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SERUM TRYPTASE AND TUMOR NECROSIS FACTOR ALPHA LEVELS IN PATIENTS WITH ACUTE CORONARY SYNDROMES

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Author(s): Filipiak Krzysztof J. | Kapłon-Cieślicka Agnieszka | Rdzanek Adam | Rancic B. Milan | Grabowski Marcin | Tarchalska-Kryńska Bozena | Opolski Grzegorz

Journal: Acta Facultatis Medicae Naissensis
ISSN 0351-6083

Volume: 24;
Issue: 4;
Start page: 173;
Date: 2007;
Original page

Keywords: acute coronary syndromes | tryptase | mast cells | tumor necrosis factor alpha

ABSTRACT
Inflammation plays a key role in atherosclerotic plaque formation and destabilization. Inflammatory markers, including C-reactive protein (CRP) and fibrinogen are known risk factors of an unfavorable prognosis in patients with ischemic heart disease and acute coronary syndromes (ACS). Tumor necrosis factor alpha (TNFa) is a proinflammatory cytokine, which promotes post-infarction cardiac remodeling and progression to heart failure. Recently, allergic processes have been implicated in the pathogenesis of ACS. Cardiac mast cell (MC) degranulation after myocardial ischemia has been documented in animal models. Human heart MCs express a highly profibrinolytic profile and release tryptase, their specific proteinase, after ischemic events. The aim of our study was, first, to investigate the relation of patient's allergic profile and tryptase concentration to the clinical course of ACS, and second, to establish the correlation between tryptase concentrations and serum levels of selected inflammatory markers: CRP, fibrinogen and TNF. A total of 70 ACS patients was included in the study. Serum tryptase levels were measured on admission, two weeks and three months after ACS onset. Concentrations of CRP, fibrinogen and TNFα were estimated on admission and at two weeks. Total IgE levels were also measured and skin prick tests (SPT) were performed. Positive SPT results and higher serum tryptase levels were more common in patients with non-ST-segment elevation ACS (NSTE-ACS) than in patients with ST-segment elevation ACS (STE-ACS). Serum tryptase concentrations on admission were not related to CRP or fibrinogen levels, but correlated inversely with TNFα concentrations. Our findings suggest that patients with NSTE-ACS differ from patients with STE-ACS in respect to their allergic profile. Cardiac MCs may play a more important role in the pathogenesis of NSTE-ACS than in STE-ACS. Furthermore, in patients with ACS a more intensive MC degranulation was associated with lower levels of TNFα. This might potentially contribute to a more favorable form of post-infarction cardiac remodeling.
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