European Heart Journal Advance Access originally published online on February 13, 2007
European Heart Journal 2007 28(5):643-644; doi:10.1093/eurheartj/ehl532
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Is erectile dysfunction a low-grade systemic inflammatory condition?: reply
Cardiovascular Diseases and Sexual Health Unit
1st Department of Cardiology
Athens Medical School
Hippokration Hospital Athens
Greece
Institute of Cardiology
University of Milan
Centro Cardiologico Monzino
Milan
Italy
Cardiovascular Diseases and Sexual Health Unit
1st Department of Cardiology Athens Medical School
Hippokration Hospital Athens
Greece
Institute of Cardiology
University of Milan
Centro Cardiologico Monzino
Milan
Italy
Cardiovascular Diseases and Sexual Health Unit
1st Department of Cardiology
Athens Medical School
Hippokration Hospital
Athens
Greece
Institute of Cardiology
University of Milan
Centro Cardiologico Monzino
Milan
Italy
Division of Urology and Sexual Medicine
University Vita-Salute
San Raffaele Hospital
Milan
Italy
Cardiovascular Diseases and Sexual Health Unit
1st Department of Cardiology
Athens Medical School
Hippokration Hospital
Athens
Greece
Tel: +30 697 2272727 Fax:+ 30 210 7485039 Email address: cvlachop{at}otenet.gr
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.
Our data showed that fibrinogen level or even better the combination of fibrinogen and inteleukin-6 levels may be of value for excluding (ruling out) ED. However, specific cut-offs that predict the presence (ruling in) of ED are also needed. An ideal marker must conform with basic criteria recently proposed by Vasan,5 such as pathophysiological relevance, high reproducibility of measurements, incremental value over other known predictors, and, finally, ability to monitor and guide therapy. At the moment, there are no sufficient data to support the routine clinical use of any biochemical marker in the evaluation of ED patients. Clearly, further scrutiny is needed and studies providing insights into the potential role of inflammatory and endothelial substances as markers and risk predictors in subjects with ED are welcome. Especially, because ED stands not only for Erectile Dysfunction, but also for Endothelial Dysfunction and Early Detection as well, as was quoted in the accompanying editorial in the Journal.6
References
- Vlachopoulos C, Aznaouridis K, Ioakeimidis N, Rokkas K, Vasiliadou C, Alexopoulos N, Stefanadi E, Askitis A, Stefanadis C. (2006) Unfavourable endothelial and inflammatory state in erectile dysfunction patients with or without coronary artery disease. Eur Heart J 22:2640–2648.
- Montorsi P, Ravagnani PM, Galli S, Rotatori F, Veglia F, Briganti A, Salonia A, Deho F, Rigatti P, Montorsi F, Fiorentini C. (2006) Association between erectile dysfunction and coronary artery disease. Role of coronary clinical presentation and extent of coronary vessels involvement: the COBRA trial. Eur Heart J 22:2632–2639.
- Montorsi F, Briganti A, Salonia A, Rigatti P, Margonato A, Macchi A, Galli S, Ravagnani PM, Montorsi P. (2003) Erectile dysfunction prevalence, time of onset and association with risk factors in 300 consecutive patients with acute chest pain and angiographically documented coronary artery disease. Eur Urol 44:360–365.[CrossRef][Web of Science][Medline]
- Vlachopoulos C, Rokkas K, Ioakeimidis N, Aggeli C, Michaelides A, Roussakis G, Fassoulakis C, Askitis A, Stefanadis C. (2005) Prevalence of asymptomatic coronary artery disease in men with vasculogenic erectile dysfunction: a prospective angiographic study. Eur Urol 48:996–1002.[CrossRef][Web of Science][Medline]
- Vasan RS. (2006) Biomarkers of cardiovascular disease: molecular basis and practical considerations. Circulation 113:2335–2362.
- Jackson G. (2006) Erectile dysfunction: a marker of silent coronary artery disease. Eur Heart J 27:2613–2614.
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