Publications by authors named "Liuzzo G"

Aims: Unfavourable cardiac remodelling often complicates acute myocardial infarction (AMI) as a result of increased cardiomyocyte apoptosis. It is currently unclear whether ongoing or recurrent ischaemia is an independent determinant for increased apoptosis in peri-infarct viable myocardium.

Methods And Results: In order to assess the link between infarct-related artery (IRA) occlusion, ischaemia, and apoptosis, 30 subjects dying 7-120 days after AMI (16 with IRA occlusion and 14 with patent IRA) and five control subjects were selected at autopsy.

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A growing body of evidence suggests that inflammation plays a major role in the pathogenesis of unstable angina; this evidence is mainly derived from the prognostic role of the acute phase reaction proteins, such as C-reactive protein (CRP) and fibrinogen. Since the production of acute phase protein is under the control of the pro-inflammatory cytokines, it is probable that citokines, such as tumour-necrosis factor (TNF)-alpha, interleukin (IL)-1 and IL-6 are involved in the same process. Indeed, elevated levels of IL-1 and IL-6 have been found by our group and by others, in patients with acute coronary syndromes.

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Many clinical indications and different technical issues have been reported on therapeutic apheresis: much criticism has also been recorded in several instances, mainly due to the lack of large clinical trials to validate collected data. A Registry where all the available data can be organized and analyzed therefore becomes a priority for all the professionals involved in apheresis. The purpose of this report is to describe the data submitted from 1994 to 2004 from 15,285 treatments on 1,477 patients from 44 Centers, including mainly, but not exclusively, Nephrological Units, collected by the Apheresis Study Group of the Italian Society of Nephrology in 15 Italian regions.

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Aims: Recent data suggest that the administration of bone marrow-derived stem cells (BMSC) might improve myocardial perfusion and left ventricular (LV) function after acute myocardial infarction (AMI). The aim of this study was to assess spontaneous mobilization of BMSC expressing the haematopoietic and endothelial progenitor cell-associated antigen CD34+ after AMI and its relation to post-infarction remodelling.

Methods And Results: Peripheral blood concentration of CD34+ BMSC was measured by flow cytometry in 54 patients with AMI, 26 patients with chronic stable angina (CSA), and 43 normal healthy subjects.

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Laminar shear stress (LSS) represents a major athero-protective stimulus. However, the mechanisms for this effect are poorly characterized. As chemokine receptors modulate endothelial cell functions, we hypothesized that at least some LSS effects on endothelial cells (ECs) may be due to LSS-dependent changes in chemokine receptor expression and function.

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In order to investigate the likelihood of Listeria monocytogenes (serotype 4b, ATCC 19115) growth on vacuum-packaged horsemeat at refrigeration temperature, fourteen horsemeat surface/volume homogeneous 150 g weight pieces were superficially inoculated with serotype 4b L. monocytogenes and vacuum packaged. The samples were stored at 4±1 °C.

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Von Hippel-Lindau (VHL) disease is an autosomal dominant syndrome characterized by germline mutations in the VHL tumor suppressor gene located at chromosome 3p25-26 and pleomorphic clinical picture. The major clinical manifestations include retinal angiomas, central nervous system hemangioblastomas, pheopleochromocytoma, pancreatic cysts, epididymal cystoadenomas and renal lesions. Recently, we observed a 58-year-old male patient with macrohematuria and a history of nephrectomy due to renal cell carcinoma (RCC).

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Background: Diffuse coronary vascular inflammation is associated with acute coronary syndromes. However, it is unknown whether inflammation also occurs within the myocardium. Therefore, this study was aimed at assessing the presence of activated cells in unaffected remote myocardium of patients with acute myocardial infarction (AMI), in comparison to the peri-infarct region from the same cases, and in comparison to myocardial specimens from control hearts.

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Despite diagnostic and therapeutic advances, the rate of event recurrence is still relatively high and short- and long-term prediction of risk is necessary although extremely challenging to provide optimal treatment to patients with acute coronary syndromes. Available data recommend the use of C-reactive protein (CRP) as a prognostic marker in patients with acute coronary syndromes in addition to other prognostic factors including troponin levels. Evaluation of CRP levels at time of admission should be included in the evaluation of the patient's risk profile, including clinical data, associated diseases, markers of myocardial necrosis (especially troponin levels), left ventricle performance, and age.

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Background: Multiple complex stenoses, plaque fissures, and widespread coronary inflammation are common in acute coronary syndromes. A systemic cause of atherosclerotic plaque instability is also suggested by studies of ischemic cerebrovascular disease. We investigated the association between coronary and carotid plaque instability and the potential common causal role of inflammation.

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Inflammation plays a pivotal role in the pathogenesis of atherosclerosis and its complications. In particular, atherosclerosis is an active process and the inflammatory component appears to be particularly correlated with the development of acute coronary syndromes (ACS). Accumulating data demonstrate that in ACS, elevated levels of circulating inflammatory markers, such as C-reactive protein, predict an unfavorable cardiovascular outcome.

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Background: Cyclo-oxygenase-2 (COX-2) is induced in cardiomyocytes only in response to stress, such as ischaemia.

Objective: To assess COX-2 expression at the site of recent myocardial infarction.

Methods: COX-2 expression was evaluated by specific immunostaining in cardiomyocytes from 23 subjects who died 10-60 days after acute myocardial infarction.

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Background: Heat shock proteins (HSPs) are a family of proteins with immunogenic and proinflammatory properties. Human and Chlamydia pneumoniae (Cp) HSP60 were found in patients with stable coronary disease.

Methods And Results: We measured the levels of anti-Cp-HSP60 and anti-Cp immunoglobulin G (IgG) in 179 patients with unstable angina, 40 with acute myocardial infarction, and 40 with stable angina (SA), as well as 100 control subjects.

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Inflammation plays a pivotal role in both the development of atherosclerosis and the acute activation of the vascular wall with consequent local thrombosis and vasoconstriction (with or without plaque fissure). In many patients with unstable angina and acute myocardial infarction, systemic signs of inflammation are detectable. The use of systemic inflammatory markers, such as C-reactive protein as marker of disease activity and short- and long-term prognosis, seems to be of clinical value.

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Diabetes represents a major cause of cardiovascular morbidity and mortality in developed countries, and atherothrombosis accounts for most deaths among diabetics. Recent evidence has reliably shown the relevant etiopathogenetic role of inflammation in atherothrombotic disease. This review summarizes and discusses the possible synergistic effects of diabetes and inflammation in promoting atherothrombosis and its complications, as well as potential avenues for diagnostic, preventive, and therapeutic benefits in the modulation of inflammatory mechanisms in diabetic atherothrombotic disease.

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Objectives: The goal of this study was to assess the prognostic role of the Lewis antigenic system, Chlamydia pneumoniae (CP) seropositivity (CP+), and C-reactive protein (CRP) levels in unstable angina (UA).

Background: The role of CP infection in acute coronary syndromes is contradictory. The Lewis antigenic system, a genetically determined blood group system associated with infections and several disorders, including ischemic heart disease, might influence the susceptibility to CP infection, inflammatory response, and risk of cardiac ischemic events.

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Inflammatory mechanisms and infectious agents, in association with "classic" cardiovascular risk factors, may be involved in the development of coronary atherosclerosis; moreover, recent studies demonstrated a direct role of inflammation in the pathogenesis of acute coronary syndromes, in which the intensity of the individual response to potential environmental inflammatory stimuli seems to influence the magnitude of the inflammatory reaction and the clinical outcome. The variability of this response may be modulated by genetic determinants, in particular by functional polymorphisms of the genes codifying for molecules involved in the inflammatory process. In this review we discuss the association between these polymorphisms and various aspects of ischemic heart disease.

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Inflammatory mechanisms play a pivotal role in the atherosclerotic process. At the base of atherogenesis there are complex interactions between macrophages, T lymphocytes and smooth muscle cells. A growing body of experimental evidences suggest that inflammation is involved in the pathogenesis of acute coronary syndromes (ACS) and influences their clinical evolution.

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Background: Inflammation within vulnerable coronary plaques may cause unstable angina by promoting rupture and erosion. In unstable angina, activated leukocytes may be found in peripheral and coronary-sinus blood, but it is unclear whether they are selectively activated in the vascular bed of the culprit stenosis.

Methods: We measured the content neutrophil myeloperoxidase content in the cardiac and femoral circulations in five groups of patients: two groups with unstable angina and stenosis in either the left anterior descending coronary artery (24 patients) or the right coronary artery (9 patients); 13 with chronic stable angina; 13 with variant angina and recurrent ischemia; and 6 controls.

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Background: Patients undergoing revascularization procedures for peripheral vascular disease (PVD) have a greatly increased risk for coronary artery disease (CAD) that is predicted only partly by clinical data and cardiovascular risk factors. We investigated whether the prognostic assessment in PVD patients could be improved by preoperative measurements of C-reactive protein (CRP).

Methods And Results: We assessed clinical and risk factors profiles, Eagle clinical scores, and preoperative CRP serum levels in 51 patients with PVD at Fontaine-Leriche stages II to IV without severe rest ventricular dysfunction or ischemia.

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Acute coronary syndromes (ACS) are complications of atherosclerotic vascular disease that are triggered by the sudden rupture of an atheroma. Atherosclerotic plaque stability is determined by multiple factors, of which immune and inflammatory pathways are critical. Unstable plaque is characterized by an infiltrate of T cells and macrophages, thereby resembling a delayed hypersensitivity reaction.

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C-reactive protein (CRP) is the prototype acute phase reactant and therefore a marker of systemic inflammation. In the last decades, accumulating data have demonstrated the role of inflammation in the pathogenesis of ischemic heart disease. High CRP levels, measured by high-sensitivity methods, on admission have a short-term negative prognostic value and are associated with a worse outcome.

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Background: C-reactive protein (CRP) plasma levels have been associated with short- and long-term occurrence of coronary events. We investigated whether circulating inflammatory cell responsiveness to low-grade stimuli could contribute to the reported association between CRP and coronary events.

Methods And Results: We studied 32 patients with unstable angina who were followed for 24 months and were free of symptoms for 6 months (group 1): 19 patients had persistently high CRP levels (>0.

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C-reactive protein (CRP), the prototypic acute phase reactant and a sensitive marker of inflammation, consistently predicts new coronary events, including myocardial infarction and death, in patients with ischemic heart disease. The data are very consistent with regard to the long-term outcome, but in many studies are also significant for in-hospital events. The predictive value of CRP is, in the majority of the studies, independent of and additive to that of the troponins.

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