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Circulation Research. 2003;92:e60
doi: 10.1161/01.RES.0000067466.48892.EC
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(Circulation Research. 2003;92:e60.)
© 2003 American Heart Association, Inc.


Letter to the Editor

Physical Training and Restenosis

Michael Ward

Department of Cardiology, Royal North Shore Hospital, Department of Cardiology, St Leonards, New South Wales, Australia, mrward@doh.health.nsw.gov.au


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

To the Editor:

I read with interest the article by Indolfi et al in the December 13, 2002, issue of Circulation Research entitled "Physical Training Increases eNOS Vascular Expression and Activity and Reduces Restenosis After Balloon Angioplasty or Arterial Stenting in Rats" in which the authors show that regular exercise reduces neointima formation after stenting and balloon angioplasty and also inhibits negative remodeling after balloon angioplasty.1 They concluded that the benefits of exercise were attributable to enhanced eNOS activity. I have some doubts on this conclusion.

First, the differences in neointima formation, remodeling, and reendothelialization could at least in part be explained by the effects of exercise on these vessels before the injury. Exercise training started 14 days before the balloon or stent injury and if this significantly increased vessel size prior to the injury, then the amount of injury created by standard techniques would be significantly reduced in the larger vessel. Data from the operated vessels 2 days after injury showed that there was little if any increase in external elastic lamina (EEL) area in the uninjured vessel, which is reassuring that the injured vessel was unlikely to be bigger 2 days prior. In studies of physiological remodeling, permanent change in arterial size is apparent 7 days after changes in flow,2 so any measurements of carotid blood flow (CBF) at varying time points after exercise training would be useful in discerning whether 14 days of training is required to result in sustained increases in CBF.

Second, the site of . . . [Full Text of this Article]

Ciro Indolfi

Division of Cardiology, Department of Clinical and, Experimental Medicine, Magna Graecia University, Catanzaro, Italy, indolfi@unicz.it

Daniele Torella

Division of Cardiology, Federico II University, Naples, Italy