👤 Arina Tyurina

Low-density lipoprotein cholesterol (LDL-C) is a major cardiovascular risk factor and an indicator of hypolipidemic therapy effectiveness. However, direct and calculated methods for determining "LDL-C" present the sum of the cholesterol in all apoB-containing lipoproteins, including lipoprotein(a) [Lp(a)]. There has been an ongoing debate about the correctness of LDL-C in patients with elevated Lp(a) concentrations up to now. The aim of this study was to evaluate the effect of Lp(a) concentration on the LDL-C calculated by different equations. The study included the results of fasting lipids and Lp(a) concentration of 566 measurements from 283 patients (before and after lipid-lowering therapy prescribing, after exclusion of 17 patients with incomplete data). LDL-C and LDL-C corrected for Lp(a)-cholesterol (LDL-C We assessed 566 measurements of lipids and Lp(a). The number of values reclassified to a higher risk category was 10% and 13% with Martin-Hopkins and Sampson equations compared to the Friedewald formula. The percentage of Lp(a)-cholesterol (Lp(a)-C) in the LDL-C calculated by three formulas was up to 90% or more depending on the concentration of LDL-C and Lp(a). When stratified by clinically significant LDL-C thresholds, the proportion of values LDL-C Comparison of LDL-C concentrations calculated by Friedewald, Martin-Hopkins, and Sampson equations showed high consistency in patients without elevated triglycerides. The LDLcorr is reasonable to use in patients with Lp(a) concentration ≥ 30 and ≥41 mg/dL when using the Martin-Hopkins and Sampson equations, respectively. These data may help clinicians interpret LDL-C goal attainment in patients with elevated Lp(a) and avoid misclassification driven by the Lp(a)-cholesterol component. Show less

To evaluate the effect of inclisiran therapy on the blood lipid profile 90 days post-injection and to describe the baseline structural and ultrasound characteristics of carotid and femoral plaques in high- and very high-risk patients who failed to achieve low-density lipoprotein cholesterol goals despite ongoing lipid-lowering treatment. This prospective observational single-center study included 22 patients (mean age 50.9±8.6 years, 50% men) with dyslipidemia and atherosclerotic plaques in peripheral arteries narrowing the lumen by 25-49%. Familial hypercholesterolemia was diagnosed in 59% of patients, and statin intolerance in 36%. Duplex scanning of the carotid and femoral arteries was performed. The gray-scale median (GSM) method is currently used for the quantitative assessment of carotid artery (CA) plaque echogenicity. Inclisiran was administered on day 1, day 90, and then every six months. Blood lipid profiles, including low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), triglycerides, and lipoprotein (a) [Lp(a)], were assessed. At baseline, median concentrations were 3.7 [2.5; 5.4] mmol/l for LDL-C, 5.4 [4.4; 6.8] mmol/l for TC, and 22.0 [5.0; 108.0] mg/dl for Lp(a). Carotid artery evaluation showed a median of 4.0 [2.0; 4.0] plaques, total stenosis of 110% [63.8; 118.8], and a GSM of 38.6 [28.6; 52.4], with a predominance of heterogeneous plaques (59%). Femoral artery assessment revealed a median of 2.0 [2.0; 3.0] plaques, 75% [42.5; 111.3] total stenosis, and a minimum echogenicity of 41.5 [33.4; 57.4] gray-scale units, with 65% heterogeneous plaques. Ninety days post-initiation of inclisiran, LDL-C was reduced by 65% (to 1.3 [1.2; 2.9] mmol/L, p<0.01), TC by 30% (p<0.01), triglycerides by 35%, and Lp(a) by 33%. Inclisiran demonstrated high efficacy in reducing LDL-C levels in patients at high and very high risk of cardiovascular disease who failed to reach targets with standard therapy. The identified plaque characteristics indicate a high risk of atherothrombosis in this cohort. The dynamics of these structural plaque changes will be assessed after completing the one-year follow-up. Show less

Previous studies suggested a certain efficiency of proteinogenic branched-chain amino acid (BCAA) and magnesium supplementations in reducing cardiovascular risk and increasing quality of life. This investigation assessed the anti-atherogenic and anti-calcific effects of BCAA (55 mg/day, corresponding to a human equivalent dose of 13.5 g/day) and magnesium citrate (MgCit, 1.85 mg/day, corresponding to a human equivalent dose of 450 mg/day) intake in male and female ApoE-knockout mice, with the treatment initiation at either 1, 3, or 6 months of age. At the 12-month time point, lipid retention and calcium deposition in the aortic valve, lipid burden in the aorta, and serum ionized calcium were evaluated. The early BCAA intake (from 1/3 to 12 months of age) significantly reduced lipid retention in the aortic valve, whilst MgCit decreased ionized calcium. Both of these protective effects were higher in male than in female mice. Furthermore, it was tested whether human serum albumin (HSA) or MgCit can be applied to decrease the serum calcification propensity in 100 patients with myocardial infarction. A dual supplementation with HSA and MgCit reduced serum calcification propensity in 68% of cases. Collectively, these results highlight the potential benefits of BCAA/HSA and magnesium supplementations for cardiovascular prevention and justify further clinical trials in this regard. Show less

Peripheral artery disease (PAD) is a major global health issue. This study investigated the relationship between lipoprotein(a) [Lp(a)], high-density lipoprotein cholesterol (HDL-C) to blood cells ratios, and PAD development. The study included 361 patients categorized into groups based on the presence of stenotic atherosclerosis in lower limb arteries (LLAs) diagnosed via duplex ultrasound. Group 1 (n = 238) had atherosclerosis at the first visit. A second visit involved 281 patients: 158 from Group 1, 32 new diagnoses (Group 2), and 91 with no atherosclerosis at either visit (Group 3). Laboratory analysis included lipid profiles, Lp(a), and complete blood counts, calculating ratios like Lp(a)/HDL-C and monocyte-to-HDL-C ratio (MHR). Showed patients with stenotic atherosclerosis had significantly higher Lp(a) (20.2 vs. 12.1 mg/dL, Show less