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Soon after intervention for an MI, remaining high-risk vulnerable plaques can be identified from catheter-based imaging, according to a natural history study.

Most of the 13.22% of major cardiac events that happened over 4 years among a cohort of 898 MI survivors stemmed from untreated lesions deemed angiographically benign and non-flow-limiting at the time of the index MI, reported the PROSPECT II team led by David Erlinge, MD, PhD, of Lund University in Sweden, in the March 13 issue of .

Fully 8.0% of people had their cardiac death, MI, unstable angina, or progressive angina events arising from non-culprit lesions identified from a dedicated intracoronary near-infrared spectroscopy (NIRS) and intravascular ultrasound (IVUS) catheter.

"By contrast, in the original and the LRP study, an equal proportion of events within 3 years were attributed to previously treated culprit lesions and untreated non-culprit lesions. The lower rate of new events arising during follow-up from the previously treated culprit lesion in our study is probably attributable to improved stent technology, more effective pharmacotherapy, and use of IVUS guidance for stent placement," the group noted.

In a , two editorialists raised questions of what practical lessons can be gleaned from the three studies.

"How do health professionals translate this series of studies, which added labour-intensive, measured intracoronary-derived imaging variables to the daily catheterisation laboratory's busy practice? Do we need both [IVUS and NIRS]? Or will a simplistic identification of plaque vulnerability be sufficient?" posited Ron Waksman, MD, of MedStar Washington Hospital Center in Washington D.C., and Rebecca Torguson, MPH, of Icahn School of Medicine at Mount Sinai in New York City.

And once a vulnerable plaque has been detected, the question then is how it should be handled.

Waksman and Torguson noted that PCKS9 inhibitors are being tested in this setting in the and trials, while local stenting is being compared against optimal medical therapy in .

"The answer could well be a patient-centric approach with a combination of therapies tailored to the patient's specific anatomy, number of non-culprit lesions with plaque vulnerability, and plaque composition," according to the duo.

was conducted from 2014 to 2017 at 16 hospitals in Denmark, Norway, and Sweden. Its main findings were first reported at the TCT Connect meeting in 2020, showing the impact of the Absorb bioresorbable vascular scaffold stent on vulnerable plaques.

Participants included 898 patients (17% women, median age 63 years) who had survived an MI in the 4 weeks prior to enrollment. After treatment of all flow-limiting coronary lesions, each person was found to have a median of 4.0 non-culprit lesions.

Untreated lesions averaged 46.9% in baseline angiographic diameter stenosis and grew to a mean 68.4% diameter stenosis at the time of event.

Independent predictors of non-culprit lesion-related major adverse cardiovascular events (MACE) were highly lipidic lesions (MaxLCBI_4mm ≥324.7 on NIRS) and large plaque burden (70% or higher on IVUS). Minimal lumen area 4.0 mm² or less missed statistical significance as a predictor after adjustment.

Even so, all three factors may be used to define vulnerable plaque characteristics in future studies, Erlinge's group said. "Thus, combined NIRS and IVUS are complementary in that they overcome the limitations of each other."

Highly lipidic lesions with large plaque burden had a 7% MACE rate per lesion by 4 years, and patients with at least one of these plaques had a 13% risk of MACE.

"A user-friendly approach for identifying such so-called vulnerable plaques before they progress could enable pharmacological or other strategies to stabilise the plaque, prevent atherosclerosis progression, and improve outcomes," Erlinge's group said.

An embedded analysis within the study had suggested that percutaneous coronary intervention on non-obstructive vulnerable plaques could be safe and effective.

"However, until large-scale, adequately powered, randomised trials are done, the routine treatment of non-ischaemic vulnerable plaques (whether with intensified pharmacotherapy or focal intervention), as identified by either non-invasive or invasive imaging, cannot be endorsed," the authors emphasized.

Additionally, PROSPECT II's selection for recent MI survivors with non-culprit lesions (defined by having at least 40% plaque burden) may have excluded non-culprit lesions with high lipid content and low plaque burden, which would result in missing crucial vulnerable plaques, Waksman and Torguson cautioned.

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