Why the study?
Does percutaneous transluminal coronary angioplasty induce the release of vasoactive substances and markers of endothelial injury compared to diagnostic angiography in patients with ischemic heart disease?
Does percutaneous transluminal coronary angioplasty induce the release of vasoactive substances and markers of endothelial injury compared to diagnostic angiography in patients with ischemic heart disease?
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PTCA induces coronary endothelial injury, reflected by the release of ET-1, ANG II, and vWF into the coronary sinus, regardless of the specific interventional modality used.
Endothelial injury plays critical roles in acute and chronic complications after percutaneous transluminal coronary angioplasty (PTCA). We investigated coronary endothelial injury and the release of vasoactive substances induced by PTCA. We examined 44 patients with ischemic heart disease who underwent elective PTCA to isolated stenotic lesions in left coronary arteries. Eleven patients received balloon angioplasty (BA), 14 percutaneous transluminal rotational atherectomy (PTRA), and 19 stent implantation. Blood samples were drawn from the coronary sinus immediately before and after as well as 4 hr and 24 hr after PTCA. Plasma levels of endothelin (ET) 1, angiotensin (ANG) II, von Willebrand factor (vWF), and thrombomodulin (TM) were measured. Seven control subjects who underwent diagnostic coronary angiography (CAG) were used as controls. In all patients, ET-1 levels in the coronary sinus blood significantly increased immediately after PTCA. ANG II levels and vWF activity showed significant increases 4 hr after PTCA. Changes in levels of these markers were similar among the BA, PTRA, and stent groups. TM levels were elevated in all groups of patients, including those simply undergoing diagnostic CAG. Changes in ET-1, ANG II, and vWF levels in the coronary sinus reflect coronary endothelial injury induced by PTCA.
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Hojo et al. (2000) studied this question.
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