Preventive PCI of vulnerable intracoronary plaque leads to favourable outcomes

Adding percutaneous coronary intervention (PCI) to optimal medical treatment (OMT) reduced revascularisations for high-risk vulnerable coronary plaques in the PREVENT trial. At 2 years, the cumulative incidence of target vessel failure was 0.4% for those receiving PCI and 3.4% without PCI, showing a statistically significant difference.

“An intracoronary, imaging-defined vulnerable plaque tends to increase major adverse cardiac events, and OMT is the standard approach to stabilise the vulnerability of the plaque,” Prof. Seung-Jung Park (University of Ulsan College of Medicine; Asan Medical Center, South Korea) explained [1]. The multicentre, randomised-controlled PREVENT trial (NCT02316886) compared OMT alone with OMT plus preventive PCI of vulnerable non-flow-limiting coronary plaques [1,2].

The 1,606 participants from research hospitals in South Korea, Japan, Taiwan, and New Zealand were randomised 1:1 to PCI and OMT or OMT alone. Among the inclusion criteria were stenosis >50% and a negative fractional flow reserve (FFR) of ≥0.80. The primary endpoint was a composite of death from cardiac causes, target vessel myocardial infarction (MI), ischaemic-driven target vessel revascularisation, or hospitalisation for unstable/progressive angina, summarised as target vessel failure at 2 years.

The results showed a cumulative incidence of target vessel failure in 0.4% of the OMT plus PCI arm, compared with 3.4% on OMT alone (see Figure). This resulted in a significant HR of 0.11 (95% CI 0.03–0.36; P=0.0003). After a longer follow-up at 7 years, a consistent advantage of preventive PCI was seen with target vessel failure rates of 6.5% versus 9.4%, respectively (HR 0.54; 95% CI 0.33–0.87; P=0.0097).

Figure: Target vessel failure at 2 years of follow-up in the PREVENT trial [1]



CI, confidence interval; OMT, optimal medical treatment; PCI, percutaneous coronary intervention.

Furthermore, the composite of any-cause death, any MI, or any repeat revascularisation through 7 years was significantly reduced in the intervention group (HR 0.69; 95% CI 0.50–0.95; P=0.022). Among the individual primary outcome components, only ischaemia-driven revascularisation and hospitalisation for angina were significantly in favour of the PCI group, other components showed no between-group difference. Also, no statistical differences were determined for secondary endpoints like bleeding events and stroke.

“Our key findings might provide a novel insight into the role of a preventive PCI on non-flow-limiting high-risk vulnerable plaques in the future,” concluded Prof. Park. Further information with regard to the definition of optimal medical therapy in this open-label trial may shed further light on the efficacy and safety of this strategy.

1. 
   
   1. Park SJ. Preventive PCI or medical therapy alone for atherosclerotic coronary vulnerable plaques. LB5, Session 412, ACC 2024 Scientific Session, 6–8 April, Atlanta, USA.
   2. Park SJ, et al. Lancet 2024; April 8. DOI: 10.1016/S0140-6736(24)00413-6.

Copyright ©2024 Medicom Medical Publishers



Posted on 16 May 202417 May 2024