Key result
Tadalafil administration significantly increased cGMP levels in all ED patients (P<0.01), but increased cAMP (P<0.05) and decreased P-selectin (P<0.01) only in those without cardiovascular risk factors.
Why the study?
Does tadalafil improve markers of endothelial and platelet activation in patients with erectile dysfunction with or without cardiovascular risk factors?
Does tadalafil improve markers of endothelial and platelet activation in patients with erectile dysfunction with or without cardiovascular risk factors?
p-value: p=<.01
Tadalafil exerts beneficial effects on platelet activation in erectile dysfunction patients without cardiovascular risk factors, suggesting that the presence of risk factors blunts this response.
Tadalafil effects on platelet markers may differ by CV risk in ED; hypothesis-generating and should not yet change practice.
Activation of endothelial cells and platelets is an initial step toward the development of cardiovascular disease. Erectile dysfunction (ED) may be an early manifestation of endotheliopathy. We evaluated the effects of tadalafil on cyclic nucleotides (cGMP and cAMP) and soluble adhesion molecules (E- and P-selectin [ES and PS]). The patients were divided into 2 groups on the basis of the presence (10 patients) or absence (9 patients) of cardiovascular risk factors (dyslipidemia, hypertension, and smoking). Nitric oxide (NO) was unmeasurable in all the patients. Tadalafil administration induced a significant increase in cGMP levels in both groups (P < .01). In contrast, cAMP significantly increased (P < .05) and PS decreased (P < .01) only in patients without cardiovascular risk factors. Tadalafil induced a beneficial effect on platelet activation in patients with ED without cardiovascular risk factors; this effect was not mediated by NO.
No takes yet. Share an insight, caveat, or question.
Bon et al. (2010) studied Erectile dysfunction (n=19). Tadalafil vs. Presence vs absence of cardiovascular risk factors was evaluated on Levels of cyclic nucleotides (cGMP and cAMP) and soluble adhesion molecules (E- and P-selectin) (p=<.01). Tadalafil administration significantly increased cGMP levels in all ED patients (P<0.01), but increased cAMP (P<0.05) and decreased P-selectin (P<0.01) only in those without cardiovascular risk factors.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: