Platelet aggregation and response to aspirin therapy in cardiac allograft vasculopathy

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 pla...

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Veröffentlicht in:The Journal of heart and lung transplantation 2020-04, Vol.39 (4), p.371-378
Hauptverfasser: Bjerre, Kamilla P., Clemmensen, Tor S., Berg, Katrine, Poulsen, Steen H., Hvas, Anne-Mette, Grove, Erik L., Løgstrup, Brian B., Jakobsen, Lars, Thim, Troels, Kristensen, Steen D., Eiskjær, Hans
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container_end_page 378
container_issue 4
container_start_page 371
container_title The Journal of heart and lung transplantation
container_volume 39
creator Bjerre, Kamilla P.
Clemmensen, Tor S.
Berg, Katrine
Poulsen, Steen H.
Hvas, Anne-Mette
Grove, Erik L.
Løgstrup, Brian B.
Jakobsen, Lars
Thim, Troels
Kristensen, Steen D.
Eiskjær, Hans
description 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. 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). 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). 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.
doi_str_mv 10.1016/j.healun.2020.01.1344
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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. 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). Off-aspirin, HTx patients with CAV (n = 21) had higher ADP-induced platelet aggregation than healthy controls (p &lt; 0.01) and HTx patients without CAV (n = 36) (p &lt; 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 &lt; 0.05). Platelet turnover did not differ between HTx patients with CAV and HTx patients without CAV (p &gt; 0.34). HTx patients with lower CFVR values had higher platelet aggregation than HTx patients with higher CFVR values (p &lt; 0.05). 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.</description><identifier>ISSN: 1053-2498</identifier><identifier>EISSN: 1557-3117</identifier><identifier>DOI: 10.1016/j.healun.2020.01.1344</identifier><identifier>PMID: 32067865</identifier><language>eng</language><publisher>NEW YORK: Elsevier Inc</publisher><subject>Aged ; Allografts ; aspirin ; Aspirin - therapeutic use ; Cardiac &amp; Cardiovascular Systems ; cardiac allograft vasculopathy ; Cardiovascular System &amp; Cardiology ; Coronary Angiography ; coronary artery disease ; Cross-Sectional Studies ; Denmark - epidemiology ; Female ; Follow-Up Studies ; Graft Rejection - diagnosis ; Graft Rejection - drug therapy ; Graft Rejection - mortality ; heart transplantation ; Heart Transplantation - adverse effects ; Humans ; Life Sciences &amp; Biomedicine ; Male ; Middle Aged ; Platelet Aggregation - drug effects ; Platelet Aggregation Inhibitors - therapeutic use ; Respiratory System ; Retrospective Studies ; Science &amp; Technology ; Surgery ; Survival Rate - trends ; Time Factors ; Transplantation ; treatment</subject><ispartof>The Journal of heart and lung transplantation, 2020-04, Vol.39 (4), p.371-378</ispartof><rights>2020 International Society for Heart and Lung Transplantation</rights><rights>Copyright © 2020 International Society for Heart and Lung Transplantation. 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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. 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). Off-aspirin, HTx patients with CAV (n = 21) had higher ADP-induced platelet aggregation than healthy controls (p &lt; 0.01) and HTx patients without CAV (n = 36) (p &lt; 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 &lt; 0.05). Platelet turnover did not differ between HTx patients with CAV and HTx patients without CAV (p &gt; 0.34). HTx patients with lower CFVR values had higher platelet aggregation than HTx patients with higher CFVR values (p &lt; 0.05). 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. 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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. 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). Off-aspirin, HTx patients with CAV (n = 21) had higher ADP-induced platelet aggregation than healthy controls (p &lt; 0.01) and HTx patients without CAV (n = 36) (p &lt; 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 &lt; 0.05). Platelet turnover did not differ between HTx patients with CAV and HTx patients without CAV (p &gt; 0.34). HTx patients with lower CFVR values had higher platelet aggregation than HTx patients with higher CFVR values (p &lt; 0.05). 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. 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subjects Aged
Allografts
aspirin
Aspirin - therapeutic use
Cardiac & Cardiovascular Systems
cardiac allograft vasculopathy
Cardiovascular System & Cardiology
Coronary Angiography
coronary artery disease
Cross-Sectional Studies
Denmark - epidemiology
Female
Follow-Up Studies
Graft Rejection - diagnosis
Graft Rejection - drug therapy
Graft Rejection - mortality
heart transplantation
Heart Transplantation - adverse effects
Humans
Life Sciences & Biomedicine
Male
Middle Aged
Platelet Aggregation - drug effects
Platelet Aggregation Inhibitors - therapeutic use
Respiratory System
Retrospective Studies
Science & Technology
Surgery
Survival Rate - trends
Time Factors
Transplantation
treatment
title Platelet aggregation and response to aspirin therapy in cardiac allograft vasculopathy
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