This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Crottogini, A. Articles by Laguens, R. Search for Related Content PubMed PubMed Citation Articles by Crottogini, A. Articles by Laguens, R.

(Circulation Research. 2007;100:e58.)
© 2007 American Heart Association, Inc.

Letter to the Editor

VEGF165 Gene-Mediated Arteriogenesis and Cardioprotection in Large Mammals With Acute Myocardial Infarction. Confirmation of Previous Results From Other Authors

Alberto Crottogini, Rubén Laguens

Departments of Physiology and Pathology, Favaloro University, Buenos Aires, Argentina

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

In a recent article, Ferrarini et al¹ report that direct intramyocardial transfer of the human vascular endothelial growth factor (VEGF) 165 gene in dogs with acute myocardial infarction exerts a beneficial effect by enhancing both arteriologenesis and cardiomyocyte viability in the infarcted myocardium.

With regard to the arteriogenic effects of the VEGF gene in large mammalian models of ischemic heart disease, we have previously demonstrated that the direct intramyocardial injection of a plasmid encoding human VEGF165 in pigs with Ameroid-induced circumflex artery occlusion² (a model which combines myocardial infarction with peri-infarct ischemia) promotes a remarkable proliferation of arterioles measuring 8 to 50 um in diameter.

In addition to this effect, VEGF165 gene substantially increased the mitotic index of adult cardiomyocytes³ and induces cardiomyocyte hyperplasia⁴ at 35 days posttreatment. So, the supposition of Ferrarini et al that "... VEGF might have an effect on resident cells, either by protecting the differentiated cardiomyocytes from apoptosis or by promoting their proliferation", is likely true.

Moreover, in a study published concomitantly with Ferrarini’s article (and therefore not available at the time of resubmission), we showed that in sheep with acute myocardial infarction, in addition to the increase in adult cardiomyocyte mitosis, VEGF165 gene transfer increased the number myoblasts in the peri-infarct zone⁵ at 10 days after occlusion. Most of these precursors were undergoing mitosis and even cytokinesis. Consequently, Ferrarini’s speculation that "VEGF might have a role in the recruitment or activation of a putative population of cardiac stem cells, which could . . . [Full Text of this Article]