A lack of effect of captopril on platelet aggregation in patients with congestive heart failure

Gow, Iain F; Flapan, A. D.; Morris, Mariana; Davies, Eleanor; Williams, Brent C.; Padfield, P. L.; Shaw, T. R. D.; Edwards, C. R. W.

doi:10.1007/bf00280105

Cited by 4 publications

(1 citation statement)

References 20 publications

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“…Novel techniques for the assessment of platelets, including whole-blood flow cytometry, should be applied in order to establish the real antiplatelet characteristics of various pharmaceuticals, and to avoid confusing claims, which, for instance, happened with captopril. This compound was first declared to be a strong antiplatelet agent [76], but was later found to be an ineffective platelet inhibitor in patients with heart failure [77].…”

Section: Platelet Markersmentioning

confidence: 99%

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

Serebruany¹,

Davis

Meister

et al. 2001

Heart Drug

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Knowledge of the pathogenesis of congestive heart failure (CHF) has improved greatly in recent years. Nevertheless, this disease still causes high morbidity and mortality in the Western world. In particular, there have been many advancements in our understanding, treatment and prophylaxis of CHF in recent years, yet the incidence of this disease continues to rise. Due to the staggering numbers of patients afflicted, CHF is becoming the most expensive burden on the health care system. The relationship between the deterioration of cardiac function and ongoing ischemic events has not been fully investigated and could conceivably be both monitored and modulated via various biomarkers. Recent data also indicate that heart failure is associated with altered hemostasis, i.e. a prothrombotic state which can lead to complications arising from occlusive and/or thromboembolic phenomena. Although the incidence of overt and clinically apparent thrombotic events is low, it is possible that subclinical events contribute to the increasing morbidity and mortality from this disease. These subclinical events may include silent ischemic events or microinfarcts which are being recognized as contributing to the progression of heart failure. As far as nonpharmacologic approaches to heart failure are concerned, the use of uniform exercise training regimens in heart failure is still a very controversial topic. Before more definitive recommendations can be made regarding the justification of such procedures, further large-scale studies investigating the effects of physical exercise on the development and progression of heart failure are needed. Furthermore, these studies must have sufficient statistical power to detect effects on clinical outcomes, specifically mortality. The purpose of this review article is to bridge the gap between biomarkers, exercise training and heart failure by discussing our current knowledge of different markers of platelet activation, thrombin generation, inflammation, endothelial dysfunction and myocardial necrosis in CHF patients undertaking physical exercise.

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Section: Platelet Markersmentioning

confidence: 99%

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

Serebruany¹,

Davis

Meister

et al. 2001

Heart Drug

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The sensitivity of human blood platelets to the aggregating agent ADP during different dietary sodium intakes in healthy men

Gow

Dockrell

Edwards

et al. 1992

Eur J Clin Pharmacol

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We have investigated the effect of varying sodium intake on the renin-angiotensin system, ADP-induced platelet aggregation in vitro, and blood 5-HT concentrations in 9 male volunteers. Systolic blood pressure was slightly reduced during a low sodium diet, whereas the diastolic pressure remained unchanged. Plasma renin activity and aldosterone concentration both fell significantly when sodium intake was increased; plasma angiotensin II concentration also fell, but not significantly. There was a significant fall in haematocrit after an increased sodium intake, but there was no change in the whole-blood platelet count after correcting for this. There were no significant changes in either total (i.e. PRP) or platelet 5-HT concentrations. The extent of platelet aggregation induced by 5 and 20 mumol.l-1 of ADP increased significantly when dietary sodium intake was increased. When compared with low or normal sodium intakes, lower concentrations of ADP were required to produce 50% of maximum aggregation after a high sodium intake. The 5-HT2 receptor antagonist ketanserin (1 mumol.l-1 in vitro) reduced the extent of aggregation induced by 5 mumol.l-1 ADP after the volunteers had taken a high sodium diet, whereas the angiotensin II receptor antagonist saralasin (1 nmol.l-1) increased the rate of aggregation after the low sodium diet. Thus, during a high sodium intake, human platelets become more sensitive to the aggregating agent ADP. It is possible that this effect is mediated via platelet 5-HT2 receptors, since ketanserin abolished the increase in salt-induced aggregation seen with 5 mumol.l-1 ADP.

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Usefulness of soluble and surface-bound P-selectin in detecting heightened platelet activity in patients with congestive heart failure

O’Connor

Gurbel

Serebruany

1999

The American Journal of Cardiology

116

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A lack of effect of captopril on platelet aggregation in patients with congestive heart failure

Cited by 4 publications

References 20 publications

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

The sensitivity of human blood platelets to the aggregating agent ADP during different dietary sodium intakes in healthy men

Usefulness of soluble and surface-bound P-selectin in detecting heightened platelet activity in patients with congestive heart failure

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