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J Am Coll Cardiol, 2008; 51:1323-1324, doi:10.1016/j.jacc.2007.11.066 © 2008 by the American College of Cardiology Foundation |
* Department of Cardiology, John Radcliffe Hospital Headley Way, Headington, OX3 9DU, Oxford, United Kingdom (Email: Adrian.Banning{at}orh.nhs.uk).
In our opinion, these studies have a number of limitations. Kawaguchi et al. (1) chose ST-segment re-elevation immediately after stent implantation as a proxy for embolization. This parameter has not previously been linked to the more recognized end points of myocardial blush grade or 90-min ST-segment resolution (3). Additionally, the limited ability of the 20-MHz Eagle Eye IVUS catheter (Volcano Therapeutics, San Diego, California) to identify luminal thrombus may be particularly relevant in their patients who received only aspirin as a procedural antiplatelet therapy. Moreover, the possibility of side branch occlusion during stent deployment as a cause of myocardial necrosis does not appear to have been considered. In patients with stable angina, Kawamoto et al. (2) suggested that plaques with larger necrotic cores were more likely to exhibit high-intensity transient signals detected by a Doppler guidewire. Histopathological correlates between VH-IVUS and pathology are questionable, and neither study uses post-procedure IVUS imaging of residual plaque. Using 40-MHz IVUS imaging, a direct relationship has been demonstrated between the change in plaque volume and evidence of new myocardial necrosis (4). Thus, although it is perhaps intuitive that friable plaque elements are more likely to be liberated than are more readily compressed fibrotic components, further investigation is required.
In the accompanying editorial, Shah (5) questions whether no reflow is merely a marker of myocardial injury or whether it is the cause of further myocardial damage. There is currently no data to support the notion that, in established no reflow, administration of any pharmacologic agent has any impact on subsequent prognosis, and perfusion in areas of new myocardial necrosis remains impaired for at least 24 h despite normal perfusion in viable areas of myocardium subtended by the same vessel (6). These data suggest that no reflow is predominantly a marker of downstream myocardial necrosis. As more diffuse and challenging diseases are being tackled by percutaneous coronary intervention (PCI), further research into the prevention of plaque embolization is essential to allow further improvement in PCI outcomes.
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