Abstract
Background
Lipoprotein(a) [Lp(a)] is a highly atherogenic particle that significantly increases overall cardiovascular risk. Evidence regarding concentrations of Lp(a) in the Polish general population remains limited, as well as the association between Lp(a) and various clinical characteristics. The aim in this study was to analyze Lp(a) concentration in a Polish population hospitalized in a tertiary referral hospital, compare clinical characteristics between patients with low and high Lp(a) and find the predictors of increased Lp(a) concentrations.
Methods
This was an observational, cross-sectional study. All patients hospitalized in the Clinical Department of Internal Medicine, Endocrinology, Diabetology, and Nephrology in the Czerniakowski Hospital between 01.03.2024 and 08.10.2024 and with measured Lp(a) concentration were consecutively included. Patients were divided into two groups: those with high Lp(a) (≥ 30 mg/dL) and those with low Lp(a) (< 30 mg/dL). The groups were compared in terms of multiple clinical characteristics. Multiple logistic regression was used to determine independent predictors of high Lp(a). The p-value below 0.05 was considered statistically significant.
Results
Out of 562 patients, 117 had high Lp(a) concentration (20.8%). The groups did not differ in terms of age, sex, or clinical examination findings. In a multiple logistic regression, male sex was associated with a decreased odds ratio of high Lp(a) (OR = 0.2857, 95% CI: 0.1107–0.6468, p = 0.01).
Conclusions
High Lp(a) is prevalent in the Polish population, and thus it is important to measure it routinely in each individual at least once in a lifetime and control all other known cardiovascular risk factors to decrease the overall risk. (Cardiology Journal 2026; 33: e00226010)
Keywords: lipoprotein(a), atherosclerotic cardiovascular disease, risk factor, cross-sectional study, coronary artery disease
Graphical abstract
Introduction
Lipoprotein(a) [Lp(a)] is a variant of the low-density lipoprotein (LDL) [1], exposing both apolipoprotein B and apolipoprotein(a) [apo(a)]. Lp(a) is a highly atherogenic particle, which significantly increases the overall cardiovascular risk. However, increased Lp(a) concentration is often underdiagnosed or ignored, which leads to an underestimation of the actual cardiovascular risk and undertreatment. According to the 2022 European Atherosclerosis Society (EAS) Consensus Statement, elevated Lp(a) is defined as > 50 mg/dL, but it also highlights the relevance of the “grey zone” of 30–50 mg/dL [2].
There is a causal continuous association between Lp(a) concentration and atherosclerotic cardiovascular disease (ASCVD) risk, with a hazard ratio of 1.11 per 50 nmol/L increment in Lp(a) concentration [3]. Moreover, increased Lp(a) is a new risk factor for aortic stenosis. In turn, very low Lp(a) concentrations (the bottom quintile) are associated with the increased risk of type 2 diabetes mellitus (DM2) compared to the top quintile of Lp(a) concentrations [2]. The relationship between Lp(a) and atrial fibrillation remains inconclusive [4].
Noteworthily, Lp(a) concentration is 90% determined by genetics and only partially influenced by lifestyle, ethnicity, comorbidities or pharmacotherapy [5]. For example, hyperthyroidism causes a decrease, while hypothyroidism — an increase in Lp(a) concentration [6]. Nephrotic syndrome can lead to an even 5-fold increase in Lp(a) concentrations [7]. Statins may lead to a slight increase in Lp(a) concentration, although the findings are inconsistent [8, 9].
Novel potent treatments lowering Lp(a) concentrations have been developed, reaching an outstanding efficacy of an almost 80% concentration reduction. These drugs are small interfering RNAs (siRNAs) that affect the production of apo(a) and, in this way, decrease Lp(a) concentration. However, the effect of this impressive Lp(a) reduction on ASCVD risk remains under investigation and the first results from the Lp(a)HORIZON trial investigating pelacarsen will be presented in 2026 [10].
Considering that no dedicated Lp(a)-lowering therapies are currently available, decreasing the overall ASCVD is the most important intervention in patients with high Lp(a). Lp(a) should be measured in each adult once in a lifetime. Still, the wide implementation of this recommendation is hindered by little awareness of the risks associated with increased Lp(a) concentration [11]. Further, data regarding the distribution of Lp(a) concentration in the Polish population are scarce. The results of Polish Lp(a) registries including the Polish Mother’s Memorial Hospital Research Institute -Lp(a) Registry and the Zabrze-Lipoprotein(a) Registry showed that Lp(a) concentration is commonly increased [12, 13], further calling for increased awareness regarding the need to determine the Lp(a) concentration in all adults. Considering this evidence gap, as well as limited data regarding the association between Lp(a) and various clinical characteristics, the aim of the present study was to analyze Lp(a) concentrations in a Polish population hospitalized in a tertiary referral hospital, compare clinical characteristics between patients with low and high Lp(a) and find the predictors of increased Lp(a) concentrations.
Methods
Study design and participants
This was an observational, cross-sectional study. All patients hospitalized in the Clinical Department of Internal Medicine, Endocrinology, Diabetology, and Nephrology in the Czerniakowski Hospital between 01.03.2024 and 08.10.2024 and with measured Lp(a) concentration were consecutively included. A threshold of 30 mg/dL was used for further analyses. Patients were divided into two groups: those with high Lp(a) (≥ 30 mg/dL) and those with low Lp(a) (< 30 mg/dL).
Due to the study’s observational and non-interventional character, ethics committee approval and written informed consent was not required. Following the consultation with the local Bioethics Committee, no formal waiver was requested.
Patient data handling
Patient data were retrieved directly from the hospital electronic medical record system (Medicus). During extraction, only the unique national identification number (PESEL) was temporarily used to link records. Immediately after transfer into an Excel spreadsheet, the PESEL identifiers were replaced by study-specific codes, and no other personally identifiable information (such as names, addresses, or contact details) was collected. The final dataset used for analysis contained only anonymized clinical variables, without any possibility of re-identifying individual patients.
The investigators had authorized direct access to the Medicus hospital database, granted by the hospital IT administrator. Access was protected by individual login credentials, password authentication, and role-based permissions. All data extraction and handling were performed exclusively on secure hospital computers within the institutional network environment. The dataset was accessible only to the research team, and after anonymization, it no longer contained any identifiers that could enable patient re-identification. In accordance with GDPR and local data protection regulations, the analysis was conducted solely on anonymized data, which did not require prior approval from the ethics committee.
Data collection
Demographic and clinical data, medical history and comorbidities, pharmacotherapy, laboratory findings and echocardiographic data were collected from medical records. The laboratory findings that were analyzed in the current study included hemoglobin concentration [mg/dL], white blood cell (WBC) count [103/μL], platelet count [103/μL], creatinine [mg/dL], HbA1c [%], NT-proBNP [pg/mL], C-reactive protein [mg/L], homocysteine [μmol/L], total cholesterol [mg/dL], high-density lipoprotein (HDL) cholesterol [mg/dL], non-HDL cholesterol [mg/dL], low-density lipoprotein (LDL) cholesterol [mg/dL] and triglycerides [mg/dL].
Echocardiographic parameters included left ventricle end-diastolic diameter (LVEDD), left ventricle end-systolic diameter (LVESD), posterior wall diameter (PWD), interventricular septal thickness at end-diastole (IVSd), left atrium (LA), left ventricle ejection fraction (LVEF), right ventricular end-diastolic diameter (RVEDD), and tricuspid annular plane systolic excursion (TAPSE).
Study endpoints
The primary endpoint was the association (for categorical data) or the difference (for continuous data) of the patient characteristics analyzed with increased Lp(a) concentration. The secondary endpoint was the odds ratio of the parameters associated with the increased Lp(a) concentration.
Statistical methods
All analyses were done with GraphPad Prism for MacOS version 10.4.2 (534). Continuous data were assessed for normality with the Shapiro–Wilk test. Then, normally distributed data was analyzed with the Student’s t-test and presented as mean±SD. Data not normally distributed were analyzed using the Mann–Whitney test and presented as a median with an interquartile range (IQR). The Fisher exact test was used for categorical data. Sex, age, and variables differing between the groups of patients with high and low Lp(a) concentrations with a p-value below 0.10 were included in the multiple logistic regression and analyzed. The p-value below 0.05 was considered statistically significant.
Results
Baseline characteristics
The present cohort included 562 patients, of which 117 had high Lp(a) concentration (20.8%). Detailed baseline characteristics of included patients are presented in Table 1. Patients with and without high Lp(a) did not differ in terms of age, sex, and clinical examination findings. Among all analyzed comorbidities, prior coronary artery bypass grafting (CABG) was the only one that differed in frequency between the groups, being more common in patients with high Lp(a) (2.6% vs. 0.2%, p = 0.03). There was a non-significant trend towards more common prevalence of ischemic heart disease and atrial fibrillation in patients with high Lp(a) (17.1% vs. 10.3%, p = 0.052 and 17.9% vs. 11.2%, p = 0.06, respectively).
Table 1.
The baseline characteristics of patients with high (≥ 30 mg/dL) and low (< 30 mg/dL) lipoprotein(a) [Lp(a)] concentration
| Parameter | High Lp(a) (n = 117) | Low Lp(a) (n = 445) | P-value |
|---|---|---|---|
| Demographic data | |||
| Sex [female] | 84 (71.8%) | 283 (63.6%) | 0.10 |
| Age [years] | 56.0 (41.5–71.5) | 52.0 (40.0–69.0) | 0.17 |
| Clinical findings | |||
| Height [m] | 1.65 (1.60–1.76) | 1.68 (1.63–1.75) | 0.09 |
| Weight [kg] | 86.0 (69.0–105.0) | 85.0 (70.0–101.0) | 0.70 |
| BMI [kg/m2] | 30.8 (24.6–37.2) | 29.5 (25.0–35.5) | 0.46 |
| Comorbidities and risk factors | |||
| Prior myocardial infarction | 12 (10.3%) | 24 (5.4%) | 0.09 |
| Prior PCI | 8 (6.8%) | 20 (4.5%) | 0.34 |
| Prior CABG | 3 (2.6%) | 1 (0.2%) | 0.03 |
| Prior stroke | 4 (3.4%) | 12 (2.7%) | 0.75 |
| Kidney transplantation | 0 (0.0%) | 1 (0.2%) | > 0.99 |
| Nephrectomy | 0 (0.0%) | 1 (0.2%) | > 0.99 |
| Familial hypercholesterolemia | 0 (0.0%) | 0 (0.0%) | n/a |
| Aortic stenosis | 4 (3.4%) | 11 (2.5%) | 0.53 |
| Ischemic heart disease | 20 (17.1%) | 46 (10.3%) | 0.05 |
| Atrial fibrillation | 21 (17.9%) | 50 (11.2%) | 0.06 |
| Chronic kidney disease | 14 (12.0%) | 49 (11.0%) | 0.74 |
| Diabetes mellitus | 39 (33.3%) | 147 (33.0%) | > 0.99 |
| Type 1 | 3 | 19 | |
| Type 2 | 35 | 127 | 0.34 |
| Type 3 | 1 | 1 | |
| Hypertension | 71 (60.7%) | 240 (53.9%) | 0.21 |
| COPD | 7 (6.0%) | 19 (4.3%) | 0.46 |
| Hyperthyroidism | 3 (2.6%) | 12 (2.0%) | 0.72 |
| Hypothyroidism | 28 (23.9%) | 93 (20.9%) | 0.53 |
| Chronic liver disease | 0 (0.0%) | 9 (2.0%) | 0.22 |
| Smoker | 0.38 | ||
| Current | 26 (23.6%) | 94 (22.4%) | |
| Previous | 7 (6.4%) | 46 (11.0%) | |
| Never | 77 (70.0%) | 280 (66.7%) | |
Categorical data is presented as the number (percentage) of patients. Continuous data is presented as median (IQR); BMI — body mass index; CABG — coronary artery bypass grafting; COPD — chronic obstructive pulmonary disease; n/a — not applicable; PCI — percutaneous coronary intervention. Significant differences are bolded
Drug intake and Lp(a) concentration
A comparison of pharmacotherapy between patients with and without increased Lp(a) concentrations is shown in Table 2.
Table 2.
Drug intake of patients with high (≥ 30 mg/dL) and low (< 30 mg/dL) Lp(a) concentration
| Parameter | High Lp(a) (n = 117) | Low Lp(a) (n = 445) | P-value |
|---|---|---|---|
| Statins | 42 (35.9%) | 122 (27.4%) | 0.09 |
| Ezetimibe | 4 (3.4%) | 11 (2.5%) | 0.53 |
| Alirocumab | 0 (0.0%) | 0 (0.0%) | n/a |
| Evolocumab | 0 (0.0%) | 0 (0.0%) | n/a |
| Inclisiran | 0 (0.0%) | 1 (0.2%) | > 0.99 |
| Insulin | 14 (12.0%) | 45 (10.1%) | 0.61 |
| Metformin | 32 (27.4%) | 106 (23.8%) | 0.47 |
| Sulfonylureas | 3 (2.6%) | 16 (3.6%) | 0.78 |
| GLP-1 agonists | 23 (19.7%) | 68 (15.3%) | 0.26 |
| DPP-4 inhibitors | 3 (2.6%) | 14 (3.1%) | > 0.99 |
| SGLT2 inhibitors | 17 (14.5%) | 56 (12.6%) | 0.64 |
| Pioglitazone | 0 (0.0%) | 0 (0.0%) | n/a |
| Acarbose | 0 (0.0%) | 0 (0.0%) | n/a |
| Growth hormone | 0 (0.0%) | 0 (0.0%) | n/a |
| Levothyroxine | 24 (20.5%) | 90 (20.2%) | > 0.99 |
| Antithyroid agents | 0 (0.0%) | 2 (0.4%) | > 0.99 |
| Radioactive iodine | 3 (2.6%) | 7 (1.6%) | 0.44 |
| Tocilizumab | 0 (0.0%) | 0 (0.0%) | n/a |
| Proteases inhibitors and/or antiretroviral drugs | 0 (0.0%) | 1 (0.2%) | > 0.99 |
| Hormonal replacement therapy | 0 (0.0%) | 8 (1.8%) | 0.22 |
| Peritoneal dialysis | 0 (0.0%) | 0 (0.0%) | n/a |
| Lipoprotein apheresis | 0 (0.0%) | 0 (0.0%) | n/a |
Categorical data is presented as the number (percentage) of patients; DPP-4 — dipeptidyl peptidase-4; GLP-1 — glucagon-like peptide-1; n/a — not applicable; SGLT2 — sodium/glucose cotransporter 2. Significant differences are bolded
There was no difference in the frequency of use of any analyzed drug between patients with high and low Lp(a) concentrations, including statins (35.9% vs. 27.4%, p = 0.09).
Laboratory findings
A summary of laboratory findings in patients with high and low Lp(a) concentrations is shown in Table 3. There was no difference found in the analyzed laboratory parameters between patients with high and low Lp(a) concentrations. There was a trend towards higher white blood cell count in patients with high Lp(a) [median (IQR) = 7.3 (5.8–9.6) vs. 6.7 (5.5–8.7); p = 0.06].
Table 3.
The laboratory findings of patients with high (≥ 30 mg/dL) and low (< 30 mg/dL) Lp(a) concentration
| Parameter | High Lp(a) (n = 117) | Low Lp(a) (n = 445) | P-value |
|---|---|---|---|
| Hemoglobin [g/dL] | 13.5 (12.2–14.7) | 13.7 (12.6–14.7) | 0.23 |
| WBC [103/μL] | 7.3 (5.8–9.6) | 6.7 (5.5–8.7) | 0.06 |
| PLT [103/μL] | 240 (205–287) | 240 (204–290) | 0.54 |
| Creatinine [mg/dL] | 0.8 (0.7–1.0) | 0.8 (0.7–1.0) | 0.93 |
| HbA1c [%] | 5.7 (5.3–6.4) | 5.6 (5.3–6.4) | 0.44 |
| NT-proBNP [pg/mL] | 142 (39–1764) | 173 (53–981) | 0.95 |
| CRP [mg/L] | 0.31 (0.10–1.05) | 0.26 (0.11–0.84) | 0.35 |
| Homocysteine [μmoL/L] | 10.12 (8.19–12.0) | 9.7 (7.7–13.3) | 0.95 |
| Total cholesterol [mg/dL] mean (SD) | 175.1 (45.2) | 174.1 (46.5) | 0.83 |
| HDL cholesterol [mg/dL] | 43.0 (36.0–54.0) | 45.0 (37.0–53.5) | 0.55 |
| Non-HDL cholesterol [mg/dL] | 125.0 (101.0–157.0) | 127.0 (97.0–156.0) | 0.79 |
| LDL cholesterol [mg/dL] | 104.0 (77.5–130.0) | 103.0 (77.0–129.8) | 0.85 |
| Triglycerides [mg/dL] | 115.0 (87.0–160.0) | 106.0 (73.5–149.5) | 0.12 |
Categorical data is presented as the number (percentage) of patients. Continuous data is presented as median (IQR) unless indicated otherwise; CRP — C-reactive protein; HDL — high-density lipoprotein; LDL — low-density lipoprotein; NT-proBNP — N-terminal prohormone of brain natriuretic peptide; PLT — platelets; SD — standard deviation; WBC — white blood cells count
Echocardiographic findings
The comparison of echocardiographic parameters between the groups is presented in Table 4. Patients with high Lp(a) had higher IVSd [median (IQR) = 12.0 (11.0–13.0) vs. 12.0 (10.0–12.0); p = 0.01].
Table 4.
The echocardiographic findings of patients with high (≥ 30 mg/dL) and low (< 30 mg/dL) Lp(a) concentration
| Parameter | High Lp(a) (n = 117) | Low Lp(a) (n = 445) | P-value |
|---|---|---|---|
| LVEDD [mm] | 47.0 (45.0–50.0) | 47.0 (45.0–50.0) | 0.89 |
| LVESD [mm] | 28.0 (26.0–31.0) | 27.0 (25.0–31.0) | 0.58 |
| PWD [mm] | 11.0 (10.0–12.0) | 11.0 (9.1–12.0) | 0.04 |
| IVSd [mm] | 12.0 (11.0–13.0) | 12.0 (10.0–12.0) | 0.01 |
| LA [mm] | 40.0 (37.0–43.0) | 39.0 (35.0–43.0) | 0.21 |
| LVEF [%] | 60.0 (57.5–65.0) | 65.0 (60.0–65.0) | 0.14 |
| RVEDD [mm] | 30.0 (26.0–32.0) | 30.0 (27.0–34.0) | 0.42 |
| TAPSE [mm] | 22.5 (20.0–24.0) | 23.0 (21.0–25.0) | 0.07 |
Categorical data is presented as the number (percentage) of patients. Continuous data is presented as median (IQR); IVSd — interventricular septal thickness at end-diastole; LA — left atrium; LVEDD — left ventricle end-diastolic diameter; LVEF — left ventricle ejection fraction; LVESD — left ventricle end-systolic diameter; PWD — posterior wall diameter; RVEDD — right ventricular end-diastolic diameter; TAPSE — tricuspid annular plane systolic excursion. Significant differences are bolded
Multiple logistic regression
Multiple logistic regression findings are presented in Table 5. Male sex was associated with a decreased odds ratio of high Lp(a) (OR = 0.2309; 95% CI: 0.0865 to 0.5455; p < 0.001). No other parameter was associated with high Lp(a) concentration.
Table 5.
The findings from the multiple logistic regression between the parameters below and having high lipoprotein(a) concentration (≥ 30 mg/dL)
| Parameter | OR | 95% CI (profile likelihood) | P-value |
|---|---|---|---|
| Age [years] | 0.9909 | 0.9697–1.012 | 0.40 |
| Sex [male] | 0.2309 | 0.08653–0.5455 | < 0.001 |
| Height [m] | 2.855 | 0.05743–298.2 | 0.64 |
| Prior MI | 2.594 | 0.8909–7.420 | 0.08 |
| Prior CABG | 10.29 | 0.8532–242.1 | 0.07 |
| Ischemic heart disease | 1.509 | 0.6247–3.545 | 0.35 |
| Atrial fibrillation | 0.8464 | 0.3499–1.955 | 0.70 |
| Statins intake | 1.066 | 0.5467–2.036 | 0.85 |
| WBC [103/μL] | 1.011 | 0.9337–1.087 | 0.78 |
| PWD [mm] | 1.053 | 0.6649–1.679 | 0.83 |
| IVSd [mm] | 1.282 | 0.8421–1.943 | 0.24 |
| TAPSE [mm] | 0.9967 | 0.9191–1.072 | 0.93 |
CABG — coronary artery bypass grafting; CI — confidence interval; IVSd — interventricular septal thickness at end-diastole; MI — myocardial infarction; OR — odds ratio; PWD — posterior wall diameter; TAPSE — tricuspid annular plane systolic excursion; WBC — white blood cell count. Statistically significant predictors are bolded
Discussion
The main findings of this study are: (i) elevated Lp(a) is prevalent in Polish population and requires special attention, (ii) prior CABG was the only comorbidity that differed between patients with high and low Lp(a), (iii) there were no differences in laboratory parameters or pharmacotherapy between high and low Lp(a) groups.
In the current cohort, 20.8% of patients had high Lp(a) concentration (≥ 30 mg/dL), which is consistent with other Polish studies. For example, 27% of the patients had Lp(a) > 30 mg/dL in the Zabrze-Lipoprotein(a) Registry [13] and 27.8% in the Polish Mother’s Memorial Hospital Research Institute (PMMHRI) Lp(a) Registry [12]. The difference in high Lp(a) concentration prevalence between the present cohort and those from the registries above may be due to the specific profile of patients included in this study. First, the prevalence of diabetes mellitus, which is associated with low Lp(a), was 33.1% in the present cohort compared to 20.6% and 29.3% in Zabrze and PMMHRI Lp(a) registries, respectively. Second, patients with very high Lp(a) levels, who may have experienced some ASCVD events, could have been referred to other departments or hospitals, particularly those having the catheterization laboratory.
Although increased Lp(a) is a common problem and accounts for residual ASCVD risk, it has been neglected for many years. The high prevalence of high Lp(a) in the Polish population calls for action regarding the implementation of the new guidelines, recommending measuring Lp(a) level in each individual at least once in a lifetime [14].
Prior CABG was the only comorbidity that differed between the groups of patients with high and low Lp(a). Ischemic heart disease was also more frequent in patients with high Lp(a), but it did not reach statistical significance (p = 0.05). There was also a nonsignificant trend towards a higher frequency of prior myocardial infarction (10.3% vs. 5.4%; p = 0.09) and prior percutaneous coronary intervention (6.8% vs. 4.5%; p = 0.34) in patients with high Lp(a). This is consistent with previous findings that patients with high Lp(a) tend to have more advanced, multivessel coronary artery disease, which may be reflected in more frequent qualification for the CABG procedure [15].
Importantly, patients with high and low Lp(a) did not differ in the concentration of total cholesterol, HDL cholesterol, non-HDL cholesterol, LDL cholesterol, or triglycerides, which further proves that Lp(a) is an independent ASCVD risk factor. Since LDL levels do not reflect the Lp(a) levels, it is crucial to determine the Lp(a) concentration in every adult patient independently of the standard lipid profile. Concurrently, there were no significant differences in the use of lipid-lowering drugs in patients with high and low Lp(a), despite more frequent ischemic heart disease and prior revascularization, which further aggravated the risk in patients with high Lp(a) and calls for action to optimize the treatment of all other concomitant cardiovascular risk factors. Of note, patients with high and low Lp(a) concentration did not differ in terms of factors such as body mass index, DM2 or hypertension prevalence, which further highlights the independence of Lp(a) from other known risk factors, being responsible for the residual risk discussed before.
Atrial fibrillation was numerically more frequent in patients with high Lp(a) and close to reaching statistical significance (17.9% vs. 11.2%; p = 0.06). Research assessing Lp(a) in atrial fibrillation is conflicting [4], but Mendelian randomization studies showed a causal relationship between high Lp(a) concentrations and atrial fibrillation [16–18].
Several limitations of this study must be noted. First, the retrospective nature hinders drawing conclusions regarding the causal relationship between Lp(a) and clinical variables. Second, this was a single-center study and it was conducted in a tertiary referral hospital, which influences the generalizability of the results. These cannot be directly translated to the broader Polish population of ambulatory patients due to a potential selection bias.
Conclusions
The present study provides important data regarding the epidemiology of Lp(a) concentration in Polish patients hospitalized in a tertiary referral hospital. High Lp(a) is prevalent in the Polish population, and thus it is important to measure it routinely in each individual at least once in a lifetime. The Lp(a) measurement should become a standard element of cardiovascular risk assessment in the Polish population, given that demographic and lifestyle factors have an influence on its level. It is important to identify individuals who are at increased ASCVD risk. Although there is no Lp(a) targeted treatment to date, such options are expected along with the results of ongoing clinical trials. Currently, it is crucial to control all other known cardiovascular risk factors to decrease the overall risk.
Acknowledgments
None.
Footnotes
Ethics statement: Ethical committee approval was waived due to the observational character of the study.
Authors’ contributions: All authors participated in the research and preparation of the manuscript. Conceptualization, T.S., G.P., M.L., A.G.; writing — original draft preparation, T.S., G.P.; writing — review and editing, J.Z., O.W., B.M., M.L., A.G.; visualization, G.P.; supervision, M.L., A.G.; funding acquisition, T.S. All authors edited and approved the final version of the manuscript. Figure 1 was created with BioRender.com (licensed version by GP).
Funding: None.
Conflict of interest: The authors have no competing interest to declare.
Supplementary material: None.
Data availability statement
All raw data are available from the corresponding author upon request.
References
- 1.Lampsas S, Xenou M, Oikonomou E, et al. Lipoprotein(a) in Atherosclerotic Diseases: From Pathophysiology to Diagnosis and Treatment. Molecules. 2023;28(3) doi: 10.3390/molecules28030969. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Kronenberg F, Mora S, Stroes ESG, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. Eur Heart J. 2022;43(39):3925–3946. doi: 10.1093/eurheartj/ehac361. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Patel AP, Wang M, Pirruccello J, et al. Lp(a) (Lipoprotein[a]) Concentrations and Incident Atherosclerotic Cardiovascular Disease. Arteriosclerosis, Thrombosis, and Vascular Biology. 2021;41(1):465–474. doi: 10.1161/atvbaha.120.315291. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Procyk G, Grabowski M, Gąsecka A. The role of lipoprotein(a) in atrial fibrillation: a systematic review. Pol Arch Intern Med. 2025;135(2) doi: 10.20452/pamw.16924. [DOI] [PubMed] [Google Scholar]
- 5.Schmidt K, Noureen A, Kronenberg F, et al. Structure, function, and genetics of lipoprotein (a) J Lipid Res. 2016;57(8):1339–1359. doi: 10.1194/jlr.R067314. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Kotwal A, Cortes T, Genere N, et al. Treatment of Thyroid Dysfunction and Serum Lipids: A Systematic Review and Meta-analysis. J Clin Endocrinol Metab. 2020;105(12) doi: 10.1210/clinem/dgaa672. [DOI] [PubMed] [Google Scholar]
- 7.Stenvinkel P, Berglund L, Heimbürger O, et al. Lipoprotein(a) in nephrotic syndrome. Kidney International. 1993;44(5):1116–1123. doi: 10.1038/ki.1993.357. [DOI] [PubMed] [Google Scholar]
- 8.Willeit P, Ridker PM, Nestel PJ, et al. Baseline and on-statin treatment lipoprotein(a) levels for prediction of cardiovascular events: individual patient-data meta-analysis of statin outcome trials. Lancet. 2018;392(10155):1311–1320. doi: 10.1016/S0140-6736(18)31652-0. [DOI] [PubMed] [Google Scholar]
- 9.Tsimikas S, Gordts PL, Nora C, et al. Statin therapy increases lipoprotein(a) levels. Eur Heart J. 2020;41(24):2275–2284. doi: 10.1093/eurheartj/ehz310. [DOI] [PubMed] [Google Scholar]
- 10.Cho L, Nicholls SJ, Nordestgaard BG, et al. Design and Rationale of Lp(a)HORIZON Trial: Assessing the Effect of Lipoprotein(a) Lowering With Pelacarsen on Major Cardiovascular Events in Patients With CVD and Elevated Lp(a) Am Heart J. 2025;287:1–9. doi: 10.1016/j.ahj.2025.03.019. [DOI] [PubMed] [Google Scholar]
- 11.Catapano AL, Daccord M, Damato E, et al. How should public health recommendations address Lp(a) measurement, a causative risk factor for cardiovascular disease (CVD)? Atherosclerosis. 2022;349:136–143. doi: 10.1016/j.atherosclerosis.2022.02.013. [DOI] [PubMed] [Google Scholar]
- 12.Sosnowska B, Lewek J, Adach W, et al. The prevalence, patients characteristics and risk factors of hyper-Lp(a)-emia in the Polish population. The first results from the PMMHRI-Lp(a) Registry. Prog Cardiovasc Dis. 2024;86:54–61. doi: 10.1016/j.pcad.2024.08.004. [DOI] [PubMed] [Google Scholar]
- 13.Dyrbuś K, Mędrala Z, Konsek K, et al. Lipoprotein(a) and its impact on cardiovascular disease - the Polish perspective: design and first results of the Zabrze-Lipoprotein(a) Registry. Arch Med Sci. 2024;20(4):1069–1076. doi: 10.5114/aoms/188294. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14.Arsenault BJ, Kamstrup PR. Eight reasons why lipoprotein(a) should be measured in everyone at least once in a lifetime. Eur Heart J. 2024;45(30):2692–2694. doi: 10.1093/eurheartj/ehae191. [DOI] [PubMed] [Google Scholar]
- 15.Farnier M, Chagué F, Maza M, et al. High lipoprotein(a) levels predict severity of coronary artery disease in patients hospitalized for acute myocardial infarction. Data from the French RICO survey. J Clin Lipidol. 2022;16(5):685–693. doi: 10.1016/j.jacl.2022.07.006. [DOI] [PubMed] [Google Scholar]
- 16.Jiang Qi, Qin D, Yang L, et al. Causal effects of plasma lipids on the risk of atrial fibrillation: A multivariable mendelian randomization study. Nutr Metab Cardiovasc Dis. 2021;31(5):1569–1578. doi: 10.1016/j.numecd.2021.02.011. [DOI] [PubMed] [Google Scholar]
- 17.Mohammadi-Shemirani P, Chong M, Narula S, et al. Elevated Lipoprotein(a) and Risk of Atrial Fibrillation: An Observational and Mendelian Randomization Study. J Am Coll Cardiol. 2022;79(16):1579–1590. doi: 10.1016/j.jacc.2022.02.018. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Satterfield BA, Dikilitas O, Safarova MS. Associations of Genetically Predicted Lp(a) (Lipoprotein [a]) Levels With Cardiovascular Traits in Individuals of European and African Ancestry. Circulation Genomic and precision medicine. 2021;14(4):e003354. doi: 10.1161/CIRCGEN.120.003354. [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
All raw data are available from the corresponding author upon request.