INTRACORONARY ULTRASOUND - THE NEW GOLD-STANDARD

Intravascular ultrasound (IVUS) has evolved to a research tool to an i ntrinsic part of modern invasive cardiology. The main reason is the ca pability to obtain ''in-vivo'' micro anatomy by means of miniaturized echo-transducers with an outer diameter of 2.9-3.5 French. For the fir st time it is possible to base decisions not only on lumenograms but a lso on vessel wall assessment. The capabilities of IVUS can be divided in its diagnostic and intervention associated potentials. The diagnos tic strength of IVUS is the ability to monitor compensatory coronary a rtery enlargement as a response to arteriosclerosis, to assess interme diate lesions, to reveal occult left main stem disease, and angiograph ically ''silent'' arteriosclerosis. In conjunction with the estimation of intracoronary flow reserve, patients with the diagnosis of coronar y ''syndrome X'' can be better classified into those with or without e arly signs of arteriosclerosis. Additionally, IVUS is at present the o nly method allowing the classification of coronary artery lesions acco rding to the AHA/ACC Stary classification.The intervention associated potentials of IVUS are the ability to allow optimal device selection, i.e. rotablators in calcified lesions or atherectomy devices in large plaque burden. The effects of PTCA on vessel wall morphology can be st udied in great detail and the effect on luminal gain can be assessed a lmost on-line. The correlation between IVUS and angiography for estima tion of luminal dimensions is inferior, because angiography is not abl e to describe complex luminal geometries. Several groups showed that t he residual plaque area even after angiographically successful PTCA li es still in the range of 60 %. A significant reduction of this number may influence long-term outcome after PTCA. Minimal luminal areas and residual plaque area after PTCA seem to be an indicator of restenosis, while the presence or absence of dissections seem to be less predicti ve. Additionally, the main mechanism of restenosis after PTCA is vesse l shrinkage, not intimal hyperplasia. Intravascular monitoring of sten t expansion led to high-pressure stent deployment with significant inc rease in post-procedural luminal diameters and finally the ability to withhold anticoagulation in patients with optimal stent deployment and to lower subacute stent thrombosis rates. First results for IVUS guid ed PTCA show a superior gain in post procedural free lumen without an increased complication rate. In the future, integrated devices, like b alloons on IVUS catheters, steerable catheters, integrated flow and pr essure transducers, tissue characterisation, and 0.018 inch IVUS guide wires will further enhance the usefulness of IVUS.