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Mazo EB, Gamidov SI, Iremashvili VV. Does the clinical efficacy of vardenafil correlate with its effect on the endothelial function of cavernosal arteries? A pilot study. BJU Int 2006;98:1054-1058.

This study from Russia addresses an important question, namely whether we can assess who will and who won’t respond to PDE5 inhibitors. Whilst it is easy to give patients oral medication, 30-40% won’t respond and they will be required to take the drug at least six times before becoming treatment failures, incurring expense and exposure to potential side effects. 122 men who attended an ED clinic over a six month period were recruited. All were assessed with detailed history taking, International index of Erectile function (IIEF) questionnaire, physical examination and laboratory tests (glucose, lipids, testosterone) and Doppler USS of the penis after prostaglandin E1 injection. On the basis of the latter, patients were divided into arteriogenic (peak systolic velocity <35cm/s) and veno-occlusive (end diastolic flow >5cm/s) ED. Those with normal values and ED were diagnosed as psychogenic ED.
Post occlusive changes in the diameter of the cavernosal arteries were measured before and then one hour after the administration of 20mg vardenafil. This was achieved by applying a 2cm wide sphygmomanometric cuff around the penis and inflating it until there was no flow in the cavernosal arteries. Occlusion was maintained for 5 minutes. The reactive hyperaemic scans were performed around one minute after removing the cuff.
Whilst there was no statistically significant difference in the percentage increase in cavernosal artery diameter (PICAD) pre vardenafil in those patients who were subsequently shown to be either responders or non responders at follow up, there was a significant difference in PICAD in responders – 76% - and non-responders – 55% - post vardenafil. The relationship was best seen in arteriogenic ED where a PICAD > 50% predicted a positive response to vardenafil with a sensitivity of  95% and specificity of 91%. Post occlusive arterial dilatation is due to NO release from the endothelium. It therefore follows that PDE5 inhibitors by increasing the NO bioactivity, also increase the PICAD and this reflection of endothelial function would correlate with clinical efficacy. This does appear to be the case.  It is obviously considerably easier to simply give a patient a PDE5 inhibitor and see if they respond, however this is one of the few studies that has tried to assess which patients will respond to oral PDE5 inhibitors allowing us to potentially tailor our treatments accordingly in the future.