doi: 10.1161/CIRCRESAHA.109.201376
© 2009 American Heart Association, Inc.
Editorials |
Limits to Growth of Native Collateral Vessels
Just One Mouse CLIC Away From Unlimited Collateral Perfusion?
From the Department of Cardiology, Maastricht University Medical Centre and Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands.
Correspondence to Johannes Waltenberger, MD, PhD, Department of Cardiology, Maastricht University Medical Centre, P. Debyelaan 25, POB 5800, 6202 AZ Maastricht, The Netherlands. E-mail j.waltenberger@mumc.nl
See related article, pages 89–98
Key Words: collaterals • arteriogenesis • genetics • vascular endothelial growth factor
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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The presence of a functional collateral circulation can have great importance for clinical symptoms as well as for clinical decision making. When experiencing an acute myocardial infarction, most patients have severe symptoms, call for emergency, and are treated rapidly and effectively given a functioning infrastructure for primary percutaneous coronary interventions. In contrast, other individuals experience few symptoms, and some may not even notice their infarction.
One possible explanation for the attenuated symptoms in the second group of patients is the presence of functional coronary collateral vessels, which are capable of supplying significant amounts of blood into an otherwise completely ischemic myocardium. In fact, the significant variability of native collateral conductance in humans is well established.1 Moreover, the genetic background had been identified as a denominator of the presence of collateral vessels in mice as different mouse strains show major differences with regard to the presence of collaterals.2,3
The study by Chalothorn et al, published in this issue of Circulation Research,4 provides a potential explanation for the interindividual variability of the presence of functional collateral vessels. In fact, data from both the peripheral circulation (hindlimb model), as well as from the cerebral circulation of a mouse model support the idea that the absence of the CLIC4 gene, ie, the gene encoding chloride intracellular channel-4, is related to the presence of fewer (approximately one-third) collateral vessels in adult mice. Likewise, the diameter of the collaterals was slightly (roughly 30%) reduced. Of interest, hemizygous CLIC+/– mice showed an intermediate phenotype with regard
Related Article:
Circ. Res. 2009 105: 89-98.