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ANTIPHOSPHOLIPID SYNDROME AS A MODIFIER OF CLINICAL PHENOTYPES IN ATHEROSCLEROTIC CARDIOVASCULAR DISEASE: A
N Archaia1, V Chumburidze2, N Kakauridze3
11Faculty of Medicine, Ivane Javakhishvili Tbilisi State University, Georgia.
Insights
Antiphospholipid syndrome (APS) significantly increases venous and central nervous system thrombosis risk in atherosclerotic cardiovascular disease (ASCVD) patients. APS modifies ASCVD by promoting thrombosis rather than causing atherosclerosis.
Area of Science:
- Immunology
- Cardiology
- Hematology
Background:
- Antiphospholipid syndrome (APS) is an autoimmune disorder linked to thrombosis.
- The role of APS in atherosclerotic cardiovascular disease (ASCVD) phenotypes is not fully understood.
Purpose of the Study:
- To investigate the association between APS and clinical, thrombotic, and laboratory features in ASCVD patients.
Main Methods:
- A single-center case-control study included 355 ASCVD patients (92 with APS, 92 without).
- Evaluated clinical characteristics, vascular involvement, risk factors, coagulation parameters, and antiphospholipid antibodies.
- Utilized correlation and multivariable regression analyses.
Main Results:
- APS prevalence was 25.9% in ASCVD patients.
- APS-positive patients had higher rates of venous thrombosis (OR 4.02) and CNS arterial thrombosis (OR 2.40).
- Lupus anticoagulant was the most common antibody; IgG antibodies correlated with activated partial thromboplastin time.
Conclusions:
- APS is linked to a distinct thrombotic phenotype in ASCVD, including increased venous and cerebrovascular thrombosis.
- Findings suggest APS acts as an immunothrombotic modifier of ASCVD, influencing atherosclerosis development.
Background:
Antiphospholipid syndrome (APS) is an autoimmune prothrombotic disorder characterized by persistent antiphospholipid antibodies and vascular thrombosis. Its contribution to clinical phenotypes of atherosclerotic cardiovascular disease (ASCVD) remains incompletely defined.
Objective:
To evaluate the association between APS and clinical, thrombotic, and laboratory characteristics in patients with ASCVD.
Methods:
A single‑center case-control study (2019-2023) included 355 patients with confirmed ASCVD. Ninety‑two patients (25.9%) fulfilled revised Sydney APS criteria and were included as cases. Ninety‑two age‑ and sex‑matched APS‑negative ASCVD patients served as controls. Clinical characteristics, vascular involvement, cardiovascular risk factors, coagulation parameters, lipid profile, and antiphospholipid antibodies (anticardiolipin, anti‑β2‑glycoprotein I, and lupus anticoagulant) were analyzed. Correlation and multivariable regression analyses were performed.
Results:
APS prevalence among ASCVD patients was 25.9%. APS‑positive patients demonstrated significantly higher rates of venous thrombosis (OR 4.02; p=0.037) and central nervous system arterial thrombosis (OR 2.40; p=0.044). Cerebral arterial involvement was more frequent in APS patients (OR 3.12; p=0.036). Lupus anticoagulant was the most prevalent antibody (57.6%). IgG isotype antibodies showed strong correlations with activated partial thromboplastin time, particularly anti‑β2GPI IgG (r=0.709; p<0.001). APS patients exhibited prolonged prothrombin time, reduced prothrombin index, and significantly elevated D‑dimer levels. Multivariable regression models (adjusted R² 0.35-0.44) identified thrombotic localization, coagulation parameters, and lipid indices as independent predictors of antiphospholipid antibody levels.
Conclusion:
APS is associated with a distinct thrombotic phenotype in ASCVD characterized by increased venous and cerebrovascular thrombosis and coagulation dysregulation. These findings support the concept that APS acts as an immunothrombotic modifier of ASCVD rather than a primary cause of atherosclerosis.
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