Comparison of the Effects of Ramipril Versus Telmisartan on High-Sensitivity C-Reactive Protein and Endothelial Progenitor Cells After Acute Coronary Syndrome

2009 ◽  
Vol 103 (11) ◽  
pp. 1500-1505 ◽  
Author(s):  
Italo Porto ◽  
Luca Di Vito ◽  
Giovanni Luigi De Maria ◽  
Ilaria Dato ◽  
Alessandra Tritarelli ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
High Sensitivity ◽  
C Reactive Protein ◽  
Endothelial Progenitor ◽  
Reactive Protein ◽  
Coronary Syndrome

scholarly journals Circulating endothelial progenitor cells are not affected by acute systemic inflammation

2010 ◽  
Vol 298 (6) ◽  
pp. H2054-H2061 ◽  
Author(s):  
Gareth J. Padfield ◽  
Olga Tura ◽  
Marlieke L. A. Haeck ◽  
Abigail Short ◽  
Elizabeth Freyer ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Systemic Inflammation ◽  
Vascular Injury ◽  
High Sensitivity ◽  
Vegf Receptor ◽  
C Reactive Protein ◽  
Endothelial Progenitor ◽  
Double Blind ◽  
Reactive Protein

Vascular injury causes acute systemic inflammation and mobilizes endothelial progenitor cells (EPCs) and endothelial cell (EC) colony-forming units (EC-CFUs). Whether such mobilization occurs as part of a nonspecific acute phase response or is a phenomenon specific to vascular injury remains unclear. We aimed to determine the effect of acute systemic inflammation on EPCs and EC-CFU mobilization in the absence of vascular injury. Salmonella typhus vaccination was used as a model of acute systemic inflammation. In a double-blind randomized crossover study, 12 healthy volunteers received S. typhus vaccination or placebo. Phenotypic EPC populations enumerated by flow cytometry [CD34+VEGF receptor (VEGF)R-2+CD133+, CD14+VEGFR-2+Tie2+, CD45−CD34+, as a surrogate for late outgrowth EPCs, and CD34+CXCR-4+], EC-CFUs, and serum cytokine concentrations (high sensitivity C-reactive protein, IL-6, and stromal-derived factor-1) were quantified during the first 7 days. Vaccination increased circulating leukocyte (9.8 ± 0.6 vs. 5.1 ± 0.2 × 109cells/l, P < 0.0001), serum IL-6 [0.95 (0–1.7) vs. 0 (0–0) ng/l, P = 0.016], and VEGF-A [60 (45–94) vs. 43 (21–64) pg/l, P = 0.006] concentrations at 6 h and serum high sensitivity C-reactive protein at 24 h [2.7 (1.4–3.6) vs. 0.4 (0.2–0.8) mg/l, P = 0.037]. Vaccination caused a 56.7 ± 7.6% increase in CD14+cells at 6 h ( P < 0.001) and a 22.4 ± 6.9% increase in CD34+cells at 7 days ( P = 0.04). EC-CFUs, putative vascular progenitors, and the serum stromal-derived factor-1 concentration were unaffected throughout the study period ( P > 0.05 for all). In conclusion, acute systemic inflammation causes nonspecific mobilization of hematopoietic progenitor cells, although it does not selectively mobilize putative vascular progenitors. We suggest that systemic inflammation is not the primary stimulus for EPC mobilization after acute vascular injury.

Higher level of high sensitivity C-reactive protein is associated with more fibrocalcific plaque and longer lesion in patients with acute coronary syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Katamine ◽  
Y Minami ◽  
K Asakura ◽  
A Kato ◽  
A Katsura ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Morphological Characteristics ◽  
High Sensitivity ◽  
Current Smoker ◽  
Lesion Length ◽  
Culprit Lesion ◽  
C Reactive Protein ◽  
Hscrp Level ◽  
Reactive Protein ◽  
Coronary Syndrome

Abstract Background The association between the level of high sensitivity C-reactive protein (hsCRP) and coronary plaque characteristics in patients with acute coronary syndrome (ACS) remains to be elucidated. Purpose To clarify the morphological characteristics of culprit lesion in patients with ACS according to the hsCRP levels using optical coherence tomography (OCT). Methods A total of 215 consecutive patients with ACS, who underwent OCT imaging of culprit lesions were included. The patients were classified into either the higher hsCRP group (hsCRP ≥0.14 mg/dL, n=108) or the lower hsCRP group (hsCRP &lt;0.14 mg/dL, n=107) according to the median preprocedural hsCRP level. The morphological characteristics of culprit lesion assessed by OCT were compared between the two groups. Results The higher hsCRP group had higher prevalence of insulin therapy (14 vs. 6%, p=0.037) and current smoker than the lower hsCRP group (37 vs. 18%, p=0.002). The prevalence of long lesion (≥25 mm, 67 vs. 53%, p=0.041) and fibrocalcific plaque (53 vs. 33%, p=0.003) was significantly higher in the higher hsCRP group than in the lower hsCRP group (Figure). On the other hand, the prevalence of plaque rupture (36 vs. 46%, p=0.174) and lipid-rich plaque (47 vs. 64%, p=0.011) was rather lower in the higher hsCRP group than in the lower hsCRP group (Figure). In a multivariate analysis, fibrocalcific plaque (odds ratio [OR]: 2.098, 95% confidence interval [CI]: 1.125–3.913, p=0.019), lesion length (mm, OR: 1.036, 95% CI: 1.010–1.061, p=0.004) and current smoker (OR: 2.757, 95% CI: 1.388–5.476, p=0.003) was independently associated with higher hsCRP level. Conclusions ACS patients with high hsCRP levels had more fibrocalcific plaque and longer lesion than those with low hsCRP levels. The association between high hsCRP levels and vulnerable characteristics of culprit plaque was not demonstrated. Funding Acknowledgement Type of funding source: None

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