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The ABO locus is associated with increased platelet aggregation in patients with stable coronary artery disease
Morten Krogh Christiansen1, Sanne Bøjet Larsen1, Mette Nyegaard2
1Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Insights
The ABO blood group risk variant increases platelet aggregation, potentially explaining its stronger link to myocardial infarction (MI) risk compared to coronary artery disease (CAD). This study investigated genetic risk factors for cardiovascular events.
Area of Science:
- Cardiovascular Genetics
- Platelet Biology
- Genetics of Atherosclerosis
Background:
- Genome-wide association studies (GWAS) identify numerous risk loci for coronary artery disease (CAD) and myocardial infarction (MI).
- The ABO blood group locus shows a disproportionately stronger association with MI risk than with CAD, with underlying mechanisms remaining unclear.
Purpose of the Study:
- To investigate the association between the ABO risk variant (rs495828) and platelet activation and aggregation.
- To explore the impact of other common CAD-associated genetic risk variants on platelet function.
Main Methods:
- Genotyping of 45 genome-wide significant CAD risk variants in 879 stable CAD patients.
- Assessment of platelet activation via serum soluble P-selectin (sP-selectin) and thromboxane B2 levels.
- Measurement of platelet aggregation using multiple electrode aggregometry (MEA) and VerifyNow assays with arachidonic acid and collagen stimulation.
Main Results:
- The rs495828 risk allele was significantly associated with increased platelet aggregation (14.9% higher AUC with arachidonic acid, 13.1% with collagen).
- Conversely, sP-selectin levels were lower (7.5%) per risk allele, suggesting a complex effect on platelet activation.
- No significant associations were found for other CAD variants or the calculated genetic risk score (GRS) with platelet parameters.
Conclusions:
- The ABO risk allele is linked to heightened platelet aggregation, as measured by MEA.
- This finding provides a potential mechanistic explanation for the elevated MI risk observed in carriers of the ABO risk variant.
Background:
Genome-wide association studies of patients with coronary artery disease (CAD) suggest that several risk loci increase the risk of CAD and myocardial infarction (MI) equally. In contrast, the ABO locus is stronger associated with MI than with CAD, but the underlying mechanisms are unknown.
Purpose:
To investigate the association between the ABO risk variant and platelet activation and aggregation. Moreover, to explore the effects of other CAD-associated risk variants.
Methods:
We included 879 stable CAD patients receiving low-dose aspirin. All patients were genotyped for 45 genome-wide significant CAD risk variants, including rs495828 at the ABO locus. A genetic risk score (GRS) was calculated to assess the combined risk of all genetic variants. Serum soluble P-selectin (sP-selectin) and thromboxane B2 were used as measures of platelet activation, and platelet aggregation was assessed by multiple electrode aggregometry (MEA) using arachidonic acid and collagen as agonists and VerifyNow.
Results:
The rs495828 CAD risk allele was associated with higher MEA platelet aggregation; arachidonic acid: 14.9% (6.7-23.7%, p = 0.0002) higher AUC (Area Under aggregation Curve) per risk allele, and collagen: 13.1% (5.8%-20.9%, p = 0.0003). Conversely, sP-selectin levels were 7.5% (3.1%-11.7%, p = 0.001) lower per risk allele. Rs495828 genotypes were not associated with aggregation assessed by VerifyNow (p = 0.30) or S-thromboxane B2 levels (p = 0.98). None of the remaining variants or the GRS were associated with platelet activation or aggregation.
Conclusions:
The ABO risk allele was associated with increased platelet aggregation as assessed by MEA. This finding may contribute to explain the increased MI risk in ABO risk variant carriers.
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Antigens in the ABO Blood Group System
Antigens are substances that can trigger an immune response, leading to the production of antibodies. In the ABO blood group system,...