Effect of Evolocumab on Coronary Plaque Phenotype and Burden in Statin-Treated Patients Following Myocardial Infarction

Stephen J. Nicholls; Yu Kataoka; Steven E. Nissen; Francesco Prati; Stephan Windecker; Rishi Puri; Thomas Hucko; Daniel Aradi; Jean Paul R. Herrman; Renicus S. Hermanides; Bei Wang; Huei Wang; Julie Butters; Giuseppe Di Giovanni; Stephen Jones; Gianluca Pompili; Peter J. Psaltis

doi:10.1016/j.jcmg.2022.03.002

Effect of Evolocumab on Coronary Plaque Phenotype and Burden in Statin-Treated Patients Following Myocardial Infarction

Stephen J. Nicholls, Yu Kataoka, Steven E. Nissen, Francesco Prati, Stephan Windecker, Rishi Puri, Thomas Hucko, Daniel Aradi, Jean Paul R. Herrman, Renicus S. Hermanides, Bei Wang, Huei Wang, Julie Butters, Giuseppe Di Giovanni, Stephen Jones, Gianluca Pompili, Peter J. Psaltis

Victorian Heart Institute (VHI)

Research output: Contribution to journal › Article › Research › peer-review

192 Citations (Scopus)

Abstract

Objectives: The purpose of this study was to determine the effect of evolocumab on optical coherence tomography (OCT) measures of plaque composition. Background: The proprotein convertase subtilisin kexin type-9 inhibitor evolocumab produced coronary atheroma regression in statin-treated patients. Methods: Patients with a non–ST-segment elevation myocardial infarction were treated with monthly evolocumab 420 mg (n = 80) or placebo (n = 81) for 52 weeks. Patients underwent serial OCT and intravascular ultrasound imaging within a matched arterial segment of a nonculprit vessel. The primary analysis determined the change in the minimum fibrous cap thickness and maximum lipid arc throughout the imaged arterial segment. Additional analyses determined changes in OCT features in lipid-rich plaque regions and plaque burden. Safety and tolerability were evaluated. Results: Among treated patients, (age 60.5 ± 9.6 years; 28.6% women; low-density lipoprotein cholesterol [LDL-C], 141.3 ± 33.1 mg/dL), 135 had evaluable imaging at follow-up. The evolocumab group achieved lower LDL-C levels (28.1 vs 87.2 mg/dL; P < 0.001). The evolocumab group demonstrated a greater increase in minimum fibrous cap thickness (+42.7 vs +21.5 μm; P = 0.015) and decrease in maximum lipid arc (−57.5^o vs. −31.4^o; P = 0.04) and macrophage index (−3.17 vs −1.45 mm; P = 0.04) throughout the arterial segment. Similar benefits of evolocumab were observed in lipid-rich plaque regions. Greater regression of percent atheroma volume was observed with evolocumab compared with placebo (−2.29% ± 0.47% vs −0.61% ± 0.46%; P = 0.009). The groups did not differ regarding changes in microchannels or calcium. Conclusions: The combination of statin and evolocumab after a non–ST-segment elevation myocardial infarction produces favorable changes in coronary atherosclerosis consistent with stabilization and regression. This demonstrates a potential mechanism for the improved clinical outcomes observed achieving very low LDL-C levels following an acute coronary syndrome. (Imaging of Coronary Plaques in Participants Treated With Evolocumab; NCT03570697)

Original language	English
Pages (from-to)	1308-1321
Number of pages	14
Journal	JACC: Cardiovascular Imaging
Volume	15
Issue number	7
DOIs	https://doi.org/10.1016/j.jcmg.2022.03.002
Publication status	Published - Jul 2022

Keywords

acute coronary syndromes
atherosclerosis
clinical trials
lipid lowering
PCSK9 inhibitor

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10.1016/j.jcmg.2022.03.002

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Nicholls, S. J., Kataoka, Y., Nissen, S. E., Prati, F., Windecker, S., Puri, R., Hucko, T., Aradi, D., Herrman, J. P. R., Hermanides, R. S., Wang, B., Wang, H., Butters, J., Di Giovanni, G., Jones, S., Pompili, G., & Psaltis, P. J. (2022). Effect of Evolocumab on Coronary Plaque Phenotype and Burden in Statin-Treated Patients Following Myocardial Infarction. JACC: Cardiovascular Imaging, 15(7), 1308-1321. https://doi.org/10.1016/j.jcmg.2022.03.002

@article{ee7839285b714583bdbb610fcda0670c,

title = "Effect of Evolocumab on Coronary Plaque Phenotype and Burden in Statin-Treated Patients Following Myocardial Infarction",

abstract = "Objectives: The purpose of this study was to determine the effect of evolocumab on optical coherence tomography (OCT) measures of plaque composition. Background: The proprotein convertase subtilisin kexin type-9 inhibitor evolocumab produced coronary atheroma regression in statin-treated patients. Methods: Patients with a non–ST-segment elevation myocardial infarction were treated with monthly evolocumab 420 mg (n = 80) or placebo (n = 81) for 52 weeks. Patients underwent serial OCT and intravascular ultrasound imaging within a matched arterial segment of a nonculprit vessel. The primary analysis determined the change in the minimum fibrous cap thickness and maximum lipid arc throughout the imaged arterial segment. Additional analyses determined changes in OCT features in lipid-rich plaque regions and plaque burden. Safety and tolerability were evaluated. Results: Among treated patients, (age 60.5 ± 9.6 years; 28.6% women; low-density lipoprotein cholesterol [LDL-C], 141.3 ± 33.1 mg/dL), 135 had evaluable imaging at follow-up. The evolocumab group achieved lower LDL-C levels (28.1 vs 87.2 mg/dL; P < 0.001). The evolocumab group demonstrated a greater increase in minimum fibrous cap thickness (+42.7 vs +21.5 μm; P = 0.015) and decrease in maximum lipid arc (−57.5o vs. −31.4o; P = 0.04) and macrophage index (−3.17 vs −1.45 mm; P = 0.04) throughout the arterial segment. Similar benefits of evolocumab were observed in lipid-rich plaque regions. Greater regression of percent atheroma volume was observed with evolocumab compared with placebo (−2.29% ± 0.47% vs −0.61% ± 0.46%; P = 0.009). The groups did not differ regarding changes in microchannels or calcium. Conclusions: The combination of statin and evolocumab after a non–ST-segment elevation myocardial infarction produces favorable changes in coronary atherosclerosis consistent with stabilization and regression. This demonstrates a potential mechanism for the improved clinical outcomes observed achieving very low LDL-C levels following an acute coronary syndrome. (Imaging of Coronary Plaques in Participants Treated With Evolocumab; NCT03570697)",

keywords = "acute coronary syndromes, atherosclerosis, clinical trials, lipid lowering, PCSK9 inhibitor",

author = "Nicholls, {Stephen J.} and Yu Kataoka and Nissen, {Steven E.} and Francesco Prati and Stephan Windecker and Rishi Puri and Thomas Hucko and Daniel Aradi and Herrman, {Jean Paul R.} and Hermanides, {Renicus S.} and Bei Wang and Huei Wang and Julie Butters and {Di Giovanni}, Giuseppe and Stephen Jones and Gianluca Pompili and Psaltis, {Peter J.}",

note = "Funding Information: In patients undergoing coronary angiography in the setting of an NSTEMI, we observed that the majority had at least 1 image containing a minimum FCT <65 ?m and more than 90% had a lipid-rich plaque in a nonculprit artery. This supports the systemic nature of high-risk features within atherosclerotic disease in patients with ACS. In the comparator group, where the majority of patients were treated with high-intensity statins, we also observed a significant increase in FCT and reduction in lipid arc. This finding underscores the benefits of intensive statins in patients following an ACS.2 However, in the group that also received evolocumab, lowering LDL-C to <30 mg/dL was associated with greater improvements in these plaque features, with only 12.5% of patients demonstrating any image containing an FCT <65 ?m. This suggests that more intensive lipid-lowering following an ACS may favorably affect high-risk plaques.After 12 months of treatment, with high treatment adherence, we observed an average LDL-C of 28.1 mg/dL with addition of evolocumab to a statin, with most patients achieving guideline mandated LDL-C goals for high-risk <70 mg/dL (94%) and very high-risk <55 mg/dL (86%). The likely role of intensive lipid lowering in the finding of plaque stabilization is supported by observations of a direct relationship between the degree of LDL-C lowering or achieved LDL-C levels and increasing FCT. This reaffirms the benefits of maintaining intensive lipid lowering for the first year after an ACS on the natural history of coronary atherosclerosis. The early benefits on plaque phenotype complement the favorable effects of the combination of evolocumab and statins on plaque progression in longer-term imaging studies.16Serial IVUS demonstrated that intensive statin therapy promotes coronary atheroma regression, with the degree of benefit directly proportional to the extent of lipid lowering.13,14 These benefits were extended with combination therapy, in which use of either ezetimibe15 or a PCSK9 inhibitor,16 in addition to background statin treatment, produced incremental plaque regression compared with statin alone. In those patients with evaluable IVUS imaging at both time points in HUYGENS, we observed a greater degree of regression with evolocumab than previously reported in the GLobal Assessment of Plaque reGression With a PCSK9 antibOdy as Measured by intraVascular Ultrasound (GLAGOV) study. This may reflect the presence of greater plaque burden at baseline in patients following an ACS. The importance of these findings is supported by the association between both plaque burden and progression with cardiovascular events.26,27 There is also interest in understanding the impact of these therapies on atheroma composition given the role of high-risk plaques, with a large accumulation of lipid and inflammatory material covered by a thin fibrous cap, in ACS.24 We extend reports that statins have a favorable effect on FCT17 to demonstrate that addition of evolocumab to intensive statin therapy promotes greater thickening of the fibrous cap and reduction in plaque lipid content, compared with statin monotherapy. This complements a small observational study demonstrating early increases in FCT and a reduction in lipid arc in patients treated with the combination of statin and evolocumab following an ACS.28 Funding Information: This study was sponsored by Amgen Inc. Dr Nicholls is a recipient of a Principal Research Fellowship from the National Health and Medical Research Council of Australia; has received research support from AstraZeneca, Amgen, Anthera, CSL Behring, Cerenis, Eli Lilly, Esperion, Resverlogix, Novartis, InfraReDx, and Sanofi-Regeneron; and is a consultant for Amgen, Akcea, AstraZeneca, Boehringer Ingelheim, CSL Behring, Eli Lilly, Esperion, Kowa, Merck, Takeda, Pfizer, Sanofi-Regeneron and Novo Nordisk. Dr Kataoka has received research support from Kowa; and has received speaker honoraria from Abbott Vascular, Amgen, CSL Behring, Daiichi Sankyo, Kowa, Nipro, and Takeda. Dr Nissen has reported that the Cleveland Clinic Center for Clinical Research has received funding to perform clinical trials from AbbVie, AstraZeneca, Amgen, Cerenis, Eli Lilly, Esperion, Medtronic, MyoKardia, Novartis, Pfizer, The Medicines Company, Silence Therapeutics, Takeda, and Orexigen; is involved in these clinical trials but receives no personal remuneration for his participation; and has served as a consultant for many pharmaceutical companies, but requires them to donate all honoraria or consulting fees directly to charity so that he receives neither income nor a tax deduction. Dr Prati has received consulting fees from Amgen and Abbott Vascular. Dr Windecker has received research and educational grants to the institution from Abbott, Amgen, AstraZeneca, Bristol Myers Squibb, Bayer, Biotronik, Boston Scientific, Cardinal Health, CardioValve, CSL Behring, Daiichi Sankyo, Edwards Lifesciences, Guerbet, InfraRedx, Johnson & Johnson, Medicure, Medtronic, Novartis, Polares, OrPha Suisse, Pfizer, Regeneron, Sanofi-Aventis, Sinomed, Terumo, and V-Wave; has served as unpaid advisory board member and/or unpaid member of the steering/executive group of trials funded by Abbott, Abiomed, Amgen, AstraZeneca, Bayer, Bristol Myers Squibb, Boston Scientific, Biotronik, Cardiovalve, Edwards Lifesciences, MedAlliance, Medtronic, Novartis, Polares, Sinomed, Terumo, V-Wave, and Xeltis, but has not received personal payments by pharmaceutical companies or device manufacturers; and is a member of the steering/executive committee group of several investigator-initiated trials that receive funding by industry without impact on his personal remuneration. Dr Puri has received speaker fees from Amgen and Sanofi; has served as a consultant for Cerenis, Medtronic, Philips, Boston Scientific, and Shockwave; has served on advisory boards for Centerline Biomedical, Medtronic, and Bioventrix; and holds minor equity in Centerline Biomedical. Drs Hucko, Wang, and Wang are employees of Amgen and hold Amgen stock/stock options. Dr Aradi has received speaker fees from AstraZeneca, Bayer, Pfizer, Merck Sharp & Dohme Pharma, Boehringer, Vascular Venture, and Amgen. Dr Psaltis is a recipient of a L2 Future Leader Fellowship from the National Heart Foundation of Australia (FLF102056) and a L2 Career Development Fellowship from the National Health and Medical Research Council of Australia (CDF1161506); has received research support from Abbott Vascular; has received consulting fees from Amgen and Esperion; and has received speaker honoraria from AstraZeneca, Bayer, Boehringer Ingelheim, Merck Schering-Plough, and Pfizer. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Publisher Copyright: {\textcopyright} 2022 American College of Cardiology Foundation",

year = "2022",

month = jul,

doi = "10.1016/j.jcmg.2022.03.002",

language = "English",

volume = "15",

pages = "1308--1321",

journal = "JACC: Cardiovascular Imaging",

issn = "1876-7591",

publisher = "Elsevier",

number = "7",

}

Nicholls, SJ, Kataoka, Y, Nissen, SE, Prati, F, Windecker, S, Puri, R, Hucko, T, Aradi, D, Herrman, JPR, Hermanides, RS, Wang, B, Wang, H, Butters, J, Di Giovanni, G, Jones, S, Pompili, G & Psaltis, PJ 2022, 'Effect of Evolocumab on Coronary Plaque Phenotype and Burden in Statin-Treated Patients Following Myocardial Infarction', JACC: Cardiovascular Imaging, vol. 15, no. 7, pp. 1308-1321. https://doi.org/10.1016/j.jcmg.2022.03.002

TY - JOUR

T1 - Effect of Evolocumab on Coronary Plaque Phenotype and Burden in Statin-Treated Patients Following Myocardial Infarction

AU - Nicholls, Stephen J.

AU - Kataoka, Yu

AU - Nissen, Steven E.

AU - Prati, Francesco

AU - Windecker, Stephan

AU - Puri, Rishi

AU - Hucko, Thomas

AU - Aradi, Daniel

AU - Herrman, Jean Paul R.

AU - Hermanides, Renicus S.

AU - Wang, Bei

AU - Wang, Huei

AU - Butters, Julie

AU - Di Giovanni, Giuseppe

AU - Jones, Stephen

AU - Pompili, Gianluca

AU - Psaltis, Peter J.

N1 - Funding Information: In patients undergoing coronary angiography in the setting of an NSTEMI, we observed that the majority had at least 1 image containing a minimum FCT <65 ?m and more than 90% had a lipid-rich plaque in a nonculprit artery. This supports the systemic nature of high-risk features within atherosclerotic disease in patients with ACS. In the comparator group, where the majority of patients were treated with high-intensity statins, we also observed a significant increase in FCT and reduction in lipid arc. This finding underscores the benefits of intensive statins in patients following an ACS.2 However, in the group that also received evolocumab, lowering LDL-C to <30 mg/dL was associated with greater improvements in these plaque features, with only 12.5% of patients demonstrating any image containing an FCT <65 ?m. This suggests that more intensive lipid-lowering following an ACS may favorably affect high-risk plaques.After 12 months of treatment, with high treatment adherence, we observed an average LDL-C of 28.1 mg/dL with addition of evolocumab to a statin, with most patients achieving guideline mandated LDL-C goals for high-risk <70 mg/dL (94%) and very high-risk <55 mg/dL (86%). The likely role of intensive lipid lowering in the finding of plaque stabilization is supported by observations of a direct relationship between the degree of LDL-C lowering or achieved LDL-C levels and increasing FCT. This reaffirms the benefits of maintaining intensive lipid lowering for the first year after an ACS on the natural history of coronary atherosclerosis. The early benefits on plaque phenotype complement the favorable effects of the combination of evolocumab and statins on plaque progression in longer-term imaging studies.16Serial IVUS demonstrated that intensive statin therapy promotes coronary atheroma regression, with the degree of benefit directly proportional to the extent of lipid lowering.13,14 These benefits were extended with combination therapy, in which use of either ezetimibe15 or a PCSK9 inhibitor,16 in addition to background statin treatment, produced incremental plaque regression compared with statin alone. In those patients with evaluable IVUS imaging at both time points in HUYGENS, we observed a greater degree of regression with evolocumab than previously reported in the GLobal Assessment of Plaque reGression With a PCSK9 antibOdy as Measured by intraVascular Ultrasound (GLAGOV) study. This may reflect the presence of greater plaque burden at baseline in patients following an ACS. The importance of these findings is supported by the association between both plaque burden and progression with cardiovascular events.26,27 There is also interest in understanding the impact of these therapies on atheroma composition given the role of high-risk plaques, with a large accumulation of lipid and inflammatory material covered by a thin fibrous cap, in ACS.24 We extend reports that statins have a favorable effect on FCT17 to demonstrate that addition of evolocumab to intensive statin therapy promotes greater thickening of the fibrous cap and reduction in plaque lipid content, compared with statin monotherapy. This complements a small observational study demonstrating early increases in FCT and a reduction in lipid arc in patients treated with the combination of statin and evolocumab following an ACS.28 Funding Information: This study was sponsored by Amgen Inc. Dr Nicholls is a recipient of a Principal Research Fellowship from the National Health and Medical Research Council of Australia; has received research support from AstraZeneca, Amgen, Anthera, CSL Behring, Cerenis, Eli Lilly, Esperion, Resverlogix, Novartis, InfraReDx, and Sanofi-Regeneron; and is a consultant for Amgen, Akcea, AstraZeneca, Boehringer Ingelheim, CSL Behring, Eli Lilly, Esperion, Kowa, Merck, Takeda, Pfizer, Sanofi-Regeneron and Novo Nordisk. Dr Kataoka has received research support from Kowa; and has received speaker honoraria from Abbott Vascular, Amgen, CSL Behring, Daiichi Sankyo, Kowa, Nipro, and Takeda. Dr Nissen has reported that the Cleveland Clinic Center for Clinical Research has received funding to perform clinical trials from AbbVie, AstraZeneca, Amgen, Cerenis, Eli Lilly, Esperion, Medtronic, MyoKardia, Novartis, Pfizer, The Medicines Company, Silence Therapeutics, Takeda, and Orexigen; is involved in these clinical trials but receives no personal remuneration for his participation; and has served as a consultant for many pharmaceutical companies, but requires them to donate all honoraria or consulting fees directly to charity so that he receives neither income nor a tax deduction. Dr Prati has received consulting fees from Amgen and Abbott Vascular. Dr Windecker has received research and educational grants to the institution from Abbott, Amgen, AstraZeneca, Bristol Myers Squibb, Bayer, Biotronik, Boston Scientific, Cardinal Health, CardioValve, CSL Behring, Daiichi Sankyo, Edwards Lifesciences, Guerbet, InfraRedx, Johnson & Johnson, Medicure, Medtronic, Novartis, Polares, OrPha Suisse, Pfizer, Regeneron, Sanofi-Aventis, Sinomed, Terumo, and V-Wave; has served as unpaid advisory board member and/or unpaid member of the steering/executive group of trials funded by Abbott, Abiomed, Amgen, AstraZeneca, Bayer, Bristol Myers Squibb, Boston Scientific, Biotronik, Cardiovalve, Edwards Lifesciences, MedAlliance, Medtronic, Novartis, Polares, Sinomed, Terumo, V-Wave, and Xeltis, but has not received personal payments by pharmaceutical companies or device manufacturers; and is a member of the steering/executive committee group of several investigator-initiated trials that receive funding by industry without impact on his personal remuneration. Dr Puri has received speaker fees from Amgen and Sanofi; has served as a consultant for Cerenis, Medtronic, Philips, Boston Scientific, and Shockwave; has served on advisory boards for Centerline Biomedical, Medtronic, and Bioventrix; and holds minor equity in Centerline Biomedical. Drs Hucko, Wang, and Wang are employees of Amgen and hold Amgen stock/stock options. Dr Aradi has received speaker fees from AstraZeneca, Bayer, Pfizer, Merck Sharp & Dohme Pharma, Boehringer, Vascular Venture, and Amgen. Dr Psaltis is a recipient of a L2 Future Leader Fellowship from the National Heart Foundation of Australia (FLF102056) and a L2 Career Development Fellowship from the National Health and Medical Research Council of Australia (CDF1161506); has received research support from Abbott Vascular; has received consulting fees from Amgen and Esperion; and has received speaker honoraria from AstraZeneca, Bayer, Boehringer Ingelheim, Merck Schering-Plough, and Pfizer. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Publisher Copyright: © 2022 American College of Cardiology Foundation

PY - 2022/7

Y1 - 2022/7

N2 - Objectives: The purpose of this study was to determine the effect of evolocumab on optical coherence tomography (OCT) measures of plaque composition. Background: The proprotein convertase subtilisin kexin type-9 inhibitor evolocumab produced coronary atheroma regression in statin-treated patients. Methods: Patients with a non–ST-segment elevation myocardial infarction were treated with monthly evolocumab 420 mg (n = 80) or placebo (n = 81) for 52 weeks. Patients underwent serial OCT and intravascular ultrasound imaging within a matched arterial segment of a nonculprit vessel. The primary analysis determined the change in the minimum fibrous cap thickness and maximum lipid arc throughout the imaged arterial segment. Additional analyses determined changes in OCT features in lipid-rich plaque regions and plaque burden. Safety and tolerability were evaluated. Results: Among treated patients, (age 60.5 ± 9.6 years; 28.6% women; low-density lipoprotein cholesterol [LDL-C], 141.3 ± 33.1 mg/dL), 135 had evaluable imaging at follow-up. The evolocumab group achieved lower LDL-C levels (28.1 vs 87.2 mg/dL; P < 0.001). The evolocumab group demonstrated a greater increase in minimum fibrous cap thickness (+42.7 vs +21.5 μm; P = 0.015) and decrease in maximum lipid arc (−57.5o vs. −31.4o; P = 0.04) and macrophage index (−3.17 vs −1.45 mm; P = 0.04) throughout the arterial segment. Similar benefits of evolocumab were observed in lipid-rich plaque regions. Greater regression of percent atheroma volume was observed with evolocumab compared with placebo (−2.29% ± 0.47% vs −0.61% ± 0.46%; P = 0.009). The groups did not differ regarding changes in microchannels or calcium. Conclusions: The combination of statin and evolocumab after a non–ST-segment elevation myocardial infarction produces favorable changes in coronary atherosclerosis consistent with stabilization and regression. This demonstrates a potential mechanism for the improved clinical outcomes observed achieving very low LDL-C levels following an acute coronary syndrome. (Imaging of Coronary Plaques in Participants Treated With Evolocumab; NCT03570697)

AB - Objectives: The purpose of this study was to determine the effect of evolocumab on optical coherence tomography (OCT) measures of plaque composition. Background: The proprotein convertase subtilisin kexin type-9 inhibitor evolocumab produced coronary atheroma regression in statin-treated patients. Methods: Patients with a non–ST-segment elevation myocardial infarction were treated with monthly evolocumab 420 mg (n = 80) or placebo (n = 81) for 52 weeks. Patients underwent serial OCT and intravascular ultrasound imaging within a matched arterial segment of a nonculprit vessel. The primary analysis determined the change in the minimum fibrous cap thickness and maximum lipid arc throughout the imaged arterial segment. Additional analyses determined changes in OCT features in lipid-rich plaque regions and plaque burden. Safety and tolerability were evaluated. Results: Among treated patients, (age 60.5 ± 9.6 years; 28.6% women; low-density lipoprotein cholesterol [LDL-C], 141.3 ± 33.1 mg/dL), 135 had evaluable imaging at follow-up. The evolocumab group achieved lower LDL-C levels (28.1 vs 87.2 mg/dL; P < 0.001). The evolocumab group demonstrated a greater increase in minimum fibrous cap thickness (+42.7 vs +21.5 μm; P = 0.015) and decrease in maximum lipid arc (−57.5o vs. −31.4o; P = 0.04) and macrophage index (−3.17 vs −1.45 mm; P = 0.04) throughout the arterial segment. Similar benefits of evolocumab were observed in lipid-rich plaque regions. Greater regression of percent atheroma volume was observed with evolocumab compared with placebo (−2.29% ± 0.47% vs −0.61% ± 0.46%; P = 0.009). The groups did not differ regarding changes in microchannels or calcium. Conclusions: The combination of statin and evolocumab after a non–ST-segment elevation myocardial infarction produces favorable changes in coronary atherosclerosis consistent with stabilization and regression. This demonstrates a potential mechanism for the improved clinical outcomes observed achieving very low LDL-C levels following an acute coronary syndrome. (Imaging of Coronary Plaques in Participants Treated With Evolocumab; NCT03570697)

KW - acute coronary syndromes

KW - atherosclerosis

KW - clinical trials

KW - lipid lowering

KW - PCSK9 inhibitor

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U2 - 10.1016/j.jcmg.2022.03.002

DO - 10.1016/j.jcmg.2022.03.002

M3 - Article

C2 - 35431172

AN - SCOPUS:85128112048

SN - 1876-7591

VL - 15

SP - 1308

EP - 1321

JO - JACC: Cardiovascular Imaging

JF - JACC: Cardiovascular Imaging

IS - 7

ER -

Effect of Evolocumab on Coronary Plaque Phenotype and Burden in Statin-Treated Patients Following Myocardial Infarction

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