PTX3 expression in the heart tissues of patients with myocardial infarction and infectious myocarditis.

INTRODUCTION: The long pentraxin 3 is involved in innate resistance to pathogens, controlling inflammation and extracellular matrix remodeling. Moreover, pentraxin 3 plays a nonredundant role in the regulation of cardiac tissue damage in mice and, recently, it has been proposed as a new candidate marker for acute and chronic heart diseases. However, the actual localization and cellular sources of pentraxin 3 in ischemic and infectious cardiac pathology have not been carefully defined. METHODS: In this study, using immunohistochemistry, we analyzed pentraxin 3 expression in the heart tissues of patients with acute myocardial infarction at different time points after the ischemic event. In addition, we studied the heart tissues of patients with infectious myocarditis (fungi, bacteria, and protozoa) and patients who died of noncardiac events with normal heart histology. RESULTS: In acute myocardial infarction cases, we observed pentraxin 3 localized within and around ischemic lesions. On the contrary, no pentraxin 3 was observed in normal heart areas. In early ischemic lesions, pentraxin 3 was localized primarily in granulocytes; in more advanced acute myocardial infarction, pentraxin 3 positivity was found in the interstitium and in the cytoplasm of macrophages and the endothelium, whereas most granulocytes did not express pentraxin 3, presumably as a consequence of degranulation. In infectious myocarditis, pentraxin 3 was present and localized within and around histological lesions, associated with macrophage, endothelial cell, and, more rarely, myocardiocyte and granulocyte positivities. As observed in acute myocardial infarction patients, no pentraxin 3 staining was found in normal heart areas. CONCLUSIONS: Thus, neutrophils are an early source of pentraxin 3 in acute myocardial infarction and presumably other inflammatory heart disorders. Subsequently, in acute myocardial infarction and infectious myocarditis, pentraxin 3 is produced by macrophages, the endothelium, and, to a lesser extent, myocardiocytes, and localized in the interstitium.

Preliminary investigation of the clinical value of vascular endothelial growth factor and hypoxia-inducible factor-1alpha in pericardial fluid in diagnosing malignant and tuberculous pericardial effusion.

OBJECTIVES: To investigate the clinical value of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1alpha (HIF-1alpha) in diagnosing malignant and tuberculous pericardial effusion. METHODS: Eighty patients with exudative pericardial effusion undergoing pericardiocentesis and drainage were divided into 2 groups, namely those with malignancy and those with tuberculosis. The levels of HIF-1alpha, VEGF, lactate dehydrogenase (LDH) and adenosine deaminase (ADA) in pericardial fluid and serum were measured. Routine and cytological examination of pericardial fluid, clinical characteristics and some blood parameters were compared between the 2 groups. RESULTS: There were 33 patients with tuberculous pericardial effusion and 47 with malignant pericardial effusion. The levels of VEGF and HIF-1alpha in pericardial fluid in the malignancy group were significantly higher than those in the tuberculosis group (p < 0.01), and there was a moderate positive correlation between the levels of VEGF and HIF-1alpha (r = 0.79, p < 0.01). The sensitivity and specificity of combining VEGF and HIF-1alpha were 90.8 and 88.3%, respectively. The 2 groups showed no differences with regard to gender distribution, occurrence of fever, erythrocyte sedimentation rate or the levels of hemoglobin, LDH, ADA, serum HIF-1alpha and VEGF. CONCLUSIONS: Both VEGF and HIF-1alpha in pericardial fluid have determinative value in the differential diagnosis of malignant and tuberculous pericardial effusion.