Slow-Flow Phenomenon Caused by Distal Embolization Should Be Predicted and Prevented to Maximize the Efficacy of Coronary Intervention
論文ID: CJ-23-0702
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論文ID: CJ-23-0702
Percutaneous coronary intervention (PCI) by either balloon dilatation or stent implantation sometimes causes distal embolization of plaque debris, which causes the slow-flow phenomenon and periprocedural myocardial infarction (MI). The latter deteriorates left ventricular function and can be a cause of future heart failure. Therefore, distal embolization caused by PCI should be prevented to maximize the treatment effect of PCI. Embolic protection devices (EPD) have been developed and can now be used in the daily practice of PCI. However, their use is not recommended in guidelines in general.
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EPD were demonstrated as effective at preventing distal embolization during PCI of the saphenous vein graft by the Saphenous Vein Graft Angioplasty Free of Emboli (SAFER) trial.1 However, the Enhanced Myocardial Efficacy and Recovery by Aspiration of Liberated Debris (EMERALD) trial showed that EPD were not effective in the PCI of acute MI (AMI) patients in general.2 An imaging study using angioscopy reported that EPD were effective in AMI patients with angioscopically defined ruptured plaque,3 and recently, the Vacuum Aspiration Thrombus Removal 3 (VAMPIRE 3) trial4 demonstrated that EPD were useful in acute coronary syndrome (ACS) patients with a culprit lesion of attenuated plaque ≥5 mm longitudinal length on intravascular ultrasound (IVUS). The most important limitation for the use of EPD is that we do not know who benefits among all the patients who undergo PCI. In other words, there is no reliable method of selecting patients at high risk of distal embolization/slow-flow phenomenon/periprocedural MI.
Theoretically, PCI of lesions with a large embolic source (i.e., large lipid-rich plaque) would be a high-risk procedure in which an EPD may be beneficial. Coronary computed tomography angiography can non-invasively identify the high-risk lesions for plaque debris embolization such as low-attenuation plaques with positive remodeling.5 Angioscopy demonstrates the embolic source as a massive ruptured yellow plaque, but detection by IVUS is not as easy. Furthermore, quantitative evaluation of the embolic source has not been reliably achieved by these imaging modalities.
Near-infrared spectroscopy (NIRS) was developed to quantitatively and more easily evaluate the lipid-rich plaques detected by angioscopy as yellow plaques.6,7 Furthermore, the NIRS catheter can be combined with IVUS for use in the daily practice of PCI. Quantitative evaluation of lipid-rich plaque by NIRS with a lipid core burden index (LCBI) maximum 4 mm (maxLCBI4mm) correlates well with the yellow color grade of the plaque on angioscopy.8 The maxLCBI4mm is a marker of vulnerable plaques, and identified high-risk plaques and patients for future events in the Lipid-Rich Plaque (LRP) study.9 Multiple studies have demonstrated the association between lipid-rich plaque detected by NIRS and the slow-flow phenomenon/periprocedural MI/microvascular obstruction in both chronic coronary syndrome (CCS) and ACS patients10–14 (Table).
Detection of High-Risk Lesions of Distal Embolization Using NIRS
| Name of investigator | No. ACS lesions |
No. CCS lesions |
Endpoint for distal embolization |
|---|---|---|---|
| James A. Goldstein (COLOR Registry)10 | 17 | 45 | Periprocedural MI |
| Gregg W. Stone (CANARY Trial)11 | 52 | 33 | Periprocedural MI |
| Takao Sato12 | 32 | 0 | Filter no-reflow |
| Takaaki Matsuoka13 | 14 | 127 | Periprocedural MI |
| Hyoung-Mo Yang14 | 20 | 19 | Microvascular dysfunction |
| Nobuaki Suzuki15 | 115 | 64 | Slow-flow phenomenon |
ACS, acute coronary syndrome; CCS, chronic coronary syndrome; MI, myocardial infarction; NIRS, near-infrared spectroscopy.
In this issue of the Journal, Suzuki et al15 demonstrate the association between maxLCBI4mm and the slow-flow phenomenon in their study that included the largest total number of CCS and ACS lesions for comparison. The best maxLCBI4mm cutoff value in ACS and CCS lesions is reported as 578 and 480, respectively, with sensitivity of 100% for predicting slow-flow phenomenon. They found that the maxLCBI4mm cutoff value for CCS was smaller than that for ACS, the reason for which requires discussion. Furthermore, the authors suggest that maxLCBI4mm is not sufficient to evaluate the total amount of embolic source and the risk of distal embolization and that the addition of the information on lesion length is important to evaluate it more precisely.
Using these findings, we should go to the next stage of a randomized trial to test if the use of EPD in these high-risk patients detected by NIRS is beneficial to prevent distal embolization/slow-flow phenomenon/microvascular obstruction/periprocedural MI and, furthermore, to prevent death or heart failure.
The author received research grant from Abbott, Daiichi-Sankyo, Teijin, Japan Lifeline, OrbusNeich, Janssen, Otsuka, Ono, Eli Lilly, Astellas, Amgen, Boehringer Ingelheim, and Novartis; and lecture fees from Abbott, Kowa, Bayer, Daiichi-Sankyo, Nipro, Takeda, AstraZeneca, Japan Lifeline, Novartis, Ono, Boehringer Ingelheim, and Amgen.
