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Cardiovascular Research 2001 49(3):582-587; doi:10.1016/S0008-6363(00)00246-7
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Transepicardial or transendocardial injury: controversies regarding angiogenic potential and mechanism of action

Shmuel Fuchs and Ran Kornowski*

The Cardiovascular Research Institute, Medlantic Research Institute, Washington Hospital Center, 110 Irving St. NW, 4B-1 Washington, DC 20010, USA

* Corresponding author. Tel.: +1-202-877-3321; fax: +1-202-877-2715 rxk3@mhg.edu

Received 29 June 2000; accepted 15 September 2000

KEYWORDS Angiogenesis

The first 150 words of the full text of this article appear below.


   1 Introduction
 
Over the past decade, surgical and now catheter-based approaches using various mechanical devices and energy sources aimed to enhance tissue perfusion are being explored as new adjunctive therapies in patients with refractory ischemic coronary disease [1,2]. It has been suggested that the likely mechanism associated with the initiation of angiogenesis is the induction of local inflammatory processes, and that tissue changes trigger endogenous expression of variety of angiogenic cytokines acting in concert to initiate and maintain microvessel formation (i.e. angiogenesis) [3]. The improved collateral pathways may change the local ischemic milieu in a way that may culminate in a long-standing therapeutic effect in selected patients. Since angiogenesis was assumed to be a primary mechanism associated with ‘direct’ myocardial revascularization (DMR) procedures, it has been termed ‘the mechanical approach for myocardial angiogenesis’. Nevertheless, the evidence for a therapeutically significant angiogenesis following mechanical myocardial injury is inconclusive.

In the current . . . [Full Text of this Article]

1.1 Myocardial tissue responses to mechanical injury
1.1.1 Laser energy
1.1.2 Radiofrequency energy
1.1.3 Mechanical myocardial channeling
1.1.4 Needle insertion

   2 Immunohistochemistry assessment
 

   3 Physiological assessment of collateral perfusion
 

   4 Perfusion changes following clinical direct myocardial revascularization
 

   5 Local cardiac denervation mechanism
 

   6 Combined mechanical and angiogenic therapy
 

   7 Conclusions
 

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