Search

Accurate estimation of low‐density lipoprotein cholesterol (LDL‐C) is important for monitoring cardiovascular disease (CVD) risk and guiding lipid‐lowering therapy. This study aimed to evaluate the magnitude of discordance of LDL‐C levels calculated by different equations and its effect on CVD incidence. The study sample consisted of 2354 CVD‐free individuals (49% males, mean age 45 ± 14 years); 1600 were re‐evaluated at 10 years and 1570 at 20 years. LDL‐C was estimated using the Friedewald, Martin/Hopkins, and Sampson equations. Participants were categorized as discordant if estimated LDL‐C was below the CVD‐risk specific cut‐off for one equation and equal/above for its comparator. The Friedewald and Martin/Hopkins equations presented a similar performance in estimating LDL‐C; however, both yielded lower values compared to the Sampson. In all pairwise comparisons, differences were more pronounced at lower LDL‐C levels, while the Friedewald equation significantly underestimated LDL‐C in hypertriglyceridemic participants. Discordance was evident in 11% of the study population, and more specifically 6%, 22%, and 20% for Friedewald versus Martin/Hopkins, Friedewald versus Sampson and Martin/Hopkins versus Sampson equations, respectively. Among discordant participants, median (1st, 3rd quartile) difference in LDL‐C was −4.35 (−10.1, 1.95), −10.6 (−12.3, −9.53) and −11.3 (−11.9, −10.6) mg/dL for Friedewald versus Martin/Hopkins, Friedewald versus Sampson and Martin/Hopkins versus Sampson equations, respectively. The 10‐ and 20‐year CVD survival model that included LDL‐C values of the Martin‐Hopkins equation outperformed the predictive ability of those based on the Friedewald or Sampson equations. Significant differences in estimated LDL‐C exist among equations, which may result in LDL‐C underestimation and undertreatment. [ABSTRACT FROM AUTHOR]

Background: Our aim was to systematically investigate the effect of upadacitinib, an oral JAK-1 selective inhibitor, on lipid profile and cardiovascular disease risk. Methods: PubMed, PubMed Central and ClinicalTrials.gov databases were searched for relevant randomized controlled trials (RCTs) up to 31 July 2022. We performed a qualitative synthesis of published RCTs to investigate the associations of upadacitinib with lipoprotein changes, along with a quantitative synthesis of MACE and mean lipoprotein changes where there were available data. Results: Nineteen RCTs were eligible for the present systematic review, which included 10,656 patients with a mean age of 51 years and a follow-up period of 12–52 weeks. Increases in low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) were noted upon upadacitinib administration (3–48 mg/day) in 15 studies, while the LDL-C:HDL-C ratio remained unchanged. The pooled analyses of three placebo-controlled RCTs (n = 2577) demonstrated that upadacitinib at 15 mg increased the LDL-C by 15.18 mg/dL (95% CI: 7.77–22.59) and HDL-C by 7.89 mg/dL (95% CI: 7.08–8.69). According to the pooled analysis of 15 placebo-controlled RCTs (n = 7695), upadacitinib had no effect on MACE (risk ratio, RR: 0.62; 95% CI: 0.24–1.60). A sub-analysis focusing on upadacitinib at 15 mg (12 studies, n = 5395) demonstrated similar results (RR: 0.67; 95% CI: 0.19–2.36). Conclusions: Treatment with upadacitinib increases both LDL-C and HDL-C levels. Nevertheless, upadacitinib had no significant effect on the cardiovascular disease risk during a ≤52-week follow-up. [ABSTRACT FROM AUTHOR]

Hyperlipidemia is a well-established risk factor for cardiovascular disease (CVD) which is the major cause of mortality associated with a high socioeconomic burden in the developed countries. Despite the available lipid-lowering therapies, a plethora of studies have demonstrated poor lipid target attainment in clinical practice. This has been attributed mainly to the decreased patients' compliance with lipid-lowering therapy along with physicians' reluctance to prescribe more aggressive statin therapy or novel lipid-lowering drugs. According to global experience, the implementation of national hyperlipidemia management policies could help overcome these issues. Guidelines proposing lower targets for the management of dyslipidemias, national initiatives increasing public health check, and aiming at public education for CVD and its associated risk factors, along with reimbursement policies reducing the cost of lipid-lowering therapies could help improve lipid target attainment in clinical practice and reduce the burden of cardiovascular disease. [ABSTRACT FROM AUTHOR]

This was a retrospective study that assessed achievement of lipid-lowering treatment targets in the setting of a University Hospital Lipid Clinic. Low-density lipoprotein cholesterol (LDL-C) goal attainment according to National Cholesterol Education Program-Adult Treatment Panel III (NCEP ATP III) and European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) guidelines was recorded in 1000 consecutive adult patients followed for ≥3 years (mean 8 years). The LDL-C targets according to the NCEP ATP III were attained by 66% and 86% of patients with “very high” (n = 477) and “high” (n = 408) cardiovascular risk, respectively. Fewer patients were within LDL-C goals according to the ESC/EAS guidelines: 25% and 42%. Overall, 92% of the patients were on statins: 67% were on statin monotherapy, while 33% were on combinations with ezetimibe (25%), ω-3 fatty acids (5%), fibrates (4%), or colesevelam (2%). Even in a specialist lipid clinic, a large proportion of patients are not at goal according to the recent ESC/EAS guidelines. [ABSTRACT FROM PUBLISHER]

Objective. Data regarding the effect of lipid parameters on repolarization are sparse. Recent data indicate that reconstituted HDL administration shortens repolarization in cardiomyocytes as well as the corrected QT (QTc) interval in human subjects. We investigated the potential association of high-density lipoprotein cholesterol (HDL-C) levels with conventional and novel electrocardiographic markers of ventricular repolarization in patients with hypercholesterolemia. Methods. Consecutive subjects with primary hypercholesterolemia were recruited. We recorded clinical and laboratory parameters as well as electrocardiographic indexes. With regard to ventricular repolarization, we calculated the QTc interval, the T peak-to-end (Tpe) interval, and the Tpe/QT ratio. Results. The study population consisted of 440 patients (199 men) with a median age of 56 [48-65] years. The correlation analysis (Spearman's) failed to show any association between HDL-C and any of the studied electrocardiographic parameter. Moreover, no correlation between other lipid parameters and the electrocardiograhic indexes was evident. Also, a comparison of the ventricular repolarization parameters between different HDL-C quartile groups (HDL-Q1: ≤ 1.11 mmol/L; HDL-Q2: 1.12-1.29 mmol/L; HDL-Q3: 1.30-1.53 mmol/L; HDL-Q4: ≥ 1.54 mmol/L) was performed. Specifically, the differences in QTc ( p: 0.372), Tpe in leads II ( p: 0.356), V2 ( p: 0.372), V5 ( p: 0.112), and Tpe/QT in leads II ( p: 0.348), V2 ( p: 0.162), V5 ( p: 0.122) were not significant. Conclusion. HDL-C levels are not associated with the QTc interval or indexes of repolarization dispersion in patients with primary hypercholesterolemia. The potential antiarrhythmic efficacy of HDL should be further evaluated in the setting of myocardial ischemia where dynamic changes in the heterogeneity of ventricular repolarization ensue. [ABSTRACT FROM AUTHOR]