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Thromboxane and prostacyclin biosynthesis in heart failure of ischemic origin: effects of disease severity and aspirin treatment
Author(s) -
SANTILLI F.,
DAVÌ G.,
BASILI S.,
LATTANZIO S.,
CAVONI A.,
GUIZZARDI G.,
DE FEUDIS L.,
TRAISCI G.,
PETTINELLA C.,
PALOSCIA L.,
MINUZ P.,
MENEGUZZI A.,
CIABATTONI G.,
PATRONO C.
Publication year - 2010
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2010.03820.x
Subject(s) - aspirin , medicine , prostacyclin , thromboxane , cardiology , thromboxane b2 , heart failure , urinary system , thromboxane a2 , platelet activation , platelet , gastroenterology
Summary. Background : Thromboembolism is a relatively common complication of chronic heart failure (HF) and the place of antiplatelet therapy is uncertain. Objectives: We characterized the rate of thromboxane and prostacyclin biosynthesis in chronic HF of ischemic origin, with the aim of separating the influence of HF on platelet activation from that of the underlying ischemic heart disease (IHD). Patients and Methods : We compared urinary 11‐dehydro‐thromboxane (TX)B 2 , 2,3 dinor 6‐keto‐PGF 1α, 8‐iso‐prostaglandin (PG)F 2α , and plasma N‐terminal pro‐brain natriuretic peptide (NT‐pro‐BNP), asymmetric dimethylarginine (ADMA), and soluble CD40 ligand (sCD40L), in 84 patients with HF secondary to IHD, 61 patients with IHD without HF and 42 healthy subjects. Results : HF patients not on aspirin had significantly higher urinary 11‐dehydro‐TXB 2 as compared with healthy subjects ( P < 0.0001) and IHD patients not on aspirin ( P = 0.028). They also showed significantly higher 8‐iso‐PGF 2α ( P = 0.018), NT‐pro‐BNP ( P = 0.021) and ADMA ( P < 0.0001) than IHD patients not on aspirin. HF patients on low‐dose aspirin had significantly lower 11‐dehydro‐TXB 2 ( P < 0.0001), sCD40L ( P = 0.007) and 2,3‐dinor‐6‐keto‐PGF 1α ( P = 0.005) than HF patients not treated with aspirin. HF patients in NYHA classes III and IV had significantly higher urinary 11‐dehydro‐TXB 2 than patients in classes I and II, independently of aspirin treatment ( P < 0.05). On multiple linear regression analysis, higher NT‐pro‐BNP levels, lack of aspirin therapy and sCD40L, predicted 11‐dehydro‐TXB 2 excretion rate in HF patients (R 2 = 0.771). Conclusions : Persistent platelet activation characterizes HF patients. This phenomenon is related to disease severity and is largely suppressable by low‐dose aspirin. The homeostatic increase in prostacyclin biosynthesis is impaired, possibly contributing to enhanced thrombotic risk in this setting.