Analysis of Radiofrequency Ultrasound Signals: Tissue Characterization With Virtual Histology and Palpography

Introduction

Ischemic heart disease often presents as an acute coronary syndrome (ACS), even in patients with prior percutaneous treatment of a flow-limiting stenosis (Glaser et al., 2005). Pathological substrate for an ACS is a (sub)occlusive thrombus filling the lumen which might stem from a segment of atherosclerotic coronary artery showing mild or borderline stenosis (often with complex morphological pattern) on a previous angiogram (Ambrose et al., 1986; Goldstein et al., 2000). These fragile (prone to rupture) foci of the coronary wall causing subsequent events(Falk, Shah, & Fuster, 1995) have been attributed as “vulnerable plaques” (VP) (Naghavi et al., 2003) and identified as “thin-cap fibroatheromas” (TCFA) as a major substrate by pathologists(Virmani, Burke, Farb, & Kolodgie, 2006). Coronary artery disease (CAD) is a diffuse atheromatosus process of the epicardial coronary arteries (sometimes also with flow-limiting stenoses or multiple ruptures(Goldstein et al., 2000)). Accordingly, the number of these VPs (manifesting in non-flow limiting stenosis) might be numerous(Rioufol et al., 2002) and they present variable with time (as acute worsening is related to actual inflammatory alterations)(Goldstein et al., 2000; Libby & Theroux, 2005). These notions may render efforts identification of a VP (before rupture!) in the catheterization laboratory a mission hard to accomplish(Ambrose, 2008). Pathological, imaging and clinical findings demonstrated that occlusive coronary thrombi tend to cluster in the proximal segments of coronary arteries(Wang, Normand, Mauri, & Kuntz, 2004) and pathology study showed TCFAs limited in number(Cheruvu et al., 2007) make the hunt for VP timely identification justified. Moreover, traditional secondary preventive measures are limited in efficacy(Libby, 2005) and local treatment may well prove to be effective in the (near) future(Ramcharitar et al., 2009).