For more information EECP Study Contact at AHA215-759-0103 (pager)
ContactTony Peacock, Vasomedical, Inc.908-500-4403
EECP therapy may generate a new blood supply in the diseased heart
(Westbury, NY, November 12) New research presented at the American Heart Association's Scientific Sessions 2001 conference provides further evidence that EECP therapy stimulates the release of angiogenic factors, and offers hope of noninvasive treatment based on rejuvenating circulation in the diseased heart.
Angiogenesis is the formation and growth of new blood vessels. Examples of angiogenesis include capillary proliferation in the healing of wounds or new vessel growth along the borders of myocardial infarction scars. The process stimulates growth of new capillaries in response to inflammatory reactions or to increased shear forces such as those that may occur in vessels proximal to a stenosis. Collateral vessel creation and growth may therefore; take place in response to severe coronary artery stenosis but ischemia itself may not be the key stimulus in initiation of the angiogenic response. Reactions to shear stress, however, include the expression of several growth factors that modulate structural changes in the vessels. These changes are complemented by the activation of other pathways that affect the actin cytoskeleton and lead to endothelial cell migration. Increased shear stress at the site of native reserve vessels is also thought to trigger maturation of these vessels; a process called "vasculogenesis".
Diastolic augmentation produced by EECP therapy, is believed to increase pulsatile shear stress on the intima. An increase in endothelial cell surface shear stress releases biochemical factors that trigger and control growth processes. In the study presented at the current Scientific Sessions, EECP therapy was found to produce an increase in three angiogenic factors in treated patients: HGF by 26.6 percent, bFGF by 18.8%, and VEGF by 15.6%.
This new, independent study strengthens previous research suggesting that mechanism by which EECP produces long-term benefit, is by increasing the formation of collateral vessels. During treatment, EECP therapy raises the pressure gradient between ischemic and non-ischemic regions of the heart. It is hypothesized that, at the same time, endothelial cell-mediated vessel growth factors expressed as a result of EECP-induced stimulation, render the vessels permanently functional. These changes may underlie improvement in myocardial perfusion and exercise tolerance reported in earlier studies of EECP therapy.
This same study also found, EECP therapy improved both myocardial perfusion at rest, and coronary flow reserve, (CFR), measured quantitatively with 13N-ammonia positron emission tomography (PET). Additionally nitric oxide levels were doubled by 1 month post-treatment, although the change was not statistically significant. Nitric oxide is a potent vasodilator, which, like growth factors, is also expressed by endothelial cells in reaction to shear stress.
For additional information or to interview the Principle Investigator and patients, please contact [email protected]. or see eecp.com.
Vasomedical, Inc. designs, manufactures, and, supports external counter pulsation systems based on the Company's proprietary technology currently indicated for use in cases of angina, cardiogenic shock and acute myocardial infarction.
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