Abstract
Although algorithms such as the Framingham Risk Score have been instrumental in helping to stratify cardiovascular disease (CVD) susceptibility, it is estimated that 15% to 20% of patients presenting with myocardial infarction (MI) may lack any history of traditional risk factors.1 These and other observations have prompted investigators to develop additional biological and genetic assays that might improve risk prediction or capture risks that might be orthogonal to well-known and traditional factors such as diabetes, smoking, hypercholesterolemia, and hypertension. One promising but confusing area appears to be the interrogation of circulating cells that have been deemed endothelial progenitor cells (EPCs). In some studies, the levels of these circulating cells appear to provide predictive power about vascular function in healthy people2,3 and future cardiovascular events in patients with disease.4,5 It is tempting to speculate that the quantitative or functional assessment of cells in the circulation with angiogenic or vascular reparative properties might eventually provide a useful biological measurement that could aid in risk assessment. Yet, significant questions remain regarding the true nature of EPCs and the actual role of these cells in disease progression.6 Answers to these and related questions are therefore urgently needed before the tantalizing promise of EPCs can be fully incorporated into any assessment of CVD risk. Article see p 296 The current report by Shaw et al7 in this issue of Circulation: Cardiovascular Genetics provides an elegant blueprint of how a combined biological and genetic approach might aid in our efforts to better understand EPC biology and ultimately better define and understand CVD risk. The current study analyzed nearly 1800 participants in the Framingham Heart Study. For the most part, these individuals were healthy and free of overt CVD. The authors performed a simple biological assay to determine …
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