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Platelet aggregation and response to aspirin therapy in cardiac allograft vasculopathy
Kamilla P Bjerre1, Tor S Clemmensen1, Katrine Berg1
1Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Insights
Heart transplant recipients with cardiac allograft vasculopathy (CAV) show increased platelet aggregation. Low-dose aspirin may not sufficiently inhibit platelet activity in these patients, highlighting potential risks for coronary thrombosis.
Area of Science:
- Cardiology
- Immunology
- Transplantation
Background:
- Cardiac allograft vasculopathy (CAV) compromises long-term survival after heart transplantation (HTx).
- The exact pathogenesis of CAV, including the role of coronary thrombosis, remains unclear.
- This study investigates platelet aggregation and turnover in HTx patients with and without CAV.
Purpose of the Study:
- To compare platelet aggregation and turnover between HTx patients with CAV, HTx patients without CAV, and healthy controls.
- To assess the anti-platelet effect of low-dose aspirin in HTx patients.
- To explore the relationship between microvascular function and platelet aggregation in HTx patients.
Main Methods:
- Enrolled 57 HTx patients (median 8.3 years post-transplant) and 57 healthy controls.
- Measured platelet aggregation (off- and on-aspirin) using adenosine diphosphate (ADP) and arachidonic acid (AA).
- Assessed platelet turnover, CAV burden, and microvascular function (coronary flow velocity reserve - CFVR).
Main Results:
- HTx patients with CAV exhibited higher ADP-induced platelet aggregation than controls and HTx patients without CAV (off-aspirin).
- Aspirin reduced AA-induced aggregation, but CAV patients still showed higher on-aspirin aggregation compared to non-CAV HTx patients.
- No significant difference in platelet turnover was observed between HTx groups; lower CFVR correlated with higher platelet aggregation.
Conclusions:
- Elevated platelet aggregation is present in HTx patients with CAV, both off- and on-aspirin.
- Aspirin monotherapy may be insufficient for adequate platelet inhibition in HTx patients with CAV.
- These findings suggest a potential role for enhanced anti-platelet strategies in managing CAV.
Background:
Long-term survival after heart transplantation (HTx) is compromised by cardiac allograft vasculopathy (CAV) characterized by coronary macro- and microvascular disease. The pathogenesis of CAV is unclear and may involve coronary thrombosis. We investigated whether HTx patients with CAV had higher platelet aggregation and turnover than HTx patients without CAV and healthy controls. Furthermore, we investigated the anti-platelet effect of low-dose aspirin in HTx patients.
Methods:
We included 57 patients who had undergone HTx (median 8.3 years from HTx) and 57 healthy controls. Platelet aggregation was measured on-aspirin and off-aspirin using impedance aggregometry with adenosine diphosphate (ADP) and arachidonic acid (AA). We evaluated platelet turnover by flow cytometry, CAV burden by coronary angiography and echocardiography, and microvascular function by echocardiographic coronary flow velocity reserve (CFVR).
Results:
Off-aspirin, HTx patients with CAV (n = 21) had higher ADP-induced platelet aggregation than healthy controls (p < 0.01) and HTx patients without CAV (n = 36) (p < 0.05). Aspirin treatment reduced AA-induced platelet aggregation in both HTx groups, but HTx patients with CAV had higher platelet aggregation on-aspirin than HTx patients without CAV (p < 0.05). Platelet turnover did not differ between HTx patients with CAV and HTx patients without CAV (p > 0.34). HTx patients with lower CFVR values had higher platelet aggregation than HTx patients with higher CFVR values (p < 0.05).
Conclusions:
Off-aspirin, platelet aggregation was higher in HTx patients with CAV than in HTx patients without CAV and healthy controls. On-aspirin, platelet aggregation was higher in HTx patients with CAV than in HTx patients without CAV. Aspirin monotherapy may not provide sufficient platelet inhibition in HTx patients with CAV.
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