The Association Between Different Monocyte Subsets and Coronary Collateral Development
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.
Coronary Artery Disease
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Study Start Date:||January 2011|
|Study Completion Date:||May 2011|
|Primary Completion Date:||May 2011 (Final data collection date for primary outcome measure)|
Patients who had good and poor collaterals formed 2 groups
|Good collateral, Poor collateral|
Please refer to this study by its ClinicalTrials.gov identifier: NCT01356836
|1Türkiye Yüksek İhtisas Education and Research Hospital, Department of Cardiology|
|Ankara, Turkey, 06550|