Journal of clinical lipidology最新文献

Background: Chylomicronemia is characterized by fasting triglyceride (TG) ≥1000 mg/dL; its longitudinal course is not well studied.

Methods: Using National Health and Nutrition Examination Survey (NHANES) data (1999-2018; n = 21,998), we determined chylomicronemia prevalence and temporal trend. Using Mayo Clinic data (4,524,506 TG measurements for 1,294,044 individuals), we studied the longitudinal course and ascertained persistent chylomicronemia (PC), defined as TG ≥1000 mg/dL in more than half the measurements for individuals with ≥3 measurements. We used logistic regression to assess factors associated with PC.

Results: In NHANES, the prevalence of chylomicronemia was 0.20% overall, with higher prevalence in men (0.32%) and Hispanics (0.33%). Chylomicronemia prevalence declined from 0.34% in 1999-2004 to 0.11% in 2013-2018, while lipid-lowering pharmacotherapy use in chylomicronemia patients increased from 5.3% to 51.9%. In the Mayo Clinic data, 5618 individuals (0.43%) had at least 1 episode of chylomicronemia. Of these, 8.8% (390 of 4443 with ≥3 measurements) met the operational definition for PC. In individuals with TG <150 mg/dL, 1.3% had a diagnosis of acute pancreatitis, and 0.6% had chronic pancreatitis. Respective figures for individuals with nonpersistent chylomicronemia were 12.5% and 5.1%, and for individuals with PC were 26.2% and 11.5%. Younger age, Hispanic ethnicity, prior pancreatitis, and higher TG levels were associated with PC.

Conclusion: In the US, 1 in ∼500 adults has chylomicronemia and 1 in ∼5500 has PC. Individuals with PC have high occurrence of acute and chronic pancreatitis and may need more effective treatment.

Background: Lipoprotein(a) (Lp[a]) has been identified as a significant risk factor for aortic stenosis (AS). However, its impact on outcomes post-transcatheter aortic valve replacement (TAVR) remains unknown.

Objective: To investigate the association between Lp(a) levels and long-term outcomes as well as its impact on the bioprosthetic valve degeneration in patients post-TAVR.

Methods: Patients with severe AS who underwent TAVR were consecutively recruited. Lp(a) was measured before TAVR procedure. The subjects were divided according to levels of Lp(a). The outcomes were all-cause mortality and possible structural valve degeneration (SVD) measured by Doppler echocardiography. Cox regression models and competing risk models were used to explore the association between Lp(a) levels and outcomes.

Results: Of the 601 included patients (mean age: 75.5 ± 7.2, male: 58.7%), 137 patients (22.7%) experienced mortality after a median follow-up of 3.9 years. After multivariable adjustment, elevated Lp(a) (defined as ≥30 mg/dL) was identified as an independent predictor of all-cause mortality (hazard ratio [HR]: 1.81, 95% CI: 1.27-2.57, P = .001) and cardiovascular mortality (HR: 2.02, 95% CI: 1.12-3.66, P = .020). Elevated Lp(a) was also associated with increased risk of possible SVD (subdistribution HR: 3.40, 95% CI: 1.32-8.79, P = .012). Using a threshold value of 50 mg/dL for elevated Lp(a) still supported the main findings.

Conclusions: Elevated baseline Lp(a) levels are associated with poor clinical outcomes and possible SVD in patients with severe AS undergoing TAVR. Further research is warranted to confirm these findings.

Background: Hypertriglyceridemia (HTG) is a prevalent metabolic disorder closely linked to cardiovascular diseases, diabetes, and other metabolic conditions. However, research examining the relationship between Helicobacter pylori (H. pylori) and HTG is limited. This study aimed to investigate the influence of H. pylori on HTG.

Methods: The study participants were individuals who underwent health examinations at Taizhou Hospital between 2017 and 2024. The subjects underwent hematological tests, anthropometric measurements, and urea breath tests. Logistic regression analysis was used to assess the relationship between H. pylori and HTG. Kaplan-Meier curves were utilized to compare HTG incidence between groups, and Cox regression models were applied to calculate associated hazard ratios.

Results: Logistic regression confirmed that H. pylori was a risk factor for HTG. Further cohort study indicated that prolonged H. pylori infection increased the risk of HTG, whereas H. pylori eradication led to a decrease in HTG incidence. Subgroup analyses demonstrated that the impact of H. pylori on HTG did not exhibit heterogeneity.

Conclusion: H. pylori was associated with an increased risk of HTG, and its eradication was crucial for reducing this risk.

Prediabetes affects more than 1 in 3 adults in the United States and is associated with increased risks of type 2 diabetes, cardiovascular diseases, chronic kidney disease, and dementia. Excess adiposity is the strongest risk factor for prediabetes, and can contribute to several other cardiometabolic risk factors, such as dyslipidemia and insulin resistance. This Journal of Clinical Lipidology Roundtable presents a conversation between Drs. Jaime P. Almandoz, Carol F. Kirkpatrick, and Kevin C. Maki, who discussed lifestyle and pharmacologic interventions for the management of prediabetes and the prevention of associated health risks. The discussion highlights the importance of interventions for addressing excess adiposity in those with prediabetes, including lifestyle, pharmacotherapy, and metabolic surgery, along with involving patients in shared decision-making conversations to identify, implement, and maintain an effective treatment plan.

Lifestyle intervention is the cornerstone of the prevention of atherosclerotic cardiovascular disease (ASCVD). Several health authorities and scientific organizations have provided dietary guidance for ASCVD prevention, including recommendations for healthful dietary patterns. Recently, intermittent fasting and time-restricted eating (TRE) have become popular dietary approaches. Findings from clinical studies suggest that intermittent fasting and TRE may result in improvements in cardiometabolic risk factors, especially in patients with metabolic dysfunction. This Journal of Clinical Lipidology Roundtable presents a conversation between Drs. Carol F. Kirkpatrick, Kevin C. Maki, Kristina S. Petersen, and Michael J. Wilkinson about dietary recommendations, intermittent fasting, and TRE. The discussion highlights the current dietary recommendations for ASCVD prevention and the potential roles of intermittent fasting and TRE for improving cardiometabolic health.

Background: This study analyzed the cross-sectional association of elevated concentrations of low-density lipoprotein particles (LDLp) and triglyceride-rich lipoprotein particles (TRLp) with carotid artery plaque (CAP) in the ELSA-Brasil cohort.

Methods: Data from 3801 participants (median age: 50.0 years [interquartile range 44.0-57.0], 54.3% women) with no prior history of cardiovascular disease nor use of lipid-lowering medications were analyzed. CAP was assessed by ultrasonography, while nuclear magnetic resonance (NMR) spectroscopy was used to measure LDLp and TRLp concentrations according to size. Poisson regression models characterized the association of elevated lipid concentrations (≥1 SD above the mean) with CAP, adjusted for sociodemographic variables, cardiovascular risk factors, and for the concentration of high-density lipoprotein particles (HDLp), LDLp, and TRLp.

Results: The frequency of CAP was 33.9% (n = 1,287). Elevated concentrations of total TRLp (prevalence ratio [PR]:1.05 [95% CI:1.01-1.10]) and small-sized TRLp (PR:1.23 [95% CI:1.11-1.36]) were associated with CAP, but lost significance after adjustment for LDLp. Elevated LDLp concentration was associated with CAP in total (PR:1.10 [95% CI:1.05-1.15]) and in all the different sizes (large [PR:1.09], medium [PR:1.11] and small [PR:1.09]), regardless of TRLp. When both LDLp and TRLp were simultaneously included in a dedicated model, only LDLp remained associated with CAP (PR:1.11 [95% CI: 1.06-1.16]). By particle size, elevated small TRLp and elevated LDLp in all sizes were associated with CAP even when mutually adjusted.

Conclusion: The elevated concentration of small TRLp seems to portend an incremental residual likelihood of prevalent CAP beyond LDLp, whereas the association of LDLp with CAP remained consistent beyond classical risk factors and NMR-assessed HDLp and TRLp concentration.

Background and aims: Tofacitinib, a Janus kinase inhibitor, has been associated with increased cardiovascular (CV) risk in rheumatoid arthritis (RA). This study evaluated tofacitinib's effects on lipid parameters and the impact of prior biological agents' therapy in RA patients.

Methods: Thirty female RA patients starting tofacitinib were assessed at baseline and after 3 months. Clinical assessments, health assessment questionnaire (HAQ), disease activity score 28 (DAS28), inflammatory markers, lipid profile, oxidized low-density lipoprotein (LDL), activities of paraoxonase 1 (PON 1), lipoprotein-associated phospholipase A₂ (Lp-PLA₂), cholesteryl ester transfer protein (CETP), high-density lipoprotein (HDL) composition, and HDL functions (cholesterol efflux and free cholesterol uptake from triglyceride-rich lipoproteins [TGRL]) upon lipolysis were measured.

Results: After 3 months, HAQ and DAS28 scores improved significantly. Total cholesterol (TC), HDL-C, non-HDL-C, and HDL capacity to acquire free cholesterol from TGRL increased, while enzyme activities and cholesterol efflux capacity remained unchanged. At baseline, patients with prior biological therapy (n = 19) had lower triglycerides, TC, non-HDL-C, and apolipoprotein (apo) B compared to biologic-naïve patients (n = 11). This group exhibited no lipid changes after tofacitinib, whereas biologic-naïve patients showed atherogenic increases in TC, LDL-C, non-HDL-C, apo B, Lp-PLA₂, and CETP, alongside beneficial increases in PON 1 activity.

Conclusion: Tofacitinib improved disease activity and functional status in RA patients with minimal lipid changes. Patients previously treated with biological agents experienced no significant lipid alterations, while biologic-naïve patients showed atherogenic lipid changes and increased PON 1 activity. Prior biologic therapy may confer a more favorable CV profile before and after tofacitinib treatment.

The National Lipid Association (NLA) is currently conducting a study to improve the uptake of evidence-based guidelines into clinical practice through the deployment of case-based online learning modules to participating health systems nationwide. The Translating Evidence-based Approaches into optimal Care of High-risk atherosclerotic cardiovascular disease patients (TEACH-ASCVD) will evaluate the impact of electronic learning modules on clinician practices related to ASCVD management. In the design phase of TEACH-ASCVD, expert lipidologists created a series of 7 cases informed by recent guidelines intended to provide common clinical scenarios that evaluate participant knowledge of evidence-based practices for high-risk ASCVD and familial hypercholesterolemia. In this manuscript, we present 4 primary prevention-focused cases in high-risk patients and discuss pertinent clinical teaching points. These cases are intended for individuals with clinical lipidology training. We encourage lipidologists to disseminate this manuscript and utilize these cases as a teaching tool for nonlipid specialists to hone their knowledge of common clinical ASCVD risk management scenarios.

Objective: Familial hypercholesterolemia (FH) is a genetic disorder characterized by elevated plasma cholesterol and an increased risk of early-onset coronary artery disease (CAD). FH has a complex genetic basis. Advances in molecular genetic techniques have deepened our understanding of FH, which is critical for accurate classification, CAD risk assessment, and optimized treatment strategies. This study aimed to evaluate the monogenic etiologies of FH and polygenic background as a possible cause of clinical FH phenotype and their relationship to clinical outcomes in a Turkish cohort.

Methods: Patients were selected based on the Simon Broome Criteria. Various molecular techniques were employed, including Sanger sequencing, multiplex-ligation dependent probe amplification (MLPA), next-generation sequencing (NGS) panel analysis, and RNA-based studies. For the first time in a Turkish FH cohort, we calculated 6-single nucleotide polymorphism (SNP) and 12-SNP scores and compared them with a control group.

Results: Multiple variants were identified, including 2 novel variants and a synonymous splice region variant in LDLR, which was shown to disrupt splicing through RNA analysis. The 6-SNP and 12-SNP scores displayed patterns consistent with other populations.

Conclusion: Our findings suggest subtle differences in the monogenic etiology of FH in the Turkish population, with variant negative patients predominantly exhibiting polygenic background. Additionally, polygenic factors appear to influence the phenotype even in variant-positive individuals.

Background: Previous studies have investigated the relationship between remnant cholesterol (RC) and mortality outcomes in the general population, but the majority have focused on Western populations.

Objective: This study aims to evaluate the association between RC and mortality-related outcomes in a relatively young and middle-aged Korean population.

Methods: This cohort study included 268,219 participants (mean age, 38 years; 50.6% men) who were enrolled in the Kangbuk Samsung Health Study between 2003 and 2016. Fasting RC was calculated as total cholesterol minus low-density lipoprotein cholesterol minus high-density lipoprotein cholesterol.

Results: The median RC was 0.47 mmol/L (18 mg/dL) and the prevalence of ≥1 mmol/L RC was 11.4%. During the median follow-up of 6.7 years, compared with the lowest quintile (RC <0.31 mmol/L), the hazard ratios (HRs) and 95% CIs for cardiovascular mortality were 1.95 [0.78, 4.84], 2.47 [1.03, 5.91], 2.39 [1.00, 5.72], and 2.84 [1.19, 6.78] in the second, third, fourth, and highest quintiles, respectively. The HRs for all-cause mortality in the third, fourth, and highest quintiles remained significant but were not significant for the risk of cancer mortality. Subgroup analyses showed that the high RC group with high-sensitivity C-reactive protein (hsCRP) or high lipoprotein(a) levels had more than 2-fold and 3-fold increased risks of cardiovascular mortality than the low RC group with low hsCRP or low lipoprotein(a) levels.

Conclusion: High RC levels were significantly associated with an increased risk of cardiovascular and all-cause mortality, but not with cancer mortality. Specifically, high hsCRP and lipoprotein(a) levels weighted the risk association between high RC and cardiovascular mortality.