[Ultrasound coronary angioplasty: state of the art and new clinical aspects].

Therapeutic ultrasound was shown to ablate thrombi and to disrupt atherosclerotic plaques in vitro and recently to recanalize occluded coronary arteries in acute myocardial infarction (AMI). The goal of this article is to update collective experience and to weigh the promising and unresolved aspects of this newly developed technology and its clinical results. As therapeutic ultrasound was for long known a synonym for lithotripsy of calculi diseases, it lastly received high attention as a catheter-based ultrasound method to ablate thrombi and disrupt atherosclerotic plaques in interventional cardiology (Figure 1). The effect of therapeutic ultrasound to ablate selectively pathological tissue depends on its bioselectivity for elastic fibers: After ultrasound sonication, healthy tissue-rich in elastin and collagen-including arterial wall remains intact whereas thrombus and plaque with their minimal elastic support are found to be highly susceptible to ablation. Our catheter for coronary ultrasound thrombolysis (Figure 2) consists of a solid metal probe and is connected to a piezo-electric transducer at its proximal end. The distal part ends in a three-wire flexible segment with a 1.6 mm tip ball to guarantee maximal wire flexibility and optimal transmission of ultrasound energy. The initial in vitro studies resulted in a fundamental understanding of the destructive effect of ultrasound on tissue based on 4 factors: mechanical vibration, thermal effects, microcurrents, and cavitation. The first studies on human peripheral vessels were published in 1991 being performed during femoral bypass surgery on occluded and partially obstructed arteries. The procedure was performed without perforation, no adverse side effects emerged, restenosis rate was 20%. The clinical application of coronary ultrasound angioplasty was initiated in 1991; Siegel published his data on 44 patients. In his study, 30 patients with chronic atherosclerotic occlusive lesions and 14 with unstable or stable angina or AMI were treated by ultrasound angioplasty. Residual stenosis after ultrasound treatment was 71%, after balloon dilation reduced to 34%. In the 6-month follow-up angiograms showed no major adverse effect or restenosis. Our experience with coronary ultrasound thrombolysis (CUT) is based on the analysis of 33 patients' data in the feasibility (Table 1) plus multicenter phase of the ACUTE trial (Analysis of Coronary Ultrasound Thrombolysis Endpoints) (Figure 3). Our patients were exclusively treated for AMI by ultrasound angioplasty and afterwards by PTCA if required (Figure 4). The average final percent stenosis was 20% (Figure 5). The main efficacy parameters, device success and angiographic success rates were 100%, clinical success rate was 91.7% (Figure 6 and Table 2). The adverse clinical events of CUT are limited--at least in our studies--to reocclusion of infarct-related artery and ischemia and could be reversed by additional PTCA. No adverse clinical side effects were observed during sonication of the coronary tree. Final angiography revealed residual stenosis of 20% without morphological signs. These excellent results suggest that bioselectivity of ultrasound together with the developed skills of the catheter system induces rapid and selective thrombolysis with no need to cross the target lesion before sonication. But what is the better solution for thrombosis and which for plaque disruption? The development of transluminal balloon catheter really modified therapeutic approach to obstructive coronary and peripheral arterial disease but it is still accompanied by a high rate of abrupt closure, AMI and death. Although the use of intravenous thrombolytic agents is well established in the treatment of AMI and these agents are widely used, a large patient collective remains (up to 33% and more) in whom their use is inadvisable due to recent stroke, surgery, trauma or other contraindications. (ABSTRACT TRUNCATED)