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Biomedical subjects

V Rizzello

Publications and source records attributed to V Rizzello.

6 recordsLinked to original sources

C-reactive protein and primary prevention of ischemic heart disease.

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. In epidemiological studies, minor elevations of CRP are associated with future risk of myocardial infarction, stroke and peripheral vascular disease. This increased risk is independent of other biochemical and clinical risk factors, and the association between high CRP and an abnormal cholesterol ratio significantly increases the risk in the individual patient. Finally, the observation of an increased level of CRP may be of clinical utility in primary prevention, because these subjects favourably benefit from statin therapy.

Biomarkers↗

Enhanced response of blood monocytes to in vitro lipopolysaccharide-challenge in patients with recurrent unstable angina.

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 (>0.3 mg/dL) (group 1A); 13 patients had normal CRP levels (group 1B). During the follow-up, 12 (63%) group 1A but no group 1B patients developed an infarction or recurrence of unstable angina (P<0.001). Eighteen patients with chronic stable angina (group 2) and 18 healthy subjects (group 3) were studied as controls. Interleukin (IL)-6 production (median, range) by peripheral blood mononuclear cells after 4 hours of in vitro stimulation with 1 ng/mL lipopolysaccharide (LPS) was significantly higher in group 1A (4526 pg/mL, 3042 to 10 583 pg/mL) than in group 1B (1752 pg/mL, 75 to 3981 pg/mL), group 2 (707 pg/mL, 41 to 3275 pg/mL), and group 3 (488 pg/mL, 92 to 3503 pg/mL) (all P<0.001). No significant differences were observed among the other groups. IL-6 production after LPS-challenge was correlated with baseline CRP levels (r=0.42, P=0.005). CONCLUSIONS: Mononuclear cells of patients with recurrent phases of instability exhibit an enhanced production of IL-6 in response to low-dose of LPS, correlated with baseline CRP levels, 6 months after the last acute event. This persisting enhanced acute-phase responsiveness may help explain the association between CRP and acute coronary events.

Angina, Unstable↗

Clinical use of C-reactive protein for the prognostic stratification of patients with ischemic heart disease.

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. Moreover recent data suggest that CRP may be a reliable marker of the risk of restenosis after percutaneous coronary interventions and that its levels can be modulated by statins. Taken together, all these data suggest that CRP, probably with different cut-offs, should be used as a marker of risk and as a guide to therapy in patients hospitalized for acute coronary syndromes and in outpatients suffering from ischemic heart disease.

Acute Disease↗

In vitro hyperreactivity to lipopolysaccharide in patients with history of unstable angina is not associated with seropositivity for Cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae.

BACKGROUND: Inflammation and possibly chronic infections are associated with acute coronary syndromes; however, the mechanisms responsible for this association are not yet fully elucidated. The aim of this study was to assess whether the hyperreactivity of the inflammatory system, that we have shown in unstable patients with persistently elevated C-reactive protein and with recurrence of symptoms, was associated with chronic infection. METHODS: In 20 unstable angina patients seropositivity and antibody levels vs Cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae were measured and correlated with the interleukin-6 production in vivo in 1 ml of whole blood stimulated with 0.1 microgram lipopolysaccharide for 4 hours. RESULTS: No positive correlation was found between antibody titer and interleukin-6 levels. No correlation was also found between seropositivity to Cytomegalovirus, Helicobacter pylori or Chlamydia pneumoniae and interleukin-6 levels. CONCLUSIONS: Our study suggests that seropositivity for infective agents, including Chlamydia pneumoniae, does not affect the monocyte response to lipopolysaccharide and thus cannot account for the enhanced interleukin-6 production observed in unstable angina patients with raised levels of C-reactive protein and worse prognosis, and suggests the predominant role of the individual response to different stimuli.

Aged↗

Role of inflammation in the pathogenesis of unstable coronary artery diseases.

Inflammation has been shown to play a pivotal role in ischemic heart disease, in particular unstable angina. The instability that characterizes this syndrome is related to the waxing and waning of ischemic stimuli, especially thrombotic ones. Angiographically and autoptically the severity of the atherosclerotic background in unstable angina does not differ from that in chronic stable angina, but in the former mural thrombi are often found and coronary atherosclerotic plaques are characterized by an inflammatory infiltrate, mostly consisting of activated lymphocytes, macrophages and mast-cells. In addition to these local findings, systemic evidence also suggests the importance of the role of inflammation in unstable angina as platelets, neutrophils and monocytes are activated, and elevated levels of serum markers of inflammation, e.g. C-Reactive Protein, have been consistently found. CRP has been demonstrated to be a reliable marker of prognosis in coronary heart disease. The consequences of inflammation are a disruption in the dynamic balance between antithrombotic and prothrombotic activities, an altered extracellular matrix metabolism, hyper-reactivity of cells such as monocytes and smooth muscle cells, all important features of unstable angina. These findings have important prognostic implications, since markers of inflammation are associated to a worse prognosis, and may also have therapeutic implications in the near future.

Angina, Unstable↗