Systemic Mastocytosis and Cardiovascular Risk

Acute cardiovascular syndromes such as myocardial infarction and stroke are a
major cause of death in Western society and are generally triggered by rupture
of an atherosclerotic plaque1. Inflammation, matrix degradation and lipid
accumulation are generally considered key processes in atherosclerosis and the
pathogenesis of plaque rupture2. The mast cell, a prominent inflammatory cell
type and a major effector cell in allergy and asthma, has been shown to
accumulate both in the rupture-prone shoulder region of human atheromas3,4 and
in the perivascular tissue (adventitia) during atherosclerotic lesion
progression5-7. Because of the work in animal studies in which activated mast
cells appeared to be causally associated to atherogenesis, we hypothesize that
patients with SM have increased atherosclerosis and potentially an impaired
lipid profile compared to controls.

Our objective is to assess whether patients with SM compared to controls have
more advanced atherosclerosis assessed by carotid intima-media thickness
(C-IMT) and carotid plaques and have a more adverse cardiovascular risk
profile.

The study design to be applied is a cross sectional study at the outpatient
clinic of the department Immunology of the Erasmus MC.

The burden associated with participation is as follows: 1 site visit, a
physical examination, 6 bloodsamples, 2 urine samples and a C-IMT measurement.
The risks are small to negligible.