scholarly journals Overexpression of Human C-Reactive Protein Exacerbates Left Ventricular Remodeling in Diabetic Cardiomyopathy

2011 ◽  
Vol 75 (7) ◽  
pp. 1717-1727 ◽  
Author(s):  
Yoshinori Mano ◽  
Toshihisa Anzai ◽  
Hidehiro Kaneko ◽  
Yuji Nagatomo ◽  
Toshiyuki Nagai ◽  
...  
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
C Reactive Protein ◽  
Reactive Protein

scholarly journals Metabolomic Approach in STEMI-Patients Undergoing Left Ventricular Remodeling

2019 ◽  
Vol 20 (2) ◽  
pp. 289 ◽  
Author(s):  
Gabriel Garcia ◽  
Juan Chao de la Barca ◽  
Delphine Mirebeau-Prunier ◽  
Pascal Reynier ◽  
Alain Furber ◽  
...  
Keyword(s):  
Inflammatory Markers ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
C Reactive Protein ◽  
St Segment Elevation ◽  
Reactive Protein ◽  
St Segment ◽  
Alpha Risk ◽  
Metabolomic Approach

Left ventricular remodeling (LVR) occurring after ST-segment elevation myocardial infarction (STEMI) is frequent and severe. We present a metabolomic approach as an attempt to reveal unknown biomarkers associated with post-STEMI LVR. Out of 192 consecutive patients with successfully revascularized STEMI, 32 presented LVR and were clinically matched with 32 no-LVR patients. They underwent cardiac magnetic resonance at baseline, three months and 12 months. Blood samples were collected during index hospitalization. Creatine kinase (CK) peak and inflammatory markers were higher for LVR patients compared to no-LVR patients (mean 3466 ± 2211 and 2394 ± 1615 UI/L respectively, p = 0.005 for CK peak; mean 35.9 ± 44.3 vs. 21.7 ± 30.4 mg/L respectively, p = 0.020 for C-reactive protein). Leukocyte and neutrophil counts were also higher for LVR patients (mean 12028 ± 2593/mL vs. 10346 ± 3626/mL respectively, p = 0.028 and mean 9035 ± 3036/mL vs. 7596 ± 3822/mL respectively, p < 0.001). For metabolomic analysis, sphingomyelin C20:2 and symmetrical dimethylarginine were higher for LVR patients, but did not reach significance after the correction for the alpha risk. The metabolomic approach did not discriminate patients with and without LVR. However, common parameters that focus on infarction severity, such as infarct size and inflammatory markers, differed between the groups.

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

scholarly journals Mst1 Knockout Alleviates Mitochondrial Fission and Mitigates Left Ventricular Remodeling in the Development of Diabetic Cardiomyopathy

2021 ◽  
Vol 8 ◽  
Author(s):  
Xinyu Feng ◽  
Shanjie Wang ◽  
Xingjun Yang ◽  
Jie Lin ◽  
Wanrong Man ◽  
...  
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Ventricular Remodeling ◽  
Mitochondrial Dynamics ◽  
Left Ventricular Remodeling ◽  
Mitochondrial Fission ◽  
Left Ventricular ◽  
Neonatal Cardiomyocytes ◽  
Primary Neonatal Cardiomyocytes ◽  
Hemodynamic Measurements ◽  
Medium Culture

The disruption of mitochondrial dynamics is responsible for the development of diabetic cardiomyopathy (DCM). However, the mechanisms that regulate the balance of mitochondrial fission and fusion are not well-understood. Wild-type, Mst1 transgenic and Mst1 knockout mice were induced with experimental diabetes by streptozotocin injection. In addition, primary neonatal cardiomyocytes were isolated and cultured to simulate diabetes to explore the mechanisms. Echocardiograms and hemodynamic measurements revealed that Mst1 knockout alleviated left ventricular remodeling and cardiac dysfunction in diabetic mice. Mst1 knockdown significantly decreased the number of TUNEL-positive cardiomyocytes subjected to high-glucose (HG) medium culture. Immunofluorescence study indicated that Mst1 overexpression enhanced, while Mst1 knockdown mitigated mitochondrial fission in DCM. Mst1 participated in the regulation of mitochondrial fission by upregulating the expression of Drp1, activating Drp1S616 phosphorylation and Drp1S637 dephosphorylation, as well as promoting Drp1 recruitment to the mitochondria. Furthermore, Drp1 knockdown abolished the effects of Mst1 on mitochondrial fission, mitochondrial membrane potential and mitochondrial dysfunction in cardiomyocytes subjected to HG treatment. These results indicated that Mst1 knockout inhibits mitochondrial fission and alleviates left ventricular remodeling thus prevents the development of DCM.

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.

Sign in / Sign up

Export Citation Format

Share Document