C-Reactive Protein Binds to Cholesterol Crystals and Co-Localizes with the Terminal Complement Complex in Human Atherosclerotic Plaques

Background: C-reactive protein (CRP) has been suggested as a risk factor in cardiovascular disease. Recently, it has been shown that CRP binds to ligands exposed in ischaemic damaged tissue and activates the complement system. Furthermore, CRP was demonstrated to be strongly and independently associated with the occurrence of heart failure in men. In this study we have investigated the presence of CRP and the Terminal Complement Complex (C5b-9) in the myocardium of patients suffering from non-ischaemic heart failure. Methods and Results: Endomyocardial biopsies were taken from 151 patients suffering from dilated cardiomyopathy. Biopsies were immunohistochemically analysed for the presence and distribution pattern of CRP and C5b-9. In 39 patients plasma levels of hsCRP and NT-proBNP were measured and correlated with myocardial biopsy findings. In 47 patients a positive staining for CRP and in 141 patients a positive staining for C5b-9 was detected. CRP and C5b-9 significantly co-localised within the myocardium. A negative correlation was observed for plasma hsCRP levels and myocardial CRP. Conclusions: This study shows for the first time that CRP is frequently present in the myocardium of patients suffering from non-ischaemic dilated cardiomyopathy and co-localises with the Terminal Complement Complex. CRP may contribute to myocardial damage in dilated cardiomyopathy via activating the complement system.

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Different Distribution of Pentraxin 3 and C-Reactive Protein in Coronary Atherosclerotic Plaques

Journal of Atherosclerosis and Thrombosis ◽

10.5551/jat.12526 ◽

2012 ◽

Vol 19 (9) ◽

pp. 837-845 ◽

Cited By ~ 19

Author(s):

Yunosuke Matsuura ◽

Kinta Hatakeyama ◽

Takuroh Imamura ◽

Toshihiro Tsuruda ◽

Yoshisato Shibata ◽

...

Keyword(s):

Atherosclerotic Plaques ◽

Pentraxin 3 ◽

C Reactive Protein ◽

Reactive Protein

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Low Testosterone Concentration and Atherosclerotic Disease Markers in Male Patients With Type 2 Diabetes

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2014-2585 ◽

2014 ◽

Vol 99 (12) ◽

pp. 4698-4703 ◽

Cited By ~ 21

Author(s):

Javier M. Farias ◽

Matias Tinetti ◽

Marina Khoury ◽

Guillermo E. Umpierrez

Keyword(s):

Atherosclerotic Disease ◽

Atherosclerotic Plaques ◽

C Reactive Protein ◽

Aged Patients ◽

Carotid Imt ◽

Reactive Protein ◽

Disease Markers ◽

Highly Sensitive ◽

Male Patients

Background: Low total T is associated with an increased risk of atherosclerotic complications. However, the magnitude of this association in middle-aged patients with type 2 diabetes (T2D) has not been determined. Materials and Methods: This cross-sectional study evaluated atherosclerotic disease markers in T2D patients with normal and low plasma total T. A total of 115 male patients, aged younger than 70 years, without a history of cardiovascular events, and with normal [≥3.5 ng/mL (≥12.1 nmol/L), n = 79] or low [< 3.5 ng/mL (≤12.1 nmol/L), n = 36] total T underwent the measurement of highly sensitive C-reactive protein, carotid artery carotid intima-media thickness (IMT), and atherosclerotic plaque by high-resolution B-mode ultrasound and to asses endothelial function by brachial artery flow-mediated dilation. Results: Carotid IMT was negatively correlated with total T concentration (r = −0.39, P < .0001). Compared with subjects with normal T, a higher proportion of patients with low total T had carotid IMT of 0.1 cm or greater [80% vs 39%, odds ratio (OR) 6.41; 95% CI 2.5–16.4, P < .0001], atherosclerotic plaques (68.5% vs 44.8%, OR 2.60, 95% CI 1.12–6.03, P < .0001); endothelial dysfunction (80.5% vs 42.3%, OR 5.77, 95% CI 2.77–14.77, P < .003), and higher highly sensitive C-reactive protein levels (2.74 ± 5.82 vs 0.89 ± 0.88 mg/L, P < .0001). Similar results were found when free T was considered. Multiple logistic regression analyses adjusted for age, diabetes mellitus duration, hemoglobin A1c, lipids, treatment effect, and body mass index reported that a low total T level was independently associated with greater IMT [OR 8.43 (95% CI 2.5–25.8)] and endothelial dysfunction [OR 5.21 (95% CI 1.73–15.66)] but not with the presence of atherosclerotic plaques (OR 1.77, 95% CI 0.66–4.74). Conclusions: Low T is associated with more advanced atherosclerotic disease markers in middle-aged patients with T2D.

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Plasma levels of high-sensitive C-reactive protein do not correlate with inflammatory activity in carotid atherosclerotic plaques

Journal of Internal Medicine ◽

10.1111/joim.12133 ◽

2013 ◽

Vol 275 (2) ◽

pp. 127-133 ◽

Cited By ~ 11

Author(s):

H. Grufman ◽

I. Gonçalves ◽

A. Edsfeldt ◽

M. Nitulescu ◽

A. Persson ◽

...

Keyword(s):

Plasma Levels ◽

Inflammatory Activity ◽

Atherosclerotic Plaques ◽

C Reactive Protein ◽

Reactive Protein

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Evaluation of the Effect of Andrographolide on Atherosclerotic Rabbits Induced byPorphyromonas gingivalis

BioMed Research International ◽

10.1155/2014/724718 ◽

2014 ◽

Vol 2014 ◽

pp. 1-11 ◽

Cited By ~ 5

Author(s):

Rami Al Batran ◽

Fouad Al-Bayaty ◽

Mazen M. Jamil Al-Obaidi ◽

Saba F. Hussain ◽

Tengku Z. Mulok

Keyword(s):

Smooth Muscle Actin ◽

Atherosclerotic Plaques ◽

C Reactive Protein ◽

Alpha Smooth Muscle Actin ◽

Reactive Protein ◽

Epidemiologic Evidence ◽

Cd36 Expression ◽

Group 3 ◽

Histological Results ◽

Group 1

Epidemiologic evidence has demonstrated significant associations between atherosclerosis andPorphyromonas gingivalis(Pg). We had investigated the effect of andrographolide (AND) on atherosclerosis induced byPgin rabbits. For experimental purpose, we separated thirty male white New Zealand rabbits into 5 groups. Group 1 received standard food pellets; Groups 2–5 were orally challenged withPg; Group 3 received atorvastatin (AV, 5 mg/kg), and Groups 4-5 received 10 and 20 mg/kg of AND, respectively, over 12 weeks. Groups treated with AND showed significant decrease in TC, TG, and LDL levels (P<0.05) and significant increase in HDL level in the serum of rabbits. Furthermore, the treated groups (G3–G5) exhibited reductions in interleukins (IL-1βand IL-6) and C-reactive protein (CRP) as compared to atherogenicgroup (G2). The histological results showed that the thickening of atherosclerotic plaques were less significant in treated groups (G3–G5) compared with atherogenicgroup (G2). Also, alpha-smooth muscle actin (α-SMA) staining decreased within the plaques of atherogenicgroup (G2), while it was increased in treated groups (G3–G5). Lastly, groups treated with AV and AND (G3–G5) showed significant reduction of CD36 expression (P<0.05) compared to atherogenicgroup (G2). These results substantially proved that AND contain antiatherogenic activity.

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Immune-Mediated Inflammation in Vulnerable Atherosclerotic Plaques

Molecules ◽

10.3390/molecules24173072 ◽

2019 ◽

Vol 24 (17) ◽

pp. 3072 ◽

Cited By ~ 8

Author(s):

Harald Mangge ◽

Gunter Almer

Keyword(s):

Blood Lipids ◽

Atherosclerotic Plaques ◽

Conventional Imaging ◽

C Reactive Protein ◽

Blood Biomarkers ◽

Clinical Endpoints ◽

Reactive Protein ◽

Immune Mediated ◽

Life Threatening ◽

Per Se

Atherosclerosis is a chronic long-lasting vascular disease leading to myocardial infarction and stroke. Vulnerable atherosclerotic (AS) plaques are responsible for these life-threatening clinical endpoints. To more successfully work against atherosclerosis, improvements in early diagnosis and treatment of AS plaque lesions are required. Vulnerable AS plaques are frequently undetectable by conventional imaging because they are non-stenotic. Although blood biomarkers like lipids, C-reactive protein, interleukin-6, troponins, and natriuretic peptides are in pathological ranges, these markers are insufficient in detecting the critical perpetuation of AS anteceding endpoints. Thus, chances to treat the patient in a preventive way are wasted. It is now time to solve this dilemma because clear results indicate a benefit of anti-inflammatory therapy per se without modification of blood lipids (CANTOS Trial, NCT01327846). This fact identifies modulation of immune-mediated inflammation as a new promising point of action for the eradication of fatal atherosclerotic endpoints.

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