Home About us Contact
|
Home About us Contact | ||
|
|
||
Arterial Lesions (arterial + lesion)
Selected AbstractsPlasma brain natriuretic peptide concentrations in patients with Kawasaki diseasePEDIATRICS INTERNATIONAL, Issue 3 2000Takashi Kawamura Abstract Background: Brain natriuretic peptide (BNP) is a cardiac hormone and plasma levels of it increase in patients with congestive heart failure and in those with acute myocardial infarction. Kawasaki disease (KD) is a well-known generalized vasculitis and the most prominent features of this disease are the cardiovascular manifestations, which involve the pericardium, myocardium, endocardium and coronary arteries. It was hypothesized that the plasma concentrations of BNP in patients with KD might be increased and that plasma BNP might be a useful biological marker of cardiovascular manifestations in patients with KD. Methods: Blood was obtained to measure and compare plasma BNP concentrations in the acute (n=32) and convalescent (n=35) phases of KD and in the acute phase of the patients with viral infection (n=26), which included adenovirus, influenza, measles and herpes group virus infection. In patients with KD, two-dimensional echocardiography was performed to check for pericardial effusion and coronary arterial lesions and to measure the dimensions of the left ventricle at diastole and the shortening fraction of the left ventricle (LVSF). Results: The mean plasma BNP concentration in patients with KD in the acute phase was 55.0~39.5 pg/mL, but was 6.8~7.3 pg/mL in patients with viral infection. The plasma BNP concentration in patients with KD in the acute phase was significantly higher than in patients with viral infection (P<0.0001). In 31 cases of KD, the plasma BNP concentrations were measured both in the acute and convalescent phases. The mean plasma BNP concentration in the acute phase of KD was 55.3~40.1 pg/mL and in the convalescent phase was 5.9~5.7 pg/mL. The level of plasma BNP decreased significantly in the convalescent phase (P<0.0001). The mean BNP level in patients with KD with pericardial effusion (n=8) in the acute phase was 80.3~43.4 pg/mL and that in patients without pericardial effusion (n=24) was 46.5~35.1 pg/mL. The BNP level in patients with pericardial effusion was significantly higher than that of patients without pericardial effusion (P<0.05). There was no significant correlation between the plasma concentrations of BNP in the acute phase of KD and LVSF (r=, 0.161, P=0.39, n=31). Conclusion: It was shown that the plasma BNP concentration increased in the acute phase of KD and decreased to within normal range in the convalescent phase. Further examinations are needed to clarify the mechanism by which the elevated levels of plasma BNP occur in the acute phase of KD. However, plasma BNP might be a useful biological marker of the cardiovascular manifestations in patients with KD. [source] A case of pulmonary arteritis with stenosis of the main pulmonary arteries with positive myeloperoxidase-antineutrophil cytoplasmic autoantibodiesRESPIROLOGY, Issue 4 2000Hiroyuki Nakayama A 53-year-old woman was referred to our hospital with the main symptoms of productive cough, fever and exertional dyspnoea. Chest X-ray revealed enlargement of the left hilar shadow and cavitary infiltration in the right upper lobe. 99mTechnetium-macroaggregated albumin (99mTc-MAA) perfusion scintigram showed complete hypoperfusion through the entire right lung. A pulmonary angiogram revealed stenotic lesions in the right and left main pulmonary arteries. Right cardiac catheterization showed an elevated right ventricular systolic pressure. There was no evidence of systemic arterial lesions nor vasculitis. The patient was positive for myeloperoxidase (MPO)antineutrophil cytoplasmic autoantibodies (ANCA) (168 EU). The Mycobacterium avium complex sputum culture was positive. The pulmonary stenotic lesions were surgically resected. The resected pulmonary arterial lesions were pathologically diagnosed as non-specific vasculitis. The cavitary lesion disappeared 6 months after the surgery. Two years after the surgery, although the MPO-ANCA level had decreased to 12 EU, stenosis of the pulmonary arteries reappeared. It is suggested that the patient became positive for MPO-ANCA in association with the Mycobacterium avium complex infection, and that the presence of MPO-ANCA may not be related to the development of pulmonary stenosis of the main pulmonary arteries. [source] Complement Independent Antibody-Mediated Endarteritis and Transplant Arteriopathy in MiceAMERICAN JOURNAL OF TRANSPLANTATION, Issue 3 2010T. Hirohashi Complement fixation, as evidenced by C4d in the microvasculature, is a widely accepted criterion of antibody-mediated rejection. Complement fixation has been shown to be essential in acute antibody-mediated rejection, but its role in chronic rejection has not been addressed. Previous studies showed that passive transfer of complement fixing monoclonal IgG2a anti-H-2Kk into B6.RAG1,/, KO recipients of B10.BR hearts led to progressive chronic transplant arteriopathy (CTA) over 14,28 days, accompanied by C4d deposition. The present studies were designed to test whether complement was required for these lesions. We report that a noncomplement fixing donor-specific alloantibody (DSA, monoclonal IgG1 anti-H-2Kk) injected into B6.RAG1 -/- KO recipients of B10.BR hearts also promotes CTA, without C4d deposition. Furthermore, a passive transfer of DSA (monoclonal IgG2a anti-H-2Kk) initiated endarteritis followed by CTA in B6.RAG1,/- mice genetically deficient in the third component of complement (RAG1,/,C3,/,). These studies indicate that antibody to class I MHC antigens can trigger chronic arterial lesions in vivo without complement participation, in contrast to acute antibody-mediated rejection. This pathway may be relevant to C4d-negative chronic rejection sometimes observed in patients with DSA, and argues that lack of C4d deposition does not exclude antibody-mediated chronic rejection. [source] Association of a nonsynonymous single-nucleotide polymorphism of matrix metalloproteinase 9 with giant cell arteritisARTHRITIS & RHEUMATISM, Issue 6 2008A. Rodríguez-Pla Objective Giant cell arteritis (GCA) is the most common type of primary vasculitis. Matrix metalloproteinase 9 (MMP-9) is present in arterial lesions of GCA and may be involved in its pathogenesis. We investigated whether certain genotypes of 4 single-nucleotide polymorphisms (SNPs) of MMP-9 are overrepresented in patients with histologically confirmed GCA. Methods Four SNPs of MMP-9, rs3918242 in the promoter region and 3 nonsynonymous coding SNPs (rs3918252, rs17576, and rs2250889) were genotyped by polymerase chain reaction,restriction fragment length polymorphism analysis in 58 white patients for whom there was a clinical suspicion of GCA. Thirty of these patients had histologically confirmed GCA (group 1), and 28 patients had negative results of a temporal artery biopsy for GCA (group 2). Estimates of the genotype distributions of each of these SNPs in a white population were determined using publicly available genotype data for a panel of 23 individuals (group 3). Results Although 1 SNP was monomorphic in all 3 groups, we observed statistically significant differences in the genotype distributions for rs2250889 between group 1 and group 2 (P = 0.005) and between group 1 and group 3 (P = 0.009), but not between groups 2 and 3 (P = 0.965). Conclusion These data derived from a sample of patients with GCA suggest that the G allele of MMP-9 polymorphism rs2250889 is overrepresented in patients with histologically confirmed GCA. Clearly, larger sample sizes will be necessary to confirm this suggestive association and better characterize a possible linkage disequilibrium structure among polymorphisms. [source] Reactivity of ,/, T cells to human 60-kd heat-shock protein and their cytotoxicity to aortic endothelial cells in Takayasu arteritisARTHRITIS & RHEUMATISM, Issue 8 2007Sunil Kumar Chauhan Objective Increased numbers of circulating ,/, T cells with a restricted T cell receptor repertoire, as well as colocalization of the expression of heat-shock protein Hsp60/65 and ,/, T cells in the arterial lesions of patients with Takayasu arteritis (TA), indicate that ,/, T cells may react to Hsp60 and cause damage to the arterial endothelium. In this study we investigated the proliferative responses of ,/, T cells to human Hsp60 and their cytotoxicity to human aortic endothelial cells (ECs) in patients with TA. Methods Blood samples were obtained from 12 patients with TA, 8 patients with systemic lupus erythematosus (SLE) (as disease controls), and 10 healthy control subjects. Proliferative responses of circulating ,/, T cells to human Hsp60 were detected by flow cytometry,based bromodeoxyuridine incorporation assay. Cytotoxicity of the ,/, T cells to human aortic ECs was analyzed by colorimetric lactate dehydrogenase release assay. Results The ,/, T cells of 11 of 12 patients with TA exhibited reactivity to Hsp60, whereas none of the ,/, T cells from patients with SLE or healthy controls showed reactivity (both P < 0.001). The mean ± SD proliferative response of ,/, T cells in patients with TA was 21.4 ± 11.3%, compared with 4.2 ± 1.2% in patients with SLE and 4.01 ± 1.82% in healthy controls (both P < 0.001). In addition, compared with the control groups, the ,/, T cells of patients with TA had increased spontaneous cytotoxicity to aortic ECs (22.1 ± 15.0% versus 9.6 ± 2.13% in SLE patients and 8.1 ± 4.7% in healthy controls; both P < 0.005), which was further enhanced following stimulation of ,/, T cells with Hsp60. The cytotoxicity of the ,/, T cells was significantly inhibited by treatment of these cells with concanamycin A and anti,Fas ligand,blocking antibodies. Conclusion The results show that ,/, T cells in patients with TA are reactive to Hsp60 and exhibit cytotoxicity to aortic ECs, suggesting a key role of Hsp60 and ,/, T cells in the pathogenesis of TA. [source] Translational Mini-Review Series on Immunology of Vascular Disease: Inflammation, infections and Toll-like receptors in cardiovascular diseaseCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2009J. R. Ward Summary Cardiovascular disease, in which atherosclerosis is the major underlying cause, is currently the largest cause of death in the world. Atherosclerosis is an inflammatory disease characterized by the formation of arterial lesions over a period of several decades at sites of endothelial cell dysfunction. These lesions are composed of endothelial cells, vascular smooth muscle cells, monocytes/macrophages and T lymphocytes (CD4+). As the lesions progress some can become unstable and prone to disruption, resulting in thrombus formation and possibly a myocardial infarction or stroke depending upon the location. Although the exact triggers for plaque disruption remain unknown, much recent evidence has shown a link between the incidence of myocardial infarction and stroke and a recent respiratory tract infection. Interestingly, many reports have also shown a link between a family of pattern recognition receptors, the Toll-like receptors, and the progression of atherosclerosis, suggesting that infections may play a role in both the progression of atherosclerosis and in inducing the more severe complications associated with the disease. [source] | ||||||||||