. The control group consisted of 23 patients with stable coronary artery disease. In addition to the standard examination, enzyme-linked immunosorbent assay was used to determine the levels of interleukins (IL)-6, -10, tumor necrosis factor alpha (TNF-α), C-reactive protein.Results. Significant increase in plasma IL-6, TNF-α and C-reactive protein levels in MI patients compared with the control group. The increase in the concentration of IL-6, TNF-α, as well as the IL-6/IL-10 ratio occurs in proportion to coronary atherosclerosis severity. A direct correlation of Gensini score with IL-6, TNF-α, and IL-6/IL-10 ratio was established.Conclusion. Further study of cytokine profile parameters in MI patients will help a clearer understanding pathogenesis of coronary artery atherosclerosis. An increase in concentrations of IL-6, TNF-α, and IL-6/IL-10 ratio is associated with an increase in coronary atherosclerosis severity and can be used in practice for its prediction.


2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Archana Rajdev ◽  
Oana Penciu ◽  
Jacqueline Bradley ◽  
Cristina Mihu ◽  
Alan Siqueros ◽  
...  

INTRODUCTION Implantation of bare metal or drug eluting stents supported by dual antiplatelet therapy (DAPT) is standard treatment for the management of patients with ST elevation myocardial infarction (STEMI). Individual response to aspirin and clopidogrel is heterogeneous, and decreased response is associated with thrombotic events following stenting. We postulated that systemic inflammation at the time of STEMI would diminish responsiveness to DAPT. The aim of this study is to evaluate the correlation between elevated high-sensitivity C-reactive protein (hs-CRP) as a marker of inflammation and decreased platelet sensitivity to DAPT in STEMI. METHODS We recruited patients with STEMI undergoing percutaneous coronary intervention (PCI) who received oral clopidogrel 600 mg loading dose followed by 75 mg daily maintenance dose and aspirin 325 mg daily. Platelet reactivity and hs-CRP were measured within 72 hours of PCI and at 6 weeks. For patients receiving eptifibatide, blood samples were taken 48 hours after discontinuation. Platelet reactivity was assessed using the VerifyNow platelet function analyzer. A cut-off value of 208 platelet reaction units (PRU) was used to define high on-clopidogrel platelet reactivity (HCPR) and a value of 454 aspirin reaction units (ARU) was used to define high on-aspirin platelet reactivity (HAPR). RESULTS In 20 patients aged 31 to 85, in hospital and 6 weeks after STEMI, hs-CRP was 6.7 (SD 4.0) and 2.6 (SD 3.2) respectively, p< 0.01. Changes in ARU from 408.3 (SD 54.3) to 425.2 (SD 68.2) and PRU from 157.8 (SD 74.7) to 164.2 (SD 75) were not statistically significant. 2 patients had HAPR in hospital; 1 became sensitive at follow up. 2 patients developed HAPR and HCPR. We saw a trend towards higher PRU in diabetic patients and those prescribed statins. CONCLUSIONS Although we found a significant difference in hs-CRP levels between the first and second time point, no significant difference was found in on-aspirin and on-clopidogrel platelet reactivity between the time points.Thus, in this small series, the acute inflammatory state associated with STEMI did not appear to influence the on-DAPT reactivity at the dosages used. Trends among those with diabetics and prescribed statins will be discussed


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Heidi T May ◽  
Jeffrey L Anderson ◽  
Benjamin D Horne ◽  
Robert R Pearson ◽  
Robert L Wolfert ◽  
...  

Background : Inflammation plays a role in the development and progression of coronary artery disease (CAD), with circulating markers of vascular inflammation being used in risk assessment including high sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A 2 (LpPLA 2 ). While hsCRP responds to the systemic inflammatory stimulus of acute myocardial infarction (AMI), LpPLA 2 has been proposed to be more vascular-specific and to vary minimally based upon clinical presentation. To test this hypothesis, we evaluated both biomarkers among CAD patients presenting with stable angina (SA), unstable angina (USA) or acute myocardial infarction (AMI). Methods : LpPLA 2 (PLAC TM test, diaDexus, Inc.) and hsCRP were measured from samples donated by consenting patients (N=1,010) enrolled in the registry of the Intermountain Heart Collaborative Study that underwent angiographic evaluation for CAD. Patients were categorized by presentation status (SA=637; USA=205; and AMI=168), stratified according to median levels of LpPLA 2 (350.2 ng/mL) and hsCRP above and below 3 mgl/L and followed for 7.5 ± 2.4 years for CAD death. Results : Age averaged 64 ± 12 years and 70% were male. While median hsCRP (mg/L) levels differed significantly by presentation [2.86, 2.80, and 13.7 for SA, USA, and AMI, respectively (p<0.0001)], median LpPLA 2 (ng/mL) levels [350.2, 353.1, and 348.1 for SA, USA, and AMI, respectively (p=0.67)], did not. LpPLA 2 was not only a better predictor of CAD death among the entire cohort (LpPLA 2 : adjusted Hazard Ratio [HR]= 1.47, p=0.04; hsCRP: adjusted HR=0.95, p=0.81), it was a better predictor among patients presenting with AMI (LpPLA 2 : adjusted HR3 1.80, p=0.30; hsCRP adjusted HR=0.76, p=0.63). Conclusions : Among CAD patients, LpPLA 2 varies minimally among differing presentations compared to hsCRP and is a better a predictor of CAD death among those presenting with AMI. This information supports the hypothesis that LpPLA 2 is a vascular specific marker of inflammation and independent of transient systemic inflammatory effects.


2014 ◽  
Vol 55 (1) ◽  
pp. 132 ◽  
Author(s):  
Yong Un Kang ◽  
Min Jee Kim ◽  
Joon Seok Choi ◽  
Chang Seong Kim ◽  
Eun Hui Bae ◽  
...  

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