No long-lasting or intermittent mast cell activation in acute coronary syndromes

Haelst, P.L. van; Timmer, Jorik R.; Crijns, H.J.G.M.; Kauffman, Henk F.; Gans, Rijk O. B.; Doormaal, Jasper J. van

doi:10.1016/s0167-5273(00)00475-7

Cited by 21 publications

(13 citation statements)

References 18 publications

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“…In a number of studies, plasma tryptase levels have been shown to correlate with the severity of cardiovascular diseases 30–33 and interestingly, plasma tryptase levels were significantly higher in patients that had a secondary cardiovascular event after carotid endarterectomy 20 , thus being a marker with certain predictive value in cardiovascular diseases. However, as other studies failed to show any increase in systemic tryptase levels during cardiovascular events 34,35 , tryptase effects may be more evident locally within the culprit lesion without any measurable release of tryptase into the systemic circulation. Interestingly, in an autopsy study plaque tryptase and chymase levels were shown to increase proportionally with lesion size 36 , and in a recent in vivo study, overexpression of tryptase led to an increase in intraplaque hemorrhage, which was inhibited by a tryptase-targeting siRNA in mice 37 .…”

Section: Mast Cell Effector Mechanismsmentioning

confidence: 68%

Mast Cells as Effectors in Atherosclerosis

Bot

Shi

Kovanen

2015

ATVB

127

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The mast cell is a potent immune cell known for its functions in host defense responses and diseases such as asthma and allergies. In the past years, accumulating evidence established the contribution of the mast cell to cardiovascular diseases as well, in particular by its effects on atherosclerotic plaque progression and destabilization. Through its release of mediators, such as the mast cell-specific proteases chymase and tryptase, but also of growth factors, histamine and chemokines, activated mast cells can have detrimental effects on its immediate surroundings in the vessel wall. This results in matrix degradation, apoptosis and enhanced recruitment of inflammatory cells, thereby actively contributing to cardiovascular diseases. In this review, we will discuss the current knowledge on mast cell function in cardiovascular diseases and speculate on potential novel therapeutic strategies to prevent acute cardiovascular syndromes via targeting of mast cells.

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Section: Mast Cell Effector Mechanismsmentioning

confidence: 68%

Mast Cells as Effectors in Atherosclerosis

Bot

Shi

Kovanen

2015

ATVB

127

View full text Add to dashboard Cite

show abstract

“…However, we found no changes in serum tryptase levels even in those patients whose samples were collected only 2-5 h after the onset of chest pain. Neither could the authors of a recent study, including 23 patients with acute coronary syndromes and 14 controls, find any differences in serum tryptase level between the patients and the controls [24]. In another study, allergic asthmatic patients were challenged with specific allergen, which resulted in bronchial mast cell degranulation and in an asthmatic reaction, but no accompanying increase in serum tryptase concentration was observed [25].…”

Section: Discussionmentioning

confidence: 99%

Serum tryptase levels in acute coronary syndromes

Kervinen

Kaartinen

Mäkynen

et al. 2005

International Journal of Cardiology

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“…6) In contrast, van Haelst et al reported that the serum levels of tryptase are not elevated in patients with acute coronary syndromes. 7) In these cases, since the amount of tryptase released by ischemia from cardiac mast cells was low, there is a possibility that it was diluted in the whole blood.…”

Section: Discussionmentioning

confidence: 99%