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Residual Cardiovascular Risk Despite Optimal LDL Cholesterol Reduction with Statins: The Evidence, Etiology, and Therapeutic Challenges
Open accessAbstract
This review captures the existence, cause, and treatment challenges of residual cardiovascular risk (CVR) after aggressive low-density lipoprotein cholesterol (LDL-C) reduction. Scientific evidence implicates low high-density lipoprotein cholesterol (HDL-C) and high triglycerides (TG) in the CVR observed after LDL-C lowering. However, the Action to Control Cardiovascular Risk in Diabetes (ACCORD) lipid trial with fenofibrate, the Investigation of Lipid Level Management to Understand its Impact in Atherosclerotic Events (ILLUMINATE) study with torcetrapib, and the recently terminated Atherothrombosis Intervention in Metabolic Syndrome with Low HDL Cholesterol/High Triglyceride and Impact on Global Health Outcomes (AIM-HIGH) study with niacin, do not clearly attribute risk reduction value to HDL-C/TG modulation. The optimum approach to long-term lipid-modifying therapies for CVR reduction remains uncertain. Consequently, absolute risk modulation via lifestyle changes remains the centerpiece of a strategy addressing the physiologic drivers of CVR associated with HDL-C/TG, especially in the context of diabetes/metabolic syndrome.
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“Residual risk persists in many individuals, especially those with features of metabolic syndrome (MetS) or diabetes mellitus (DM), suggesting the need to address additional lipoprotein abnormalities such as elevated triglycerides (TGs) and TG-rich lipoproteins (TRLs) [6, 7].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [7]
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1 retracted
Arsenault, B. J., Barter, P. J., DeMicco, D. A., Bao, W., Preston, G. M., LaRosa, J. C., Grundy, S. M., DEEDWANIA, P. C., Greten, H., WENGER, N. K., et al. (2010) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2010.06.052 · Cited by 36
RetractedGrundy, S. M., Bilheimer, D. W., Chait, A., Clark, L. T., Denke, M. A., Havel, R. J., Hazzard, W. R., Hulley, S. B., Hunninghake, D. B., Kreisberg, R. A., et al. (1993) · JAMA · doi:10.1001/jama.269.23.3015 · Cited by 27,944
Expert Panel on Detection, E. (2001) · JAMA: The Journal of the American Medical Association · doi:10.1001/jama.285.19.2486 · Cited by 26,011
Detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III)
Grundy, S. M., Becker, D. M., Clark, L. T., Cooper, R., Denke, M. A., Howard, J. L., Hunninghake, D. B., Illingworth, D. R., Luepker, R. V., McBride, P. E., et al. (2002) · Civil War Book Review · Cited by 12,198
Yusuf, S., Hawken, S., Ôunpuu, S., Dans, T., Avezum, A., Lanas, F., McQueen, M., Budaj, A., Pais, P., Varigos, J., et al. (2004) · The Lancet · doi:10.1016/s0140-6736(04)17018-9 · Cited by 12,026
OLSSON, A. G., McMurray, J. J. V., Thorgeirsson, G., Spaulding, C. M., Slattery, J., Pyörälà, K., Færgeman, O., Wright, R. S., Berg, K. M., Wilhelmsen, L., et al. (1994) · The Lancet · Cited by 8,467
Inflammation and Atherosclerosis
Libby, P., Ridker, P. M., & Maseri, A. (2002) · Circulation · doi:10.1161/hc0902.104353 · Cited by 7,724
Prevention of Coronary Heart Disease with Pravastatin in Men with Hypercholesterolemia
Shepherd, J., Cobbe, S. M., Ford, I., Isles, C. G., Lorimer, A. R., Macfarlane, P. W., McKillop, J. H., & Packard, C. J. (1995) · New England Journal of Medicine · doi:10.1056/nejm199511163332001 · Cited by 7,449
Sacks, F. M., Pfeffer, M. A., Moye, L. A., Rouleau, J. L., Rutherford, J. D., Cole, T. G., Brown, L., Warnica, J. W., Arnold, J. M. O., Wun, C.-C., et al. (1996) · New England Journal of Medicine · doi:10.1056/nejm199610033351401 · Cited by 7,439
Cited by
Sorted by citations
Items 201–300 of 438
Frigerio, B., Werba, J. P., Amato, M., Ravani, A. L., Sansaro, D., Coggi, D., Vigo, L., Tremoli, E., & Baldassarre, D. (2019) · Current Pharmaceutical Design · doi:10.2174/1381612825666191213120339 · Cited by 13
Lipid Profiles in Out-of-Hospital Sudden Unexpected Death
Hosadurg, N., Bogle, B. M., Joodi, G., Sadaf, M. I., Pursell, I. W., Mendys, P., Mounsey, J. P., & Simpson, R. J. (2018) · Mayo Clinic Proceedings Innovations Quality & Outcomes · doi:10.1016/j.mayocpiqo.2018.06.010 · Cited by 13
“It may also be indicative of a residual sudden death risk in the community despite adequate control of TC and/or LDL-C levels with medication, as previously suggested.(28) High TG(29) and low HDL(30) levels, the hallmarks of combined dyslipidemia, are established predictors of adverse cardiovascular events, but their…”
Sterol carrier protein 2: A promising target in the pathogenesis of atherosclerosis
Xu, C., Li, H., & Tang, C. (2022) · Genes & Diseases · doi:10.1016/j.gendis.2021.12.007 · Cited by 12
“Although statins therapy is effective in improving plasma lipid profile in patients with cardiovascular disease, the residual cardiovascular risk is still representing a challenge worthy of attention.(8,9) Therefore, it is necessary to develop new promising therapeutic strategies aiming to target critical molecules in…”
BackgroundWelty, F. K., Hariri, E. H., Asbeutah, A. A., Daher, R., Amangurbanova, M., Chedid, G., Elajami, T. K., Alfaddagh, A., & Malik, A. (2023) · Journal of the American Heart Association · doi:10.1161/jaha.123.030071 · Cited by 13
Kim, N. H., Kim, J. Y., Choi, J., & Kim, S. G. (2023) · European Heart Journal - Cardiovascular Pharmacotherapy · doi:10.1093/ehjcvp/pvad090 · Cited by 13
High-Density Lipoproteins and Coronary Artery Disease
Schaffer, A., Verdoia, M., Barbieri, L., Aprami, T. M., Suryapranata, H., Marino, P. N., & Luca, G. D. (2013) · Angiology · doi:10.1177/0003319713502253 · Cited by 12
“However, a residual event rate was demonstrated in most trials using statins, ranging from 9% to even 20% according to established target level of LDL-C and dosage of statin.(5,6,15) High-density lipoprotein cholesterol has been identified over the past 60 years as an independent modifier of the atherosclerotic proces…”
BackgroundJiang, J., Zhou, Y.-J., Li, J., Ge, J., Feng, Y., & Huo, Y. (2018) · Therapeutics and Clinical Risk Management · doi:10.2147/tcrm.s178318 · Cited by 12
“Both epidemiological and interventional clinical trials have shown a strong association between elevated LDL-C level and cardiovascular events.(4,5) A large observational study (DYSIS-China) showed that although the majority (88.”
BackgroundOrekhov, A. N., & Myasoedova, V. A. (2019) · Vessel Plus · doi:10.20517/2574-1209.2018.80 · Cited by 12
“Over the past two decades, data demonstrating the non-linear dependence of the reduction in the risk of atherosclerosis from the therapeutic reduction in total LDL level are widely discussed([52-61]).”
BackgroundVallecillo, G., Pedro‐Botet, J., Fernández, S. F., Román, I., Elosúa, R., Camps, A., Torrens, M., & Marrugat, J. (2022) · Drug and Alcohol Review · doi:10.1111/dar.13449 · Cited by 12
Chan, Y., & Ramji, D. P. (2022) · Methods in molecular biology · doi:10.1007/978-1-0716-1924-7_2 · Cited by 13
Zhao, Z., Zhu, Y., Fang, Y.-T., Ye, W., & McCollam, P. L. (2015) · Journal of Medical Economics · doi:10.3111/13696998.2015.1041966 · Cited by 12
“15, or a pharmacy claim for cilostazol or pentoxifylline; or (4) Patients with diabetes mellitus (250.”
BackgroundWu, J., Wang, Y., Wang, A., Xie, J., & Zhao, X. (2018) · Scientific Reports · doi:10.1038/s41598-018-24157-w · Cited by 11
Fernández‐Cidón, B., Candás‐Estébanez, B., Gil, M., Amigó, N., Corbella, E., Rodríguez-Sánchez, M. A., Padró‐Miquel, A., Brotons, C., Hernández‐Mijares, A., Calmarza, P., et al. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10071379 · Cited by 11
“Premature cardiovascular disease (PVCD) remains an important public health issue and dyslipidemia is the most common risk factor of this condition [1] Patients with premature cardiovascular disease (PCVD) have non-conventional risk factors, both lipid and non-lipid [2,3], which entail a residual cardiovascular risk th…”
BackgroundHu, Y. P., Wang, X., Luo, C., Zheng, T., & Tian, G. (2023) · Lipids in Health and Disease · doi:10.1186/s12944-022-01767-y · Cited by 11
“However, the cardiovascular risk remains considerable after LDL-C reduction [29].”
BackgroundA Potential Role of NFIL3 in Atherosclerosis
Zeng, G.-G., Zhou, J., Jiang, W.-L., Yu, J., Nie, G.-Y., Li, J., Zhang, S., & Tang, C. (2023) · Current Problems in Cardiology · doi:10.1016/j.cpcardiol.2023.102096 · Cited by 11
Downregulation of adipose LPL by PAR2 contributes to the development of hypertriglyceridemia
Huang, Y., Chen, L., Li, L., Qi, Y., Tong, H., Wu, H., Xu, J., Leng, L., Cheema, S. K., Sun, G., et al. (2024) · JCI Insight · doi:10.1172/jci.insight.173240 · Cited by 11
“It also increases the risk of cardiovascular disease even in the presence of optimized LDL cholesterol levels (23).”
Li, G., Wu, X., Lü, W., Ai, R., Chen, F., & Tang, Z. (2014) · BMC Cardiovascular Disorders · doi:10.1186/1471-2261-14-145 · Cited by 11
Emerging biologic therapies for hypercholesterolaemia
Pucci, G., Cicero, A. F. G., Borghi, C., & Schillaci, G. (2017) · Expert Opinion on Biological Therapy · doi:10.1080/14712598.2017.1341485 · Cited by 11
“On a greater extent, however, residual risk is determined in many high-risk patients by the failure to reach optimal levels of LDL-C [6].”
BackgroundUnni, S. K., Quek, R. G. W., BISKUPIAK, J. E., Lee, V. C., Ye, X., & Gandra, S. R. (2015) · Journal of clinical lipidology · doi:10.1016/j.jacl.2015.09.008 · Cited by 11
The Emerging Role of PCSK9 Inhibitors in Preventive Cardiology
Pitts, R., & Eckel, R. H. (2014) · European Cardiology Review · doi:10.15420/ecr.2014.9.2.65 · Cited by 11
Han, H., Dai, D., Wang, W., Zhu, J., Zhu, Z., Lu, L., & Zhang, R. (2019) · Journal of interventional medicine · doi:10.1016/j.jimed.2019.05.005 · Cited by 11
Bazarbashi, N., & Miller, M. J. (2020) · Expert Review of Cardiovascular Therapy · doi:10.1080/14779072.2020.1749596 · Cited by 11
Masson, W. M., Lobo, M., Siniawski, D. A., Molinero, G., Huerin, M. S., & Nogueira, J. P. (2019) · High Blood Pressure & Cardiovascular Prevention · doi:10.1007/s40292-019-00330-8 · Cited by 10
Retargeting the management of hypercholesterolemia – focus on evolocumab
Cicero, A. F. G., Colletti, A., & Derosa, G. (2016) · Therapeutics and Clinical Risk Management · doi:10.2147/tcrm.s116679 · Cited by 10
“Then, statins are the first drugs suggested,(2) and it has been estimated that statins are able to reduce atherosclerotic cardiovascular disease (ASCVD) risk by 15%–37%, but residual 60%–80% risk still remains and a significant part of this risk is probably related to an insufficient reduction of LDL-C.(4) Corresponde…”
InfluentialLipids and Lipoproteins in Risk Prediction
Hadjiphilippou, S., & Ray, K. K. (2018) · Cardiology Clinics · doi:10.1016/j.ccl.2017.12.002 · Cited by 10
Summarizing the FIELD study: lessons from a ‘negative' trial
Tsimihodimos, V., Mikhailidis, D. P., & Elisaf, M. (2013) · Expert Opinion on Pharmacotherapy · doi:10.1517/14656566.2013.850075 · Cited by 10
“In addition, even in statin-treated patients a residual cardiovascular risk remains that has been partially attributed to the aforementioned lipid abnormalities [8].”
BackgroundGliozzi, M., Maiuolo, J., Oppedisano, F., & Mollace, V. (2015) · PharmaNutrition · doi:10.1016/j.phanu.2015.11.003 · Cited by 10
Murphy, B. A., Tadin‐Strapps, M., Jensen, K., Mogg, R., Liaw, A. I., Herath, K. B., Bhat, G., McLaren, D. G., Previs, S. F., & Pinto, S. (2017) · Metabolism · doi:10.1016/j.metabol.2017.02.015 · Cited by 10
Chen, H., Lee, W., Fang, H., Fang, C.-Y., Chen, C.-J., Yang, C., & Wu, C. (2020) · Medicine · doi:10.1097/md.0000000000022848 · Cited by 10
“Different letters (a, b, c, d) associated with different groups indicate significant difference (at 0.05 leve DM=diabetes mellitus, HDL-C=high-density lipoprotein cholesterol, MACE=major adverse cardiac eve concentration of HDL-C.”
BackgroundInfluentialYoshida, M., Nakamura, K., Miyoshi, T., Yoshida, M., Kondo, M., Akazawa, K., Kimura, T., Ohtsuka, H., Ohno, Y., Miura, D., et al. (2020) · Cardiovascular Diabetology · doi:10.1186/s12933-020-01181-7 · Cited by 10
Bibliometric analysis of residual cardiovascular risk: trends and frontiers
Wang, L., Wang, S., Song, C., Yu, Y., Jiang, Y., Wang, Y., & Li, X. (2023) · Journal of Health Population and Nutrition · doi:10.1186/s41043-023-00478-z · Cited by 11
“The third most cited article was a review on residual cardiovascular risk [3].”
BackgroundYang, M., Jiao, H., Li, Y., Zhang, L., Zhang, J., Zhong, X., & Xue, Y. (2022) · Drug Design Development and Therapy · doi:10.2147/dddt.s372143 · Cited by 9
“However, there is still a residual cardiovascular risk after effectively lowering LDL-C levels using statins or combined lipid-lowering strategies.(63,64) Recent studies have shown that inflammation and cholesterol are both pathogenic factors of AS.”
BackgroundHigh-density lipoprotein infusion therapy: A review
Brewer, H. B., Schaefer, E. J., Foldyna, B., & Ghoshhajra, B. B. (2024) · Journal of clinical lipidology · doi:10.1016/j.jacl.2024.01.009 · Cited by 9
Risk factors associated with atherogenic dyslipidemia in the presence of optimal statin therapy
Wang, Z., Zheng, X., Jiang, Z., Liao, X., & Zhao, S. (2017) · International Journal of Cardiology · doi:10.1016/j.ijcard.2017.06.105 · Cited by 9
Effects of 3,4-Dihydroxyacetophenone on the Hypercholesterolemia-Induced Atherosclerotic Rabbits
Zhang, D., Liu, J., Wang, L., Wang, J., Li, W., Baoxiang, Z., Hou, J.-P., & Liu, T. (2013) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.b12-00710 · Cited by 9
Targeted Therapies: The Role of Monoclonal Antibodies in Disease Management
Salah, A. N., Hashem, A. H., Zaki, M. B., Abulsoud, A. I., Atta, A. M., Elkalla, W. S., Moustafa, H. A. M., El‐Dakroury, W. A., El-Tokhy, F. S., ElBoghdady, J. A., et al. (2025) · Journal of Biochemical and Molecular Toxicology · doi:10.1002/jbt.70163 · Cited by 9
“C) concentrations even with optimized statin treatment remains a concern [221].”
Atherogenic dyslipidemia and incident cardiovascular events in high-risk hypertension
Kazibwe, R., Jehopio, J., Schaich, C. L., Rikhi, R. R., Mirzai, S., Chevli, P. A., Namutebi, J. H., Chebrolu, S., O'Connor, S., Yeboah, J., et al. (2025) · Progress in Cardiovascular Diseases · doi:10.1016/j.pcad.2025.05.006 · Cited by 12
Nakao, K., Noguchi, T., Asaumi, Y., Morita, Y., Kanaya, T., Fujino, M., Hosoda, H., Yoneda, S., Kawakami, S., Nagai, T., et al. (2018) · Trials · doi:10.1186/s13063-017-2353-1 · Cited by 7
“Discussion Although the results of many randomized controlled trials using statins have shown the usefulness of LDL-cholesterol-lowering therapy, the extent of coronary artery disease suppression did not exceed approximately 30% [27].”
BackgroundAtherogenic markers in predicting cardiovascular risk and targeting residual cardiovascular risk
Catapano, A. L., Tokgözoğlu, L. S., Silva, A. M. E., & Bruckert, É. (2019) · Atherosclerosis Supplements · doi:10.1016/j.athx.2019.100001 · Cited by 8
“Despite this, there remains a residual risk of CV events with statin treatment in clinical trials, even in patients achieving target LDL-C levels [19,20].”
BackgroundMetzner, T., Leitner, D. R., Mellitzer, K., Beck, A., Sourij, H., Stojaković, T., Reishofer, G., März, W., Landmesser, U., Scharnagl, H., et al. (2022) · Biomedicines · doi:10.3390/biomedicines10010193 · Cited by 9
“However, despite substantial reductions in LDL cholesterol with statins and newer lipid-lowering agents, patients continue to experience recurrent major cardiovascular events [4].”
BackgroundAssociation between Lipoprotein Subfractions, Hemostatic Potentials, and Coronary Atherosclerosis
Flerin, T. P., Mijovski, M. B., & Jug, B. (2022) · Disease Markers · doi:10.1155/2022/2993309 · Cited by 9
“However, despite aggressive LDL-C lowering, substantial residual atherosclerotic risk remains and may possibly be associated with lipid metabolism derangements not captured by measuring LDLC [4].”
BackgroundEfficacy and safety of pemafibrate in patients with chronic kidney disease: A retrospective study
Iwasaki, M., Suzuki, H., Umezawa, Y., Koshida, T., Saito, M., Fukuda, H., Takahara, H., Matsuzaki, K., & Suzuki, Y. (2023) · Medicine · doi:10.1097/md.0000000000032818 · Cited by 10
“Notably, additional treatment with fibrate for high TG was associated with reduced CVD risk independent of the LDL-C level among patients treated with statins.[5,6] Bezafibrate (Beza-F) and fenofibrate (Feno-F) are highly effective in lowering plasma TG levels and moderately effective in raising HDL-C.”
BackgroundVerdoia, M., Cassetti, E., Schaffer, A., Giovine, G. D., & Luca, G. D. (2014) · Platelets · doi:10.3109/09537104.2014.948839 · Cited by 8
Rondini, E. A., Duniec‐Dmuchowski, Z., Cukovic, D., Dombkowski, A. A., & Kocarek, T. A. (2016) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.116.233312 · Cited by 8
“Additionally, despite aggressive statin therapy, certain populations have a high residual risk for CVD (Campbell et al., 2007; Sampson et al., 2012), so alternative lipid-modifying agents are needed.”
BackgroundNovel lipid-modifying therapies addressing unmet needs in cardiovascular disease
Kosmas, C. E., Sourlas, A., Silverio, D., Montan, P. D., & Guzman, E. (2019) · World Journal of Cardiology · doi:10.4330/wjc.v11.i11.256 · Cited by 8
Xiao, Q., Wang, L., Wang, J., Wang, M., Wang, D. W., & Ding, H. (2024) · Molecular Metabolism · doi:10.1016/j.molmet.2024.102011 · Cited by 8
“TRLs and remnants have been identi fi ed as signi fi cant contributors to the residual cardiovascular risk in patients receiving optimal LDL-lowering medication [8,9].”
Kenkre, J. S., Mazaheri, T., Neely, R. D. G., Soran, H., Datta, D. B. N., Penson, P. E., Downie, P., Yates, A. M., Hayden, K., Patel, M., et al. (2025) · Annals of Clinical Biochemistry International Journal of Laboratory Medicine · doi:10.1177/00045632251315303 · Cited by 8
Association between remnant cholesterol and arterial stiffness: Evidence from NHANES 1999–2018
Lai, T., Liang, Y., Guan, F., Chen, Y., & Hu, K. (2025) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2025.104013 · Cited by 7
Ran, X., Wu, Z., Guo, D., Zhang, S., Liu, L., Chen, S., Song, C., Zhang, C., & Yang, J. (2025) · European journal of medical research · doi:10.1186/s40001-025-02796-w · Cited by 7
“Nevertheless, despite controlling patients’ LDL-C to recommended levels, patients still had residual cardiovascular risk[28].”
(2013) · Journal of Liver · doi:10.4172/2167-0889.1000132 · Cited by 7
“Despite extensive clinical research on the association of Low- and High-Density Lipoprotein (LDL and HDL) levels with cardiovascular risk, a proportion of patients optimally treated with statins remain at a high risk [6, 7].”
BackgroundPharmacokinetic drug evaluation of anacetrapib for the treatment of dyslipidemia
Borghi, C., & Cicero, A. F. G. (2016) · Expert Opinion on Drug Metabolism & Toxicology · doi:10.1080/17425255.2017.1262347 · Cited by 7
Cho, I. Y., Chang, Y., Sung, E., Kim, Y., Kang, J., Shin, H. C., Wild, S. H., Byrne, C. D., & Ryu, S. (2022) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2022.03.018 · Cited by 7
Lipid Profile and Atrial Fibrillation: Is There Any Link?
Jiang, Q., Yang, L., Chen, M., Hua, F., & Li, J. (2022) · Reviews in Cardiovascular Medicine · doi:10.31083/j.rcm2308272 · Cited by 7
“Statin therapy has been used to reduce the concentration of LDL-C levels [41].”
BackgroundRonca, A., Pellegrini, N., Pagliai, G., Dinu, M., Manfredini, M., Incerti, M., Favari, E., & Sofi, F. (2022) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2022.11.012 · Cited by 7
Wang, H., Guo, Y., Zhang, H., Wang, X., & Zheng, X. (2024) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2024.05.011 · Cited by 9
Zhang, C., Zhang, H., Yang, Z., Sheng, Y., & Ji, N. (2025) · BMC Cardiovascular Disorders · doi:10.1186/s12872-024-04410-z · Cited by 8
“It has been shown that Non-HDL-C is a better predictor of atherosclerotic cardiovascular events than LDL-C [6].”
Li, S., Du, Y., Chen, G., Mao, Y., Zhang, W., Kang, M., Zhu, S., & Wang, D. (2025) · Nutrients · doi:10.3390/nu17061090 · Cited by 7
Kimura, T., Akahori, H., Tanaka, T., Yanaka, K., Yoshihara, N., Miki, K., Imanaka, T., Asakura, M., & Ishihara, M. (2022) · Journal of Cardiology · doi:10.1016/j.jjcc.2022.03.004 · Cited by 7
Sakai, R., Sekimoto, T., Koba, S., Mori, H., Matsukawa, N., Arai, T., Yokota, Y., Sato, S., Tanaka, H., Masaki, R., et al. (2023) · Journal of clinical lipidology · doi:10.1016/j.jacl.2023.01.004 · Cited by 7
Weaver, O. R., Ye, M., Vena, J. E., Eurich, D. T., & Proctor, S. D. (2023) · Diabetic Medicine · doi:10.1111/dme.15133 · Cited by 7
Novel Hypolipidaemic Drugs: Mechanisms of Action and Main Metabolic Effects
Filippatos, T. D., Liontos, A., Christopoulou, E. C., & Elisaf, M. (2018) · Current Vascular Pharmacology · doi:10.2174/1570161116666180209112351 · Cited by 7
Monguillon, V., Marston, N., Bohula, E. A., Park, J., Kuder, J., Murphy, S. A., Ferrari, G. M. D., Leiter, L. A., Nicolau, J. C., Ebenbichler, C. F., et al. (2026) · Circulation · doi:10.1161/circulationaha.126.080999 · Cited by 7
Taboun, Z., Naik, N., Brown, V., Lin, P., Padarath, M., Hegele, R. A., & Gupta, M. (2023) · CJC Open · doi:10.1016/j.cjco.2023.02.002 · Cited by 6
“Lowering of LDL-C level is fundamental to risk reduction in high-risk patients, including those with ASCVD or diabetes, yet lipid management in high-risk patients remains challenging in Canada and beyond.(11,12) The 2021 CCS lipid guidelines included stronger recommendations for combination LDL-C-lowering therapies in…”
BackgroundKim, H., Kim, J., Lee, J. S., Kim, B. J., Kang, J., Lee, K., Park, J., Kang, K., Lee, S. J., Kim, J. G., et al. (2024) · Scientific Reports · doi:10.1038/s41598-024-73851-5 · Cited by 6
“While the reduction of LDL-C through statin therapy diminishes a patient’s cardiovascular risk, a residual risk persists even when LDL-C levels are adequately controlled 14 .”
BackgroundCheng, J., Wang, H., Song, C., Qiao, Z., Bian, X., Yin, D., Feng, L., Zhu, C., Yang, M., Gao, G., et al. (2025) · American Journal of Preventive Cardiology · doi:10.1016/j.ajpc.2025.100965 · Cited by 6
“…residual CV risk despite achieving LDL-C targets, incorporating biomarker-based high-risk conditions into the VHR definition may enhance risk stratification and guide more personalized treatment strategies, particularly in diverse populations where current criteria may be insufficient [9,10].”
Huwait, E. A., Al-Gharawi, N., Al-Ghamdi, M. A., Gari, M. A., Prola, A., Pushparaj, P. N., & Gauthaman, K. (2022) · Current Issues in Molecular Biology · doi:10.3390/cimb44040120 · Cited by 6
Fonseca, A. F., Byrne, H., Laguna-Fernández, A., Itani, T., Studer, R. L., Heo, J., Dillon, A., Ferber, P. C., & Costa‐Scharplatz, M. (2023) · Journal of Managed Care & Specialty Pharmacy · doi:10.18553/jmcp.2023.29.5.519 · Cited by 6
Wang, Z., Zhang, X., Qu, Y., Zhang, S., Chen, Y., Chen, X., Qi, X., Liu, P., Liu, S., Jiang, S., et al. (2023) · Lipids in Health and Disease · doi:10.1186/s12944-023-01838-8 · Cited by 7
Liu, X., Yang, Y., Kang, F., Li, J., Zhou, M., Ma, X., Yu, T., Zhang, T., & Xue, F. (2019) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2019.05.058 · Cited by 5
Lipid parameters and vitamin A modify cardiovascular risk prediction by plasma neopterin
Dhar, I., Siddique, S., Pedersen, E. R., Svingen, G. F. T., Lysne, V., Olsén, T., Nilsen, D. W. T., Nordrehaug, J. E., Midttun, Ø., Ueland, P. M., et al. (2020) · Heart · doi:10.1136/heartjnl-2019-316165 · Cited by 6
Li, Y., Wang, S., Liu, L., Cai, H., Huang, Y., Gao, M., Zhang, X., Wu, Q., & Qiu, G. (2025) · Advanced Science · doi:10.1002/advs.202413491 · Cited by 6
Gagnon, É., Gill, D., Burgess, S., & Arsenault, B. J. (2025) · European Heart Journal Open · doi:10.1093/ehjopen/oeaf018 · Cited by 5
“36 This residual risk could be attributed to other risk factors not adequately addressed by licenced therapies.”
Solanki, J., Makwana, A., Mehta, H., Desai, C., & Gandhi, P. (2015) · Journal of Obesity and Metabolic Research · doi:10.4103/2347-9906.151755 · Cited by 5
Zhou, T., Lin, W., Yang, B., Liu, Y., Huang, W., Xie, N., Yang, F., Lin, Z., Hu, Z., Luo, S., et al. (2025) · Lipids in Health and Disease · doi:10.1186/s12944-025-02466-0 · Cited by 5
Ehrlich, J., Gliozzi, M., Carresi, C., Musolino, V., Palma, E., Muscoli, C., Vitale, C., Muscianisi, G., Janda, E., Ragusa, S., et al. (2015) · IJC Metabolic & Endocrine · doi:10.1016/j.ijcme.2015.05.015 · Cited by 5
Influence of Baseline Psychological Health on Muscle Pain During Atorvastatin Treatment
Zaleski, A. L., Taylor, B. A., Pescatello, L. S., Dornelas, E. A., White, C. M., & Thompson, P. D. (2016) · The Journal of Cardiovascular Nursing · doi:10.1097/jcn.0000000000000382 · Cited by 5
How to Interpret Recent CV Outcome Trials and Future: PCSK9 Inhibitors
Lee, E. Y., & Yoon, K. (2018) · Journal of Lipid and Atherosclerosis · doi:10.12997/jla.2018.7.1.1 · Cited by 5
Dyslipidemia and Cardiometabolic Syndrome
Hsiao, Y.-C., & Wu, C. (2021) · CardioMetabolic Syndrome Journal · doi:10.51789/cmsj.2021.1.e2 · Cited by 5
Targeting Triglycerides: The Rise of Apolipoprotein C3 and Angiopoietin-Like Protein 3 Inhibitors
Mansoor, T., Nambi, V., Parikh, S. S., Misra, A., Ismayl, M., Sullivan, C., Sperling, L. S., Virani, S. S., Rifai, M. A., Koshy, S. K. G., et al. (2025) · American Journal of Cardiovascular Drugs · doi:10.1007/s40256-025-00748-7 · Cited by 4
qi, X., Cao, S., Chen, J., & yin, X. (2025) · Journal of Inflammation Research · doi:10.2147/jir.s529581 · Cited by 4
“The key transcription factor for Tfh cells is B-cell lymphoma 6.”
Yu, B., Zhao, J., Zhang, W., Wang, L., Zheng, X. S., Li, X., Yao, Z., Sun, Y., Ren, Z., & Liang, B. (2025) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1650319 · Cited by 4
de la Cruz, S., Leon‐Acuña, A., Yubero‐Serrano, E. M., Torres-Peña, J. D., Larriva, A. P. A.-D., Cardelo, M. P., Rangel-Zúñiga, O. A., Luque, R. M., Alcala-Diaz, J. F., Ordovás, J. M., et al. (2022) · Clinica Chimica Acta · doi:10.1016/j.cca.2022.06.002 · Cited by 4
“…umbrella of dyslipidemia exists a dramatic heterogeneity and complexity, such as the numerous, and potentially significant lipoprotein subfractions pre-sent in the fasting and postprandial states [9,10], but we lack full understanding of their contributions and informativeness as CHD risk factors.”
Li, S., Liu, P., Feng, X., Du, M., Zhang, Y., Wang, Y., & Wang, J. (2023) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2023.1111475 · Cited by 4
Menezes, A. D. S., Oliveira, V. M. R., Oliveira, I. C., de Sousa, A. M., Santana, A. J. P., Carvalho, D. P. C., Piai, R. F. P., Matos, F. H., de Paiva, A. M., & Reis, G. B. B. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12175674 · Cited by 4
“considerable residual cardiovascular risk persists [6].”
Maiti, R., Mohanty, R. R., Dey, A., Maji, S., Padhan, M., & Mishra, A. (2023) · Journal of the American Nutrition Association · doi:10.1080/27697061.2023.2256816 · Cited by 4
Vu, T., Yano, Y., Pham, H. K. T., Mondal, R. K., Ohashi, M., Kitaoka, K., Moniruzzaman, M., Torii, S., Shiino, A., Tsuji, A. B., et al. (2024) · Scientific Reports · doi:10.1038/s41598-024-59523-4 · Cited by 4
Jiang, Y. (2025) · Scientific Reports · doi:10.1038/s41598-025-87281-4 · Cited by 4
Joint exposure to multiple air pollutants and residual cardiovascular risk in hypertension
Li, Y., Hong, W., Wu, J., Wang, J., Liu, S., Yuan, H., Cai, J., Miao, R., Wang, J., & Lu, Y. (2025) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2025.117782 · Cited by 4
Mechanisms and implications of vascular-homing CD8 T cells in atherosclerosis
Su, X., O’Hare, K. A., & Freeman, M. L. (2025) · npj Cardiovascular Health · doi:10.1038/s44325-025-00056-8 · Cited by 6
“Despitethe widespreaduseofstatinstomitigatelipidlevels,atherosclerosis-related mortalityhascontinuedtorise 3,4 , highlighting the need for a more comprehensive treatment approach.”
PCSK9, a novel target for lowering LDL cholesterol: promise and progress
Tavori, H., Fazio, S., & Linton, M. F. (2012) · Clinical Lipidology · doi:10.2217/clp.12.72 · Cited by 4
Self-citationKłosiewicz−Latoszek, L., Cybulska, B., & Tyszko, P. Z. (2020) · Annals of Agricultural and Environmental Medicine · doi:10.26444/aaem/126674 · Cited by 4
Proposal for a Multidisciplinary Clinical Approach to Obesity
Rosero, R., Polanco, J. P., Ciro, V., Uribe, A., Manrique, H., & Sánchez, P. E. (2020) · Journal of Medical - Clinical Research & Reviews · doi:10.33425/2639-944x.1185 · Cited by 7
“A single altered value of the lipid profile already classifies the patient as being at moderate risk, which together with the patient’s morphotype may suggest that the patient is at an even greater risk [43].”
BackgroundPCSK9 Targeting in the Management of Hypercholesterolaemia
Kosmas, C. E., Papakonstantinou, E. J., Carreño, J., Uceta, R. E., Guzman, E., & Sourlas, A. (2023) · EMJ Cardiology · doi:10.33590/emjcardiol/10303462 · Cited by 4
“7 In this regard, the addition of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors in the lipid-lowering armamentarium was monumental, irrevocably changing the scope of lipid-lowering treatment, and closing the gap in optimal LDL-C reduction.”
BackgroundLipid-lowering activity of Cow urine ark in guinea pigs fed with a high cholesterol diet.
Chawda, H. M., Rasiklal, M. D., Baxi, S., Kishorbhai, V. V., & Tripathi, C. R. (2014) · Europe PMC (PubMed Central) · Cited by 4
Lampropoulou, A., Zannis, V. I., & Kypreos, K. E. (2012) · Biochemical Pharmacology · doi:10.1016/j.bcp.2012.09.006 · Cited by 3
Bermúdez, V., Torres, W., Salazar, J. J., Martínez, M. S., Rojas, E., Olivar, L. C., Lameda, V., Ortega, Á., Ramírez, P., Rojas, M., et al. (2018) · F1000Research · doi:10.12688/f1000research.13005.1 · Cited by 4
Alam, U., Mathai, S. V., Filtz, A., Kuno, T., Badimon, J. J., Sniderman, A. D., Virani, S. S., Toth, P. P., Shapiro, M. D., Lavie, C. J., et al. (2026) · Current Cardiology Reports · doi:10.1007/s11886-025-02337-1 · Cited by 4
“Residual risk persists in many individuals, especially those with features of metabolic syndrome (MetS) or diabetes mellitus (DM), suggest - ing the need to address additional lipoprotein abnormalities such as elevated triglycerides (TGs) and TG-rich lipoproteins (TRLs) [ 6, 7 ].”
Walking the VLDL tightrope in cardiometabolic diseases
Kim, M., & Zheng, Z. (2024) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2024.07.020 · Cited by 4
Karadimas, T., & Meier, H. C. S. (2024) · BMJ Public Health · doi:10.1136/bmjph-2023-000455 · Cited by 5
Kacemi, M. E., Orche, A. E., Bourakadi, K. E., Benchekroun, Y. H., Echerfaoui, F., Karrouchi, K., Bouatia, M., & Karbane, M. E. (2024) · Journal of AOAC International · doi:10.1093/jaoacint/qsae060 · Cited by 3
Metadata
- Authors
- Sampson, U. K., Fazio, S., & Linton, M. F.
- Affiliations
- Vanderbilt University Medical Center (US)
- Corresponding author
- Linton, MacRae F.
- Venue
- Current Atherosclerosis Reports
- Published
- 2011-11-19
- Volume
- 14
- Issue
- 1
- Pages
- 1-10
- ISSN
- 1523-3804 (ISSN-L)
- 1534-6242
- PMC
- PMC3697085
- OpenAlex
- W2079979713
- Cited by
- 439
- References
- 117
- Citations by year
- 2026: 37 · 2025: 36 · 2024: 38 · 2023: 50 · 2022: 43 · 2021: 36 · 2020: 34 · 2019: 36 · 2018: 33 · 2017: 25 · 2016: 19 · 2015: 18 · 2014: 15 · 2013: 11 · 2012: 7
- FWCI
- 1.91
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Current Atherosclerosis Reports (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL065709, R01HL086988, HL086988, HL105375, HL65709, R01HL105375)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- residual cardiovascular risk, LDL cholesterol lowering, statins, HDL cholesterol, triglycerides, fenofibrate, torcetrapib, nicotinic acid, AIM-HIGH trial, ILLUMINATE trial, diabetes mellitus, metabolic syndrome, lifestyle modification, lipid therapy
- MeSH terms
- Cardiovascular Diseases, Humans, Life Style, Cholesterol, LDL, Morbidity, Risk Factors, Risk Assessment, Hydroxymethylglutaryl-CoA Reductase Inhibitors
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