Lipoprotein-Associated Phospholipase A2 – Pathophysiological Role and Clinical Significance as a Cardiovascular Biomarker

Within the last decade, a broad range of biomarkers associated with an increased risk for death and cardiovascular/cerebrovascular endpoints have been identified. Epidemiological studies clearly indicate that lipoprotein-associated phospholipase A2 (Lp-PLA2) has the potential to become clinically useful emerging biomarker in the true sense, linking plaque biology with cardiovascular/cerebrovascular event rate. Lipoprotein-associated phospholipase A2 is a specific vascular inflammatory marker, a risk factor, a prognostic biomarker, and also a therapeutic target. This chapter will summarize our current knowledge on Lp-PLA2 with emphasis on its potential pathophysiological mechanisms of action and on clinical relevance as cardiovascular/cerebrovascular biomarker. This chapter gives comprehensive, systematic review of studies assessing the significance of Lp-PLA2 in cardiovascular/cerebrovascular diseases with emphasis on clinical benefit of pharmacologic inhibition of Lp-PLA2

Biomarkers in Idiopathic Pulmonary Fibrosis

Numerous published papers are investigating the utility of biomarkers in Idiopathic Pulmonary Fibrosis (IPF) diagnosis, treatment, and outcome prediction. This chapter will summarize our current knowledge about biomarkers associated with alveolar epithelial cell damage and dysfunction (Krebs von den Lungen, surfactant proteins, the mucin MUC5B, CA 15-3, CA 125, CA 19-9, defensins, Clara cell protein (CC16), telomere shortening), biomarkers associated with fibrogenesis, fibroproliferation and extracellular matrix (ECM) remodeling (MMPs and their inhibitors, osteopontin, periostin, insulin-like growth factors, fibulin-1, heat shock protein 47, lysyl oxidase-like 2, circulating fibroblasts, extracellular matrix neoepitopes) and biomarkers related to immune dysfunction and inflammation (C-C chemokine ligand-18, C-C chemokine 2, YKL-40, C-X-C motif chemokine 13, S100A4, S100A8/9, S100A12, autoantibodies to heat shock protein 72, toll-like receptor 3, soluble receptor for advanced glycosylated end products, endothelial damage (vascular endothelial growth factor, interleukin 8, endothelin 1). The future directions in incorporating IPF biomarkers into clinical practice will be reviewed

Sex and age differences and outcomes in acute coronary syndromes

Background: There is conflicting information about sex differences in presentation, treatment, and outcome after acute coronary syndromes (ACS) in the era of reperfusion therapy and percutaneous coronary intervention. The aim of this study was to examine presentation, acute therapy, and outcomes of men and women with ACS with special emphasis on their relationship with younger age ( lt = 65 years). Methods: From January 2010 to June 2015, we enrolled 5140 patients from 3 primary PCI capable hospitals. Patients were registered according to the International Survey of Acute Coronary Syndrome in Transitional Countries (ISACS-TC) registry protocol (ClinicalTrials.gov: NCT01218776). The primary outcome was the incidence of in-hospital mortality. Results: The study population was constituted by 2876 patients younger than 65 years and 2294 patients older. Women were older than men in both the young (56.2 +/- 6.6 vs. 54.1 +/- 7.4) and old (74.9 +/- 6.4 vs. 73.6 +/- 6.0) age groups. There were 3421 (66.2%) patients with ST elevation ACS (STE-ACS) and 1719 (33.8%) patients without ST elevation ACS (NSTE-ACS). In STE-ACS, the percentage of patients who failed to receive reperfusion was higher in women than in men either in the young (21.7% vs. 15.8%) than in the elderly (35.2% vs. 29.6%). There was a significant higher mortality in women in the younger age group (age-adjusted OR 1.52, 95% CI: 1.01-2.29), but there was no sex difference in the older group (age-adjusted OR 1.10, 95% CI: 0.87-1.41). Significantly sex differences in mortality were not seen in NSTE-ACS patients. Conclusions: In-hospital mortality from ACS is not different between older men and women. A higher short-term mortality can be seen only in women with STEMI and age of 65 or less