IVUS max

Despite numerous clinical studies detailing improved clinical outcome using IVUS to guide PCI, its use has remained infrequent. Many of us have wondered why. Perhaps IVUS gave us too much information: beyond angiography, beyond measurements, we could actually interrogate the vessel wall. However, short of crushing, grinding, or cutting the plaque, we didn’t know what else to do with this information. So, why bother? Fast-forward to the era of the vulnerable patient, the vulnerable plaque, local and systemic antiatherogenic drugs. Fast-forward to ‘‘IVUS-max’’: accurate dimensions and plaque composition from a single IVUS run. Rodriguez-Granillo et al. [1] describe a basic validation study employing Virtual Histology IVUS (IVUS-VH), a technique that analyzes not only the IVUS radiofrequency amplitude, but also backscatter frequency domain. The correlation with amplitude-based traditional gray-scale imaging is excellent after correction for imaging sheath-induced ultrasound distortion. Such a validation means that IVUS-VH could be used to quantify the volume of particular atheromatous components in a given segment of artery. While we can still use IVUS to measure for stent sizes and treat the culprit hemodynamically significant lesion, we can also use IVUS-VH to evaluate the remaining artery for vulnerable plaque. As interventional physicians become increasingly aware of the systemic nature of atherosclerosis, the ability to target nonculprit lesion therapy based on objective information is useful. Many years ago, our group described a rough correlation of certain gray-scale lesion patterns with clinical presentation [2]; however, more recently, both IVUS [3] and optical coherence tomography [4] have more carefully detailed the nature of ruptured plaques in patients with unstable and stable clinical presentations. It is clear that unstable patients often have additional ruptured plaques or thin-cap vulnerable plaques distant from the culprit lesion. Rioufol et al. [5] recently demonstrated that 50% of these nonculprit ruptured plaques heal within 2 years, whereas 50% remain persistently ulcerated but clinically stable on oral antithrombotic and statin therapy. These lesions have already degenerated at the time of first study. What of the nonruptured but potentially vulnerable plaque? To date, we have only inferential data; however, registries are ongoing to assess the natural history of IVUS-defined plaque morphology and clinical outcome. Some insight on this question is provided by a recent database review from the NHLBI Dynamic registry. In that review of incidental nontarget lesions seen at index PCI [6], nearly 6% of all patients represented for a clinically indicated nontarget lesion PCI within 1 year. More importantly, 59% presented with unstable angina and 9.3% with a nonfatal myocardial infarction. The ability to identify which incidental lesions might lead to a future acute coronary syndrome would be most welcome. Our ability to alter the progression and stability of coronary atheroma with aggressive statin use is seen in the complementary REVERSAL [7] and PROVE-IT [8] studies. Atheroma progression was significantly retarded and clinical event rates lower in the aggressive statin group. In the LACMART trial [9], plasmapheresis in patients with familial hypercholesterolemia actually resulted in atheroma reversal. The smaller GAIN study [10], using a similar statin regimen, demonstrated increased plaque echogenicity after 12 months of therapy, suggesting plaque compositional changes may be detectable. While much groundwork remains before this approach can be recommended, a new paradigm of culprit lesion treatment followed by IVUS-VH screening for vulnerable plaques followed by aggressive pharmocotherapy (possibly locally delivered, possibly systemic) seems plausible. Perhaps this paradigm would give us reason to ‘‘bother’’ with ultrasound once again. The Rotterdam group is to be commended for pushing the envelope and encouraging us to think beyond the donut hole.