# LDL-verlaging en lesie-niveau effecten na acuut MI

*geplaatst 2024-12-01 · Cholesterol · JAMA cardiology · doi 10.1001/jamacardio.2024.3200 · https://hartvaat.nl/2024/12/01/ldl-verlaging-en-lesie-niveau-effecten-na-acuut-mi/*

Post-hoc analyse onderzocht het effect van LDL-verlaging op individuele coronaire lesies na MI. Lagere LDL-waarden waren geassocieerd met minder plaquepubressie en meer stabilisatie op lesieniveau.

## English: Lesion-Level Effects of LDL-C-Lowering Therapy in Patients With Acute Myocardial Infarction: A Post Hoc Analysis of the PACMAN-AMI Trial.

This post-hoc analysis examined the lesion-level effects of LDL cholesterol lowering after MI, showing that lower achieved LDL is associated with greater plaque regression in individual coronary lesions.

## Abstract (original, from the publication)

IMPORTANCE: Previous studies investigated atherosclerotic changes induced by lipid-lowering therapy in extensive coronary segments irrespective of baseline disease burden (a vessel-level approach). OBJECTIVE: To investigate the effects of lipid-lowering therapy on coronary lesions with advanced atherosclerotic plaque features and presumably higher risk for future events. DESIGN, SETTING, AND PARTICIPANTS: The PACMAN-AMI randomized clinical trial (enrollment: May 2017 to October 2020; final follow-up: October 2021) randomized patients with acute myocardial infarction to receive alirocumab or placebo in addition to high-intensity statin therapy. In this post hoc lesion-level analysis, nonculprit lesions were identified as segments with plaque burden 40% or greater defined by intravascular ultrasound (IVUS). IVUS, near-infrared spectroscopy, and optical coherence tomography images at baseline and the 52-week follow-up were manually matched by readers blinded to treatment allocation. Data for this study were analyzed from October 2022 to November 2023. INTERVENTIONS: Alirocumab or placebo in addition to high-intensity statin therapy. MAIN OUTCOMES AND MEASURES: Lesion-level imaging outcome measures, including high-risk plaque characteristics and phenotypes. RESULTS: Of the 245 patients in whom lesions were found, 118 were in the alirocumab group (mean [SD] age, 58.2 [10.0] years; 101 [85.6%] male and 17 [14.4%] female) and 127 in the placebo group (mean [SD] age, 57.7 [8.8] years; 104 [81.9%] male and 23 [18.1%] female). Overall, 591 lesions were included: 287 lesions (118 patients, 214 vessels) in the alirocumab group and 304 lesions (127 patients, 239 vessels) in the placebo group. Lesion-level mean change in percent atheroma volume (PAV) was -4.86% with alirocumab vs -2.78% with placebo (difference, -2.02; 95% CI, -3.00 to -1.05; P < .001). At the minimum lumen area (MLA) site, mean change in PAV was -10.14% with alirocumab vs -6.70% with placebo (difference, -3.36; 95% CI, -4.98 to -1.75; P < .001). MLA increased by 0.15 mm2 with alirocumab and decreased by 0.07 mm2 with placebo (difference, 0.21; 95% CI, 0.01 to 0.41; P = .04). Among 122 lipid-rich lesions, 34 of 55 (61.8%) in the alirocumab arm and 27 of 67 (41.8%) in the placebo arm showed a less lipid-rich plaque phenotype at follow-up (P = .03). Among 63 lesions with thin-cap fibroatheroma at baseline, 8 of 26 (30.8%) in the alirocumab arm and 3 of 37 (8.1%) in the placebo arm showed a fibrous/fibrocalcific plaque phenotype at follow-up (P = .02). CONCLUSIONS AND RELEVANCE: At the lesion level, very intensive lipid-lowering therapy induced substantially greater PAV regression than described in previous vessel-level analyses. Compared with statin therapy alone, alirocumab treatment was associated with greater enlargement of the lesion MLA and more frequent transition of presumably high-risk plaque phenotypes into more stable, less lipid-rich plaque phenotypes. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT03067844.

Auteurs: Flavio G Biccirè, Ryota Kakizaki, Konstantinos C Koskinas, Yasushi Ueki, Jonas Häner, Hiroki Shibutani, Jacob Lønborg, Ernest Spitzer, Juan F Iglesias, Tatsuhiko Otsuka, George C M Siontis, Stefan Stortecky, Christoph Kaiser, Maria Ambühl, Laura Morf, Anna S Ondracek, Robert-Jan van Geuns, David Spirk, Joost Daemen, François Mach, Stephan Windecker, Thomas Engstrøm, Irene Lang, Sylvain Losdat, Lorenz Räber

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Bron: JAMA cardiology, https://doi.org/10.1001/jamacardio.2024.3200. Bijgewerkt 2026-07-03T13:30:21Z. Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.