Abstract

Background:

Early detection of peripheral atherosclerosis remains a clinical challenge, especially in asymptomatic individuals. This study aimed to evaluate the predictive value of systemic inflammatory indices and lipid-related biomarkers for early atherosclerosis.

Objectives:

To investigate the diagnostic value of systemic inflammation indices, fibrinogen, and lipoprotein(a) as individual biomarkers and as a combined predictive model for early peripheral arterial disease.

Methods:

A prospective case-control study was conducted in 54 individuals: 20 patients diagnosed with early peripheral atherosclerosis (<55 years) and 34 healthy controls. Laboratory data included complete blood count, lipid profile, fibrinogen, lipoprotein(a), angiopoietin-like protein 3 (ANGPTL3), and Lp-PLA₂. Inflammatory indices, including NLR, PLR, SII, SIRI, AISI, and MLR, were calculated. Logistic regression and ROC analysis were performed. A two-sided p-value < 0.05 was considered statistically significant.

Results:

SIRI (1.70 vs. 0.93, p = 0.0039) and AISI (431.6 vs. 236.4, p = 0.0128) were significantly higher in the atherosclerosis group. Fibrinogen showed the most robust association (5.46 vs. 3.71 g/L, p < 0.00001). Lp(a) alone was not statistically different between groups but improved the multivariate model (AUC 0.85 vs. 0.82). The final model, including age, inflammatory indices, LDL, Lp (a), and fibrinogen, achieved an AUC of 0.91.

Conclusion:

Systemic inflammation and fibrinogen levels are strongly associated with early atherosclerosis. Their combination with lipoprotein(a) enhances diagnostic performance, offering a simple, cost-effective strategy for early vascular risk assessment.

Abstract

Background:

Coronavirus disease (COVID-19) can cause permanent damage to vascular structures by directly or indirectly affecting the cardiopulmonary system. Lipoprotein(a) [Lp(a)] is an important identified risk factor for vascular endothelial cell dysfunction.

Objective:

The aim of this study was to reveal the relationship between Lp(a) levels measured at the time of COVID-19 diagnosis and the pulmonary artery (PA) to the ascending aorta (Ao) ratio (PA:Ao ratio) in survivors evaluated by transthoracic echocardiography (TTE).

Methods:

The study sample consisted of 100 patients who recovered from COVID-19 in the past 3 to 6 months. The relationship between the change in the PA:Ao ratio (ΔPA:Ao) and the Lp(a) levels measured at the time of diagnosis was evaluated. Diameter measurements at baseline and follow-up were evaluated with TTE.

Results:

A significant increase was found in PA, Ao, and epicardial adipose tissue (EAT) thickness in TTE (p< 0.001 for all). There was a weak correlation between D-dimer and high-sensitivity cardiac troponin measured at the time of diagnosis and ΔPA:Ao and ΔEAT in survivors. However, a positive and strong correlation was observed between Lp(a) levels and ΔPa:Ao (r = 0.628, p< 0.001) and ΔEAT (r = 0.633, p< 0.001).

Conclusion:

There may be dysfunction in vascular structures due to COVID-19. For the first time in the literature, a strong correlation was shown between the Lp(a) levels measured at the time of diagnosis and ΔPA:Ao and ΔEAT values in patients with COVID-19.

Over the last decades, numerous studies have demonstrated that elevated lipoprotein (Lp)(a) is a powerful and independent risk factor for coronary heart disease,^, ischemic stroke, and calcific aortic stenosis. Even in patients treated with statins who achieve LDL-cholesterol goals below 70 mg/dL, elevated Lp(a) levels remain independently related to an increased risk of atherosclerotic events.

The LDL particle has a unique molecular structure, as exemplified by its covalent bond with an apolipoprotein(a) that bears resemblance to plasminogen and may well represent an evolutionary deviation of this well-known plasmin precursor. Lp(a) is synthesized by the liver and the amount of circulating particles in the bloodstream is almost exclusively determined by inheritance, leaving very little space for environmental influence. The distribution of Lp(a) levels in the population is highly skewed with approximately 80% of people exhibiting plasma concentrations below 50 mg/dL, and the remaining 20% with a wide range of values above that limit.

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