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. 2024 Oct;17(10):e017066.
doi: 10.1161/CIRCIMAGING.124.017066. Epub 2024 Sep 30.

Coronary Plaque Characteristics in Patients With Chronic Kidney Failure: Impact on Cardiovascular Events and Mortality

Jonathan Nørtoft Dahl  1   2 , Marie B Nielsen  3   4 , Laust D Rasmussen  1   5 , Per Ivarsen  2   4 , Michelle C Williams  6   7 , My Hanna Sofia Svensson  8   9 , Henrik Birn  2   3   4 , Morten Bøttcher  1   2 , Simon Winther  1   2
Affiliations

Coronary Plaque Characteristics in Patients With Chronic Kidney Failure: Impact on Cardiovascular Events and Mortality

Jonathan Nørtoft Dahl et al. Circ Cardiovasc Imaging. 2024 Oct.

Abstract

Background: In patients with coronary artery disease, coronary plaques with high-risk features and low-attenuation plaque burden are independent measures associated with major adverse cardiovascular events (MACEs). Patients with chronic kidney failure may have different coronary artery disease characteristics. The aim was to assess the association of coronary plaque characteristics and coronary artery disease extent with MACE and all-cause mortality in patients with chronic kidney failure.

Methods: Potential kidney transplant candidates who underwent coronary computed tomography angiography as part of the cardiac screening program before kidney transplantation were included. We evaluated high-risk plaques and diameter stenosis semiqualitatively and quantified coronary artery calcium score and plaque burden (percentage atheroma volume).

Results: In 484 patients with chronic kidney failure and few or no symptoms of coronary artery disease (mean age, 53±12 years; 62% men; 32% on dialysis), 56 (12%) patients suffered MACE and 69 (14%) patients died during a median follow-up of 4.9 years. High-risk plaques were present in 39 (70%) patients with MACE. Median calcified plaque burden was 3.7% in patients with MACE versus 0.2% in patients without MACE. The median low-attenuation plaque burden was 0.3% versus 0.03%, respectively. In semiqualitative analyses, the presence of high-risk plaque and a higher coronary artery calcium score were associated with increased risk of MACE (hazard ratio (HR), 2.0 [95% CI, 1.0-3.7]; P=0.040; HR, 1.2 [95% CI, 1.0-1.3]; P=0.014), respectively. Neither were associated with all-cause mortality. In quantified analysis, increasing levels of both calcified and low-attenuation plaque burdens were associated with risk of MACE (HR, 2.6 [95% CI, 1.8-3.7]; P<0.001; HR, 2.6 [95% CI, 1.5-4.5]; P=0.001 [per variable doubling, respectively]) and all-cause mortality (HR, 1.6 [95% CI, 1.2-2.1]; P=0.002; HR, 1.8 [95% CI, 1.1-3.0]; P=0.028, respectively).

Conclusions: In patients with chronic kidney failure, calcified and low-attenuation plaque burdens were independently associated with MACE and all-cause mortality, while high-risk plaques and coronary artery calcium score were only associated with MACE.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT01344434.

Keywords: cardiovascular diseases; cause of death; computed tomography angiography; coronary artery disease; kidney transplantation; renal insufficiency, chronic.

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Conflict of interest statement

Dr Winther had a nonfinancial collaboration agreement with Medis, the Netherlands, which sponsored the QAngio software. The provider had no role in the collection or the analysis of data nor in the interpretation of the results or writing of the article. Aside from this, the authors’ disclosures are unrelated to the present study. Dr Winther acknowledges support from the Novo Nordisk Foundation Clinical Emerging Investigator grant (NNF21OC0066981). Dr Rasmussen acknowledges support in terms of a research grant (PD5Y-2023001-DCA) from the Danish Cardiovascular Academy, which is funded by the Novo Nordisk Foundation (grant NNF20SA0067242) and the Danish Heart Foundation. Dr Ivarsen discloses consultancy/advisory board participation for CSL Vifor Pharma, Otsuka, and Novartis, speaker’s honorarium from Otsuka, and research grants from the Augustinus Foundation and CSL Vifor Pharma. Dr Svensson discloses funding from Novo Nordisk and the Augustinus Foundation. Dr Birn discloses consultancy and advisory board participation for NOVO Nordisk, AstraZeneca, Boehringer Ingelheim, Bayer, Alexion, Vifor Pharma, Otsuka, and Galapagos; speaker’s honorarium from AstraZeneca, Astellas, Novartis, and MSD; and research grants from Vifor Pharma, GSK, the NOVO Foundation, the Karen Elise Jensen Foundation, and the Augustinus Foundation. Dr Bøttcher discloses advisory board participation for NOVO Nordisk, AstraZeneca, Pfizer, Boehringer Ingelheim, Bayer, Sanofi, Novartis, Amgen, CSL Behring, and Acarix. The other authors report no conflicts.

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