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4. Discovery of an embryonically derived bipotent population of endothelial-macrophage progenitor cells in postnatal aorta

Author

Williamson, Anna E., Liyanage, Sanuri, Hassanshahi, Mohammadhossein, Dona, Malathi S. I., Toledo-Flores, Deborah, Tran, Dang X. A., Dimasi, Catherine, Schwarz, Nisha, Fernando, Sanuja, Salagaras, Thalia, Long, Aaron, Kazenwadel, Jan, Harvey, Natasha L., Drummond, Grant R., Vinh, Antony, Chandrakanthan, Vashe, Misra, Ashish, Neufeld, Zoltan, Tan, Joanne T. M., Martelotto, Luciano, Polo, Jose M., Bonder, Claudine S., Pinto, Alexander R., Sharma, Shiwani, Nicholls, Stephen J., Bursill, Christina A., and Psaltis, Peter J.

Published
2024
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7. Discovery of potent small-molecule inhibitors of lipoprotein(a) formation

Author

Diaz, Nuria, Perez, Carlos, Escribano, Ana Maria, Sanz, Gema, Priego, Julian, Lafuente, Celia, Barberis, Mario, Calle, Luis, Espinosa, Juan Felix, Priest, Birgit T., Zhang, Hong Y., Nosie, Amanda K., Haas, Joseph V., Cannady, Ellen, Borel, Anthony, Schultze, Albert E., Sauder, J. Michael, Hendle, Jörg, Weichert, Ken, Nicholls, Stephen J., and Michael, Laura F.

Published
2024
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10. Patient-Specific Myocardial Infarction Risk Thresholds From AI-Enabled Coronary Plaque Analysis

Author

Miller, Robert J.H., Manral, Nipun, Lin, Andrew, Shanbhag, Aakash, Park, Caroline, Kwiecinski, Jacek, Killekar, Aditya, McElhinney, Priscilla, Matsumoto, Hidenari, Razipour, Aryabod, Grodecki, Kajetan, Kwan, Alan C., Han, Donghee, Kuronuma, Keiichiro, Flores Tomasino, Guadalupe, Geers, Jolien, Goeller, Markus, Marwan, Mohamed, Gransar, Heidi, Tamarappoo, Balaji K., Cadet, Sebastien, Cheng, Victor Y., Achenbach, Stephan, Nicholls, Stephen J., Wong, Dennis T., Chen, Lu, Cao, J. Jane, Berman, Daniel S., Dweck, Marc R., Newby, David E., Williams, Michelle C., Slomka, Piotr J., and Dey, Damini

Published
2024
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12. Contributors

Author

Agha, Ali M., primary, Alexander, Lydia C., additional, Ballantyne, Christie M., additional, Bays, Harold, additional, Bhatt, Deepak L., additional, Blumenthal, Roger S., additional, Boffa, Michael B., additional, Bond, Rachel M., additional, Brandts, Julia M., additional, Brinton, Eliot A., additional, Brothers, Julie A., additional, Catapano, Alberico L., additional, Chan, Dick C., additional, Chiavaroli, Laura, additional, Cho, Laura Browning, additional, Cho, Leslie, additional, Cummings, Danielle, additional, Daniels, Stephen R., additional, Deshotels, Matthew R., additional, Dove, Erik, additional, Feldman, David I., additional, Fellström, Bengt, additional, Ferdinand, Keith C., additional, Fichtenbaum, Carl J., additional, Fitch, Angela, additional, Gaudet, Daniel, additional, Ginsberg, Henry N., additional, Gluckman, Ty J., additional, Hegele, Robert A., additional, Hoogeveen, Ron C., additional, Hussain, Aliza, additional, Jardine, Alan G., additional, Jenkins, David J.A., additional, Jones, Peter H., additional, Jones, Peter, additional, Kachur, Sergey M., additional, Kendall, Cyril W.C., additional, Knowles, Joshua W., additional, Kobashigawa, Jon A., additional, Koschinsky, Marlys L., additional, Kris-Etherton, Penny M., additional, Lavie, Carl J., additional, Libby, Peter, additional, Marcovina, Santica M., additional, Mark, Patrick B., additional, Marston, Nicholas A., additional, Martin, Seth Shay, additional, Michos, Erin D., additional, Mirrahimi, Arash, additional, Mora, Samia, additional, Moriarty, Patrick M., additional, Nambi, Vijay, additional, Nelson, Adam J., additional, Nicholls, Stephen J., additional, Nissen, Steven E., additional, Nordestgaard, Børge Grønne, additional, Norata, Giuseppe Danilo, additional, Orringer, Carl, additional, Palmisano, Brian T., additional, Patel, Darshna, additional, Patel, Rajan K., additional, Pulipati, Vishnu Priya, additional, Raal, Frederick J., additional, Rader, Daniel J., additional, Ray, Kausik K., additional, Richter, Chesney, additional, Ridker, Paul M., additional, Sabatine, Marc S., additional, Safarova, Maya S., additional, Santos, Raul D., additional, Saseen, Joseph J., additional, Schwartz, Gregory G., additional, Shustak, Rachel J., additional, Sievenpiper, John L., additional, Singh, Nickpreet, additional, Skulas-Ray, Ann C., additional, Srichaikul, Kristie, additional, Stone, Neil J., additional, Tokgözoğlu, Lale, additional, Tybjærg-Hansen, Anne, additional, Virani, Salim S., additional, Watson, Karol, additional, Watts, Gerald F., additional, Wenger, Nanette K., additional, and Wong, Julia M.W., additional

Published
2024
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14. Aspirin for Primary Prevention of Cardiovascular Events in Relation to Lipoprotein(a) Genotypes

Author

Lacaze, Paul, Bakshi, Andrew, Riaz, Moeen, Polekhina, Galina, Owen, Alice, Bhatia, Harpreet S, Natarajan, Pradeep, Wolfe, Rory, Beilin, Lawrence, Nicholls, Stephen J, Watts, Gerald F, McNeil, John J, Tonkin, Andrew M, and Tsimikas, Sotirios

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Research, Cardiovascular, Prevention, Clinical Trials and Supportive Activities, Patient Safety, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Good Health and Well Being, Aged, Aspirin, Cardiovascular Diseases, Genotype, Humans, Lipoprotein(a), Primary Prevention, aspirin, cardiovascular disease, genetics, lipoprotein(a), primary prevention, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundThe role of aspirin in reducing lipoprotein(a)-mediated atherothrombotic events in primary prevention is not established.ObjectivesThis study sought to assess whether low-dose aspirin benefits individuals with elevated plasma lipoprotein(a)-associated genotypes in the setting of primary prevention.MethodsThe study analyzed 12,815 genotyped individuals ≥70 years of age of European ancestry and without prior cardiovascular disease events enrolled in the ASPREE (ASPirin in Reducing Events in the Elderly) randomized controlled trial of 100 mg/d aspirin. We defined lipoprotein(a)-associated genotypes using rs3798220-C carrier status and quintiles of a lipoprotein(a) genomic risk score (LPA-GRS). We tested for interaction between genotypes and aspirin allocation in Cox proportional hazards models for incidence of major adverse cardiovascular events (MACE) and clinically significant bleeding. We also examined associations in the aspirin and placebo arms of the trial separately.ResultsDuring a median 4.7 years (IQR: 3.6-5.7 years) of follow-up, 435 MACE occurred, with an interaction observed between rs3798220-C and aspirin allocation (P = 0.049). rs3798220-C carrier status was associated with increased MACE risk in the placebo group (HR: 1.90; 95% CI: 1.11-3.24) but not in the aspirin group (HR: 0.54; 95% CI: 0.17-1.70). High LPA-GRS (vs low) was associated with increased MACE risk in the placebo group (HR: 1.70; 95% CI: 1.14-2.55), with risk attenuated in the aspirin group (HR: 1.41; 95% CI: 0.90-2.23), but the interaction was not statistically significant. In all participants, aspirin reduced MACE by 1.7 events per 1,000 person-years and increased clinically significant bleeding by 1.7 events per 1,000 person-years. However, in the rs3798220-C and high LPA-GRS subgroups, aspirin reduced MACE by 11.4 and 3.3 events per 1,000 person-years respectively, without significantly increased bleeding risk.ConclusionsAspirin may benefit older individuals with elevated lipoprotein(a) genotypes in primary prevention.

Published
2022

15. Lipoprotein(a) levels in a global population with established atherosclerotic cardiovascular disease

Author

Nissen, Steven E, Wolski, Kathy, Cho, Leslie, Nicholls, Stephen J, Kastelein, John, Leitersdorf, Eran, Landmesser, Ulf, Blaha, Michael, Lincoff, A Michael, Morishita, Ryuichi, Tsimikas, Sotirios, Liu, Junhao, Manning, Brian, Kozlovski, Plamen, Lesogor, Anastasia, Thuren, Tom, Shibasaki, Taro, Matei, Florin, Silveira, Fábio Serra, Meunch, Andreas, Bada, Aysha, Vijan, Vinod, Bruun, Niels Eske, Nordestgaard, Borge G, and Investigators, For the LpHERITAGE

Subjects
Clinical Research, Atherosclerosis, Cardiovascular, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Good Health and Well Being, Female, Humans, Male, Middle Aged, Brain Ischemia, Cardiovascular Diseases, Cholesterol, LDL, Cross-Sectional Studies, Lipoprotein(a), Stroke, Aged, Lp(a)HERITAGE Investigators, atherosclerosis, global burden of disease, hyperlipidemias
Abstract

ObjectiveLipoprotein(a) (Lp(a)) is an important genetically determined risk factor for atherosclerotic vascular disease (ASCVD). With the development of Lp(a)-lowering therapies, this study sought to characterise patterns of Lp(a) levels in a global ASCVD population and identify racial, ethnic, regional and gender differences.MethodsA multicentre cross-sectional epidemiological study to estimate the prevalence of elevated Lp(a) in patients with a history of myocardial infarction, ischaemic stroke or peripheral artery disease conducted at 949 sites in 48 countries in North America, Europe, Asia, South America, South Africa and Australia between April 2019 and July 2021. Low-density lipoprotein cholesterol (LDL-C) and Lp(a) levels were measured either as mass (mg/dL) or molar concentration (nmol/L).ResultsOf 48 135 enrolled patients, 13.9% had prior measurements of Lp(a). Mean age was 62.6 (SD 10.1) years and 25.9% were female. Median Lp(a) was 18.0 mg/dL (IQR 7.9-57.1) or 42.0 nmol/L (IQR 15.0-155.4). Median LDL-C was 77 mg/dL (IQR 58.4-101.0). Lp(a) in women was higher, 22.8 (IQR 9.0-73.0) mg/dL, than in men, 17.0 (IQR 7.1-52.2) mg/dL, p50 mg/dL, 20.7% had levels >70 mg/dL, 12.9% were >90 mg/dL and 26.0% of patients exceeded 150 nmol/L.ConclusionsGlobally, Lp(a) is measured in a small minority of patients with ASCVD and is highest in black, younger and female patients. More than 25% of patients had levels exceeding the established threshold for increased cardiovascular risk, approximately 50 mg/dL or 125 nmol/L.Trial registration number

Published
2022

16. Reduction in the risk of major adverse cardiovascular events with the BET protein inhibitor apabetalone in patients with recent acute coronary syndrome, type 2 diabetes, and moderate to high likelihood of non-alcoholic fatty liver disease

Author

Toth, Peter P, Schwartz, Gregory G, Nicholls, Stephen J, Khan, Aziz, Szarek, Michael, Ginsberg, Henry N, Johansson, Jan O, Kalantar-Zadeh, Kamyar, Kulikowski, Ewelina, Lebioda, Ken, Wong, Norman CW, Sweeney, Michael, Ray, Kausik K, and Investigators, BETonMACE

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Cardiovascular, Chronic Liver Disease and Cirrhosis, Prevention, Liver Disease, Heart Disease, Clinical Trials and Supportive Activities, Clinical Research, Heart Disease - Coronary Heart Disease, Digestive Diseases, Atherosclerosis, Diabetes, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Good Health and Well Being, Apabetalone, Cardiovascular events, Fibrosis, Nonalcoholic fatty liver disease, BETonMACE Investigators, ACS, Acute coronary syndrome, ALP, Alkaline Phosphatase, ALT, Alanine aminotransferase, APR, Acute phase reactant, AST, Aspartate aminotransferase, ApoAI, Aproprotein-AI, BD, Bromodoamin, BET, Bromodomain and extraterminal proteinfamily, BMI, Body mass index, CV, Cardiovascular, CVD, Cardiovascular Disease, FS, Fibrosis score, HDL-C, High density lipoprotein cholesterol, HHF, Hospitalization for heart Failure, HR, Hazard ratio, MACE, Major acute coronary event, NAFLD, Nonalcoholic fatty liver disease, T2DM, Type 2 diabetes mellitus, Cardiovascular medicine and haematology
Abstract

BackgroundNonalcoholic fatty liver disease (NAFLD) is common among patients with type 2 diabetes mellitus (T2DM) and is associated with increased risk for coronary atherosclerosis and acute cardiovascular (CV) events. We employed the validated, non-invasive Angulo NAFLD fibrosis score (FS) in an intervention study in patients with T2DM and recent acute coronary syndrome (ACS) to determine the association of FS with CV risk and treatment response to apabetalone. Apabetalone is a novel selective inhibitor of the second bromodomain of bromodomain and extra-terminal (BET) proteins, epigenetic regulators of gene expression.MethodsThe Phase 3 BETonMACE trial compared apabetalone with placebo in 2,425 patients with T2DM and recent ACS. In this post hoc analysis, we evaluated the impact of apabetalone therapy on CV risk, defined as a composite of major adverse cardiovascular events (MACE: CV death, non-fatal myocardial infarction [MI], or stroke) and hospitalization for heart failure (HHF) in two patient categories of FS that reflect the likelihood of underlying NAFLD. Patients were initially classified into three mutually exclusive categories according to a baseline Angulo FS 0.675 (F3-F4), where F0 through F4 connote fibrosis severity none, mild, moderate, severe, and cirrhosis, respectively. The composite of ischemic MACE and HHF in the placebo group was higher in indeterminant and F3-F4 categories compared to the F0-F2 category (17.2% vs 15.0% vs 9.7%). Therefore, for the present analysis, the former two categories were combined into an elevated NAFLD CVD risk group (FS+) that was compared with the F0-F2 group (lower NAFLD risk, FS0-2).ResultsIn 73.7% of patients, FS was elevated and consistent with a moderate-to-high likelihood of advanced liver fibrosis (FS+); 26.3% of patients had a lower FS (FS0-2). In the placebo group, FS+ patients had a higher incidence of ischemic MACE and HHF (15.4%) than FS0-2 patients (9.7%). In FS+ patients, addition of apabetalone to standard of care treatment lowered the rate of ischemic MACE compared with placebo (HR = 0.79; 95% CI 0.60-1.05; p=0.10), HHF (HR = 0.53; 95% CI 0.33-0.86; p=0.01), and the composite of ischemic MACE and HHF (HR = 0.76; 95% CI 0.59-0.98; p=0.03). In contrast, there was no apparent benefit of apabetalone in FS0-2 patients (HR 1.24; 95% CI 0.75-2.07; p=0.40; HR 1.12; 95% CI 0.30-4.14; p=0.87; and HR 1.13; 95% CI 0.69-1.86; p=0.62, respectively). Over a median duration of 26.5 months, FS increased from baseline in both treatment groups, but the increase was smaller in patients assigned to apabetalone than to placebo (p=0.04).ConclusionsAmongst patients with T2DM, recent ACS, and a moderate-to-high likelihood of advanced liver fibrosis, apabetalone was associated with a significantly lower rate of ischemic MACE and HHF and attenuated the increase in hepatic FS over time.

Published
2022

17. ApoA-I Infusions and Burden of Ischemic Events After Acute Myocardial Infarction: Insights From the AEGIS-II Trial

Author

Gibson, C. Michael, Chi, Gerald, Duffy, Danielle, Bahit, M. Cecilia, White, Harvey, Korjian, Serge, Alexander, John H., Lincoff, A. Michael, Anschuetz, Gaya, Girgis, Ihab G., Nicolau, Jose C., Lopes, Renato D., Cornel, Jan H., Bainey, Kevin R., Libby, Peter, Sacks, Frank M., Ridker, Paul M, Goodman, Shaun G., Mahaffey, Kenneth W., Nicholls, Stephen J., Pocock, Stuart J., Mehran, Roxana, and Harrington, Robert A.

Published
2024
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23. Characterization of plaque phenotypes exhibiting an elevated pericoronary adipose tissue attenuation: insights from the REASSURE-NIRS registry

Author

Kitahara, Satoshi, Kataoka, Yu, Miura, Hiroyuki, Nishii, Tatsuya, Nishimura, Kunihiro, Murai, Kota, Iwai, Takamasa, Matama, Hideo, Honda, Satoshi, Fujino, Masashi, Yoneda, Shuichi, Takagi, Kensuke, Otsuka, Fumiyuki, Asaumi, Yasuhide, Fujino, Yusuke, Tsujita, Kenichi, Puri, Rishi, Nicholls, Stephen J., and Noguchi, Teruo

Published
2023
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24. Calcified plaque harboring lipidic materials associates with no-reflow phenomenon after PCI in stable CAD

Author

Hosoda, Hayato, Kataoka, Yu, Nicholls, Stephen J., Puri, Rishi, Murai, Kota, Kitahara, Satoshi, Mitsui, Kentaro, Sugane, Hiroki, Sawada, Kenichiro, Iwai, Takamasa, Matama, Hideo, Honda, Satoshi, Takagi, Kensuke, Fujino, Masashi, Yoneda, Shuichi, Otsuka, Fumiyuki, Takamisawa, Itaru, Nishihira, Kensaku, Asaumi, Yasuhide, Kawai, Kazuya, and Noguchi, Teruo

Published
2023
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26. Obicetrapib on top of maximally tolerated lipid‐modifying therapies in participants with or at high risk for atherosclerotic cardiovascular disease: rationale and designs of BROADWAY and BROOKLYN

Author

Nicholls, Stephen J., Nelson, Adam J., Ditmarsch, Marc, Kastelein, John J.P., Ballantyne, Christie M., Ray, Kausik K., Navar, Ann Marie, Nissen, Steven E., Golberg, Anne C., Brunham, Liam R., Curcio, Danielle, Wuerdeman, Erin, Neild, Annie, Kling, Douglas, Hsieh, Andrew, Dicklin, Mary R., Ference, Brian A., Laufs, Ulrich, Banach, Maciej, Mehran, Roxana, Catapano, Alberico L., and Davidson, Michael H.

Published
2024
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27. Clinical Effectiveness and Utilisation of Cardiac Rehabilitation After Hospital Discharge: Data Linkage Analysis of 84,064 Eligible Discharged Patients (2016–2021)

Author

Beleigoli, Alline, Foote, Jonathon, Gebremichael, Lemlem G., Bulamu, Norma B., Astley, Carolyn, Keech, Wendy, Tavella, Rosanna, Gulyani, Aarti, Nesbitt, Katie, Pinero de Plaza, Maria Alejandra, Ramos, Joyce S., Ludlow, Marie, Nicholls, Stephen J., Chew, Derek P., Beltrame, John, and Clark, Robyn A.

Published
2024
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28. Effect of Reconstituted Human Apolipoprotein A-I on Recurrent Ischemic Events in Survivors of Acute MI

Author

Povsic, Thomas J., Korjian, Serge, Bahit, M. Cecilia, Chi, Gerald, Duffy, Danielle, Alexander, John H., Vinereanu, Dragos, Tricoci, Pierluigi, Mears, Sojaita Jenny, Deckelbaum, Lawrence I., Bonaca, Marc, Ridker, Paul M., Goodman, Shaun G., Cornel, Jan H., Lewis, Basil S., Parkhomenko, Alexander, Lopes, Renato D., Aylward, Philip, Lincoff, A. Michael, Heise, Mark, Sacks, Frank, Nicolau, Jose C., Merkely, Bela, Trebacz, Jaroslaw, Libby, Peter, Nicholls, Stephen J., Pocock, Stuart, Bhatt, Deepak L., Kastelein, John, Bode, Christoph, Mahaffey, Kenneth W., Steg, P. Gabriel, Tendera, Michal, Bainey, Kevin R., Harrington, Robert A., Mehran, Roxana, Duerschmied, Daniel, Kingwell, Bronwyn A., and Gibson, C. Michael

Published
2024
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30. Glucagon-like Peptide-1 analogues and delipidation of coronary atheroma in statin-treated type 2 diabetic patients with coronary artery disease: The prespecified sub-analysis of the OPTIMAL randomized clinical trial

Author

Kataoka, Yu, Kitahara, Satoshi, Funabashi, Sayaka, Makino, Hisashi, Matsubara, Masaki, Matsuo, Miki, Omura-Ohata, Yoko, Koezuka, Ryo, Tochiya, Mayu, Tamanaha, Tamiko, Tomita, Tsutomu, Honda-Kohmo, Kyoko, Noguchi, Michio, Murai, Kota, Sawada, Kenichiro, Iwai, Takamasa, Matama, Hideo, Honda, Satoshi, Fujino, Masashi, Nakao, Kazuhiro, Yoneda, Shuichi, Takagi, Kensuke, Otsuka, Fumiyuki, Asaumi, Yasuhide, Hosoda, Kiminori, Nicholls, Stephen J., Yasuda, Satoshi, and Noguchi, Teruo

Published
2024
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36. World Heart Federation Cholesterol Roadmap 2022

Author

Ray, Kausik K, Ference, Brian A, Séverin, Tania, Blom, Dirk, Nicholls, Stephen J, Shiba, Mariko H, Almahmeed, Wael, Alonso, Rodrigo, Daccord, Magdalena, Ezhov, Marat, Olmo, Rosa Fernández, Jankowski, Piotr, Lanas, Fernando, Mehta, Roopa, Puri, Raman, Wong, Nathan D, Wood, David, Zhao, Dong, Gidding, Samuel S, Virani, Salim S, Lloyd-Jones, Donald, Pinto, Fausto, Perel, Pablo, and Santos, Raul D

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Heart Disease, Health Services, Patient Safety, Prevention, Atherosclerosis, Cardiovascular, Clinical Research, Heart Disease - Coronary Heart Disease, Good Health and Well Being, Humans, Cholesterol, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Dyslipidemias, Lipoproteins, Apolipoproteins B, Cardiovascular Diseases, cholesterol, low-density lipoprotein cholesterol prevention, ASCVD, lipid lowering therapy, familial hypercholesterolaemia, Cardiorespiratory Medicine and Haematology, Cardiovascular medicine and haematology
Abstract

BackgroundAtherosclerotic cardiovascular diseases (ASCVD) including myocardial infarction, stroke and peripheral arterial disease continue to be major causes of premature death, disability and healthcare expenditure globally. Preventing the accumulation of cholesterol-containing atherogenic lipoproteins in the vessel wall is central to any healthcare strategy to prevent ASCVD. Advances in current concepts about reducing cumulative exposure to apolipoprotein B (apo B) cholesterol-containing lipoproteins and the emergence of novel therapies provide new opportunities to better prevent ASCVD. The present update of the World Heart Federation Cholesterol Roadmap provides a conceptual framework for the development of national policies and health systems approaches, so that potential roadblocks to cholesterol management and thus ASCVD prevention can be overcome.MethodsThrough a review of published guidelines and research papers since 2017, and consultation with a committee composed of experts in clinical management of dyslipidaemias and health systems research in low-and-middle income countries (LMICs), this Roadmap identifies (1) key principles to effective ASCVD prevention (2) gaps in implementation of these interventions (knowledge-practice gaps); (3) health system roadblocks to treatment of elevated cholesterol in LMICs; and (4) potential strategies for overcoming these.ResultsReducing the future burden of ASCVD will require diverse approaches throughout the life-course. These include: a greater focus on primordial prevention; availability of affordable cholesterol testing; availability of universal cholesterol screening for inherited dyslipidaemias; risk stratification moving beyond 10-year risk to look at lifetime risk with adequate risk estimators; wider availability of affordable cholesterol-lowering therapies which should include statins as essential medications globally; use of adequate doses of potent statin regimens; and combination therapies with ezetimibe or other therapies in order to attain and maintain robust reductions in LDL-C in those at highest risk. Continuing efforts are needed on health literacy for both the public and healthcare providers, utilising multi-disciplinary teams in healthcare and applications that quantify both ASCVD risk and benefits of treatment as well as increased adherence to therapies.ConclusionsThe adverse effects of LDL-cholesterol and apo B containing lipoprotein exposure are cumulative and result in ASCVD. These are preventable by implementation of different strategies, aimed at efficiently tackling atherosclerosis at different stages throughout the human life-course. Preventive strategies should therefore be updated to implement health policy, lifestyle changes and when needed pharmacotherapies earlier with investment in, and a shift in focus towards, early preventive strategies that preserve cardiovascular health rather than treat the consequences of ASCVD.

Published
2022

37. Author Correction: Optical coherence tomography in coronary atherosclerosis assessment and intervention

Author

Araki, Makoto, Park, Seung-Jung, Dauerman, Harold L., Uemura, Shiro, Kim, Jung-Sun, Di Mario, Carlo, Johnson, Thomas W., Guagliumi, Giulio, Kastrati, Adnan, Joner, Michael, Holm, Niels Ramsing, Alfonso, Fernando, Wijns, William, Adriaenssens, Tom, Nef, Holger, Rioufol, Gilles, Amabile, Nicolas, Souteyrand, Geraud, Meneveau, Nicolas, Gerbaud, Edouard, Opolski, Maksymilian P., Gonzalo, Nieves, Tearney, Guillermo J., Bouma, Brett, Aguirre, Aaron D., Mintz, Gary S., Stone, Gregg W., Bourantas, Christos V., Räber, Lorenz, Gili, Sebastiano, Mizuno, Kyoichi, Kimura, Shigeki, Shinke, Toshiro, Hong, Myeong-Ki, Jang, Yangsoo, Cho, Jin Man, Yan, Bryan P., Porto, Italo, Niccoli, Giampaolo, Montone, Rocco A., Thondapu, Vikas, Papafaklis, Michail I., Michalis, Lampros K., Reynolds, Harmony, Saw, Jacqueline, Libby, Peter, Weisz, Giora, Iannaccone, Mario, Gori, Tommaso, Toutouzas, Konstantinos, Yonetsu, Taishi, Minami, Yoshiyasu, Takano, Masamichi, Raffel, O. Christopher, Kurihara, Osamu, Soeda, Tsunenari, Sugiyama, Tomoyo, Kim, Hyung Oh, Lee, Tetsumin, Higuma, Takumi, Nakajima, Akihiro, Yamamoto, Erika, Bryniarski, Krzysztof L., Di Vito, Luca, Vergallo, Rocco, Fracassi, Francesco, Russo, Michele, Seegers, Lena M., McNulty, Iris, Park, Sangjoon, Feldman, Marc, Escaned, Javier, Prati, Francesco, Arbustini, Eloisa, Pinto, Fausto J., Waksman, Ron, Garcia-Garcia, Hector M., Maehara, Akiko, Ali, Ziad, Finn, Aloke V., Virmani, Renu, Kini, Annapoorna S., Daemen, Joost, Kume, Teruyoshi, Hibi, Kiyoshi, Tanaka, Atsushi, Akasaka, Takashi, Kubo, Takashi, Yasuda, Satoshi, Croce, Kevin, Granada, Juan F., Lerman, Amir, Prasad, Abhiram, Regar, Evelyn, Saito, Yoshihiko, Sankardas, Mullasari Ajit, Subban, Vijayakumar, Weissman, Neil J., Chen, Yundai, Yu, Bo, Nicholls, Stephen J., Barlis, Peter, West, Nick E. J., Arbab-Zadeh, Armin, Ye, Jong Chul, Dijkstra, Jouke, Lee, Hang, Narula, Jagat, Crea, Filippo, Nakamura, Sunao, Kakuta, Tsunekazu, Fujimoto, James, Fuster, Valentin, and Jang, Ik-Kyung

Published
2024
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38. Apabetalone and hospitalization for heart failure in patients following an acute coronary syndrome: a prespecified analysis of the BETonMACE study

Author

Nicholls, Stephen J, Schwartz, Gregory G, Buhr, Kevin A, Ginsberg, Henry N, Johansson, Jan O, Kalantar-Zadeh, Kamyar, Kulikowski, Ewelina, Toth, Peter P, Wong, Norman, Sweeney, Michael, and Ray, Kausik K

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Clinical Research, Clinical Trials and Supportive Activities, Diabetes, Heart Disease, Heart Disease - Coronary Heart Disease, Cardiovascular, Atherosclerosis, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Acute Coronary Syndrome, Aged, Cardiovascular Agents, Diabetes Mellitus, Type 2, Double-Blind Method, Female, Heart Failure, Humans, Male, Middle Aged, Patient Admission, Patient Readmission, Quinazolinones, Time Factors, Treatment Outcome, BET inhibitors, Acute coronary syndrome, Heart failure, Clinical trial, Cardiovascular disease, Epigenetics, BETonMACE Investigators, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundPatients with diabetes and acute coronary syndrome (ACS) are at high risk for subsequent heart failure. Apabetalone is a selective inhibitor of bromodomain and extra-terminal (BET) proteins, epigenetic regulators of gene expression. Preclinical data suggest that apabetalone exerts favorable effects on pathways related to myocardial structure and function and therefore could impact subsequent heart failure events. The effect of apabetalone on heart failure events after an ACS is not currently known.MethodsThe phase 3 BETonMACE trial was a double-blind, randomized comparison of apabetalone versus placebo on the incidence of major adverse cardiovascular events (MACE) in 2425 patients with a recent ACS and diabetes. This prespecified secondary analysis investigated the impact of apabetalone on hospitalization for congestive heart failure, not previously studied.ResultsPatients (age 62 years, 74.4% males, 90% high-intensity statin use, LDL-C 70.3 mg/dL, HDL-C 33.3 mg/dL and HbA1c 7.3%) were followed for an average 26 months. Apabetalone treated patients experienced the nominal finding of a lower rate of first hospitalization for heart failure (2.4% vs. 4.0%, HR 0.59 [95%CI 0.38-0.94], P = 0.03), total number of hospitalizations for heart failure (35 vs. 70, HR 0.47 [95%CI 0.27-0.83], P = 0.01) and the combination of cardiovascular death or hospitalization for heart failure (5.7% vs. 7.8%, HR 0.72 [95%CI 0.53-0.98], P = 0.04).ConclusionApabetalone treatment was associated with fewer hospitalizations for heart failure in patients with type 2 diabetes and recent ACS. Future studies are warranted to define the potential for BET inhibition with apabetalone to prevent heart failure in patients with diabetes and ACS.

Published
2021

39. Relation of insulin treatment for type 2 diabetes to the risk of major adverse cardiovascular events after acute coronary syndrome: an analysis of the BETonMACE randomized clinical trial

Author

Schwartz, Gregory G, Nicholls, Stephen J, Toth, Peter P, Sweeney, Michael, Halliday, Christopher, Johansson, Jan O, Wong, Norman CW, Kulikowski, Ewelina, Kalantar-Zadeh, Kamyar, Ginsberg, Henry N, and Ray, Kausik K

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Brain Disorders, Heart Disease - Coronary Heart Disease, Cardiovascular, Prevention, Diabetes, Heart Disease, Clinical Trials and Supportive Activities, Clinical Research, Atherosclerosis, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Metabolic and endocrine, Acute Coronary Syndrome, Aged, Diabetes Mellitus, Type 2, Female, Humans, Hypoglycemic Agents, Insulin, Male, Middle Aged, Quinazolinones, Recurrence, Risk Assessment, Risk Factors, Time Factors, Treatment Outcome, Acute coronary syndrome, Epigenetics, BET proteins, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundIn stable patients with type 2 diabetes (T2D), insulin treatment is associated with elevated risk for major adverse cardiovascular events (MACE). Patients with acute coronary syndrome (ACS) and T2D are at particularly high risk for recurrent MACE despite evidence-based therapies. It is uncertain to what extent this risk is further magnified in patients with recent ACS who are treated with insulin. We examined the relationship of insulin use to risk of MACE and modification of that risk by apabetalone, a bromodomain and extra-terminal (BET) protein inhibitor.MethodsThe analysis utilized data from the BETonMACE phase 3 trial that compared apabetalone to placebo in patients with T2D, low HDL cholesterol, andACS. The primary MACE outcome (cardiovascular death, myocardial infarction, or stroke) was examined according to insulin treatment and assigned study treatment. Multivariable Cox regression was used to determine whether insulin use was independently associated with the risk of MACE.ResultsAmong 2418 patients followed for median 26.5 months, 829 (34.2%) were treated with insulin. Despite high utilization of evidence-based treatments including coronary revascularization, intensive statin treatment, and dual antiplatelet therapy, the 3-year incidence of MACE in the placebo group was elevated among insulin-treated patients (20.4%) compared to those not-treated with insulin (12.8%, P = 0.0001). Insulin treatment remained strongly associated with the risk of MACE (HR 2.10, 95% CI 1.42-3.10, P = 0.0002) after adjustment for demographic, clinical, and treatment variables. Apabetalone had a consistent, favorable effect on MACE in insulin-treated and not insulin-treated patients.ConclusionInsulin-treated patients with T2D, low HDL cholesterol, and ACS are at high risk for recurrent MACE despite the use of evidence-based, contemporary therapies. A strong association of insulin treatment with risk of MACE persists after adjustment for other characteristics associated with MACE. There is unmet need for additional treatments to mitigate this risk. Trial registration ClinicalTrials.gov NCT02586155, registered October 26, 2015.

Published
2021

42. Comparison of tirzepatide and dulaglutide on major adverse cardiovascular events in participants with type 2 diabetes and atherosclerotic cardiovascular disease: SURPASS‐CVOT design and baseline characteristics

Author

Nicholls, Stephen J., Bhatt, Deepak L, Buse, John B, Prato, Stefano Del, Kahn, Steven E, Lincoff, A Michael, McGuire, Darren K, Nauck, Michael A, Nissen, Steven E, Sattar, Naveed, Zinman, Bernard, Zoungas, Sophia, Basile, Jan, Bartee, Amy, Miller, Debra, Nishiyama, Hiroshi, Pavo, Imre, Weerakkody, Govinda, Wiese, Russell J, and D'Alessio, David

Published
2024
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44. Effect of Apabetalone on Cardiovascular Events in Diabetes, CKD, and Recent Acute Coronary Syndrome

Author

Kalantar-Zadeh, Kamyar, Schwartz, Gregory G, Nicholls, Stephen J, Buhr, Kevin A, Ginsberg, Henry N, Johansson, Jan O, Kulikowski, Ewelina, Lebioda, Kenneth, Toth, Peter P, Wong, Norman, Sweeney, Michael, Ray, Kausik K, and Investigators, on behalf of the BETonMACE

Subjects
Biomedical and Clinical Sciences, Nutrition and Dietetics, Heart Disease, Heart Disease - Coronary Heart Disease, Clinical Trials and Supportive Activities, Clinical Research, Cardiovascular, Patient Safety, Diabetes, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Good Health and Well Being, Acute Coronary Syndrome, Aged, Cardiovascular Diseases, Diabetes Complications, Diabetes Mellitus, Type 2, Double-Blind Method, Female, Heart Failure, Humans, Male, Middle Aged, Quinazolinones, Renal Insufficiency, Chronic, epigenetic pharmacotherapy, apabetalone, alkaline phosphatase, major adverse cardiovascular events, CKD stage 5, chronic kidney disease, diabetes, diabetes mellitus, cardiovascular, BETonMACE Investigators, Clinical Sciences, Urology & Nephrology, Clinical sciences, Epidemiology
Abstract

Background and objectivesCKD and type 2 diabetes mellitus interact to increase the risk of major adverse cardiovascular events (i.e., cardiovascular death, nonfatal myocardial infarction, or stroke) and congestive heart failure. A maladaptive epigenetic response may be a cardiovascular risk driver and amenable to modification with apabetalone, a selective modulator of the bromodomain and extraterminal domain transcription system. We examined this question in a prespecified analysis of BETonMACE, a phase 3 trial.Design, setting, participants, & measurementsBETonMACE was an event-driven, randomized, double-blind, placebo-controlled trial comparing effects of apabetalone versus placebo on major adverse cardiovascular events and heart failure hospitalizations in 2425 participants with type 2 diabetes and a recent acute coronary syndrome, including 288 participants with CKD with eGFR

Published
2021

47. The effect of continuous glucose monitoring-guided glycemic control on progression of coronary atherosclerosis in type 2 diabetic patients with coronary artery disease: The OPTIMAL randomized clinical trial

Author

Kataoka, Yu, Kitahara, Satoshi, Funabashi, Sayaka, Makino, Hisashi, Matsubara, Masaki, Matsuo, Miki, Omura-Ohata, Yoko, Koezuka, Ryo, Tochiya, Mayu, Tamanaha, Tamiko, Tomita, Tsutomu, Honda-Kohmo, Kyoko, Noguchi, Michio, Maruki, Maki, Kanai, Emi, Murai, Kota, Iwai, Takamasa, Sawada, Kenichiro, Matama, Hideo, Honda, Satoshi, Fujino, Masashi, Yoneda, Syuichi, Takagi, Kensuke, Otsuka, Fumiyuki, Asaumi, Yasuhide, Hosoda, Kiminori, Nicholls, Stephen J., Yasuda, Satoshi, and Noguchi, Teruo

Published
2023
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49. Incorporating a polygenic risk score-triaged coronary calcium score into cardiovascular disease examinations to identify subclinical coronary artery disease (ESCALATE): Protocol for a prospective, nonrandomized implementation trial

Author

Barlow, John E., Bauer, Denis, BradfordBerman, DanaYemima, Bottá, Giordano, Figtree, Gemma A., Gilbert, Andrew, Gray, Michael P., Grieve, Stuart M., Ho, Amy, Hu, Jessica, Hyun, Karice, Jennings, Garry, Kilov, Gary, Levesque, Jean-Frederic, Meikle, Peter, Nicholls, Stephen J., Redfern, Julie, Stavreski, Bill, Suthers, Graeme, Usherwood, Tim, Wilson, Andrew, Thackway, Stephen, Rogers, Caroline, Berman, Yemima, Bottà, Giordano, Ingles, Jodie, and Vernon, Stephen T.

Published
2023
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50. Clinical Pathway for Coronary Atherosclerosis in Patients Without Conventional Modifiable Risk Factors: JACC State-of-the-Art Review

Author

Ademi, Zanfina, Avis, Suzanne Robyn, Chan, Adam, Contreras, Osvaldo, Coorey, Craig P., Fathieh, Sina, Genetzakis, Elijah, Gholipour, Alireza, Giles, Corey, Hollings, Matthew, Hyun, Karice, Kazi, Samia, Kovacic, Jason C., Larance, Mark, Marathe, Jessica A., Marquina, Clara, Nelson, Adam, Ng, Hooi Hooi, Patrick, Ellis, Peter, Karlheinz, Tran, Andy, Yang, Jean, Zhu, Dantong, Zwack, Clara, Figtree, Gemma A., Vernon, Stephen T., Harmer, Jason A., Gray, Michael P., Arnott, Clare, Bachour, Eric, Barsha, Giannie, Brieger, David, Brown, Alex, Celermajer, David S., Channon, Keith M., Chew, Nicholas W.S., Chong, James J.H., Chow, Clara K., Cistulli, Peter A., Ellinor, Patrick T., Grieve, Stuart M., Guzik, Tomasz J., Hagström, Emil, Jenkins, Alicia, Jennings, Garry, Keech, Anthony C., Kott, Katharine A., Kritharides, Leonard, Mamas, Mamas A., Mehran, Roxana, Meikle, Peter J., Natarajan, Pradeep, Negishi, Kazuaki, O’Sullivan, John, Patel, Sanjay, Psaltis, Peter J., Redfern, Julie, Steg, Philippe G., Sullivan, David R., Sundström, Johan, Vogel, Birgit, Wilson, Andrew, Wong, Dennis, Bhatt, Deepak L., and Nicholls, Stephen J.

Published
2023
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