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Near-infrared spectroscopy detected STEMI-causing plaques
For the first time, the presence of lipid core plaque has been identified in living patients, which could help physicians better identify those at risk for MI.
Prior autopsy studies have demonstrated that rupture of lipid core plaque is the cause of most STEMIs; however, lipid core plaque had previously never been detected in living patients.
Researchers identified the presence of lipid core plaque in 20 patients using intracoronary near-infrared spectroscopy (NIRS) performed with a catheter (TVC Imaging System, Infraredx).
“We have discovered a NIRS signature of the plaques which caused MI,” Ryan D. Madder, MD, interventional cardiologist at Spectrum Health’s Frederik Meijer Heart and Vascular Institute, Grand Rapids, Mich., said in a press release. “This signature is detectable at the time of cardiac catheterization using a novel intracoronary imaging device. It is our hope that this signature may be capable of predicting MI before it happens.”
The researchers first identified the culprit lesion of 20 patients with acute STEMI using an angiogram. They then performed NIRS within the culprit vessels. They compared those findings with findings in other artery segments, as well as findings in autopsy controls. All segments were analyzed for the maximum lipid core burden index in a 4-mm artery segment (maxLCBL4mm), which was the primary measure of interest.
In most cases, NIRS identified a large amount of lipid core plaque at the STEMI culprit site. MaxLCBL4mmwas 5.8-fold higher in STEMI-culprit segments than in other segments in the same vessel (median [interquartile range] 523 [445, 821] vs. 90 [6, 265]; P<.001). In addition, maxLCBL4mmwas 87-fold higher in STEMI-culprit segments than in coronary autopsy segments without large amounts of lipid core plaque (523 [445, 821] vs. 6 [0, 88]; P<.001). NIRS was able to distinguish culprit from non-culprit segments within the culprit artery (receiver operating characteristic analysis area under the curve=0.9). The researchers determined that a threshold of maxLCBL4mm >400 distinguished culprit segments from histology-negative autopsy specimens (sensitivity 85%, specificity 98%).
Further study is needed, according to Madder and colleagues. “The finding of a NIRS signature at STEMI culprit sites that differs significantly from findings in control segments contributes to the broader effort of detecting a signature of a vulnerable plaque, defined as a plaque prone to disruption and thrombosis,” they wrote. “These data provide support for the next step in evaluation of the NIRS signature of culprit lesions. … If NIRS is prospectively validated as a reliable predictor of clinical events, randomized studies of multiple promising systemic and local therapies could be conducted.”
Further, NIRS is an invasive procedure, so it should not be used for screening in the general population; however, it may be useful for secondary prevention in patients undergoing catheterization for other reasons, the researchers said.
Disclosure: Some researchers reported financial ties with Abbott Vascular, Angioscore, Boston Scientific, Bridgepoint Medical, DSI/Lilly, Gilead, Infraredx, The Medicines Company, Revascular Therapeutics, St. Jude Medical, Siemens, Terumo and Volcano.