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Charalambos Vlachopoulos, Piero Montorsi, Konstantinos Aznaouridis, Stefano Galli, Konstantinos Rokkas, Paolo Ravagnani, Francesco Montorsi, Christodoulos Stefanadis, Is erectile dysfunction a low-grade systemic inflammatory condition?: reply, European Heart Journal, Volume 28, Issue 5, March 2007, Pages 643–644, https://doi.org/10.1093/eurheartj/ehl532
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We thank Dr Das for his interest in our work. Taken together, our two studies1,2 reinforce the notion of a close link between subclinical inflammation/endothelial-prothrombotic activation, erectile dysfunction (ED), and atherosclerotic coronary artery disease (CAD). In patients with both ED and CAD, ED precedes the onset of CAD in the majority of patients,1,3 and it is associated with increased inflammatory and prothrombotic activation.1
Thus, in patients with suspected ED or at risk for ED, such as subjects with cardiometabolic risk factors, measurement of inflammatory compounds may contribute to a more comprehensive evaluation of these patients. Other substances, such as the vascular endothelial growth factor proposed by Dr Das, may also be considered. Furthermore, preliminary data from the Sexual Health Unit of Athens Medical School show that ED is associated with high level of adhesion molecules and low level of the N-terminal fragment C-type natriuretic peptide, an endothelium-derived relaxant factor.
At the moment, evidence regarding a possible direct etiological relationship between markers/mediators of inflammatory/prothrombotic activation and ED is limited. However, both ED and CAD are associated with high blood level of these compounds, and, interestingly enough, the adverse effect of each of these conditions (ED or CAD) is independent of the presence of the other condition (CAD or ED), so that men with both ED and CAD have the highest activation of inflammatory and prothrombotic mechanisms.1 In this sense, measuring the level of these compounds may contribute to the following: first, to diagnose vasculogenic ED in patients with ED of unknown etiology. This does not imply that biomarkers may substitute for penile Doppler studies, and, moreover, it presupposes that there is no (or at least much less) inflammatory activation in patients with ED secondary to hormonal, psychological, or neurological abnormalities, which is currently unknown. Secondly, the level of these markers may discriminate men with ED who are also affected by subclinical CAD.4 For both purposes, recognition of appropriate cut-offs is essential.
