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agonists mediate coronary vasoconstriction, adenosine, ATP-dependent K+-channels, endothelium-derived hyperpolarizing factor and β-adrenoceptors agonists cause coronary vasodilatation [5]. Likewise, there are several factors such as adenosine diphosphate, thromboxane A2, thrombin, epinephrine, collagen and platelet activating factor which provoke platelet activation and adhesion and prostacycline as a second major inhibitor of platelet adhesion [6]. Additionally, the reduction of NO by itself does not induce spontaneous platelet aggregation but requires prior platelet activation by cofactors as a prerequisite. Thus, the effect of absent NO remains speculative, provides only limited explanation and these other pathways described need to be taken into account. Finally, TTP and TMA are characterized by severe injury and activation of the vascular endothelium that in all likelihood will result in the release of most of these factors favouring microvascular coronary thrombosis [4]. The intriguing idea to administer NO donors as nitrates to patients with TTP certainly deserves to be studied. As no data exist on the effect of NO donation in TTP, detailed studies are required. However, we caution against applying nitrates at present outside of any trial, as TTP may induce sudden haemodynamic shock and multiorgan failure, lifethreatening situations which may be aggravated by the use of nitrates.

Sleep quality and dialysis efficacy affect functional capacity in patients receiving haemodialysis therapy