Circulating Factor VII Activating Protease (FSAP) Is Associated With Clinical Outcome in Acute Coronary Syndrome

Background: Factor VII activating protease (FSAP) is a circulating serine protease strongly expressed in unstable plaques and may serve as a marker of plaque destabilization. The aim of this study was to examine the relation between plasma concentrations of FSAP and clinical instability and outcome...

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Published in:Circulation Journal 2012, Vol.76(11), pp.2653-2661
Main Authors: Parahuleva, Mariana S., Hölschermann, Hans, Zandt, Daniel, Pons-Kühnemann, Jörn, Parviz, Behnoush, Weiskirchen, Ralf, Staubitz, Anne, Tillmanns, Harald, Erdogan, Ali, Kanse, Sandip M.
Format: Article
Language:English
Subjects:
Acute Coronary Syndrome - blood
Acute Coronary Syndrome - complications
Acute Coronary Syndrome - diagnostic imaging
Acute Coronary Syndrome - mortality
Aged
Coronary Angiography
Coronary atherosclerosis
Factor VII activating protease
Female
Follow-Up Studies
Gene Expression Regulation, Enzymologic
Humans
Inflammation
Male
Middle Aged
Monocytes - enzymology
Myocardial Infarction - blood
Myocardial Infarction - diagnostic imaging
Myocardial Infarction - etiology
Myocardial Infarction - mortality
Plaque stability
Prospective Studies
Risk Factors
RNA, Messenger - biosynthesis
Serine Endopeptidases - blood
Time Factors
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Summary:Background: Factor VII activating protease (FSAP) is a circulating serine protease strongly expressed in unstable plaques and may serve as a marker of plaque destabilization. The aim of this study was to examine the relation between plasma concentrations of FSAP and clinical instability and outcome in coronary artery disease (CAD). Methods and Results: Circulating FSAP concentration and activity, as well as FSAP mRNA expression in monocytes, were measured in 231 sequential patients who underwent coronary angiography because of stable angina pectoris (n=50), unstable angina pectoris (n=43), or acute myocardial infarction (n=87). FSAP activity, but not FSAP antigen concentration, was elevated in patients with CAD compared with a control group. Elevated FSAP activity (≥1.035 plasma equivalent units [PEU]/ml) indicated a significantly increased risk of death or non-fatal myocardial infarction during 1 year of follow-up as compared with patients with low activity of FSAP (odds ratio 1.895 [95% confidence interval 1.093–3.283]; P=0.023). Furthermore, there were no significant changes in the FSAP expression in monocytes from CAD and control subjects in the basal state but there were differences after stimulation with proinflammatory factors. Conclusions: Plasma FSAP activity was significantly increased in patients with acute coronary syndrome and may be involved in the pathogenesis of these conditions. High levels of FSAP activity were predictive of adverse events during follow-up, suggesting its potential role in risk stratification and clinical management of CAD patients.  (Circ J 2012; 76: 2653–2661)
ISSN:1346-9843
1347-4820
DOI:10.1253/circj.CJ-11-1502