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Background and aimsCurrently, less than 20% of patients at very high-risk achieve ESC/EAS dyslipidemia guideline-recommended LDL-C target levels in Europe. “Jena auf Ziel—JaZ” is a prospective cohort study in which early combination therapy with atorvastatin 80 mg and ezetimibe 10 mg was initiated on admission in patients with ST-elevation myocardial infarction (STEMI) and lipid-lowering therapy was escalated during follow-up with bempedoic acid and PCSK9 inhibitors to achieve recommended LDL-C targets in all patients. Moreover, we evaluated side-effects of lipid-lowering therapy.MethodsPatients admitted with STEMI at Jena University Hospital were started on atorvastatin 80 mg and ezetimibe 10 mg on admission. Patients were followed for EAS/ESC LDL-C target achievement during follow-up.ResultsA total of 85 consecutive patients were enrolled in the study. On discharge, 32.9% achieved LDL-C targets on atorvastatin 80 mg and ezetimibe 10 mg. After 4–6 weeks, 80% of all patients on atorvastatin 80 mg and ezetimibe started at the index event were on ESC/EAS LDL-C targets. In 20%, combined lipid-lowering therapy was escalated with either bempedoic acid or PCSK9 inhibitors. All patients achieved LDL-C levels of or below 55 mg/dL during follow-up on triple lipid-lowering therapy. Combined lipid-lowering therapy was well-tolerated with rare side effects.ConclusionsEarly combination therapy with a high-intensity statin and ezetimibe and escalation of lipid-lowering therapy with either bempedoic acid or PCSK9 inhibitors gets potentially all patients with STEMI on recommended ESC/EAS LDL-C targets without significant side effects.

In patients with stable atherosclerotic cardiovascular disease, proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9is) have shown a 50% to 60% reduction in low-density lipoprotein cholesterol (LDL-C) from baseline when added to high-intensity statin therapy. However, less is known about the impact of PCSK9is in the setting of an acute coronary syndrome (ACS). Therefore, we performed a systematic review and meta-analysis comparing PCSK9is with placebo in the setting of ACS added to guideline-directed high-intensity or maximally tolerated statin therapy. We included randomized controlled trials with initiation of a PCSK9i or placebo within 1 week of presentation or percutaneous coronary intervention for ACS. PubMed, EMBASE, and Cochrane Central were searched. This study followed the Cochrane and Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) recommendations. A total of 6 randomized controlled trials were included, with a total of 996 patients, of whom 503 (50.5%) received PCSK9is. The mean follow-up ranged from 4 to 52 weeks. The LDL-C (mean difference [MD] −44.0 mg/100 ml, CI −54.3 to −33.8, p <0.001) and lipoprotein (a) levels (MD −24.0 nmol/L, confidence interval [CI] −43.0 to −4.9, p = 0.01) were significantly lower at follow-up with PCSK9is. Similarly, the total cholesterol (MD −49.2 mg/100 ml, CI −59.0 to −39.3), triglycerides (MD −19.0 mg/100 ml, CI −29.9 to −8.2), and apolipoprotein B (MD −33.3 mg/100 ml, CI −44.4 to −22.1) were significantly reduced with PCSK9is. In conclusion, in patients with ACS, early initiation of PCSK9i added to statin significantly reduces LDL-C and lipoprotein (a) levels compared with placebo. Whether the differences in these atherogenic lipoproteins translate into a reduction in clinical end points is yet to be determined.

For a given body mass index, human immunodeficiency virus (HIV) infection was associated with an excess risk of abdominal obesity, which was exacerbated by age. People living with HIV also had higher risk of elevated low-density lipoprotein cholesterol and hypertriglyceridemia. Abstract Background People living with human immunodeficiency virus (PLWH) are characterized by excess risk of cardiovascular diseases (CVD) and CVD risk factors compared to uninfected individuals. We investigated the association between HIV infection and abdominal obesity, elevated low-density lipoprotein cholesterol (LDL-C), hypertriglyceridemia, and hypertension in a large cohort of predominantly well-treated PLWH and matched controls. Methods 1099 PLWH from the Copenhagen Co-morbidity in HIV Infection Study and 12 161 age- and sex-matched uninfected controls from the Copenhagen General Population Study were included and underwent blood pressure, waist, hip, weight, and height measurements and nonfasting blood samples. We assessed whether HIV was independently associated with abdominal obesity, elevated LDL-C, hypertriglyceridemia, and hypertension using logistic regression models adjusted for known risk factors. Results HIV infection was associated with higher risk of abdominal obesity (adjusted odds ratio [aOR], 1.92 [1.60-2.30]) for a given body mass index, elevated LDL-C (aOR, 1.32 [1.09-1.59]), hypertriglyceridemia (aOR, 1.76 [1.49-2.08]), and lower risk of hypertension (aOR, 0.63 [0.54-0.74]). The excess odds of abdominal obesity in PLWH was stronger with older age (p interaction, 0.001). Abdominal obesity was associated with elevated LDL-C (aOR, 1.44 [1.23-1.69]), hypertension (aOR, 1.32 [1.16-1.49]), and hypertriglyceridemia (aOR, 2.12 [1.86-2.41]). Conclusions Abdominal obesity was associated with proaterogenic metabolic factors including elevated LDL-C, hypertension, and hypertriglyceridemia and remains a distinct HIV-related phenotype, particularly among older PLWH. Effective interventions to reduce the apparent detrimental impact on cardiovascular risk from this phenotype are needed.

Background Small dense LDL cholesterol (sdLDL-c) has been established to be highly associated with metabolic disorder. However, the relationship between circulating sdLDL-c and the presence of metabolic syndrome (MetS) has not been fully established. Methods A total of 1065 Chinese males (45.07 ± 11.08 years old) without diabetes and general obesity was recruited into a population-based, cross-sectional study. The MetS was defined based on the updated National Cholesterol Education Program/ Adult Treatment Panel III criteria for Asian Americans. Serum sdLDL-c concentration was measured by a homogeneous assay method and its relationship with MetS and its traits was investigated. Results Serum sdLDL-c concentrations increased gradually with increasing numbers of MetS components ( p  < 0.001) and the proportion of patients with MetS increased gradually with increasing sdLDL-c levels ( p for trend< 0.001). For the second, third, and fourth sdLDL-c quartiles versus the first, the OR (95% CI) for MetS were 4.47(2.41,8.28), 5.47(2.97,10.07) and 8.39(4.58,15.38) ( p  < 0.001 for trend) after multivariate adjustment. The stratified analysis conducted according to LDL-c levels showed that the OR between serum sdLDL-c levels and MetS was greater in those LDL-c levels lower than 3.3 mmol/L (OR = 22.97; 95% CI, 7.64–69.09) than in those LDL-c levels higher than 3.3 mmol/L (OR = 17.49; 95% CI, 4.43–68.98). Mediation analysis showed sdLDL-c mediated 38.6% of the association of waist circumference with triglycerides, while the association between sdLDL-c and MetS components did not mediate by hsCRP. Conclusions This study found that high sdLDL-c concentrations were associated with the presence of MetS independently of central obesity and inflammation.

IntroductionIntensive control of LDL cholesterol (LDL-C) following myocardial infarction (MI) are recommended by European Society of Cardiology (ESC) guidelines, to improve clinical outcomes. In this retrospective analysis, we report experiences and trends of lipid management by clinical cardiologists from a UK District General Hospital.MethodsPost-MI patients on high-intensity statin not meeting Low Density Lipoprotein-Cholesterol (LDL-C) targets of <1.4 mmol/L at first post-MI clinic follow-up were included for a second follow-up 3 months later at the lipid clinic. Lipid profiles were done at baseline (MI admission), post-MI clinic follow-up and lipid clinic follow-up. Cardiovascular (CV) risk factors, lipid profiles at post-MI clinic and lipid clinic follow up, changes to lipid treatment and lipid MDT outcomes were recorded on Excel and statistically analysed.ResultsFifty six percent of patients in the lipid clinic had ST-elevation MI. Baseline CV risk factors included hypertension (41%), diabetes (18%), family Hx 291(52.8%), smoking (60%), prior CAD/ MI (9%).LDL during index admission (mean+/-standard deviation [SD]) was 3.17 +/-1.28 mmol/l; total cholesterol was 5.05+/-1.41 mmol/l. 62% of patients had LDL> 1.4 mmol/L.At first follow up (i.e. post-MI clinic), mean LDL-C was 2.12+/-0.69 mmol/l and cholesterol was 4.06 +/-0.93 mmol/l. Only 5% had met the ESC LDL target <1.4 mmol/l.At time of referral to the lipid clinic, 32% had achieved LDL targets; 94% of those referred to lipid clinic were established on atorvastatin; 82% were on Ezetimibe. Mean LDL-C was 1.82 +/-0.80 mmol/l and cholesterol was 3.76+/- 0.91 mmol/l. 82% of patients were discharged from the lipid clinic. Ezetimibe was further added in 11% of patients, 7% were started on Inclisaran,10% were started on bempedoic acid and 18% were further referred to lipid MDT at a tertiary centre.ConclusionIn this analysis, we demonstrate the feasibility and importance of follow-up clinics for optimising lipid lowering therapy to intensive targets in post-MI patients by clinical cardiologists at DGH level.Conflict of InterestNone

Background and AimHigh levels of Low Density Lipoprotein-C (LDL-C) have been associated with increased cardiovascular mortality. The introduction of Inclisiran in recent years have provided an alternative for patients on maximal dose of statins or intolerant to statins and not achieving their target LDL-C level. This study aims to determine the baseline LDL-C level as a predictor in determining the percentage of patients achieving LDL-C level less than 1.8 mmol/l at day 90 after the first dose of Inclisiran with or without statins.MethodThis is a retrospective observational study using real world data which we collected the data electronically by looking at patients who received Inclisiran as an addon to their usual lipid lowering therapy with an initial level of below 2.6 mmol/l. Their baseline LDL-C levels were then grouped into different categories and their percentage of achieving target below 1.8 mmol/l were determined and analysed. This target is the cutoff point for high cardiovascular risk as per ESC guidance.ResultsA total of 69 patients were included in the study. The greatest percentage achieving the target were those with a baseline between 2–3 mmol/l, which was 74%. Of those between 3–4 mmol/l, the percentage reduction was 44%, with 4–5 mmol/l 23% and with 1–2 mmol/l 71%. The analysis showed that none of those with a level above 5 mmol had achieved a target below 1.8 mmol/l.In addition, the percentage reduction in LDL-C in these subgroups were also determined. Those with a baseline between 2–3 mmol/l have the highest percentage reduction of 53% ±11 (95% CI), followed by those between 4–5 mmol/l with 50% ±10 (95% CI), between 3–4 mmol/l 44% ±8 (95% CI). In those with level above 5 mmol/l, they had a reduction of 32% ±11 (95% CI). Surprisingly in those with levels between 1–2 mmol/l, 3 patients had an increase in LDL-C level of 7%, 117% and 197%.ConclusionBaseline LDL-C level can potentially be used as a predictor to determine if patients may achieve the target of below 1.8 mmol/l following the first dose of Inclisiran at day 90, with the best baseline level being 2–3 mmol/l. Our study showed that adding Inclisiran in patients with baseline levels of more than 5 mmol/l did not reach target and the effect can be mitigated in those with low level of 1–2 mmol/l, both of which will need further exploration.Abstract 232 Figure 1Abstract 232 Figure 2Conflict of InterestNone

In two randomized trials, evolocumab, a monoclonal antibody that inhibits proprotein convertase subtilisin–kexin type 9 (PCSK9), reduced LDL cholesterol levels by 61%. In an exploratory analysis, the incidence of cardiovascular events was reduced in the evolocumab group. Reduction in low-density lipoprotein (LDL) cholesterol levels has proved to be highly effective in reducing rates of major cardiovascular events in numerous large outcome trials. 1 – 3 For this reason, LDL cholesterol reduction has been incorporated into practice guidelines as a fundamental means of reducing cardiovascular morbidity and mortality. 4 – 7 During the past 3 years, monoclonal antibodies that inhibit proprotein convertase subtilisin–kexin type 9 (PCSK9) have emerged as a new class of drugs that very effectively lower LDL cholesterol levels. 8 One of the members of this class is evolocumab, a fully human monoclonal antibody that typically achieves approximately a 60% reduction . . .

Familial hypercholesterolemia (FH) is the most common monogenic disorder in humans. There is a lack of data on the clinical characteristics and natural history of FH patients in Iran, which necessitates performing a longitudinal study. In this five-year prospective longitudinal cohort study, we enrolled patients with high LDL cholesterol who were registered in the Iranian Registry of Hypercholesterolemia (IFHR), diagnosed as definite and probable FH cases based on the Dutch Lipid Clinic Network Score (DLCN ≥6). General characteristics, lipid profiles, and cardiovascular disease assessments were evaluated in the baseline phase, and whole blood samples were stored for future genetic and epigenetic studies. This study will evaluate the incidence and recurrence rates of cardiovascular disease (CVD) and mortality as the main outcomes during five years of follow-up. During the initial year, we successfully identified and enrolled patients with FH. We are reporting the whole methodology and the results of the first 50 who were followed up. At the study's outset, the patients exhibited a mean age of 50.27±12.06 years, with 64% being men and 36% women. The mean LDL level recorded was 312.8 ±106.3 mg/dL, with the highest LDL concentration observed at 623.5 mg/dL. A total of 62.0% of patients were on lipid-lowering treatment mostly of the PCAD group. In this paper, we present the design and methodology of the Isfahan Familial Hypercholesterolemia Cohort (IFHC) study in detail with the aim of helping future research generate evidence from comprehensive IFHC data sources.

Cardiovascular disease is a major cause of morbidity and mortality in patients with type 2 diabetes mellitus, with a two- to fourfold increase in cardiovascular disease risk compared with non-diabetic individuals. Abnormalities in lipid metabolism that are observed in the context of type 2 diabetes are among the major factors contributing to an increased cardiovascular risk. Diabetic dyslipidaemia includes not only quantitative lipoprotein abnormalities, but also qualitative and kinetic abnormalities that, together, result in a shift towards a more atherogenic lipid profile. The primary quantitative lipoprotein abnormalities are increased triacylglycerol (triglyceride) levels and decreased HDL-cholesterol levels. Qualitative lipoprotein abnormalities include an increase in large, very low-density lipoprotein subfraction 1 (VLDL 1 ) and small, dense LDLs, as well as increased triacylglycerol content of LDL and HDL, glycation of apolipoproteins and increased susceptibility of LDL to oxidation. The main kinetic abnormalities are increased VLDL 1 production, decreased VLDL catabolism and increased HDL catabolism. In addition, even though LDL-cholesterol levels are typically normal in patients with type 2 diabetes, LDL particles show reduced turnover, which is potentially atherogenic. Although the pathophysiology of diabetic dyslipidaemia is not fully understood, the insulin resistance and relative insulin deficiency observed in patients with type 2 diabetes are likely to contribute to these lipid changes, as insulin plays an important role in regulating lipid metabolism. In addition, some adipocytokines, such as adiponectin or retinol-binding protein 4, may also contribute to the development of dyslipidaemia in patients with type 2 diabetes.

Cardiovascular diseases (CVDs) represent the leading cause of global mortality with 1.7 million deaths a year. One of the alternative systems to drug therapy to minimize the risk of CVDs is represented by alpha-linolenic acid (ALA), an essential fatty acid of the omega-3 series, known for its cholesterol-lowering effect. The main purpose of this review is to analyze the effects of ALA and investigate the relevant omega-6/omega-3 ratio in order to maintain functionally beneficial effects. Concerning the lipid-lowering preventive effects, ALA may favorably affect the values of LDL-C and triglycerides in both adult and pediatric populations. Furthermore, ALA has shown protective effects against hypertension, contributing to balancing blood pressure through customary diet. According to the 2009 EFSA statement, dietary ALA may contribute to reducing the risk of CVDs, thanks to anti-hypertensive, anti-atherosclerotic and cardioprotective effects.