BACKGROUND: The present study aimed to evaluate the effects of 24 weeks of moderate aerobic exercise on lipids and lipoprotein levels; Lipo (a) markers, and their association with cognitive performance in healthy older adults.
METHODS: A total of 150 healthy subjects (100 males and 50 females; age range: 65-95 years) were recruited for this study. Based on the LOTCA test score, subjects were classified into two groups: the control group (n = 50) and the cognitive impairment group (n = 100). Cognitive functioning, leisure-time physical activity (LTPA), lipid profile, total cholesterol, TG, HDL-c, LDL-C, and lipo(a) were assessed at baseline and post-24-week aerobic exercise interventions using LOTCA battery, pre-validated Global Physical Activity Questionnaire (GPAQ) version II, colorimetric, and immunoassay techniques, respectively.
RESULTS: Significant improvements in cognitive function and modulation in lipid profile and lipoprotein (a) markers were reported in all older subjects following 24 weeks of moderate exercise. LOTCA-7-sets scores significantly correlated with physical activity status and the regulation of lipids and Lipo (a) markers. Physically active persons showed higher cognitive performance along with a reduction in the levels of T-Cholest., TG, LDL-C, Lipo (a), and an increase in the levels of HDL-C and aerobic fitness VO2max compared with sedentary participants. Cognitive performance correlated positively with increased aerobic fitness, HDL-C, and negatively with T-Cholest., TG, LDL-C, and Lipo (a). However, a significant increase in the improvement of motor praxis, vasomotor organization, thinking operations, attention, and concentration were reported among older adults.
CONCLUSIONS: The study findings revealed that supervised moderate aerobic training for 24 weeks significantly enhances cognitive functions via mitigating older adults\' lipid profiles and lipoprotein (a). Cognitive performance is positively correlated with aerobic fitness and HDL-C level and negatively with T-Cholest., TH, LDL-C, and Lipo (a).

BACKGROUND: Serum lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerotic cardiovascular disease (ASCVD) in the general population, its association with ASCVD incidence in Chinese maintenance hemodialysis (MHD) patients remains unclear. We aimed to evaluate the relationship between Lp(a) levels and ASCVD incidence among MHD patients in Beijing, China.
METHODS: This retrospective, observational cohort study included MHD patients at Beijing Tongren Hospital from January 1, 2013 to December 1, 2020, and followed until December 1,2023. The primary outcome was ASCVD occurrence. Kaplan-Meier survival analysis was used to evaluate ASCVD-free survival in MHD patients, with stratification based on Lp(a) levels. Cox regression analyses were conducted to assess the association between Lp(a) levels and the occurrence of ASCVD.
RESULTS: A total of 265 patients were enrolled in the study. The median follow-up period were 71 months.78 (29.4%) participants experienced ASCVD events, and 118 (47%) patients died, with 58 (49.1%) deaths attributed to ASCVD. Spearman rank correlation analyses revealed positive correlations between serum Lp(a) levels and LDL-c levels, and negative correlations with hemoglobin, triglyceride, serum iron, serum creatinine, and albumin levels. Multivariate Cox regression analysis showed that Lp(a) levels ≥ 30 mg/L, increased age, decreased serum albumin levels, and a history of diabetes mellitus were significantly associated with ASCVD incidence.
CONCLUSIONS: This study demonstrated an independent and positive association between serum Lp(a) levels and the risk of ASCVD in MHD patients, suggesting that serum Lp(a) could potentially serve as a clinical biomarker for estimating ASCVD risk in this population.

Significant advances in atherosclerotic cardiovascular (ASCVD) risk stratification and treatment have occurred over the past 10 years. While the lipid panel continues to be the basis of risk estimation, imaging for coronary artery calcium is now widely used in estimating risk at the individual level. Statins remain first-line agents for ASCVD risk reduction but in high-risk patients, ezetimibe, proprotein convertase subtilisin kexin-9 inhibitors, and bempedoic acid can be added to further reduce individual cardiovascular risk based on results of cardiovascular outcomes trials. Results of randomized control trials do not support use of medications targeted at triglyceride lowering for ASCVD risk reduction, but icosapent ethyl can be considered.

The role of lipoprotein (a) [Lp(a)] in cerebrovascular disease is a topic of importance. In this narrative review, pertinent studies have been leveraged to comprehensively examine this relationship from diverse perspectives.Lp(a) shares structural traits with low-density lipoprotein cholesterol. Lp(a) is synthesized by hepatocytes, and its plasma levels are genetically determined by the LPA gene, which produces apolipoprotein (a).Numerous epidemiological studies have confirmed the positive correlation between elevated serum Lp(a) levels and the occurrence or recurrence of cerebrovascular events, especially ischemic strokes, in adults. It should be noted that the correlation strength varies among studies and is marginal in Mendelian randomization studies.Regarding pediatric patients, screening is currently limited to those with a relevant medical history. Lp(a) seems to play a significant role in the pathogenesis of arterial ischemic stroke in children because environmental thrombotic and atherogenic factors are generally not present.Phase 3 trials of novel Lp(a) targeting agents, such as pelacarsen and olpasiran, are anticipated to demonstrate their efficacy in reducing the incidence of stroke. Given the richness of the literature, new guidelines regarding Lp(a) screening and management in targeted populations are warranted to provide more effective primary and secondary prevention.

BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) primarily affects the adult population and is closely related to obesity. The most severe form of MASLD, metabolic dysfunction-associated steatohepatitis (MASH), can progress to liver fibrosis. While lipoprotein(a) (Lp(a)) is known to be associated with cardiovascular disease, its relationship with MASLD remains unclear. This study aims to determine the prevalence of MASLD in ambulatory patients and to explore the association between Lp(a) levels and advanced liver damage.
METHODS: This retrospective cross-sectional study included 130 patients older than 18 years seen in a healthcare center in Medellin, Colombia, between April 2023 and May 2024. Sociodemographic, clinical, and specific biomarker data were collected. Patients with cirrhosis, previous liver disease, frequent alcohol consumption, cancer, and other severe conditions were excluded. Continuous variables were analyzed using Student\'s t-tests or Mann-Whitney tests according to their distribution, and categorical variables were analyzed using contingency tables and chi-square tests.
RESULTS: Of the 130 patients, 57.9% (n=73) had MASLD, with a higher prevalence in patients with obesity (80%, n=32). Lp(a) levels were abnormally high in 43.1% (n=31) of patients; however, a weak but significant inverse correlation was found between Lp(a) levels and the Fibrosis-4 (FIB-4) score, which is used to assess the severity of liver fibrosis. Patients with MASLD had significantly lower high-density lipoprotein (HDL) and vitamin D levels, and higher levels of gamma-glutamyl transferase (GGT).
CONCLUSIONS: This study highlights the significant prevalence of MASLD in outpatients and its relationship with various biomarkers, including Lp(a), HDL, vitamin D, and GGT. Although the findings suggest a possible utility of Lp(a) as a biomarker in MASLD, longitudinal studies are needed to confirm these associations and clarify their role in liver disease progression. The study\'s limitations include its cross-sectional nature and potential selection bias, indicating the need for further research to validate these results.

UNASSIGNED: Lipoprotein(a) [Lp(a)] is a genetically determined risk factor for atherosclerotic cardiovascular disease (CVD). Limited data are available on Lp(a) testing from the Middle-East region. Therefore, we aim to evaluate the utilization and yield of Lp(a) testing over time and characterize CVD profiles of patients with abnormal Lp(a) tasting at a single-quaternary-care center in the United Arab Emirates.
UNASSIGNED: Unique Lp(a) tests conducted between 07/2017 and 10-2023 were included. Overtime trends in Lp(a) test utilization and abnormal Lp(a) [defined as Lp(a) > 125 nmol/L] test findings were described. CVD rates in patients with abnormal Lp(a) were compared to those with Lp(a) ≤ 125 nmol/L using appropriate methods.
UNASSIGNED: In our center, 0.95% of the patients (n = 5,677) had their Lp(a) measured, with a median level of 32 [11-82] nmol/L. Lp(a) was abnormal in 15.9% of the tests. Over the years 2018-2022, there was a 109% increase in Lp(a) testing, with concomitant up-trends in findings of abnormal Lp(a) (11.8% to 16.4%, P = 0.02). Compared to patients with Lp(a) ≤ 125 nmol/I, those with abnormal Lp(a) had higher rates of any prevalent CVD (34% vs. 25.1%, P < 0.001), CAD (25.6% vs. 17.7%, P < 0.001), HF (6.5% vs. 3.8%, P < 0.001), and stroke (7.1% vs. 4.4%, P < 0.001).
UNASSIGNED: Almost one in six patients tested for Lp(a) had abnormally elevated Lp(a), and CVD was prevalent in one-third of the patients who tested abnormal for Lp(a). The study highlights the growing awareness of the relevance of Lp(a) for CVD risk stratification and prevention.

Lipoprotein(a), or Lp(a), is a distinctive lipoprotein particle linked to various cardiovascular diseases, notably atherosclerosis and aortic stenosis. Much like plasminogen, Lp(a) hinders normal fibrinolysis, leading to increased thrombosis and slower clearance of fibrin debris. It also causes inflammation, oxidative stress, and endothelial dysfunction, contributing to the formation of atherosclerotic lesions. Epidemiological studies have consistently shown that even slight increases in Lp(a) levels correlate with a heightened risk of cardiovascular events. Furthermore, Lp(a) plays a role in aortic stenosis by binding to leaflet valves, accumulating within them, and triggering calcium deposition and nodule formation. These calcium deposits gradually narrow the arteries, impeding blood flow. By raising inflammation and oxidative stress in the valve, Lp(a) accelerates tissue damage and calcium deposition. Traditional lipid-lowering therapies have limited efficacy in reducing Lp(a) levels. However, new treatments using RNA interference and antisense oligonucleotides to decrease Lp(a) production in the liver offer promising prospects for mitigating the risks and managing atherosclerosis and aortic stenosis associated with high Lp(a) levels. As Lp(a) screening becomes more common in healthcare, physicians will be better equipped to assess patients\' risk levels and provide tailored treatments. This review aims to examine the role of Lp(a) in the development of aortic stenosis and atherosclerosis.

BACKGROUND: Diabetes mellitus (DM) and Lp(a) are well-established predictors of coronary artery disease (CAD) outcomes. However, their combined association remains poorly understood.
OBJECTIVE: To investigate the relationship between elevated Lp(a) and DM with CAD outcomes.
METHODS: Retrospective analysis of the MGB Lp(a) Registry involving patients ≥ 18 years who underwent Lp(a) measurements between 2000 and 2019. Exclusion criteria were severe kidney dysfunction, malignant neoplasms, and prior atherosclerotic cardiovascular disease (ASCVD). The primary outcome was a combination of cardiovascular death or myocardial infarction (MI). Elevated Lp(a) was defined as > 90th percentile (≥ 216 nmol/L).
RESULTS: Among 6,238 patients who met the eligibility criteria, the median age was 54, 45% were women, and 12% had DM. Patients with DM were older, more frequently male, and had a higher prevalence of additional cardiovascular risk factors. Over a median follow-up of 12.9 years, patients with either DM or elevated Lp(a) experienced higher rates of the primary outcome. Notably, those with elevated Lp(a) had a higher incidence of the primary outcome regardless of their DM status. The annual event rates were as follows: No-DM and Lp(a) < 90th% - 0.6%; No-DM and Lp(a) > 90th% - 1.3%; DM and Lp(a) < 90th% - 1.9%; DM and Lp(a) > 90th% - 4.7% (p < 0.001). After adjusting for confounders, elevated Lp(a) remained independently associated with the primary outcome among both patients with DM (HR = 2.66 [95%CI: 1.55-4.58], p < 0.001) and those without DM (HR = 2.01 [95%CI: 1.48-2.74], p < 0.001).
CONCLUSIONS: Elevated Lp(a) constitutes an independent and incremental risk factor for CAD outcomes in patients with and without DM.

BACKGROUND: Lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular diseases; however, its role in acute coronary syndrome (ACS) remains unclear.
OBJECTIVE: To investigate the hypothesis that the Lp(a) levels are altered by various conditions during the acute phase of ACS, resulting in subsequent cardiovascular events.
METHODS: From September 2009 to May 2016, 377 patients with ACS who underwent emergent coronary angiography, and 249 who completed ≥ 1000 d of follow-up were enrolled. Lp(a) levels were measured using an isoform-independent assay at each time point from before percutaneous coronary intervention (PCI) to 48 h after PCI. The primary endpoint was the occurrence of major adverse cardiac events (MACE; cardiac death, other vascular death, ACS, and non-cardiac vascular events).
RESULTS: The mean circulating Lp(a) level decreased significantly from pre-PCI (0 h) to 12 h after (19.0 mg/dL to 17.8 mg/dL, P < 0.001), and then increased significantly up to 48 h after (19.3 mg/dL, P < 0.001). The changes from 0 to 12 h [Lp(a)Δ0-12] significantly correlated with the basal levels of creatinine [Spearman\'s rank correlation coefficient (SRCC): -0.181, P < 0.01] and Lp(a) (SRCC: -0.306, P < 0.05). Among the tertiles classified according to Lp(a)Δ0-12, MACE was significantly more frequent in the lowest Lp(a)Δ0-12 group than in the remaining two tertile groups (66.2% vs 53.6%, P = 0.034). A multivariate analysis revealed that Lp(a)Δ0-12 [hazard ratio (HR): 0.96, 95% confidence interval (95%CI): 0.92-0.99] and basal creatinine (HR: 1.13, 95%CI: 1.05-1.22) were independent determinants of subsequent MACE.
CONCLUSIONS: Circulating Lp(a) levels in patients with ACS decreased significantly after emergent PCI, and a greater decrease was independently associated with a worse prognosis.

UNASSIGNED: This study aimed to examine the relationship between lipoprotein (a) (Lp[a]) and other blood lipid indexes and carotid artery atherosclerosis in patients with acute ischemic stroke (AIS).
UNASSIGNED: A total of 2,018 patients were selected from the hospital \"acute stroke intervention and secondary prevention registration database\" by identifying blood fat indexes (cholesterol, triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol and Lp[a]). Based on the results of carotid artery ultrasound examinations, the patients were divided into a \"no plaque\" group, comprising 400 patients, a \"plaque and no stenosis\" group, comprising 1,122 patients and a \"carotid stenosis\" group, comprising 496 patients. The relationship between Lp(a) and blood lipid indexes and carotid artery atherosclerosis was then investigated using multi-factor logistics regression analysis.
UNASSIGNED: There were 400 patients (19.8%) with no carotid plaque, 1,122 patients (55.6%) with plaque and no carotid stenosis and 496 patients (24.6%) with carotid stenosis. As the degree of carotid artery atherosclerosis increased, the Lp(a) level gradually increased; Lp(a) and cholesterol were identified as independent risk factors for carotid atherosclerosis.
UNASSIGNED: Lipoprotein (a) and cholesterol are independent risk factors for patients with AIS with carotid atherosclerosis, and their levels increase with the degree of carotid artery atherosclerosis; therefore, attention should focus on levels of cholesterol and Lp(a) in acute stroke patients to control atherosclerosis effectively.