Mast cells have been implicated in several types of cardiac and vascular dysfunction. Mast cells are thought to contribute to rupture of atherosclerotic plaques by mediator release. They are found around blood clots in the body. Mast cells may destabilize them and mature them by releasing heparin and degrading fibrinogen with tryptase. Increased numbers of mast cells are associated with coronary vasospasm.
Mast cell mediator levels are often higher in vascular and cardiac events. In patients who die from coronary heart disease, the histamine concentration in the coronary artery than in control subjects. Higher white blood cell, platelet and plasma histamine levels are found in patients with peripheral vascular disease. Increased histamine levels are found in patients with both stable coronary artery disease and acute coronary syndrome. Plasma histamine is elevated in the great cardiac vein of 8/11 patients with variant angina.
One study found that tryptase is higher in patients without acute coronary syndrome undergoing catheterization, compared to patients with and without obstructive coronary disease. In this study, patients in the highest 25% of tryptase values had 4.3x greater risk for coronary artery disease. Tryptase is being investigated as a marker to identify asymptomatic patients with coronary artery disease and to track efficacy of treatment.
Mast cell mediators are also elevated in non-allergic coronary events, indicating that there is a common pathway for both allergic (Kounis syndrome) and non-allergic cardiac episodes. Two cholesterol lowering medications, cervistatin and atorvastatin, inhibit stem cell factor (SCF) mediated differentiation of mast cells. Lovastatin inhibited IgE-mediated degranulation.
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