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Abstract Background Current guidelines target low-density lipoprotein cholesterol (LDL-C) concentrations to reduce atherosclerotic cardiovascular disease (ASCVD) risk, and yet clinical trials demonstrate persistent residual ASCVD risk despite aggressive LDL-C lowering. Content Non–LDL-C lipid parameters, most notably triglycerides, triglyceride-rich lipoproteins (TGRLs), and lipoprotein(a), and C-reactive protein as a measure of inflammation are increasingly recognized as associated with residual risk after LDL-C lowering. Eicosapentaenoic acid in statin-treated patients with high triglycerides reduced both triglycerides and ASCVD events. Reducing TGRLs is believed to have beneficial effects on inflammation and atherosclerosis. High lipoprotein(a) concentrations increase ASCVD risk even in individuals with LDL-C < 70 mg/dL. Although statins do not generally lower lipoprotein(a), proprotein convertase subtilisin/kexin type 9 inhibitors reduce lipoprotein(a) and cardiovascular outcomes, and newer approaches are in development. Persistent increases in C-reactive protein after intensive lipid therapy have been consistently associated with increased risk for ASCVD events. Summary We review the evidence that biochemical assays to measure TGRLs, lipoprotein(a), and C-reactive protein are associated with residual risk in patients treated to low concentrations of LDL-C. Growing evidence supports a causal role for TGRLs, lipoprotein(a), and inflammation in ASCVD; novel therapies that target TGRLs, lipoprotein(a), and inflammation are in development to reduce residual ASCVD risk.

Lipoprotein(a) is similar to LDL cholesterol but contains apolipoprotein(a). A trial tested the effects of an oligonucleotide drug targeting apo(a) mRNA on lipoprotein(a) concentrations in patients with CVD.

Background and Objectives: Diabetic retinopathy (DR) is a significant complication of Diabetes Mellitus. Several studies have indicated Lipoprotein (a) [Lp(a)] plays a role in atherosclerotic alterations. Materials and Methods: This meta-analysis/systematic review aims to investigate the connection between Lp(a) and DR. All relevant studies indexed in PubMed and Scopus from up to January 2025 were included. A total of 29 studies (7007 subjects) were included, and the results were synthesized according to the PRISMA Guidelines. The results are presented as standardized mean differences (SMDs) with 95% confidence intervals (CIs) derived using random effects models. Results: The mean age of the included subjects was 52.6 ± 9.4 years, with 52.5% being male. The primary analysis included 25 observational studies involving a total of 6291 subjects (2770 patients with DR vs. 3521 controls). Notably, Lp(a) levels were significantly higher in patients with DR compared to those in controls, with an SMD of 0.85 (95% CI: 0.48–1.22; p < 0.001, I2 = 98%). Interestingly, a secondary analysis of the patients with Proliferative Diabetic Retinopathy (PDR) and Non-Proliferative Diabetic Retinopathy (NPDR) yielded an SMD of 0.28 (95% CI: 0.09–0.47; p = 0.004, I2 = 97%) between the two compared groups. In this analysis, a total of 1066 patients (465 PDR patients vs. 601 NPDR patients) were included. Conclusions: Elevated Lp(a) levels may have a compelling relationship with the development and progression of DR based on the evidence analyzed.

Background The mechanism for hypercoagulability in malignancy is not entirely understood. Although several studies report contrasting finding about the link between elevated plasma levels of the lipoprotein(a) [Lp(a)] and the possible recurrence of venous thromboembolism, we perform a study to evaluate the impact of the Lp(a) in the development of portal vein thromboembolism (PVT) in patients with HCC. Methods We compared 44 PVT patients with 50 healthy subjects and 50 HCC patients. Results The comparison between PVT patients and HCC showed in the former the mean value of serum lipoprotein levels was higher than 37.3 mg/dl ( p  = 0.000). The comparison between PVT versus healthy controls showed that in the former, mean value of serum lipoprotein levels was higher than 75 mg/dl ( p  = 0.000). The predictive value test of serum lipoprotein(a) on PVT was 0.72 and on HCC was 0.83. The odds ratio of lipoprotein(a) was 9.21 on PVT and 6.33 on HCC. Conclusion Patients with PVT and HCC showed a statistical significant serum lipoprotein(a) level higher than the subjects with HCC and no PVT or the healthy subject. So we assume a role of lipoprotein(a) as predictor of venous thromboembolism in neoplastic patients.

Risk prediction functions for incident coronary heart disease (CHD) were estimated using data from the Atherosclerosis Risk in Communities (ARIC) Study, a prospective study of CHD in 15,792 persons recruited in 1987–1989 from four U.S. communities, with follow-up through 1998. Predictivity of which individuals had incident CHD was assessed by increase in area under ROC curves resulting from adding nontraditional risk factors and markers of subclinical disease to a basic model containing only traditional risk factors. We also assessed the increase in population attributable risk. The additional factors were body mass index; waist–hip ratio; sport activity index; forced expiratory volume; plasma fibrinogen, factor VIII, von Willebrand factor, and Lp(a); heart rate; Keys score; pack-years smoking; and subclinical disease marker carotid intima-media thickness. These factors substantially improved prediction of future CHD for men, less for women, and also increased attributable risks.

The association between Lipoprotein (a) (Lp [a]) and common carotid intima media thickness (IMT) has been evaluated in 222 menopausal women. Lp (a) and IMT were measured, carotid ultrasound examination (B-Mode imaging) was performed and mean max IMT was calculated. Lp (a) was significantly lower in women with metabolic syndrome (MS). In a multivariate analysis Lp (a) showed the following odds ratio (OR; all p < 0.05) of having common carotid IMT (≥1.30 mm): 1.03, adjusted for age, low-density lipoprotein cholesterol (LDL) and waist circumference; 1.02, adjusted for age LDL, homeostatic assessment model (HOMA). In women without MS, after controlling for age, LDL and waist circumference, we found the following OR for increased IMT (≥1.30; OR: 1.03; for Lp [a]); 1.02 adjusted for age, LDL and HOMA (all p < 0.05). In women with MS these relationships were not statistically significant. Lp (a) gives additional information in the risk assessment for atherosclerotic cardiovascular disease, especially in menopausal women without MS.

Numerous studies have identified risk factors and markers associated with incidence of cardiovascular disease (CVD). However, few studies have examined whether established risk factors, novel blood markers, carotid ultrasonography, or ankle-brachial index can predict recurrent CVD events. We analyzed the relation of established risk factors and markers of atherosclerosis with the risk of recurrent CVD in 766 participants. Over a mean of 8.7 years of follow-up, 70 women and 243 men had a recurrent CVD event (85.3% coronary heart disease and 23.7% stroke). Adjusting for age and sex, this study found that established risk factors were associated with recurrent CVD events in the anticipated direction. Being in the highest (vs lowest) quartiles of lipoprotein (a), fibrinogen, white blood cells, and creatinine at baseline were associated with 47%, 69%, 65%, and 81%, respectively, greater risk of a CVD event, and being in the highest quartile of albumin was associated with 39% lower risk. Being in the highest (vs lowest) quartile of carotid intima-media thickness (IMT) was associated with a doubling of risk, and having carotid plaque with acoustic shadowing (vs having no plaque) was associated with 83% increased risk of a CVD event. After adjustment for established risk factors, creatinine, albumin, and carotid IMT in the highest quartile (vs lowest quartile) and carotid plaque with acoustic shadowing (vs no plaque) were independently associated with recurrent CVD events. Established risk factors, but only a few of novel risk factors and markers, were independent predictors of recurrent CVD events.

Background: Inflammation contributes to the development and progression of atherosclerosis, and C-reactive protein (CRP) can be used as a marker to assess risk for cardiovascular diseases. As variability among existing high-sensitivity CRP (hsCRP) assays can lead to misclassification of patients and hamper implementation of population-based medical decision points, standardization of hsCRP assays is needed. Methods: We evaluated five proposed secondary reference materials, including two diluted preparations of Certified Reference Material 470 (CRM470), two preparations of a serum-based material with recombinant CRP added, and one serum-based material with isolated CRP added. Twenty-one manufacturers participated in the comparison with 28 different assays. We examined imprecision, linearity, and parallelism with these materials and with fresh serum. Results: All materials had similar imprecision; CVs for the undiluted materials were 2.1–3.7%. None of the materials was linear across all assays. Each had between one and three cases of nonlinearity, with one preparation of CRM470 having the fewest cases of nonlinearity. Although none of the materials was parallel across all assays, the differences in slope from fresh serum were similar across all assays. Conclusions: All materials performed similarly with regard to imprecision, linearity, and parallelism. As one preparation of CRM470 had slightly better characteristics than the other materials and because CRM470 had been certified previously as a reference material for the acute-phase reactant range, it will be used in the next phase to standardize hsCRP assays.

Lipoprotein (a) is a cholesterol-rich plasma lipoprotein with a lipid composition similar to that of low-density lipoproteins (LDL). Many prospective and case-control studies identified elevated levels of lipoprotein (a) as a risk factor for premature myocardial infarction and stroke. Elevated lipoprotein (a) has been identified as a genetically determined risk factor for stroke in young adults, but only preliminary data are available on its role as a risk factor for ischemic stroke in infants and children. Fifty two children with arterial ischemic stroke and 78 age- and sex-matched healthy children were studied. Data of this study indicate that 26.9% of children with arterial ischemic stroke had high lipoprotein (a) levels in comparison with the age matched healthy control group. Measurement of lipoprotein (a) should be included in screening programs performed in young patients suffering not only from venous thromboembolism but also arterial ischemic stroke, in addition to other thrombophilic factors.