BACKGROUND: Many complications associated with congestive heart failure (CHF) have a thrombosis-related aetiology. Platelets play an important role in thrombogenesis, but it is not clear whether circulating platelets actively participate in thrombosis-related complications associated with CHF. OBJECTIVE: To determine whether soluble P-selectin, platelet surface P-selectin, and total platelet P-selectin as indices of platelet activation in CHF patients-compared to 'disease controls' and 'healthy controls'-and to assess their prognostic value in CHF. METHODS: We measured soluble P-selectin (sP-sel, by enzyme-linked immunosorbent assay, ELISA), total platelet P-selectin (pP-sel, by a novel 'platelet lysate' assay), platelet surface P-selectin (CD62P%G) and platelet surface CD63 (CD63%G) expression by flow cytometry-in 108 patients with stable congestive heart failure (all with left ventricular ejection fraction (LVEF) <50%). Levels were compared with 50 healthy controls and 70 'disease controls' (patients with coronary artery disease with normal left ventricular systolic function). RESULTS: CHF patients and disease controls had higher sP-sel, CD62P%G and CD63%G than healthy controls. There were no significant correlations between sP-sel, pP-sel, CD62P%G and CD63%G with ejection fraction (all P>0.05). There were no differences in these markers when ischaemic and non-ischaemic aetiologies of CHF were compared. After a median follow-up of 490 days (range 340-535), there were 7 deaths, 15 hospitalizations for worsening heart failure, 1 for cardiac resynchronization therapy, 4 for revascularizations, 4 for myocardial infarctions, and 1 stroke. None of the platelet markers were predictive of the composite end-point at follow-up. CONCLUSIONS: Patients with stable CHF exhibit evidence of abnormal platelet activation, despite usage of antiplatelet agents. These abnormalities did not determine prognosis and were broadly similar to those seen in 'disease controls' indicating that platelet abnormalities in CHF may simply be related to associated comorbidities.
BACKGROUND: Many complications associated with congestive heart failure (CHF) have a thrombosis-related aetiology. Platelets play an important role in thrombogenesis, but it is not clear whether circulating platelets actively participate in thrombosis-related complications associated with CHF. OBJECTIVE: To determine whether soluble P-selectin, platelet surface P-selectin, and total platelet P-selectin as indices of platelet activation in CHFpatients-compared to 'disease controls' and 'healthy controls'-and to assess their prognostic value in CHF. METHODS: We measured soluble P-selectin (sP-sel, by enzyme-linked immunosorbent assay, ELISA), total platelet P-selectin (pP-sel, by a novel 'platelet lysate' assay), platelet surface P-selectin (CD62P%G) and platelet surface CD63 (CD63%G) expression by flow cytometry-in 108 patients with stable congestive heart failure (all with left ventricular ejection fraction (LVEF) <50%). Levels were compared with 50 healthy controls and 70 'disease controls' (patients with coronary artery disease with normal left ventricular systolic function). RESULTS:CHFpatients and disease controls had higher sP-sel, CD62P%G and CD63%G than healthy controls. There were no significant correlations between sP-sel, pP-sel, CD62P%G and CD63%G with ejection fraction (all P>0.05). There were no differences in these markers when ischaemic and non-ischaemic aetiologies of CHF were compared. After a median follow-up of 490 days (range 340-535), there were 7 deaths, 15 hospitalizations for worsening heart failure, 1 for cardiac resynchronization therapy, 4 for revascularizations, 4 for myocardial infarctions, and 1 stroke. None of the platelet markers were predictive of the composite end-point at follow-up. CONCLUSIONS:Patients with stable CHF exhibit evidence of abnormal platelet activation, despite usage of antiplatelet agents. These abnormalities did not determine prognosis and were broadly similar to those seen in 'disease controls' indicating that platelet abnormalities in CHF may simply be related to associated comorbidities.
Authors: Christopher S Lee; Quin E Denfeld; Bradley E Aouizerat; Corrine Y Jurgens; Christopher V Chien; Emily Aarons; Jill M Gelow; Shirin O Hiatt; James O Mudd Journal: Heart Lung Date: 2018-10-09 Impact factor: 2.210
Authors: Armen Yuri Gasparyan; Antonios Stavropoulos-Kalinoglou; Dimitri P Mikhailidis; Karen M J Douglas; George D Kitas Journal: Rheumatol Int Date: 2011-02 Impact factor: 2.631
Authors: Boris Bigalke; Konstantinos Stellos; Tobias Geisler; Stephan Lindemann; Andreas E May; Meinrad Gawaz Journal: Clin Res Cardiol Date: 2010-01-05 Impact factor: 5.460
Authors: Prathap Kanagala; Jayanth R Arnold; Jamal N Khan; Anvesha Singh; Gaurav S Gulsin; Iain B Squire; Gerry P McCann; Leong L Ng Journal: ESC Heart Fail Date: 2021-03-10