Tryptase levels in patients after acute coronary syndromes: The potential new marker of an unstable plaque?

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Abstract
Background: Mast cells (MCs) are multifunctional immune cells that produce a number of vasoactive or thromboactive mediators. Elevated numbers of human heart MCs are observed in the shoulder regions of coronary atherosclerotic plaques, suggesting that they play a role in plaque rupture. Cardiac MC degranulation after myocardial ischemia has been documented in animal models. Cardiac MCs are highly profibrinolytic cells and release tryptase, their specific protease, after ischemic events. Hypothesis: Mast cell activation and release of tryptase may differentiate among patients with acute coronary syndromes (ACS), potentially determining the clinical course of ACS. Tryptase levels may indirectly reflect the fibrinolytic status of patients. Methods: Mast cell activation after ACS was estimated in 10 controls and 52 patients by measuring the serum levels of tryptase in the acute phase, at 2 weeks, and at 3 months after the ACS episode. Total tryptase levels were determined by using the UniCAP® system and analyzed with respect to the patients' clinical types of ACS on admission (ACS with persistent ST‐segment elevation on electrocardiogram or with ST‐segment depression). Results: Significant differences in serum tryptase levels between the groups were found, with higher serum tryptase concentrations in the ST‐segment depression group in the acute phase, and at follow‐up. Conclusions: Serum tryptase concentration differences among patients with distinct types of ACS may indicate a more important role of human heart MCs in ACS with ST‐segment depression pathogenesis. To our knowledge, this is the first report indicating that serum tryptase levels may differentiate patients with distinct types of ACS.