And Now, Even the Stent Mongers are Starting to GET It!
Posted Aug 26 2008 4:32pm
Let's make this clear yet again. Needing a stent, any stent, is a prevention failure. But, they are effective life-savers once you are "over the edge." Perhaps the COURAGE trials (which showed that non-interventional therapy was as effective as inteventional therapy for non-acute heart disease sufferers) has helped pushed technology in the right direction.
The TRIAS HR study has shown that the new Genous R stent to be as or more effective in patients at high risk for restenosis than paclitaxel drug-eluting stents. What is noteworthy about the Genous stent is that it has been bioengineered with a coating that attracts Endothelial Progenitor Cells (EPCs). The idea is that the stent will form a natural endothelial lining similar to healthy arteries. Recall that it is the one-cell thick endothelial lining that regulates artery dilation (by producing nitric oxide) and provides a protective barrier. Once that lining is compromised the atherosclerotic process begins.
Of course, this whole area of innovation begs the question, "Can a method be devised to get EPCs to damaged endothelial sites BEFORE lesions become acute and require a stent?" If so, you might be talking about a REAL cure to heart disease before too long!
Given that hearts in my family are genetically predisposed to fail at age 65, that gives them about 13 years to figure it out.
Let's make this clear yet again. Needing a stent, any stent, is a prevention failure. But, they are effective life-savers once you are "over the edge." Perhaps the COURAGE trials (which showed that non-interventional therapy was as effective as inteventional therapy for non-acute heart disease sufferers) has helped pushed technology in the right direction.
The TRIAS HR study has shown that the new Genous R stent to be as or more effective in patients at high risk for restenosis than paclitaxel drug-eluting stents. What is noteworthy about the Genous stent is that it has been bioengineered with a coating that attracts Endothelial Progenitor Cells (EPCs). The idea is that the stent will form a natural endothelial lining similar to healthy arteries. Recall that it is the one-cell thick endothelial lining that regulates artery dilation (by producing nitric oxide) and provides a protective barrier. Once that lining is compromised the atherosclerotic process begins.
Of course, this whole area of innovation begs the question, "Can a method be devised to get EPCs to damaged endothelial sites BEFORE lesions become acute and require a stent?" If so, you might be talking about a REAL cure to heart disease before too long!
Given that hearts in my family are genetically predisposed to fail at age 65, that gives them about 13 years to figure it out.
Stay tuned,
HeartHawk