The Lipid Rich Plaque (LRP) study indicates that cardiac patients with a high lipid core plaque burden index (LBCI), identified with near infrared spectroscopy (NIRS, Infraredx), are at increased risk of a major adverse cardiac event (MACE) in a non-culprit vessel compared with those a low LCBI. Ron Waksman presented the LRP study at the 2018 Transcatheter Cardiovascular Therapeutics (TCT) meeting (21–25 September, San Diego, USA) and talks to Cardiovascular News about its findings.
Patients who have had a coronary event, such as a myocardial infarction, are known to be at increased risk of further events. Why is there a need to further assess the risk profile of these patients?
Some of these patients will go on to have further coronary events despite receiving optimal medical therapy, but others will remain event free despite their apparent risk of future events given their combination of known comorbidities. Before our study, we did not have any devices that could quickly and efficiently identify which patients would go on to have further events and which ones would not at the time of cardiac catheterization.
In this study, we evaluated the use of NIRS to identify patients and coronary segments with lipid rich plaque and determined these lipid rich plaques were vulnerable to rupture when large. Previous studies have shown that there is an association between the presence of lipid rich plaque and acute coronary syndromes, myocardial infarction, and death. Our goal was to see if NIRS could identify “vulnerable patients” and “vulnerable plaque” with 24 months after a patient had undergone the initial imaging.
How is NIRS performed?
A single, dual probe, catheter that can perform both NIRS and intravascular imaging (IVUS) is used, and this catheter is connected to one console with one screen. The NIRS provides you with a chemogram of the artery, which measures the LCBI overall and automatically identify the largest 4mm segments in one scan.
On the LBCI scale, what indicates that the patient/plaque is vulnerable?
The numbers range from 0 (meaning no lipid rich plaques; red on screen) to 1000 (the maximum that can be seen; yellow on screen), and the LCBI is then calculated within all 4mm segments to find the maximum LCBI value (maxLCBI4mm). In the study, we used a threshold maxLCBI4mm of 400 to discriminate between patients who we thought would have further events and those who we did not think would have a future event. We based this threshold on some preliminary studies that suggested 400 would be a good cutoff.
What were the key findings of the study?
We had two co-primary hypotheses—one for the vulnerable patient and one for the vulnerable plaque—and both of these were met. We found that at the patient level, the risk of non-culprit MACE increased by 18% for each 100unit increase of maxLCBI4mm after adjustment for known risk factors; it increased by 45% for each 100 unit increase at the plaque level.
Also, a patient with ≥400maxLCBI4mm had 87% higher risk of non-culprit MACE. The cumulative incidence of non-culprit MACE was 6.3% for patients with <400maxLCBI4mm but was significantly higher at 12.6% for patients with ≥400maxLCBI4mm.
Furthermore, NIRS (plus IVUS) was very safe to do; we had to very few events (0.3%).
What are the implications of the study?
For the physician there is now a diagnostic tool that is both user-friendly and already available within the cardiac catheterisation laboratory that can predict further events at the patient and plaque level. The obvious next study should explore whether NIRS can guide therapy either an intervention with a stent or pharmacologic agent to mitigate this high vulnerability.