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STATE-OF-THE-ART PAPER

A Critical Review of Clinical Arteriogenesis Research

Niels van Royen, MD, PhD^_*,_*, Jan J. Piek, MD, PhD^_*, Wolfgang Schaper, MD and William F. Fulton, MD

^_* Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
Max Planck Institute for Physiological and Clinical Research, Department of Experimental Cardiology, Bad Nauheim, Germany
Materia Medica and Therapeutics, University of Glasgow, Glasgow, Scotland

Manuscript received March 12, 2009; revised manuscript received June 5, 2009, accepted June 29, 2009.

^_* Reprint requests and correspondence: Dr. Niels van Royen, Department of Cardiology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands (Email: n.vanroyen{at}amc.uva.nl).

In human hearts, an extensive pre-existing collateral network is present. This was shown unequivocally some 50 years ago in a series of very detailed post-mortem angiographic studies. In these studies, it was also observed that the pre-existent collateral vessels enlarge upon closure of an epicardial coronary artery, resulting in large collateral conduit arteries, in sharp contrast to earlier claims that human coronary arteries are functional end arteries. These insights still form the basis for the concept of arteriogenesis as positive remodeling of pre-existent arteriolar connections. Subsequent experimental studies disclosed the putative role of circulating cells, especially monocytes, which invade the proliferating vessel wall and secrete growth factors, degrading enzymes and survival factors that are required for the development of a mature collateral circulation. Experimental stimulation of arteriogenesis is feasible but to date a relatively low number of clinical studies, with no or limited success, have been performed. The use of intracoronary derived collateral flow index can increase the sensitivity to detect the effects of pharmacological compounds on arteriogenesis, which is important in first proof-of-principle studies. These invasive measurements also allow the detection of patients with an innate defect in their arteriogenic response to coronary obstruction. In a reversed bedside-to-bench approach, the characterization of ribonucleic acid and protein expression patterns in these patients generated new targets for therapeutic arteriogenesis.

Key Words: arteriogenesis • collateral circulation • angiogenesis • intracoronary hemodynamics • genomics

Abbreviations and Acronyms   CFIp = pressure-derived collateral flow index   FGF = fibroblast growth factors   GM-CSF = granulocyte-macrophage colony-stimulating factor   LAD = left anterior descending artery   LCx = left circumflex artery   MCP = monocyte chemotactic protein   RCA = right coronary artery

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J. Am. Coll. Cardiol. 2010 55: A40. [Full Text] [PDF]