September 26, 2018
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LRP Study: IVUS plus near-infrared spectroscopy identifies patients, arteries at risk

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Ron Waksman

SAN DIEGO — The use of coronary near-infrared spectroscopy with IVUS in patients with ACS or stable angina identified people and coronary segments at risk for nonculprit-artery MACE, according to findings from the LRP Study presented at TCT 2018.

“We still see many patients that come to the cath lab for one event and have a subsequent event despite being treated with medical therapy,” Ron Waksman, MD, FACC, FSCAI, associate director in the division of cardiology at MedStar Washington Hospital Center and director of cardiovascular research and advanced education for the MedStar Heart and Vascular Institute, told Cardiology Today’s Intervention. “Some of these patients are optimally treated and still have events. The unmet need was to find an imaging technology able to detect vulnerable patients and vulnerable plaques. Doing that could be a good predictor for subsequent events.”

It is known that lipid-rich plaques are associated with risk for MI and ACS, Waksman said.

Lipid-rich plaque can be identified by near-infrared spectroscopy (NIRS; Infraredx, a Nipro company), which can be used in any IVUS procedure, he said. “It’s a combined imaging console that has both IVUS and near-infrared.”

Using NIRS with IVUS produces a chemogram that assesses agreement between histological factors and the NIRS findings, and these findings are summarized as the lipid core burden index (LCBI), according to Waksman. “If there is lipid content within the plaque, it will be colored yellow, and the quantity is on a scale from 0 to 1,000,” he said. “We believed that a low score would be associated with low risk for events and a high one would be associated with high risk.”

The primary endpoints were the association between LCBI in all imaged arteries and future nonculprit MACE at the patient level, and the association between LCBI in an artery segment and future nonculprit MACE in that segment. The researchers hypothesized that LCBI of 400 or more would identify patients and plaques at risk for nonculprit MACE; that figure had been suggested in previous studies but had never been prespecified as an outcome, Waksman told Cardiology Today’s Intervention.

Nonculprit MACE was adjudicated by a clinical events committee masked to the NIRS findings and was defined as cardiac death, cardiac arrest, nonfatal MI, ACS, revascularization via CABG or PCI or rehospitalization for progressive angina with a stenosis progression of more than 20%.

The primary endpoint analysis included 1,271 patients (mean age, 64 years; 70% men) who came to the cath lab for PCI or diagnostic angiography and 5,744 Ware segments. Mean follow-up was 732 days.

Among the study population, 46.3% had stable angina, 36.8% had unstable angina, 14.3% had non-STEMI and 2.5% had stabilized STEMI.

Patients had a mean of 2.1 vessels scanned, and 38.8% of patients and 11.5% of Ware segments had LBCI of 400 or more, Waksman said.

During the study period, nonculprit MACE occurred in 8.8% of patients, according to the researchers.

In the patient-level analysis, risk for nonculprit MACE increased 18% for every increase of 100 in LBCI, and the primary endpoint was met (HR = 1.18; 95% CI, 1.05-1.32). In addition, Waksman said, patients with LBCI of at least 400 had an 87% greater risk for nonculprit MACE than patients with LBCI less than 400 (HR = 1.87; 95% CI, 1.25-2.8), with 12.6% of patients with LBCI more than 400 having nonculprit MACE vs. 6.3% in patients who did not.

In Ware segments, risk for nonculprit MACE rose by 45% for every increase of 100 in LBCI (HR = 1.45; 95% CI, 1.28-1.64), and segments with LBCI of 400 or more were at 411% greater risk for nonculprit MACE than segments with LBCI of less than 400 (HR = 4.11; 95% CI, 2.3-7.34), Waksman said.

Cumulative nonculprit MACE incidence in plaques was 3.7% in segments with LCBI of 400 or more and 0.8% in segments of less than 400, according to the researchers.

“Events continue to occur despite medical therapy,” Waksman told Cardiology Today’s Intervention. “A NIRS chemogram can detect vulnerable plaque and vulnerable patients, and probably should be considered to be utilized more routinely to be able to discriminate patients at risk. We should try to tailor therapy guided by this technology, and see if there are any therapies that can reduce the LCBI. We also need to determine whether if we reduce LCBI, it will be associated with fewer events.” – by Erik Swain

Reference:

Waksman R, et al. Late-Breaking Trials 4. Presented at: TCT Scientific Symposium; Sept. 21-25, 2018; San Diego.

Disclosure: The study was funded by Infraredx, a Nipro company. Waksman reports he has financial ties unrelated to the present study with Abbott Vascular, Amgen, AstraZeneca, Biosensors, Biotronik, Boston Scientific, Cardioset, Chiesi, DOMed, Medtronic, Philips/Volcano and Pi-Cardia Ltd.