STUDIES OF ACUTE-PHASE PROTEIN. II. LOCALIZATION OF Cx-REACTIVE PROTEIN IN HEART IN INDUCED MYOCARDIAL INFARCTION IN RABBITS*

Kushner, Irving; Rakita, Louis; Kaplan, Melvin H.

doi:10.1172/jci104715

Cited by 100 publications

(50 citation statements)

References 4 publications

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“…Previous studies have shown that CRP localizes in infarcted human myocardium, and that CRP is co-deposited with activated complement within the area of MI. [24][25][26][27] CRP can induce complement activation via the classical pathway. 28 An experimental study showed that human CRP enhances MI size by activating complement.…”

Section: Discussionmentioning

confidence: 99%

Peak C-Reactive Protein Concentration Correlates With Left Ventricular Thrombus Formation Diagnosed by Contrast Echocardiographic Left Ventricular Opacification in Patients With a First Anterior Acute Myocardial Infarction

Seo

Maeda

Ishizu

et al. 2006

Circ J

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eft ventricular (LV) thrombus formation is a complication of acute myocardial infarction (AMI) and it is more prevalent in patients with an anterior AMI, because of the extensive area of severe apical wall motion abnormality with stagnant flow. [1][2][3] Before the era of early revascularization (ie, intravenous thrombolysis or primary coronary intervention), LV thrombus developed in 39% of patients with a first anterior AMI. 4 Although recent studies report that the prevalence has decreased because of early revascularization, 5-9 LV thrombus formation is still a risk of arterial embolism in patients with anterior wall AMI. 6,10 Apical contraction abnormalities with stagnant flow are important factors related to LV thrombus formation, but that alone is not sufficient to identify high-risk patients. Therefore, identification of additional risk factors may be useful. Recently, LV diastolic dysfunction and inflammatory reactions have been reported as associated with LV thrombus formation, 11-13 although reliable predictors have not yet been determined.LV thrombus can be diagnosed with transthoracic echocardiography, 14,15 although on occasion, either the vague nature of the thrombus or technical limitations in the examination renders confirmation difficult. 16 Contrast echocardiography is a useful modality for detecting LV thrombus, because the LV opacification can improve endocardial border delineation in the LV apex. [17][18][19][20] In addition, contrast echocardiography can visualize intraventricular flow dynamics, and recently our group reported that it is possible to determine the presence of stagnant flow with this technique. 21 However, systematic and prospective studies of contrast echocardiographic diagnosis of LV thrombus in patients with first anterior AMI have not been performed. Therefore, the purpose of this study was to prospectively study the determinants of LV thrombus using contrast echocardiography in patients with their first anterior AMI. Methods Study PopulationThis Background Wall motion abnormality in the apical legion of the left ventricle (LV) with stagnant flow alone is not sufficient to identify patients at high risk for LV thrombus formation among those with first anterior acute myocardial infarction (AMI). The aim of this study was to identify the determinants of LV thrombus formation using contrast echocardiography. Methods and ResultsIn 75 patients with first anterior AMI, standard and contrast echocardiography was performed to detect LV thrombus. Although LV thrombus was found in 10 patients (13%) using standard echocardiography, it was found in 15 patients (20%) using contrast echocardiography. Apical stagnant flow was observed in 14 patients (93%) with LV thrombus. In addition, patients with LV thrombus had a higher peak C-reactive protein (CRP) concentration (18.2±4.3 vs 7.9±5.5 mg/dl, p<0.0001). In multivariate analysis, only peak CRP concentration was identified as an independent predictor of LV thrombus (p=0.02, odds ratio: 1.400, confidence interval: 1.040-1.884). The receiv...

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Section: Discussionmentioning

confidence: 99%

Peak C-Reactive Protein Concentration Correlates With Left Ventricular Thrombus Formation Diagnosed by Contrast Echocardiographic Left Ventricular Opacification in Patients With a First Anterior Acute Myocardial Infarction

Seo

Maeda

Ishizu

et al. 2006

Circ J

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“…CRP has been localized in vivo to inflammatory lesions in rheumatoid arthritis (53), experimental allergic encephalomyelitis (54), and myocardial infarction (55,56), while in a mouse model of infection, CRP protects mice from a lethal challenge with S. pneumoniae (9,57). Although previous work described CRP as a proinflammatory agent (reviewed in Ref.…”

Section: Discussionmentioning

confidence: 99%

C-Reactive Protein Binding to Murine Leukocytes Requires Fcγ Receptors

Stein

Mold

Clos

2000

The Journal of Immunology

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Human C-reactive protein (CRP) is an acute phase protein that binds to receptors on human and mouse leukocytes. We have recently determined that the high and low affinity receptors for CRP on human leukocytes are FcγRIIa and FcγRI, respectively. Previous work by others suggested that CRP receptors on mouse macrophages are distinct from FcγR. We have taken advantage of the availability of mice deficient in one or more FcγR to reexamine the role of FcγR in CRP binding to mouse leukocytes. Three strains of FcγR-deficient mice were examined: γ-chain-deficient mice that lack FcγRI and FcγRIII, FcγRII-deficient mice, and mice deficient in both γ-chain and FcγRII that lack all FcγR. No binding of CRP was detected to leukocytes from double-deficient mice, indicating that FcγR are required for CRP binding. CRP binding to leukocytes from γ-chain-deficient and FcγRII-deficient mice was reduced compared with binding to leukocytes from wild-type mice. Further analysis of CRP binding to macrophages, neutrophils, and lymphocytes provides direct evidence that FcγRIIb1, FcγRIIb2, and FcγRI are the receptors for CRP on mouse leukocytes. These findings may have important implications in understanding the physiological function of CRP.

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“…In rabbits given typhoid vaccine intramuscularly, Kushner and Kaplan (43) found Cx-reactive proteir (CxRP) localized to the cytoplasm of necrotic myo fibers in the inflammatory area, but lymphocytes, macrohpages, and polymorphonuclear leukocytes did not contain the protein. In rabbits with myocardial infarction produced by coronary artery occlusion, CxRP localized only in necrotic cardiac myofibers (44). It is apparent that the localization of CxRP in inflammatory or necrotic sites in rabbits was different from the nuclear localization of CRP in the synovial inflammation of rheumatoid arthritis.…”

Section: Discussionmentioning

confidence: 87%

Localization of C‐reactive protein in synovium of patients with rheumatoid arthritis

Gitlin

1977

Arthritis & Rheumatism

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Synovial biopsies from 8 patients with rheumatoid arthritis, 2 patients with degenerative osteoarthritis, and 4 patients with nonarthritic disease were studied for localization of C-reactive protein (CRP) using immunofluorescence microscopy. The nuclei of many synoviocytes and histiocytes in rheumatoid synovial membrane were found to bind CRP. Cultures of rheumatoid synovium in 14C-labeled amino acids produced radioactive IgG, IgM, IgA, and C3, but not CRP, indicating the synovial-bound CRP was not of local origin. A few CRP-binding nuclei were present in one osteoarthritic synovium, but none was found in the other and none in synovium from the 4 nonarthritic patients. The nature of the nuclear CRP ligand in rheumatoid synovium was not determined.C-reactive protein (CRP) is a normal constituent of human plasma (1). It is synthesized by all normal individuals, and its average concentration ranges from

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STUDIES OF ACUTE-PHASE PROTEIN. II. LOCALIZATION OF Cx-REACTIVE PROTEIN IN HEART IN INDUCED MYOCARDIAL INFARCTION IN RABBITS*

Cited by 100 publications

References 4 publications

Peak C-Reactive Protein Concentration Correlates With Left Ventricular Thrombus Formation Diagnosed by Contrast Echocardiographic Left Ventricular Opacification in Patients With a First Anterior Acute Myocardial Infarction

Peak C-Reactive Protein Concentration Correlates With Left Ventricular Thrombus Formation Diagnosed by Contrast Echocardiographic Left Ventricular Opacification in Patients With a First Anterior Acute Myocardial Infarction

C-Reactive Protein Binding to Murine Leukocytes Requires Fcγ Receptors

Localization of C‐reactive protein in synovium of patients with rheumatoid arthritis

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