Circulating endothelial progenitor cells in patients with unstable angina: association with systemic inflammation

Abstract

Patients with unstable angina and no evidence of cardiac necrosis exhibited increased circulating EPCs. Systemic inflammation, in addition to recognised growth factors, could play a role in the peripheral mobilisation of EPCs in patients with anginal syndromes.

Level of CD14+-endothelial progenitor cells is not associated with coronary artery disease or cardiovascular risk factors

“…In addition, the level of EPCs in that study did not vary significantly with cardiovascular risk factors. George et al ( 2004) found higher number of EPC colonies in patients with UA as compared with stable angina. Massa et al (2005) showed that the number of CD34 + KDR + cells in the blood was increased in patients with acute MI compared with healthy controls or patients with stable CAD.…”

“…To date there is no uniform method or criteria for defining an EPC despite extensive research activity. Some methods of characterization are based on in vitro behavior, including the ability to form endothelial colonies with the incorporation of acetylated low-density lipoprotein and binding of lectins (Vasa et al 2001;Hill et al 2003;George et al 2004;Güven et al 2006). The majority of acetylated LDL (+) lectins (+) cells express monocyte/macrophage markers such as CD14, and a much lower percentage of cells express CD133 (Rehman et al 2003).…”

“…It follows that the number of circulating EPCs may reflect the "vascular health" of an individual, and thus represent a marker by which to assess cardiovascular disease risk. However, the lack of a uniform EPC definition complicates cross-study comparisons and may contribute to the apparent paradox of some studies that suggest that EPCs are reduced in the presence of cardiovascular risk factors and coronary artery disease (CAD) (Vasa et al 2001;Hill et al 2003;Schmidt-Lucke et al 2005), whereas others suggest that numbers are increased in those with obstructive CAD (George et al 2004;Massa et al 2005;Güven et al 2006).…”

“…More importantly, there are data indicating that the vast majority of EPCs actually arise from the CD14 + subpopulation of peripheral blood mononuclear cells (PBMCs) (Rehman et al 2003;Gulati et al 2003;Romagnani et al 2005). However, previous studies focusing on the relationship between either CAD or cardiovascular risk factors and the level of EPCs either did not distinguish between the two types of EPCs (Vasa et al 2001;Hill et al 2003;George et al 2004) or studied only CD34 + -EPCs (Schmidt-Lucke et al 2005;Massa et al 2005). Therefore, the question of whether the level of CD14 + -EPCs correlates with either CAD or cardiovascular risks remains unresolved.…”

Working hypothesis to redefine endothelial progenitor cells

“…Later studies demonstrated that the concentration of CFU-ECs was decreased in patients with type I diabetes, 48 chronic obstructive pulmonary disease, 49 congestive heart failure, 50 and rheumatoid arthritis. 51 However, some studies have contradicted the trend of lower numbers in disease susceptibility; CFU-EC concentration has been shown to be significantly increased in patients with unstable angina, 52 at the time of myocardial infarction (MI), 53 and within 7 days of an acute MI. 54 Thus, evidence points to reduced CFU-EC concentration in patients at risk for vascular disease, and increased during acute cardiovascular stress.…”