👤 Leandro Slipczuk

The prognostic value of jointly assessing lipoprotein(a) [Lp(a)] and high-sensitivity C-reactive protein (hsCRP) in primary prevention among individuals without standard modifiable risk factors (SMuRFs) remains unclear. We analyzed 50,450 UK Biobank participants free of cardiovascular disease at baseline who were SMuRF-less, defined as absence of current smoking, obesity, hypertension, dyslipidemia, and diabetes. Elevated Lp(a) and hsCRP were defined using cohort-specific 75th percentile cutoffs and established clinical thresholds. Incident atherosclerotic cardiovascular disease (ASCVD), defined as nonfatal myocardial infarction, nonfatal ischemic stroke, or cardiovascular death, was ascertained. Associations were evaluated using Fine-Gray competing-risk regression models to estimate subdistribution hazard ratios (sHRs) with 95% confidence intervals (CI), accounting for competing non-cardiovascular death. Over 15 years of follow-up, 1,104 (2.2%) incident ASCVD events occurred. Using cohort-specific cutoffs, elevated hsCRP was associated with higher ASCVD risk (sHR 1.35, 95% CI 1.16-1.57), while elevated Lp(a) showed a more modest association (sHR 1.24, 95% CI 1.06-1.45). In joint analyses, isolated elevations of hsCRP or Lp(a) were each associated with increased risk, with the highest risk observed among individuals with concurrent elevations (sHR 1.64, 95% CI 1.28-2.09), without evidence of interaction. Similar patterns were observed using clinical cutoffs (Lp(a) ≥125 nmol/L; hsCRP ≥2.0 mg/L), with concurrent elevation conferring the greatest risk (sHR 1.74, 95% CI 1.17-2.59). In SMuRF-less individuals, Lp(a) and hsCRP independently predict ASCVD risk. These findings suggest that combined assessment of Lp(a) and hsCRP may provide complementary information for risk characterization among SMuRF-less adults in primary prevention. Show less

Lipoprotein(a) (Lp(a)) is increasingly recognised as an independent and causal risk factor for atherosclerotic cardiovascular disease. Although the underlying mechanisms remain incompletely defined, evidence supports a multifactorial role for Lp(a) in atherogenesis. Lp(a) contributes to endothelial dysfunction, promotes vascular inflammation and enhances lipid retention and oxidation within the arterial wall. These changes drive foam cell formation and smooth muscle cell activation, hallmarks of early plaque development. In addition, Lp(a) exerts prothrombotic effects through structural homology with plasminogen, interfering with fibrinolysis and promoting thrombosis, which may increase the risk of plaque rupture and acute events. Collectively, these overlapping mechanisms underscore the unique contribution of Lp(a) to both the development and progression of atherosclerosis. As novel targeting therapies emerge, a deeper understanding of Lp(a) biology will be essential for translating these insights into clinical benefit. Show less

Apolipoprotein B (apoB) distribution and its implications as an atherosclerotic cardiovascular disease (ASCVD) risk-enhancing factor among individuals of diverse Hispanic or Latino backgrounds have not been described. To describe the distribution of apoB in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) cohort and to characterize associations of baseline sociodemographic and clinical variables with apoB and self-identified Hispanic or Latino background. The HCHS/SOL was a prospective, population-based cohort study of diverse Hispanic or Latino adults living in the US who were recruited and screened between March 2008 and June 2011. Sampling weights were used to generate a population-based sample of Hispanic or Latino participants aged 18 to 74 years who resided in 4 US metropolitan areas (Bronx, New York; Chicago, Illinois; Miami, Florida; and San Diego, California). ApoB concentration was measured in participants from the HCHS/SOL, and apoB tertiles were compared across demographic groups, including self-identified Hispanic or Latino background. Median percentage continental genetic ancestry (West African, Amerindian, and European) was compared across apoB tertiles. ApoB measured in mg/dL from serum or plasma using an immunoturbidimetric assay. ApoB tertiles were determined, and traditional lipids were evaluated across apoB tertiles. ApoB and traditional lipid measurements were assessed across ASCVD risk categories. Additionally, scatterplots were created to observe correlations between apoB and low-density lipoprotein cholesterol or non-high-density lipoprotein cholesterol. Overall mean (SD) apoB concentration was 99.8 (0.4) mg/dL, with male participants displaying significantly higher mean levels than female participants (102.4 vs 97.4 mg/dL, respectively). Mean (SD) participant age was 41.1 (0.8) years, and 8376 participants (51.9%) were female. ApoB levels were higher among older age groups. There was significant heterogeneity in mean apoB concentrations across self-identified Hispanic or Latino background groups, ranging from 95.1 mg/dL in Dominican individuals to 104.8 mg/dL in Cuban individuals. The prevalence of elevated apoB (≥130 mg/dL) was greater across higher predicted ASCVD risk categories. Among participants with a 10-year predicted ASCVD risk of 7.5% or higher, 26.5% had an elevated apoB. Median West African ancestry was lower across higher tertiles of apoB. In this cohort study among participants from the HCHS/SOL, elevated apoB was present in one-quarter of a diverse cohort study of Hispanic or Latino individuals who were at intermediate or high predicted ASCVD risk. Differences in apoB distribution among Hispanic or Latino individuals may have important implications for apoB's use in ASCVD risk assessment. Show less

The 2025 American Society for Preventive Cardiology meeting highlighted evolving strategies in cardiovascular disease prevention, spanning risk models based on traditional risk factors, emerging biomarkers, novel therapeutics, and digital health innovations. Key discussions addressed lipoprotein(a) [Lp(a)] and inflammation as a causal risk factor, their clinical management, and readiness for targeted therapies; optimal systolic blood pressure targets informed by recent randomized controlled trials; and ongoing debate regarding apolipoprotein B versus low-density lipoprotein cholesterol (LDL-C) as the primary lipid target. Advances in digital health emphasized prevention through artificial intelligence, health equity in technology, and the growing role of wearables. Imaging emerged as a central theme, with sessions highlighting its role in risk assessment, monitoring treatment response, and refining prevention strategies, especially in young adults. Sessions on women's cardiovascular health underscored female-specific risk enhancers and limitations of current risk prediction models. Additional debates addressed the use of polygenic risk scores in young adults and strategies for universal screening with LDL-C, hsCRP, and Lp(a). Heart failure prevention was highlighted as a critical frontier, with emphasis on stage-based risk stratification, early identification of subclinical disease, and targeted interventions to avert progression to symptomatic heart failure. Updates on renal denervation reaffirmed its safety, efficacy, and durability as an adjunctive therapy in resistant hypertension. Collectively, these highlights emphasize the rapid evolution of preventive cardiology, integrating precision risk stratification, digital tools, and novel therapies into routine care. Show less

Lipoprotein(a) [Lp(a)] is associated with atherosclerotic cardiovascular disease. An Lp(a) threshold of ≥125 nmol/L is commonly used to identify individuals at higher risk for events, but there is a paucity of data on individuals of Hispanic/Latino descent. The purpose of this study was to provide a comprehensive evaluation of Lp(a) and its association with 10-year cardiovascular disease risk and mortality among Hispanic/Latino adults in the United States. We evaluated the association between Lp(a) and myocardial infarction (MI), ischemic stroke, and all-cause mortality among 16,117 Hispanic Community Health Study/Study of Latinos individuals. Event rates were compared across Lp(a) quintiles. Multivariable Cox proportional hazards models assessed the relationship between events and Lp(a) across increasing quintiles, log-transformed Lp(a), and ≥125 nmol/L vs <125 nmol/L. Sampling weights and survey methods were used to account for the stratified probability sampling of the cohort. Among the Hispanic Community Health Study/Study of Latinos target population (median age 41.1 years, 52.4% women), the median Lp(a) was 19.7 nmol/L (Q1-Q3: 7.3-60.6 nmol/L), with 11.4% having Lp(a) ≥125 nmol/L, and the highest Lp(a) quintile defined as >77 nmol/L. Over a median follow-up of 9.8 years, 883 events (135 MI, 99 stroke, 649 all-cause mortality) occurred. The age-adjusted incidence rate of the composite events (MI, stroke, and all-cause mortality) was 505.2 per 100,000 person-years. After multivariable adjustment, each 1-SD increase in log-transformed Lp(a) was associated with a higher risk of MI (HR: 1.47; 95% CI: 1.14-1.89). Compared with Lp(a) <125 nmol/L, elevated Lp(a) ≥125 nmol/L conferred an increased risk of MI (HR: 2.29; 95% CI: 1.45-3.63), all-cause mortality (HR: 1.43; 95% CI: 1.05-1.93), and composite events (HR: 1.56; 95% CI: 1.22-2.01), but not stroke. Findings were consistent when comparing the highest Lp(a) quintile to the lower 4 quintiles, but the elevated risk was observed only for MI and composite events. Hispanic/Latino individuals with elevated Lp(a) are at an increased risk of MI and all-cause mortality. Although Lp(a) ≥125 nmol/L is a valid risk threshold, Hispanics/Latinos show a continuous relationship between increasing Lp(a) levels and MI risk. Show less