Coronary Artery Disease Clinical Trial
Collateral growth and coronary angiogenesis are chronic adaptations to myocardial ischemia.
Collateralization helps to restore blood flow and as a result salvages myocardium in
severely ischemic myocardial regions. Thus, good collateral development in patients with
severe coronary artery disease (CAD) improves ventricular function and prognosis (1-3).
However, coronary collateral development is different among patients even with similar
degrees of coronary artery stenosis. Several factors, such as diabetes mellitus (4) and
duration of myocardial ischemic symptoms (5) have been reported to effect coronary
collateral development. At the cellular level, inflammatory cells, especially monocytes have
an important role in collateralization. In a series of experimental studies with animals, it
has been shown that monocytes are important elements for development of collateral vessels
(6-7). In a recent study, it has been demonstrated that increased circulating monocyte count
is related to good collateral development in patients with stable coronary artery disease
(8).
Monocytes in human blood are heterogeneous and can be classified into two subsets according
to the presence or absence of the FcγRIII receptor CD16 (9): CD14++CD16- monocytes
characterized by high level expression of the CD14 cell surface receptor but no expression
of CD16 receptor, and CD14+CD16+ monocytes characterized by the co-expression of CD16
receptor with either high or low level expression of the CD14 receptor. These subsets differ
in function and response to several cytokines.
Our aim in this study was to find out any possible relationship between the levels of
circulating monocyte subsets and coronary collateral development.
n/a
Observational Model: Cohort, Time Perspective: Prospective
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