Coronary Artery Disease Clinical Trial
Official title:
The Effects of Age on Endothelial Progenitor Cell Mobilization in Humans
It is hypothesized that aging is associated with reduced vascular injury-induced endothelial progenitor cell activity, resulting in impaired vascular repair and increased vascular disease. Patients with stable coronary artery disease will be enrolled in this observational study and will undergo either angiography alone or angiography and angioplasty. Participants will be followed for 5 years.
Coronary artery disease is a leading cause of morbidity and mortality in our society. It is
initiated by the dysfunction of the lining of coronary arteries. Such endothelial dysfunction
permits vascular wall inflammation, smooth muscle cell proliferation, and thrombosis, which
progresses to coronary artery stenosis and occlusion, and manifests as myocardial ischemia
and infarction. Endothelial injury can be due to the damaging effects of various
cardiovascular risk factors and it can also be induced by balloon injury associated with
coronary angioplasty. Damaged endothelium can be repaired via endogenous mechanisms, such as
by the migration and proliferation of neighboring uninjured mature endothelial cells, or by
the mobilization and homing of bone-marrow-derived circulating endothelial progenitor cells
(EPCs).
There are several repair mechanisms that are now thought to involve circulating endothelial
progenitor cells that are mobilized from the bone marrow and home to sites of endothelial
injury. The researchers of this study hypothesize that aging is associated with reduced
vascular injury induced endothelial progenitor cell activity, resulting in impaired vascular
repair and increased coronary heart disease events. Patients with stable coronary artery
disease will be enrolled in this study. They will undergo either angiography alone or
angiography and angioplasty. Venous blood will be collected immediately prior to the
procedure and 20-24 hours after the procedure. The number of endothelial progenitor cells
will be assessed based on their ability to form colonies and also to migrate under the
influence of certain growth factors. These values will be compared between both samples.
Study participants will also be contacted at 6 months, and 2 and 5 years after their
participation in the study. The clinical outcomes of the participant's coronary artery
disease will be correlated with the number of endothelial progenitor cells.
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