Abstract 222: HDL-ApoA-I Exchange Rate is Inversely Correlated With Coronary Artery Disease Stability

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Mark S Borja ◽  
Yumin He ◽  
Jacques Genest ◽  
Michael N Oda

Objective: The exchange of apolipoprotein A-I between lipid-associated and lipid-free states is a key step in reverse cholesterol transport and is representative of HDL’s functional status. Reduced HDL-apoA-I exchange (HAE) is associated with the presence of cardiovascular disease. To build on this observation, we investigated the hypothesis that HAE in a coronary artery disease-identified patient decreases with increased coronary artery disease instability. Method: HAE was measured by electron paramagnetic resonance spectroscopy (EPR), wherein nitroxide-labeled lipid-free apoA-I is introduced into apolipoprotein B-depleted plasma, incubated at 37°C and measured. When added to plasma, the nitroxide-labeled apoA-I specifically interacts with HDL and displaces resident apoA-I. The EPR spectrum reports the population of lipid-bound, spin labeled apoA-I, which is directly proportional to the amount of resident apoA-I displaced. The relative level of apoA-I displaced is representative of the plasticity of HDL and its ability to make lipid-poor apoA-I available for ABCA1-mediated cholesterol efflux. We measured HAE in the plasma of three groups: stable coronary artery disease (n=22), 3 months following acute coronary syndrome (n=19), and a control group with no history of coronary artery disease (n=15). Results: HAE was significantly lower in both the stable coronary artery disease and acute coronary syndrome groups, compared to the control group (P<0.001 and, P<0.0001, respectively). Remarkably, the ACS subjects also had significantly lower HAE compared to those with stable CAD (P<0.01). By comparing HAE to apoA-I and HDL-C levels, we observed that stable CAD and ACS subjects have lower HAE per milligram/deciliter of apoA-I, consistent with a qualitative deficiency in their apoA-I. Conclusions: HAE activity is a by-product of apoA-I qualitative status, which is inversely correlated with coronary artery disease stability.

2007 ◽  
Vol 98 (08) ◽  
pp. 413-419 ◽  
Author(s):  
Pal Soltesz ◽  
Katalin Veres ◽  
Renata Laczik ◽  
Henrietta Der ◽  
Istvan Csipo ◽  
...  

SummaryThe aim was to measure the level of antibodies to oxidized LDL (oxLDL) and C-reactive protein (CRP) in the serum of patients with acute coronary syndrome (ACS). The results were correlated with data obtained from patients with stable coronary artery disease (stable CAD) and healthy controls.Thirty-three patients with ACS and 62 stable CAD patients were enrolled in the study. Fifty healthy individuals served as controls.The evaluation of anti-oxLDL autoantibodies was performed by ELISA, while CRP levels were measured by turbidimetry. The level of antibodies to oxLDL was significantly higher in both groups of patients with ACS and stable CAD compared to controls.The comparison between the acute and stable groups showed that anti-oxLDL levels were higher in the acute group,but because of high SD, the difference was not significant. By performing group analysis, anti-oxLDL levels were found to be significantly higher in ACS patients with unstable clinical state (circulatory insufficiency, malignant arrhythmias, recurring ischemic pain, need for urgent coronary intervention and death). CRP level in patients with ACS was significantly higher than in those with stable CAD. A positive correlation was found between anti-oxLDL antibodies and CRP levels both in patients with ACS and stable CAD. The association between the two biomarkers was stronger in the ACS group. In conclusion, our findings support the notion that the presence of antibodies to oxLDL, a plaquespecific antigen, plays a major role as a predictor of complicated manifestations of ACS.


Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1143
Author(s):  
Jeremy Yuvaraj ◽  
Andrew Lin ◽  
Nitesh Nerlekar ◽  
Ravi K. Munnur ◽  
James D. Cameron ◽  
...  

Background: High-risk plaques (HRP) detected on coronary computed tomography angiography (CTA) confer an increased risk of acute coronary syndrome (ACS). Pericoronary adipose tissue attenuation (PCAT) is a novel biomarker of coronary inflammation. This study aimed to evaluate the association of PCAT with HRP and subsequent ACS development in patients with stable coronary artery disease (CAD). Methods: Patients with stable CAD who underwent coronary CTA from 2011 to 2016 and had available outcome data were included. We studied 41 patients with HRP propensity matched to 41 controls without HRP (60 ± 10 years, 67% males). PCAT was assessed using semi-automated software on a per-patient basis in the proximal right coronary artery (PCATRCA) and a per-lesion basis (PCATLesion) around HRP in cases and the highest-grade stenosis lesions in controls. Results: PCATRCA and PCATLesion were higher in HRP patients than controls (PCATRCA: −80.7 ± 6.50 HU vs. −84.2 ± 8.09 HU, p = 0.03; PCATLesion: −79.6 ± 7.86 HU vs. −84.2 ± 10.3 HU, p = 0.04), and were also higher in men (PCATRCA: −80.5 ± 7.03 HU vs. −86.1 ± 7.08 HU, p < 0.001; PCATLesion: −79.6 ± 9.06 HU vs. −85.2 ± 7.96 HU, p = 0.02). Median time to ACS was 1.9 years, within a median follow-up of 5.3 years. PCATRCA alone was higher in HRP patients who subsequently presented with ACS (−76.8 ± 5.69 HU vs. −82.0 ± 6.32 HU, p = 0.03). In time-dependent analysis, ACS was associated with HRP and PCATRCA. Conclusions: PCAT attenuation is increased in stable CAD patients with HRP and is associated with subsequent ACS development. Further investigation is required to determine the clinical implications of these findings.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Paulo V Camargo ◽  
Raquel M Roman ◽  
Ana Paula W Rossini ◽  
Anderson Dedonelli ◽  
Steffan F Stella ◽  
...  

Background: The balance between pro-inflammatory cytokine IL-18 and anti-inflammatory cytokine IL-10 has been suggested to play a role in atherogenesis and in the prognosis of acute coronary syndrome (ACS). We hypothesized that stable coronary artery disease (CAD) patients have a pro-inflammatory profile prior to an acute event. Methods : A case-control study nested in a cohort of stable CAD patients was performed. Patients were consecutively included and blood samples collected at 3-months intervals. Cases were patients who presented any vascular event (death, ACS, ischemic stroke, peripheral arterial occlusion and revascularization) and controls were retrieved from a sequential list, in a 1:2 ratio, after 22 ± 9 months of follow-up. Serum hs-CRP, interleukin (IL)-10, IL-18 were measured in two serial samples, collected before the events. Results : Among 176 CAD patients, 42 developed a vascular event (cases) and 76 were selected to the control group. Serum levels of IL-18 were significantly higher among cases (411 ± 185 vs. 340 ± 133pg/ml; p = 0.037). Hs-CRP levels (5.4 vs. 5.1mg/l), IL-10 (7.4 vs. 7.2pg/ml), and IL-18/IL-10 ratio (66 vs. 61) were not different between cases and controls in both samples. Cox regression analysis showed that IL-18 levels (HR 1.75 (0.89 –3.5;p = 0.11) and IL-18/IL-10 ratio (HR 1.97; 1.0 –3.8) were predictors of worse prognosis (Figure ). Conclusion: In this study, IL-18 and IL-18/IL-10 ratio were associated with clinical outcomes and support the hypothesis that the balance between pro-inflammatory and anti-inflammatory cytokines may be an important determinant of vascular events in stable CAD patients.


2008 ◽  
Vol 31 (2) ◽  
pp. 85 ◽  
Author(s):  
Zhi-Yuan Liu ◽  
Jin-Ying Zhang ◽  
Tong-Wen Sun ◽  
Yan-Jun Zhang ◽  
Li Zhang ◽  
...  

Purpose: To investigate the levels of pregnancy-associated plasma protein A (PAPP-A) or insulin-like growth factor -1 (IGF-1) in patients with acute coronary syndrome. Methods: Serum PAPP-A and IGF-1 was measured with biotin–tyramide-amplified enzyme immunoassay and Enzyme Linked Immuoserbent Assay, respectively, in patients with ST elevation acute myocardial infarction (STEMI, n=12), unstable angina (UAP, n=15), and stable angina (n=15). PAPP-A and IGF-1 was also measured in 16 healthy subjects (control group). Results: The serum levels of PAPP-A in the STEMI (16.9±10.3 mIU/L) and UAP group (15.2±10.5 mIU/L) were higher than in the stable angina (8.5±3.1 mIU/L) or control group (8.4±2.0 mIU/L, P < 0.01). The serum levels of IGF-1 in the STEMI (132.3±40.9 µg/L) and UAP group (127.3±36.0 µg/L) were also higher than in the stable angina (44.9±18.5 µg/L) or control group (67.7±24.5µg/L, P < 0.01). There were no differences in serum levels of PAPP-A or IGF-1 among the single, double and three vessel lesion groups. The serum levels of PAPP-A (19.9±10.1 mIU/L) and IGF-1 (153.2±52.4 µg/L) after PCI were higher than those before PCI (15.1±10.0 mIU/L and 91.4±51.0 µg/L, respectively, P < 0.01). A positive correlation was found between PAPP-A and IGF-1 levels in the STEMI and UAP group before PCI (r=0.48?P < 0.01). Conclusion: PAPP-A and IGF-1 are elevated in patients with acute coronary syndrome. They may be used as biomarkers for vulnerable plaques in patients with coronary artery disease. Whether post-PCI elevation of IGF-1 can be used to predict restenosis of coronary arteries remains to be seen.


Author(s):  
Peter J. Meikle ◽  
Melissa F. Formosa ◽  
Natalie A. Mellett ◽  
Kaushala S. Jayawardana ◽  
Corey Giles ◽  
...  

2019 ◽  
Vol 32 (12) ◽  
pp. 1199-1205 ◽  
Author(s):  
Eugenia Gkaliagkousi ◽  
Eleni Gavriilaki ◽  
Ioannis Vasileiadis ◽  
Barbara Nikolaidou ◽  
Efthalia Yiannaki ◽  
...  

Abstract BACKGROUND Endothelial microvesicles (EMVs) have emerged as markers of endothelial injury. However, little is known about their levels in the coronary circulation of acute coronary syndrome (ACS) and stable coronary artery disease (CAD). We hypothesized that ACS patients exhibit a more pronounced increase of EMVs both in the peripheral and coronary circulation when compared with CAD. We also investigated possible associations of EMVs with markers preclinical target organ damage. METHODS We enrolled consecutive eligible patients undergoing coronary angiography. Blood samples were collected from the stem of the left coronary artery and the femoral artery. ΕMVs were measured by a standardized flow cytometry protocol. Central systolic blood pressure (cSBP) was measured invasively and patients’ history was recorded. RESULTS CAD patients exhibited increased levels of EMVs compared with controls. When patients with ACS and stable CAD were compared, the former had significantly increased EMVs in both coronary and peripheral circulation. Importantly, both ACS and CAD patients exhibited increased levels of EMVs in the coronary circulation compared with periphery. In addition, EMVs were associated with cSBP. CONCLUSIONS EMVs emerge as novel markers of ongoing underlying vascular damage, further augmenting the vicious cycle of inflammation and thrombosis mainly in ACS but also in stable CAD.


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