Journal of Shanghai Jiao Tong University (Medical Science) >

2026 , Vol. 46 >Issue 3: 312 - 321

DOI: https://doi.org/10.3969/j.issn.1674-8115.2026.03.005

Clinical research

Impact of apolipoprotein B control on coronary atherosclerotic plaque progression: a cohort study using intravascular ultrasound

  • Amuti Abulikemu ,
  • Li Youran ,
  • Yang Chendie ,
  • GuanPoh Tay ,
  • Feng Shuo ,
  • Zhang Ruiyan ,
  • Wang Xiaoqun
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  • 1.Department of Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
    2.Department of Cardiology, Kashgar People's Hospital, Xinjiang Uygur Autonomous Region, Kashgar 844000, China
Wang Xiaoqun, E-mail: wangxq@shsmu.edu.cn.

Received date: 2025-06-23

  Accepted date: 2026-01-08

  Online published: 2026-03-30

Supported by

National Key Research and Development Program of China(2022YFC2503502);National Natural Science Foundation of China(82170423);“Two-hundred Talents” Program of Shanghai Jiao Tong University School of Medicine(2024-0801);Shanghai Municipal Health Commission Medical New Technology Research and Transformation Seed Program(2024ZZ2042);Opening Project of National Research Center for Translational Medicine, Shanghai [NRCTM (SH)-2023-13]

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Abstract

Objective ·To investigate the correlation between apolipoprotein B (ApoB) control level and coronary plaque progression in patients with stable coronary atherosclerotic heart disease (CHD). Methods ·This study retrospectively enrolled 86 patients with stable CHD (146 lesions) who were treated in the Department of Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, from January 2020 to May 2023. At baseline, demographic characteristics, physical examination finding, medical history, and medication use were collected. At baseline and follow-up, cardiometabolic parameters (including blood lipids and blood glucose) were measured, and intravascular ultrasound (IVUS) was performed to evaluate the same untreated intermediate coronary lesions (stenosis rate 30%‒70%). Time-averaged values of cardiometabolic parameters during follow-up were calculated. Quantitative analysis was performed on IVUS images to measure total atheroma volume (TAV) and percent atheroma volume (PAV) at baseline and follow-up. Patients were divided into a plaque progression group and a non-progression group according to a cutoff value of PAV change ≥5%. Spearman correlation analysis and multivariate Logistic regression were used to evaluate the association between time-averaged ApoB control level and coronary plaque progression. Results ·During follow-up, the mean change in PAV was 3.6% (-2.7%, 9.7%), and plaque progression was detected in 65 lesions (44.5%). A positive correlation was observed between time-averaged ApoB control level and mean change in TAV (r=0.22, P=0.008). Multivariate logistic regression analysis further demonstrated that, after adjustment, each 0.1 mmol/L increase in time-averaged ApoB control level was associated with a 0.885-fold increase in the risk of plaque progression (P=0.048). Conclusion ·Higher ApoB levels remain an independent predictor of coronary plaque progression after adjustment for potential confounders. These findings suggest that comprehensive management of cardiometabolic parameters, including ApoB, should be strengthened in clinical practice to delay plaque progression and improve patient prognosis.

Key words： coronary atherosclerotic heart disease (CHD); plaque progression; apolipoprotein B (ApoB); intravascular ultrasound (IVUS)

Cite this article

Amuti Abulikemu , Li Youran , Yang Chendie , GuanPoh Tay , Feng Shuo , Zhang Ruiyan , Wang Xiaoqun . Impact of apolipoprotein B control on coronary atherosclerotic plaque progression: a cohort study using intravascular ultrasound[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2026 , 46(3) : 312 -321 . DOI: 10.3969/j.issn.1674-8115.2026.03.005

References

[1] Ahmadi A, Argulian E, Leipsic J, et al. From subclinical atherosclerosis to plaque progression and acute coronary events JACC state-of-the-art review[J]. J Am Coll Cardiol, 2019, 74(12): 1608-1617.
[2] Libby P. The changing landscape of atherosclerosis[J]. Nature, 2021, 592(7855): 524-533.
[3] Bayturan O, Kapadia S, Nicholls S J, et al. Clinical predictors of plaque progression despite very low levels of low-density lipoprotein cholesterol[J]. J Am Coll Cardiol, 2010, 55(24): 2736-2742.
[4] Pontone G, Rossi A, Baggiano A, et al. Progression of non-obstructive coronary plaque: a practical CCTA-based risk score from the PARADIGM registry[J]. Eur Radiol, 2024, 34(4): 2665-2676.
[5] Neglia D, Caselli C, Maffei E, et al. Rapid plaque progression is independently associated with hyperglycemia and low HDL cholesterol in patients with stable coronary artery disease: a PARADIGM study[J]. Circ Cardiovasc Imaging, 2024, 17(7): e016481.
[6] Nissen S E, Tuzcu E M, Schoenhagen P, et al. Statin therapy, LDL cholesterol, C-reactive protein, and coronary artery disease[J]. N Engl J Med, 2005, 352(1): 29-38.
[7] Welty F K, Hariri E, Asbeutah A A, et al. Regression of coronary fatty plaque and risk of cardiac events according to blood pressure status: data from a randomized trial of eicosapentaenoic acid and docosahexaenoic acid in patients with coronary artery disease[J]. J Am Heart Assoc, 2023, 12(18): e030071.
[8] Casta?er O, Pintó X, Subirana I, et al. Remnant cholesterol, not LDL cholesterol, is associated with incident cardiovascular disease[J]. J Am Coll Cardiol, 2020, 76(23): 2712-2724.
[9] Hagstr?m E, Steg P G, Szarek M, et al. Apolipoprotein B, residual cardiovascular risk after acute coronary syndrome, and effects of alirocumab[J]. Circulation, 2022, 146(9): 657-672.
[10] Marston N A, Giugliano R P, Melloni G E M, et al. Association of apolipoprotein B-containing lipoproteins and risk of myocardial infarction in individuals with and without atherosclerosis: distinguishing between particle concentration, type, and content[J]. JAMA Cardiol, 2022, 7(3): 250-256.
[11] Johannesen C D L, Langsted A, Nordestgaard B G, et al. Excess apolipoprotein B and cardiovascular risk in women and men[J]. J Am Coll Cardiol, 2024, 83(23): 2262-2273.
[12] Faridi K F, Lahan S, Budoff M J, et al. Serum lipoproteins are associated with coronary atherosclerosis in asymptomatic U.S. adults without traditional risk factors[J]. JACC Adv, 2024, 3(7): 101049.
[13] Mach F, Baigent C, Catapano A L, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk[J]. Eur Heart J, 2020, 41(1): 111-188.
[14] Sniderman A D, Dufresne L, Pencina K M, et al. Discordance among apoB, non-high-density lipoprotein cholesterol, and triglycerides: implications for cardiovascular prevention[J]. Eur Heart J, 2024, 45(27): 2410-2418.
[15] Mintz G S, Nissen S E, Anderson W D, et al. American college of cardiology clinical expert consensus document on standards for acquisition, measurement and reporting of intravascular ultrasound studies (IVUS). a report of the American college of cardiology task force on clinical expert consensus documents[J]. J Am Coll Cardiol, 2001, 37(5): 1478-1492.
[16] Maehara A, Cristea E, Mintz G S, et al. Definitions and methodology for the grayscale and radiofrequency intravascular ultrasound and coronary angiographic analyses[J]. JACC Cardiovasc Imaging, 2012, 5(3 Suppl): S1-S9.
[17] Garcia-Garcia H M, Costa M A, Serruys P W. Imaging of coronary atherosclerosis: intravascular ultrasound[J]. Eur Heart J, 2010, 31(20): 2456-2469.
[18] Vesterbekkmo E K, Akset?y I A, Follestad T, et al. High-intensity interval training induces beneficial effects on coronary atheromatous plaques: a randomized trial[J]. Eur J Prev Cardiol, 2023, 30(5): 384-392.
[19] Xiao J Y, Padrick M M, Jiang T, et al. Acute ischemic stroke versus transient ischemic attack: differential plaque morphological features in symptomatic intracranial atherosclerotic lesions[J]. Atherosclerosis, 2021, 319: 72-78.
[20] Melina G, Angeloni E, Refice S, et al. Clinical SYNTAX score predicts outcomes of patients undergoing coronary artery bypass grafting[J]. Am Heart J, 2017, 188: 118-126.
[21] Rampidis G P, Benetos G, Benz D C, et al. A guide for gensini score calculation[J]. Atherosclerosis, 2019, 287: 181-183.
[22] van Rosendael A R, Lin F Y, van den Hoogen I J, et al. Progression of whole-heart atherosclerosis by coronary CT and major adverse cardiovascular events[J]. J Cardiovasc Comput Tomogr, 2021, 15(4): 322-330.
[23] Nicholls S J, Hsu A, Wolski K, et al. Intravascular ultrasound-derived measures of coronary atherosclerotic plaque burden and clinical outcome[J]. J Am Coll Cardiol, 2010, 55(21): 2399-2407.
[24] Puri R, Nissen S E, Ballantyne C M, et al. Factors underlying regression of coronary atheroma with potent statin therapy[J]. Eur Heart J, 2013, 34(24): 1818-1825.
[25] Pencina M J, D′Agostino R B, Zdrojewski T, et al. Apolipoprotein B improves risk assessment of future coronary heart disease in the Framingham Heart Study beyond LDL-C and non-HDL-C[J]. Eur J Prev Cardiol, 2015, 22(10): 1321-1327.
[26] Clark D 3rd, Nicholls S J, St John J, et al. Visit-to-visit cholesterol variability correlates with coronary atheroma progression and clinical outcomes[J]. Eur Heart J, 2018, 39(27): 2551-2558.
[27] Polewczyk A, Janion M, Gasior M, et al. Benefits from revascularisation therapy in the elderly with acute myocardial infarction. Comparative analysis of patients hospitalised in 1992-1996 and in 2005-2006[J]. Kardiol Pol, 2010, 68(8): 873-881.
[28] Shanmugasundaram M. Percutaneous coronary intervention in elderly patients: is it beneficial [J]. Tex Heart Inst J, 2011, 38(4): 398-403.
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