open access

Online first
Original article
Published online: 2022-12-05
Get Citation

HDL cholesterol, triglycerides and characteristics of coronary atherosclerosis in patients with newly diagnosed significant coronary artery disease by CTCA

Anna Oleksiak1, Cezary Kępka, Cezary Kępka, Karolina Rucińska, Karolina Rucińska, Kamil Marcinkiewicz, Kamil Marcinkiewicz, Marcin Demkow, Marcin Demkow, Mariusz Kruk, Mariusz Kruk
DOI: 10.33963/KP.a2022.0279
·
Pubmed: 36475513
Affiliations
  1. Department of Intensive Cardiac Therapy, Institute of Cardiology, Warszawa, Poland

open access

Online first
Original article
Published online: 2022-12-05

Abstract

Background: Current European Society of Cardiology guidelines indicate specific target low-density lipoprotein cholesterol (LDL-C) levels for different cardiovascular risk categories in terms of prevention. However, the target for high-density lipoprotein cholesterol (HDL-C)  and triglycerides have not been established.

Aim: The study aim to investigate the associations between HDL-C, triglycerides and coronary plaques characteristics.

Methods: This is a prospective single-center study with enrolled consecutive patients with newly diagnosed significant (≥1 stenosis ≥50%) CAD on CTCA. Patients had lipids and CTCA analysis, including high-risk plaque (HRP) features: low-attenuation plaque (LAP), napkin-ring sign (NRS), positive remodeling (PR) and spotty calcium (SC), type of plaque (calcified, noncalcified, mixed), and their composition (calcified, fibrous, fibro-fatty, necrotic core).

Results: The study included 300 patients (191 men, 66 [8] years). 66% of them took lipid-lowering therapy. HRP were found in 208 patients. There was no association between LDL-C, plaque composition and HRP presence. There was a negative correlation between HDL-C and fibro-fatty and necrotic core plaque components (P = 0.0002, P = 0.0009). There was a positive correlation between triglycerides and necrotic core (P = 0.038). There were differences in HDL-C and triglycerides in patients with and without NRS (47 vs. 53 mg/dl, P = 0.0002 and 128 vs. 109 mg/dl, P = 0.02). In logistic regression, HDL-C (odds ratio [OR], 0.95; 95% confidence interval [CI], 0.93­‒0.98; P <0.001), triglycerides (OR, 1.00; 95% CI, 1.00­‒1.01; P = 0.02), and male sex (OR, 3.04; 95% CI, 1.41­‒6.52; P = 0.004) were NRS predictors. In multivariable regression only HDL-C (OR, 0.96; 95% CI, 0.93­‒0.99; P = 0.02) was an independendent predictor of NRS, despite statin therapy.

Conclusion: Lower HDL-C and higher triglycerides were associated with NRS presence and more necrotic core plaque component in coronary plaques in patients with newly diagnosed CAD.

Abstract

Background: Current European Society of Cardiology guidelines indicate specific target low-density lipoprotein cholesterol (LDL-C) levels for different cardiovascular risk categories in terms of prevention. However, the target for high-density lipoprotein cholesterol (HDL-C)  and triglycerides have not been established.

Aim: The study aim to investigate the associations between HDL-C, triglycerides and coronary plaques characteristics.

Methods: This is a prospective single-center study with enrolled consecutive patients with newly diagnosed significant (≥1 stenosis ≥50%) CAD on CTCA. Patients had lipids and CTCA analysis, including high-risk plaque (HRP) features: low-attenuation plaque (LAP), napkin-ring sign (NRS), positive remodeling (PR) and spotty calcium (SC), type of plaque (calcified, noncalcified, mixed), and their composition (calcified, fibrous, fibro-fatty, necrotic core).

Results: The study included 300 patients (191 men, 66 [8] years). 66% of them took lipid-lowering therapy. HRP were found in 208 patients. There was no association between LDL-C, plaque composition and HRP presence. There was a negative correlation between HDL-C and fibro-fatty and necrotic core plaque components (P = 0.0002, P = 0.0009). There was a positive correlation between triglycerides and necrotic core (P = 0.038). There were differences in HDL-C and triglycerides in patients with and without NRS (47 vs. 53 mg/dl, P = 0.0002 and 128 vs. 109 mg/dl, P = 0.02). In logistic regression, HDL-C (odds ratio [OR], 0.95; 95% confidence interval [CI], 0.93­‒0.98; P <0.001), triglycerides (OR, 1.00; 95% CI, 1.00­‒1.01; P = 0.02), and male sex (OR, 3.04; 95% CI, 1.41­‒6.52; P = 0.004) were NRS predictors. In multivariable regression only HDL-C (OR, 0.96; 95% CI, 0.93­‒0.99; P = 0.02) was an independendent predictor of NRS, despite statin therapy.

Conclusion: Lower HDL-C and higher triglycerides were associated with NRS presence and more necrotic core plaque component in coronary plaques in patients with newly diagnosed CAD.

Get Citation

Keywords

HDL cholesterol, coronary artery disease, high-risk plaque, cardiovascular prevention, triglycerides

Supp./Additional Files (1)
Supplementary material
Download
68KB
About this article
Title

HDL cholesterol, triglycerides and characteristics of coronary atherosclerosis in patients with newly diagnosed significant coronary artery disease by CTCA

Journal

Kardiologia Polska (Polish Heart Journal)

Issue

Online first

Article type

Original article

Published online

2022-12-05

Page views

90

Article views/downloads

42

DOI

10.33963/KP.a2022.0279

Pubmed

36475513

Keywords

HDL cholesterol
coronary artery disease
high-risk plaque
cardiovascular prevention
triglycerides

Authors

Anna Oleksiak
Cezary Kępka
Cezary Kępka
Karolina Rucińska
Karolina Rucińska
Kamil Marcinkiewicz
Kamil Marcinkiewicz
Marcin Demkow
Marcin Demkow
Mariusz Kruk
Mariusz Kruk

References (31)
  1. Authors/Task Force Members, ESC Committee for Practice Guidelines (CPG), ESC National Cardiac Societies. 2019 ESC/EAS guidelines for the management of dyslipidaemias: Lipid modification to reduce cardiovascular risk. Atherosclerosis. 2019; 290: 140–205.
  2. Visseren FLJ, Mach F, Smulders YM, et al. 2021 ESC Guidelines on cardiovascular disease prevention in clinical practice. Eur Heart J. 2021; 42(34): 3227–3337.
  3. Maurovich-Horvat P, Ferencik M, Voros S, et al. Comprehensive plaque assessment by coronary CT angiography. Nat Rev Cardiol. 2014; 11(7): 390–402.
  4. Oleksiak A, Kępka C, Kruk M. The relationship between anisocytosis, quantitative and qualitative characteristics of coronary atherosclerosis, and major adverse cardiac events in patients with coronary artery disease: Rationale and study design. Kardiol Pol. 2022; 80(6): 699–701.
  5. Bom MJ, van der Heijden DJ, Kedhi E, et al. Early detection and treatment of the vulnerable coronary plaque: can we prevent acute coronary syndromes? Circ Cardiovasc Imaging. 2017; 10(5).
  6. Nerlekar N, Ha FJ, Cheshire C, et al. Computed tomographic coronary angiography-derived plaque characteristics predict major adverse cardiovascular events: A systematic review and meta-analysis. Circ Cardiovasc Imaging. 2018; 11(1): e006973.
  7. Lee SE, Chang HJ, Sung JiM, et al. Effects of statins on coronary atherosclerotic plaques: the PARADIGM study. JACC Cardiovasc Imaging. 2018; 11(10): 1475–1484.
  8. Puchner SB, Liu T, Mayrhofer T, et al. High-risk plaque detected on coronary CT angiography predicts acute coronary syndromes independent of significant stenosis in acute chest pain: results from the ROMICAT-II trial. J Am Coll Cardiol. 2014; 64(7): 684–692.
  9. Henzel J, Kępka C, Kruk M, et al. High-Risk coronary plaque regression after intensive lifestyle intervention in nonobstructive coronary disease: a randomized study. JACC Cardiovasc Imaging. 2021; 14(6): 1192–1202.
  10. Pflederer T, Marwan M, Schepis T, et al. Characterization of culprit lesions in acute coronary syndromes using coronary dual-source CT angiography. Atherosclerosis. 2010; 211(2): 437–444.
  11. Kashiwagi M, Tanaka A, Kitabata H, et al. Feasibility of noninvasive assessment of thin-cap fibroatheroma by multidetector computed tomography. JACC Cardiovasc Imaging. 2009; 2(12): 1412–1419.
  12. Ito T, Terashima M, Kaneda H, et al. Comparison of in vivo assessment of vulnerable plaque by 64-slice multislice computed tomography versus optical coherence tomography. Am J Cardiol. 2011; 107(9): 1270–1277.
  13. Otsuka K, Fukuda S, Tanaka A, et al. Napkin-ring sign on coronary CT angiography for the prediction of acute coronary syndrome. JACC Cardiovasc Imaging. 2013; 6(4): 448–457.
  14. Narula J, Nakano M, Virmani R, et al. Histopathologic characteristics of atherosclerotic coronary disease and implications of the findings for the invasive and noninvasive detection of vulnerable plaques. J Am Coll Cardiol. 2013; 61(10): 1041–1051.
  15. 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 Am Coll Cardiol. 2019; 74(12): 1608–1617.
  16. Weber C, Deseive S, Brim G, et al. Coronary plaque volume and predictors for fast plaque progression assessed by serial coronary CT angiography-A single-center observational study. Eur J Radiol. 2020; 123: 108805.
  17. Takata K, Honda S, Sidharta SL, et al. High-density lipoprotein cholesterol associated with change in coronary plaque lipid burden assessed by near infrared spectroscopy. Atherosclerosis. 2017; 265(4): 110–116.
  18. von Birgelen C, Hartmann M, Mintz GS, et al. Relation between progression and regression of atherosclerotic left main coronary artery disease and serum cholesterol levels as assessed with serial long-term (> or =12 months) follow-up intravascular ultrasound. Circulation. 2003; 108(22): 2757–2762.
  19. Langsted A, Freiberg JJ, Nordestgaard BG. Fasting and nonfasting lipid levels: influence of normal food intake on lipids, lipoproteins, apolipoproteins, and cardiovascular risk prediction. Circulation. 2008; 118(20): 2047–2056.
  20. Jørgensen AB, Frikke-Schmidt R, Nordestgaard BG, et al. Loss-of-function mutations in APOC3 and risk of ischemic vascular disease. N Engl J Med. 2014; 371(1): 32–41.
  21. Nordestgaard BG, Benn M, Schnohr P, et al. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007; 298(3): 299–308.
  22. Tragante V, Asselbergs FW, Swerdlow DI, et al. Mendelian randomization of blood lipids for coronary heart disease. Eur Heart J. 2015; 36(9): 539–550.
  23. Faergeman O, Holme I, Fayyad R, et al. Plasma triglycerides and cardiovascular events in the treating to new targets and incremental decrease in end-points through aggressive lipid lowering trials of statins in patients with coronary artery disease. Am J Cardiol. 2009; 104(4): 459–463.
  24. Schwartz GG, Abt M, Bao W, et al. Fasting triglycerides predict recurrent ischemic events in patients with acute coronary syndrome treated with statins. J Am Coll Cardiol. 2015; 65(21): 2267–2275.
  25. Miller M, Cannon CP, Murphy SA, et al. Impact of triglyceride levels beyond low-density lipoprotein cholesterol after acute coronary syndrome in the PROVE IT-TIMI 22 trial. J Am Coll Cardiol. 2008; 51(7): 724–730.
  26. Asakura K, Minami Y, Kinoshita D, et al. Impact of triglyceride levels on plaque characteristics in patients with coronary artery disease. Int J Cardiol. 2022; 348: 134–139.
  27. Bayturan O, Kapadia S, Nicholls SJ, et al. Clinical predictors of plaque progression despite very low levels of low-density lipoprotein cholesterol. J Am Coll Cardiol. 2010; 55(24): 2736–2742.
  28. Ahmadi A, Narula J. Primary and secondary prevention, or subclinical and clinical atherosclerosis. JACC Cardiovasc Imaging. 2017; 10(4): 447–450.
  29. Tsujita K, Sugiyama S, Sumida H, et al. Impact of dual lipid-lowering strategy with ezetimibe and atorvastatin on coronary plaque regression in patients with percutaneous coronary intervention. J Am Coll Cardiol. 2015; 66(5): 495–507.
  30. O'Keefe JH, Cordain L, Harris WH, et al. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004; 43(11): 2142–2146.
  31. Seo YH, Seo DJ, Song InG, et al. Rationale of decreasing low-density lipoprotein cholesterol below 70 mg/dL in patients with coronary artery disease: A retrospective virtual histology-intravascular ultrasound study. Cardiol J. 2018; 25(6): 674–682.

Regulations

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

By VM Media Group sp. z o.o., ul. Świętokrzyska 73 , 80–180 Gdańsk, Poland

phone:+48 58 320 94 94, fax:+48 58 320 94 60, e-mail: viamedica@viamedica.pl