open access

Ahead of print
Research paper
Published online: 2018-07-13
Get Citation

Effect of moderate-intensity statin therapy on plaque inflammation in patients with acute coronary syndrome: A prospective interventional study evaluated by 18F-FDG PET/CT of the carotid artery

Chan Joon Kim, Eun Ji Han, Eun-Ho Chu, Byung-Hee Hwang, Jin-Jin Kim, Ki-Bae Seung, Sung Hoon Kim, Joon Hyun O, Kiyuk Chang
DOI: 10.5603/CJ.a2018.0069
·
Pubmed: 30009378

open access

Ahead of print
Original articles
Published online: 2018-07-13

Abstract

Background: Asian patients with acute coronary syndrome (ACS) are frequently prescribed moderate-intensity statin in real practice, even during the early stage of ACS. Under assessment herein was the effect of moderate-intensity statin therapy on the resolution of plaque inflammation during the first month after ACS, a period with highest recurrent ischemic events, using dual time point 18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT).

Methods: This prospective study included statin-naïve patients with ACS and non-calcified carotid plaques (³ 3 mm on ultrasound images). Baseline FDG PET/CT images of the carotid arteries of the patients were obtained. Then, all patients received atorvastatin (20 mg/day); follow-up FDG PET/CT images of the carotid arteries were then obtained after 1 month of therapy. The primary endpoint measurement was the change in the target-to-background ratio (TBR) of the carotid artery between the initial and follow-up FDG PET/CT scans.

Results: Thirteen ACS patients completed the initial and follow-up FDG PET/CT scans. Moderate-intensity statin therapy failed to reduce plaque inflammation at 1 month after ACS (TBR 1.60 ± 0.20 at baseline vs. 1.50 ± 0.40 after therapy; p = 0.422) but significantly reduced serum low-density lipoprotein cholesterol (LDL-C) levels (mean LDL-C 101.2 ± 21.1 mg/dL at baseline vs. 70.7 ± 12.4 mg/dL after therapy; p < 0.001). Changes in the TBR and serum LDL-C levels were not correlated (r = –0.27, p = 0.243).

Conclusions: Dual time point FDG PET/CT imaging demonstrates that moderate-intensity statin therapy was insufficient in  suppressed plaque inflammation within the first month after ACS in Asian patients, even though achieving target LDL levels.

Abstract

Background: Asian patients with acute coronary syndrome (ACS) are frequently prescribed moderate-intensity statin in real practice, even during the early stage of ACS. Under assessment herein was the effect of moderate-intensity statin therapy on the resolution of plaque inflammation during the first month after ACS, a period with highest recurrent ischemic events, using dual time point 18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT).

Methods: This prospective study included statin-naïve patients with ACS and non-calcified carotid plaques (³ 3 mm on ultrasound images). Baseline FDG PET/CT images of the carotid arteries of the patients were obtained. Then, all patients received atorvastatin (20 mg/day); follow-up FDG PET/CT images of the carotid arteries were then obtained after 1 month of therapy. The primary endpoint measurement was the change in the target-to-background ratio (TBR) of the carotid artery between the initial and follow-up FDG PET/CT scans.

Results: Thirteen ACS patients completed the initial and follow-up FDG PET/CT scans. Moderate-intensity statin therapy failed to reduce plaque inflammation at 1 month after ACS (TBR 1.60 ± 0.20 at baseline vs. 1.50 ± 0.40 after therapy; p = 0.422) but significantly reduced serum low-density lipoprotein cholesterol (LDL-C) levels (mean LDL-C 101.2 ± 21.1 mg/dL at baseline vs. 70.7 ± 12.4 mg/dL after therapy; p < 0.001). Changes in the TBR and serum LDL-C levels were not correlated (r = –0.27, p = 0.243).

Conclusions: Dual time point FDG PET/CT imaging demonstrates that moderate-intensity statin therapy was insufficient in  suppressed plaque inflammation within the first month after ACS in Asian patients, even though achieving target LDL levels.

Get Citation

Keywords

statin, 18F-FDG PET/CT, low-density lipoprotein cholesterol, acute coronary syndromes

About this article
Title

Effect of moderate-intensity statin therapy on plaque inflammation in patients with acute coronary syndrome: A prospective interventional study evaluated by 18F-FDG PET/CT of the carotid artery

Journal

Cardiology Journal

Issue

Ahead of print

Article type

Research paper

Published online

2018-07-13

DOI

10.5603/CJ.a2018.0069

Pubmed

30009378

Keywords

statin
18F-FDG PET/CT
low-density lipoprotein cholesterol
acute coronary syndromes

Authors

Chan Joon Kim
Eun Ji Han
Eun-Ho Chu
Byung-Hee Hwang
Jin-Jin Kim
Ki-Bae Seung
Sung Hoon Kim
Joon Hyun O
Kiyuk Chang

References (23)
  1. Wright RS, Anderson JL, Adams CD, et al. 2011 ACCF/AHA focused update incorporated into the ACC/AHA 2007 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines developed in collaboration with the American Academy of Family Physicians, Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons. J Am Coll Cardiol. 2011; 57: e215–e367.
  2. Timmis AD. Plaque stabilisation in acute coronary syndromes: clinical considerations. Heart. 2003; 89(10): 1268–1272.
  3. Ray KK, Cannon CP, McCabe CH, et al. PROVE IT-TIMI 22 Investigators. Early and late benefits of high-dose atorvastatin in patients with acute coronary syndromes: results from the PROVE IT-TIMI 22 trial. J Am Coll Cardiol. 2005; 46(8): 1405–1410.
  4. Wang P. Statin dose in Asians: is pharmacogenetics relevant? Pharmacogenomics. 2011; 12(11): 1605–1615.
  5. Kim MJ, Jeon DS, Gwon HC, et al. Current statin usage for patients with acute coronary syndrome undergoing percutaneous coronary intervention: multicenter survey in Korea. Clin Cardiol. 2012; 35(11): 700–706.
  6. Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014; 63(25 Pt B): 2889–2934.
  7. Tawakol A, Migrino RQ, Bashian GG, et al. In vivo 18F-fluorodeoxyglucose positron emission tomography imaging provides a noninvasive measure of carotid plaque inflammation in patients. J Am Coll Cardiol. 2006; 48(9): 1818–1824.
  8. Tahara N, Kai H, Ishibashi M, et al. Simvastatin attenuates plaque inflammation: evaluation by fluorodeoxyglucose positron emission tomography. J Am Coll Cardiol. 2006; 48(9): 1825–1831.
  9. Rudd JHF, Machac J, Fayad ZA. Simvastatin and plaque inflammation. J Am Coll Cardiol. 2007; 49(19): 1991–1992.
  10. Ogawa M, Magata Y, Kato T, et al. Application of 18F-FDG PET for monitoring the therapeutic effect of antiinflammatory drugs on stabilization of vulnerable atherosclerotic plaques. J Nucl Med. 2006; 47(11): 1845–1850.
  11. Cannon C, Braunwald E, McCabe C, et al. Intensive versus Moderate Lipid Lowering with Statins after Acute Coronary Syndromes. N Engl J Med. 2004; 350(15): 1495–1504.
  12. Navarese EP, Kowalewski M, Andreotti F, et al. Meta-analysis of time-related benefits of statin therapy in patients with acute coronary syndrome undergoing percutaneous coronary intervention. Am J Cardiol. 2014; 113(10): 1753–1764.
  13. Stenestrand U, Wallentin L. Early statin treatment following acute myocardial infarction and 1-year survival. JAMA. 2001; 285(4): 430–436.
  14. Saito M, Hirata-Koizumi M, Urano T, et al. A literature search on pharmacokinetic drug interactions of statins and analysis of how such interactions are reflected in package inserts in Japan. J Clin Pharm Ther. 2005; 30(1): 21–37.
  15. Hiro T, Kimura T, Morimoto T, et al. Effect of intensive statin therapy on regression of coronary atherosclerosis in patients with acute coronary syndrome: a multicenter randomized trial evaluated by volumetric intravascular ultrasound using pitavastatin versus atorvastatin (JAPAN-ACS [Japan assessment of pitavastatin and atorvastatin in acute coronary syndrome] study). J Am Coll Cardiol. 2009; 54(4): 293–302.
  16. Wu YW, Kao HL, Chen MF, et al. Characterization of plaques using 18F-FDG PET/CT in patients with carotid atherosclerosis and correlation with matrix metalloproteinase-1. J Nucl Med. 2007; 48(2): 227–233.
  17. Tahara N, Kai H, Yamagishi Si, et al. Vascular inflammation evaluated by [18F]-fluorodeoxyglucose positron emission tomography is associated with the metabolic syndrome. J Am Coll Cardiol. 2007; 49(14): 1533–1539.
  18. Ben-Haim S, Kupzov E, Tamir A, et al. Evaluation of 18F-FDG uptake and arterial wall calcifications using 18F-FDG PET/CT. J Nucl Med. 2004; 45(11): 1816–1821.
  19. Ben-Haim S, Kupzov E, Tamir A, et al. Changing patterns of abnormal vascular wall F-18 fluorodeoxyglucose uptake on follow-up PET/CT studies. J Nucl Cardiol. 2006; 13(6): 791–800.
  20. Menezes LJ, Kayani I, Ben-Haim S, et al. What is the natural history of 18F-FDG uptake in arterial atheroma on PET/CT? Implications for imaging the vulnerable plaque. Atherosclerosis. 2010; 211(1): 136–140.
  21. Schwartz G, Olsson A. The Case for Intensive Statin Therapy After Acute Coronary Syndromes. Am J Cardiol. 2005; 96(5): 45–53.
  22. Tawakol A, Fayad ZA, Mogg R, et al. Intensification of statin therapy results in a rapid reduction in atherosclerotic inflammation: results of a multicenter fluorodeoxyglucose-positron emission tomography/computed tomography feasibility study. J Am Coll Cardiol. 2013; 62(10): 909–917.
  23. Yang J, Li XP, Zhao SP, et al. The effect of different doses of fluvastatin on inflammatory markers in the early phase of acute coronary syndrome. Clin Chim Acta. 2006; 368(1-2): 183–187.

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 "Via Medica sp. z o.o." sp.k., ul. Świętokrzyska 73, 80–180 Gdańsk, Poland
tel.:+48 58 320 94 94, fax:+48 58 320 94 60, e-mail: viamedica@viamedica.pl