Acetylsalicylate reduces endothelial and platelet-derived microparticles in patients with coronary artery disease

2011 ◽  
Vol 89 (4) ◽  
pp. 239-244 ◽  
Author(s):  
Daniel Bulut ◽  
Vanessa Becker ◽  
Andreas Mügge

Previous studies suggest that endothelial progenitor cells (EPCs) contribute to vascular repair processes. In contrast, circulating microparticles (MPs) are reported to be part of a process that is damaging to vascular cells. Numerous studies suggest that the “balance” between EPCs and MPs is important for the integrity of vascular cells and preservation of endothelial function. In the present study, we assess the impact of acetylsalicylate (ASA) — which is, beside statins and physical exercise, a third basic column in the preventive therapy of coronary artery disease (CAD) — on EPCs and MPs in patients with CAD. We investigated the effect of treatment (8 weeks) with ASA (100 mg/d) on endothelial function (flow-mediated vasodilation, FMD), number of circulating EPCs, and endothelial- and platelet-derived microparticles (eMP, pMP) in 15 male patients (age 59.5 ± 12.3 years) with CAD but nonsignificant stenosis. The number of pMPs and eMPs decreased by 62.7% (p < 0.05) and 28.4% (p < 0.05), respectively. The number of circulating EPCs (VEGFR2+CD34+), expressed as ‰ of circulating polymorphonuclear leukocytes, remained unchanged. Despite the reduced number of pMPs and eMPs in response to the ASA therapy, the FMD responses and the maximal dilator effects of nitroglycerin were unaffected. In a control experiment, patients (n = 6) treated with the selective COX-2 inhibitor etoricoxib (90 mg/day) for 8 weeks showed no changes in the number of pMPs, eMPs, and EPCs and in FMD. We report on a novel effect of ASA treatment on the number of circulating endothelial- and platelet-derived microparticles in patients with cardiovascular disease. The mechanism remains elusive, and appears not to be associated with the COX-2 pathway.

2012 ◽  
Vol 59 (13) ◽  
pp. E1409
Author(s):  
Marina Zaromitidou ◽  
Gerasimos Siasos ◽  
Dimitris Tousoulis ◽  
Stamatios Kioufis ◽  
Evangelos Oikonomou ◽  
...  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K Mourouzis ◽  
G Siasos ◽  
E Oikonomou ◽  
M Zaromitidou ◽  
V Tsigkou ◽  
...  

Abstract Background Lipoprotein-associated Phospholipase A2 (Lp-PLA2), has inflammatory and atherogenic actions in the vascular wall. We investigate the impact of high Lp-PLA2 levels on endothelial function and arterial stiffness on patients with coronary artery disease (CAD). Methods We enrolled 374 consecutive patients with stable CAD (mean age 61±11 years). Endothelial function was evaluated by flow-mediated dilation (FMD) and reflected waves with augmentation index (AIx) of the central aortic pressure. Serum levels of Lp-PLA2 were measured with ELISA. Results In the studied population the median values of Lp-PLA2 levels was 125 (96–152) μg/L. There was no difference between subjects with Lp-PLA2 levels above and below 125μg/L concerning classical risk factors for CAD. Importantly, subjects with Lp-PLA2 values ≥125μg/L had significantly impaired FMD (4.44±2.19% vs. 4.89±2.07%, p=0.04) and AIx values (25.21±8.70% vs. 23.06±9.47%, p=0.03), compared to participants with lower Lp-PLA2 serum levels. A linear regression analysis revealed that Lp-PLA2 ≥125μg/L negatively relates to impaired FMD [b=−0.54 (95% CI: −1.05 to −0.02), p=0.04] and AIx values [b=2.14 (95% CI: 0.18–4.01), p=0.03] independently of cofounders. Conclusions Elevated Lp-PLA2 relates to endothelial dysfunction and arterial stiffness in CAD patients. These findings highlight the significant role of Lp-PlA2 in the process of atherosclerosis. Funding Acknowledgement Type of funding source: None


Circulation ◽  
2003 ◽  
Vol 107 (3) ◽  
pp. 405-409 ◽  
Author(s):  
Rémy Chenevard ◽  
David Hürlimann ◽  
Markus Béchir ◽  
Frank Enseleit ◽  
Lukas Spieker ◽  
...  

2020 ◽  
Vol 27 (7) ◽  
pp. 1052-1080 ◽  
Author(s):  
Evangelos Oikonomou ◽  
Gerasimos Siasos ◽  
Vasiliki Tsigkou ◽  
Evanthia Bletsa ◽  
Maria-Evi Panoilia ◽  
...  

Coronary artery disease is the leading cause of morbidity and mortality worldwide. The most common pathophysiologic substrate is atherosclerosis which is an inflammatory procedure that starts at childhood and develops throughout life. Endothelial dysfunction is associated with the initiation and progression of atherosclerosis and is characterized by the impaired production of nitric oxide. In general, endothelial dysfunction is linked to poor cardiovascular prognosis and different methods, both invasive and non-invasive, have been developed for its evaluation. Ultrasound evaluation of flow mediated dilatation of the branchial artery is the most commonly used method to assessed endothelial function while intracoronary administration of vasoactive agents may be also be used to test directly endothelial properties of the coronary vasculature. Endothelial dysfunction has also been the subject of therapeutic interventions. This review article summarizes the knowledge about evaluation of endothelial function in acute coronary syndromes and stable coronary artery disease and demonstrates the current therapeutic approaches against endothelial dysfunction.


2020 ◽  
Vol 18 (5) ◽  
pp. 523-530 ◽  
Author(s):  
Konstantinos Maniatis ◽  
Gerasimos Siasos ◽  
Evangelos Oikonomou ◽  
Manolis Vavuranakis ◽  
Marina Zaromytidou ◽  
...  

Background: Osteoprotegerin and osteopontin have recently emerged as key factors in both vascular remodelling and atherosclerosis progression. Interleukin-6 (IL-6) is an inflammatory cytokine with a key role in atherosclerosis. The relationship of osteoprotegerin, osteopontin, and IL-6 serum levels with endothelial function and arterial stiffness was evaluated in patients with coronary artery disease (CAD). Methods: We enrolled 219 patients with stable CAD and 112 control subjects. Osteoprotegerin, osteopontin and IL-6 serum levels were measured using an ELISA assay. Endothelial function was evaluated by flow-mediated dilation (FMD) in the brachial artery and carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness. Results: There was no significant difference between control subjects and CAD patients according to age and sex. Compared with control subjects, CAD patients had significantly impaired FMD (p<0.001) and increased PWV (p=0.009). CAD patients also had significantly higher levels of osteoprotegerin (p<0.001), osteopontin (p<0.001) and IL-6 (p=0.03), compared with control subjects. Moreover, IL-6 levels were correlated with osteoprotegerin (r=0.17, p=0.01) and osteopontin (r=0.30, p<0.001) levels. FMD was correlated with osteoprotegerin levels independent of possible confounders [b coefficient= - 0.79, 95% CI (-1.54, -0.05), p=0.04]. Conclusion: CAD patients have increased osteoprotegerin, osteopontin and IL-6 levels. Moreover, there is a consistent association between osteoprotegerin and osteopontin serum levels, vascular function and inflammation in CAD patients. These findings suggest another possible mechanism linking osteoprotegerin and osteopontin serum levels with CAD progression through arterial wall stiffening and inflammation.


2013 ◽  
Vol 11 (5) ◽  
pp. 779-784 ◽  
Author(s):  
Vasilios G. Athyros ◽  
Konstantinos Tziomalos ◽  
Niki Katsiki ◽  
Thomas D. Gossios ◽  
Olga Giouleme ◽  
...  

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
F Andre ◽  
S Seitz ◽  
P Fortner ◽  
R Sokiranski ◽  
F Gueckel ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Private company. Main funding source(s): Siemens Healthineers Introduction Coronary CT angiography (CCTA) plays an increasing role in the detection and risk stratification of patients with coronary artery disease (CAD). The Coronary Artery Disease – Reporting and Data System (CAD-RADS) allows for standardized classification of CCTA results and, thus, may improve patient management. Purpose Aim of this study was to assess the impact of CCTA in combination with CAD-RADS on patient management and to identify the impact of cardiovascular risk factors (CVRF) on CAD severity. Methods CCTA was performed on a third-generation dual-source CT scanner in patients, who were referred to a radiology centre by their attending physicians. In a total of 4801 patients, CVRF were derived from medical reports and anamnesis. Results The study population consisted of 4770 patients (62.0 (54.0-69.0) years, 2841 males) with CAD (CAD-RADS 1-5), while 31 patients showed no CAD and were excluded from further analyses. Age, male gender and the number of CVRF were associated with more severe CAD stages (all p &lt; 0.001). 3040 patients (63.7 %) showed minimal or mild CAD requiring optimization of CVRF i.e. medical therapy but no further assessment at his time. A group of 266 patients (5.6 %) had a severe CAD defined as CAD-RADS 4B/5. In the multivariate regression analysis, age, male gender, history of smoking, diabetes mellitus and hyperlipidaemia were significant predictors for severe CAD, whereas arterial hypertension and family history of CAD did not reach significance. Of note, a subgroup of 28 patients (10.5 %) with a severe CAD (68.5 (65.5-70.0) years, 26 males, both p = n.s.) had no CVRF. Conclusions CCTA in combination with the CAD-RADS allowed for effective risk stratification of CAD patients. The majority of the patients showed non-obstructive CAD and, thus, could be treated conservatively without the need for further CAD assessment. CVRF out of arterial hypertension and family history had an impact on CAD severity reflected in higher CAD-RADs gradings. Of note, a relevant fraction of patients with CAD did not have any CVRF and, thus, may not be covered by risk stratification models. CAD-RADS n Age (years) Males (%) 1 1453 56.0 (50.0-62.0) 623 (42.9 %) 2 1587 62.0 (55.0-69.0) 918 (57.8 %) 3 1067 66.0 (59.0-71.0) 749 (70.2 %) 4A 397 66.0 (59.0-72.0) 317 (79.8 %) 4B 162 67.0 (61.0-74.0) 139 (85.8 %) 5 104 66.0 (58.5.0-77.0) 95 (91.3 %)


Author(s):  
Rutao Wang ◽  
Scot Garg ◽  
Chao Gao ◽  
Hideyuki Kawashima ◽  
Masafumi Ono ◽  
...  

Abstract Aims To investigate the impact of established cardiovascular disease (CVD) on 10-year all-cause death following coronary revascularization in patients with complex coronary artery disease (CAD). Methods The SYNTAXES study assessed vital status out to 10 years of patients with complex CAD enrolled in the SYNTAX trial. The relative efficacy of PCI versus CABG in terms of 10-year all-cause death was assessed according to co-existing CVD. Results Established CVD status was recorded in 1771 (98.3%) patients, of whom 827 (46.7%) had established CVD. Compared to those without CVD, patients with CVD had a significantly higher risk of 10-year all-cause death (31.4% vs. 21.7%; adjusted HR: 1.40; 95% CI 1.08–1.80, p = 0.010). In patients with CVD, PCI had a non-significant numerically higher risk of 10-year all-cause death compared with CABG (35.9% vs. 27.2%; adjusted HR: 1.14; 95% CI 0.83–1.58, p = 0.412). The relative treatment effects of PCI versus CABG on 10-year all-cause death in patients with complex CAD were similar irrespective of the presence of CVD (p-interaction = 0.986). Only those patients with CVD in ≥ 2 territories had a higher risk of 10-year all-cause death (adjusted HR: 2.99, 95% CI 2.11–4.23, p < 0.001) compared to those without CVD. Conclusions The presence of CVD involving more than one territory was associated with a significantly increased risk of 10-year all-cause death, which was non-significantly higher in complex CAD patients treated with PCI compared with CABG. Acceptable long-term outcomes were observed, suggesting that patients with established CVD should not be precluded from undergoing invasive angiography or revascularization. Trial registration SYNTAX: ClinicalTrials.gov reference: NCT00114972. SYNTAX Extended Survival: ClinicalTrials.gov reference: NCT03417050. Graphic abstract


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