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Background: Recent guidelines on acute coronary syndromes (ACS) recommend initiating lipid-lowering therapy (LLT) as early as possible to obtain >50% low-density-lipoprotein cholesterol (LDL-c) reduction and an LDL-c < 1.4 mmol/l., Methods: A multinational European survey study of ACS patients between 2021-2022 and acquired data on LLT and lipid levels on admission and during 1-year posthospitalization. We compared plasma lipid changes and adherence to post-ACS lipid targets across two in-hospital LLT groups: high-intensity statin (HIS) monotherapy (mono-HIS) and a combination of HIS and ezetimibe (combo-HIS)., Results: Of 286 patients, 268 (94%) received in-hospital HIS and were included in the final analysis. Patients (median age: 61.1 years) had a median baseline LDL-c of 3.3 mmol/l. Mono-HIS was the predominant in-hospital LLT (72.4%). In-hospital combo-HIS was administered in 27.6% of the cases. Patients from high-income countries ( n  = 141) were more likely to receive in-hospital combo-HIS than patients from middle-income countries [ n  = 127; 38.3% vs. 15.7% patients, P  < 0.001). One-year post-ACS, 50 (26.5%) patients from the mono-HIS group received ezetimibe. The target of LDL-c ≤ 55 mg/dl was reached in 85 patients (31.7%), without significant difference between study groups [mono-HIS: 56 (28.9%) and combo-HIS: 29 (39.2%) patients, P  = 0.10]. The target of >50% reduction was achieved more frequently among the combo-HIS group than in the mono-HIS group (50.0% vs. 29.9%, respectively, P  = 0.002)., Conclusion: LDL-c targets were achieved in less than half of the patients post-ACS, regardless of the LLT regimen. Combo-HIS was initiated in-hospital post-ACS in only 28% and was associated with greater LDL-c reduction compared to a staged approach of mono-HIS with up-titration at follow-up., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

The absolute value of small dense low-density lipoprotein (sd-LDL) including small LDL (s-LDL) and very small LDL (vs-LDL) has been shown to be associated with increased incidence of atherosclerosis. However, the impact of short-timeframe increases in sd-LDL on arteriosclerosis has not yet been elucidated. Therefore, we investigated the clinical roles of ex-vivo induced sd-LDL in acute coronary syndrome (ACS) using a novel method. This is a prospective, single-blind, and observational study that screened patients who underwent coronary angiography (CAG) for the treatment of ACS or investigation of heart-failure etiology between June 2020 and April 2022 (n = 247). After excluding patients with known diabetes mellitus and advanced renal disease, the patients were further divided into the ACS (n = 34) and control (non-obstructive coronary artery, n = 34) groups. The proportion of sd-LDL (s-LDL + vs-LDL) in total lipoproteins was observed before and after 2-h incubation at 37 ℃ (to approximate physiologic conditions) using 3% polyacrylamide gel electrophoresis. The coronary plaque burden was quantified upon CAG in the ACS group. There were no significant differences between the ACS and control groups in terms of clinical coronary risk factors. The baseline of large, medium, small, and very small LDL were comparable between the two groups. Following a 2-h incubation period, significant increases were observed in the ratios of s-LDL and vs-LDL in both the ACS and control groups (ACS, p = 0.01*; control, p = 0.01*). Notably, the magnitude of increase in sd-LDL was more pronounced in the ACS group compared to the control group, with s-LDL showing a significant difference (p = 0.03*) and vs-LDL showing a tread toward significance (p = 0.08). In addition, in both groups, there was a decrease in IDL and L-LDL, while M-LDL remained unchanged. The plaque burden index and rate of short-timeframe changes in both s-LDL (p = 0.01*) and vs-LDL (p = 0.04*) before and after incubation were significantly correlated in the ACS group. The enhanced production rate of sd-LDL induced under short-term physiologic culture in an ex-vivo model was greater in patients with ACS than in the control group. The increase in sd-LDL is positively correlated with coronary plaque burden. Short-timeframe changes in sd-LDL may serve as markers for the severity of coronary artery disease., Competing Interests: Declarations. Conflict of interest: The authors declare that they do not have any conflict of interest. Ethical approval: This study was approved by the Clinical Research Appropriate Promotion Center at Saitama Medical University International Medical Center (No. 19-307), and written informed consent was obtained from all participants., (© 2024. Springer Nature Japan KK, part of Springer Nature.)

The American Diabetes Association (ADA) "Standards of Care in Diabetes" includes the ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, an interprofessional expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations and a full list of Professional Practice Committee members, please refer to Introduction and Methodology. Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC. [ABSTRACT FROM AUTHOR]

Several epidemiological studies have appreciated the impact of "duration" and "level" of hyperglycemia on the initiation and development of chronic complications of diabetes. However, glycemic profiles could not fully explain the presence/absence and severity of diabetic complications. Genetic issues and concepts of "hyperglycemic memory" have been introduced as additional influential factors involved in the pathobiology of late complications of diabetes. In the extended phase of significant diabetes randomized, controlled clinical trials, including DCCT/EDIC and UKPDS, studies have concluded that the quality of glycemic or metabolic control at the early time around the diabetes onset could maintain its protective or detrimental impact throughout the following diabetes course. There is no reliable indication of the mechanism by which the transient exposure to a given glucose concentration level could evoke a consistent cellular response at target tissues at the molecular levels. Some biological phenomena, such as the production and the concentration of advanced glycation end products (AGEs), reactive oxygen species (ROS) and protein kinase C (PKC) pathway activations, epigenetic changes, and finally, the miRNAs-mediated pathways, may be accountable for the development of hyperglycemic memory. This work summarizes evidence from previous experiments that may substantiate the hyperglycemic memory soundness by its justification in molecular terms., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)