ABSTRACT: Acute exercise has been associated with activation of thrombosis, and this risk may be accentuated in patients with heart failure. Given the relation of platelets to atherothrombosis, we tested the hypothesis that acute exercise would adversely affect platelet indices and platelet activation markers in patients with systolic and diastolic heart failure.
We studied 20 patients with systolic heart failure (17 men, 3 women; mean age 64 +/- 10 years, all with ejection fraction (EF) < or = 40%) and 20 patients with diastolic heart failure (14 men, 6 women; mean age 64 +/- 8 years, mean EF = 66%) who were exercised to maximal intensity, who were compared to 13 healthy controls (6 men, 7 women; mean age 60 +/- 4 years, mean EF = 73%). We measured platelet indices (platelet volume, mass and component) and platelet activation markers (platelet-bound CD62P%G, CD63%G and CD40L%G using flow cytometry, as well as plasma sCD40L and soluble P-selectin (sP-sel) levels).
Baseline Mean Platelet Volume (MPV), sP-sel, CD40L%G and CD63%G levels were significantly higher in patients with systolic and diastolic heart failure, when compared with controls. The mean exercise duration and VO(2 )peak in patients with systolic and diastolic heart failure were not significantly different, but lower than that seen in healthy controls. Following exercise, mean haematocrit, CD62P%G, and CD63%G significantly increased in all three subject groups (all P < 0.05). The proportional change in CD62P%G and CD63%G were not significantly different between healthy controls and heart failure patients (P > 0.05).
Acute maximal graded exercise increases platelet activation markers, with no disproportionate differences between heart failure patients and healthy controls, despite the former group having a lower exercise tolerance and VO2 peak.
European Journal of Clinical Investigation 03/2008; 38(3):150-8. · 3.02 Impact Factor
ABSTRACT: Many complications associated with congestive heart failure (CHF) have a thrombosis-related aetiology, which may involve platelets. The immune modulator pair CD40-CD40L has been proposed to be an important link between inflammation and thrombosis and may be important in the pathophysiology of CHF.
To study soluble CD40L (sCD40L), platelet surface CD40L (%GCD40L) and total platelet CD40L (pCD40L) levels in CHF patients, their relationships to other platelet indices (platelet volume, mass and component) and to assess their prognostic value.
We measured sCD40L (by ELISA); pCD40L (by a platelet lysate assay); platelet surface CD40L (%GCD40L) expression by flow cytometry; mean platelet volume (MPV), mean platelet mass (MPM) and mean platelet component (MPC); in 108 patients with stable CHF. Levels were compared with 37 'healthy controls' and 63 'disease controls'. After a median follow-up period of 490 days, clinical endpoints were determined.
pCD40L was significantly higher in CHF than disease controls, but not sCD40L or %GCD40L levels. CHF patients and disease controls had higher MPV (one-way anova, P < 0.0001), whilst MPC was significantly lower in CHF patients (P < 0.0001), compared to healthy controls. All indices related to CD40L (i.e. sCD40L, pCD40L and %GCD40L) were neither related to disease severity or left ventricular ejection function, nor to clinical endpoints at follow-ups.
Patients with stable CHF patients did not exhibit enhanced levels of CD40L and the latter did not predict clinical events at follow-up. The lack of difference in CD40L levels between CHF and disease controls suggests that CD40L may not have a major role in CHF per se, but in the comorbidities associated with CHF.
Journal of Internal Medicine 03/2008; 263(3):313-21. · 5.48 Impact Factor
ABSTRACT: Patients with congestive heart failure (CHF) are at increased risk of thromboembolic events. However, there is much debate and uncertainty over the use of antithrombotic therapy in these patients. The evidence for oral anticoagulation is limited, although large randomised trial data are forthcoming. Aspirin may be detrimental for heart failure due to a possible interaction with angiotensin-converting enzyme inhibitors, leading to increased hospitalisations from decompensated heart failure. The objective of this review article is to summarise the available evidence regarding the risk of stroke and thromboembolic events in CHF patients, as well as the effectiveness and risks of antithrombotic therapy in these patients.
International Journal of Clinical Practice 02/2006; 60(1):36-47. · 2.41 Impact Factor