scholarly journals Plasma Level of High-Sensitive C-Reactive Protein in Patients with Acute Myocardial Infarction and Arterial Hypertension

2017 ◽  
Vol 23 (1) ◽  
Author(s):  
Wael Rumaneh
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Plasma Level ◽  
Arterial Hypertension ◽  
Ventricular Remodeling ◽  
Left Ventricular ◽  
Control Group ◽  
Blood Levels ◽  
C Reactive Protein ◽  
Reactive Protein

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.

Serum C-reactive protein elevation in left ventricular remodeling after acute myocardial infarction—role of neurohormones and cytokines

2003 ◽  
Vol 88 (2-3) ◽  
pp. 257-265 ◽  
Author(s):  
Toshiyuki Takahashi ◽  
Toshihisa Anzai ◽  
Tsutomu Yoshikawa ◽  
Yuichiro Maekawa ◽  
Yasushi Asakura ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
C Reactive Protein ◽  
Reactive Protein

High-sensitivity C-reactive protein and left ventricular remodeling in patients with acute myocardial infarction

2003 ◽  
Vol 18 (2) ◽  
pp. 67-74 ◽  
Author(s):  
Kohzou Uehara ◽  
Masahiro Nomura ◽  
Yuji Ozaki ◽  
Hiroyuki Fujinaga ◽  
Hiroyuki Ikefuji ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
High Sensitivity ◽  
Left Ventricular ◽  
C Reactive Protein ◽  
Reactive Protein

Abstract 5393: Increased C-Reactive Protein Expression Exacerbates Left Ventricular Dysfunction and Remodeling after Myocardial Infarction

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Toshiyuki Takahashi ◽  
Toshihisa Anzai ◽  
Hidehiro Kaneko ◽  
Atsushi Anzai ◽  
Yoshinori Mano ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Angiotensin Ii ◽  
Left Ventricular ◽  
Receptor Expression ◽  
Border Zone ◽  
Histological Evaluation ◽  
Control Group ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Lv Remodeling

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.

Serum Endothelial Cell–Specific Molecule 1 (Endocan) Levels in Patients With Acute Myocardial Infarction and Its Clinical Significance

Angiology ◽  
2016 ◽  
Vol 68 (4) ◽  
pp. 354-359 ◽  
Author(s):  
Chong-Rong Qiu ◽  
Qiang Fu ◽  
Jian Sui ◽  
Qian Zhang ◽  
Peng Wei ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
High Sensitivity ◽  
Control Group ◽  
C Reactive Protein ◽  
Protein Levels ◽  
Reactive Protein ◽  
The Relationship

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.

scholarly journals Left Ventricular Function and C-Reactive Protein Levels in Acute Myocardial Infarction

2010 ◽  
Vol 105 (7) ◽  
pp. 917-921 ◽  
Author(s):  
Adelaide M. Arruda-Olson ◽  
Maurice Enriquez-Sarano ◽  
Francesca Bursi ◽  
Susan A. Weston ◽  
Allan S. Jaffe ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Left Ventricular ◽  
C Reactive Protein ◽  
Protein Levels ◽  
Reactive Protein

scholarly journals Galectin-3 in Acute Myocardial Infarction Patients with Atrial Fibrillation

2019 ◽  
Vol 28 (3) ◽  
pp. 284-290 ◽  
Author(s):  
Dragana Stanojevic ◽  
Svetlana Apostolovic ◽  
Dragana Stokanovic ◽  
Stefan Momčilović ◽  
Tatjana Jevtovic-Stoimenov ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Atrial Fibrillation ◽  
Acute Myocardial Infarction ◽  
Venous Blood ◽  
Control Group ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Galectin 3 ◽  
Predictive Role

Objective: Atrial fibrillation (AF) is common in acute myocardial infarction (AMI), and galectin-3 is possibly involved in its occurrence. Galectin-3 has been shown to play a central role in fibrosis and tissue remodeling and has a role in inflammatory and proliferative responses. The aim of our study was to measure galectin-3 levels in patients with myocardial infarction and to compare its levels in patients with or without AF, in order to investigate the potential predictive role of galectin-3 in this setting. Subjects and Methods: The study included 51 consecutive AMI patients with AF; 27 AMI patients (52.9%) had permanent/persistent AF, and 24 patients (47.1%) had paroxysmal AF. Thirty-eight consecutive AMI patients without AF were used as a control group. Blood samples were obtained from venous blood on the third day after reperfusion. Results: Patients with AF had higher levels of C-reactive protein (p < 0.01) and galectin-3 (p < 0.05) than those without AF. Patients with high galectin-3 had 4.4 times greater odds of having AF. Galectin-3 levels were lower in patients without AF (p < 0.01) than in those with permanent/persistent AF. Conclusion: AMI patients with AF had higher levels of galectin-3 than those without this arrhythmia. This biomarker of inflammation and fibrosis could be a potential target for treating AMI patients at high risk.

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