|Year : 2017 | Volume
| Issue : 4 | Page : 210-216
Colour doppler sonography of the penis in the evaluation of erectile dysfunction: Our experience in Abuja, Nigeria
Joshua Oluwafemi Aiyekomogbon1, Joseph Bako Igashi2, Reuben Omokafe Lawan3, Muftau Jimoh Bioku4, Musa Ameadaji3
1 Department of Radiology, College of Health Sciences, University of Abuja, Abuja, Nigeria
2 Department of Radiology, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria
3 Department of Radiology, Federal Medical Centre, Abuja, Nigeria
4 Department of Surgery, Federal Medical Centre, Abuja, Nigeria
|Date of Web Publication||18-Jan-2018|
Dr. Joshua Oluwafemi Aiyekomogbon
Department of Radiology, College of Health Sciences, University of Abuja, Abuja
Source of Support: None, Conflict of Interest: None
Background: Erectile dysfunction (ED) is an inability to achieve and maintain erectile rigidity sufficient for satisfactory sexual performance. It is either organic or psychogenic in origin. This study was aimed at establishing vasculogenic causes among patients being evaluated for ED using triplex Doppler Ultrasound. Patients and Methods: This study was conducted at the Department of Radiology, Federal Medical Centre, Abuja, Nigeria from July 2015 to January 2017. Thirty-five consecutive patients with the clinical diagnosis of ED were evaluated with colour Doppler ultrasound scan using a high-frequency linear transducer. The penile scan was done before and after intracavernosal injection of 10–20 μg prostaglandin E1. The waveforms of cavernosal arteries (CAs) were obtained alternately using angle of inclination ≤60°. The spectral waveforms and peak systolic velocities (PSV) of the CA were documented at 5-min intervals, from 5 to 50 min. Results: PSV of CA varied between 19.5 and 104.4 cm/s (mean: 42.4 ± 17.6) among the entire patients and between 19.5 and 24.7 cm/s (mean: 21.9 ± 1.7) among patients with arteriogenic ED. Arteriogenic ED was found in six patients (17%), while venogenic ED was observed in ten patients, which constituted 29% of the entire participants. None had combined arteriogenic and venogenic ED. Peyronie's disease was observed in seven patients, and none of these had vasculogenic ED. Conclusion: About 46% of the patients had vasculogenic ED. It is therefore imperative that patients with ED benefit from this safe, cheap and non-ionising diagnostic modality before initiating therapy as ED treatment is cause specific.
Keywords: Doppler ultrasound, erectile dysfunction, prostaglandin E1
|How to cite this article:|
Aiyekomogbon JO, Igashi JB, Lawan RO, Bioku MJ, Ameadaji M. Colour doppler sonography of the penis in the evaluation of erectile dysfunction: Our experience in Abuja, Nigeria. Niger Postgrad Med J 2017;24:210-6
|How to cite this URL:|
Aiyekomogbon JO, Igashi JB, Lawan RO, Bioku MJ, Ameadaji M. Colour doppler sonography of the penis in the evaluation of erectile dysfunction: Our experience in Abuja, Nigeria. Niger Postgrad Med J [serial online] 2017 [cited 2018 Apr 23];24:210-6. Available from: http://www.npmj.org/text.asp?2017/24/4/210/223462
| Introduction|| |
Erectile dysfunction (ED) is defined as consistent inability to achieve and maintain erectile rigidity sufficient for satisfactory sexual performance., A complex mechanism is required to attain penile erection, involving synchronous and coordinated interaction of nervous, arterial, venous and sinusoidal systems. A disruption of any of these components usually results in ED. There are three corporal bodies in the penis; two dorsally placed corpora cavernosa (CC) and a single ventrally placed corpus spongiosum (CS), which contains the urethra. The three are enclosed in a bulk fascia, and the two CC are enclosed by tunica albuginea. The two CC are separated by a septum which has fenestrations that allow communication between the corpora bodies., The arterial supply of the penis is from the internal pudendal arteries (IPA), which are anterior branches of the internal iliac arteries (IIA). Each IPA gives off the penile artery proper which branches into a cavernosal artery (CA) and a dorsal artery (DA) at the base of the penis. The CA primarily supplies the CC, while DA supplies the skin and the glans penis. The venous drainage of the CC is by emissary veins, which drains into the dorsal, crural and cavernosal veins.,
When the penis is flaccid, its smooth muscle is in a tonic state, the cavernous sinusoids are collapsed, and the cavernous venules are open., The emissary veins drain the sinusoidal spaces and blood circulates into the dorsal veins. There is attendant high resistance of arterial blood flow into the penis., Erection starts when an autonomic neurogenic impulse relaxes the cavernosal arterioles and sinusoidal spaces. Arterial inflow increases into the penis as cavernous arteries dilate. This is accompanied by relaxation of the smooth muscle of the CC with expansion and elongation of the cavernous sinusoids as they fill with blood. The venules and emissary veins are compressed against the taut tunica albuginea which ultimately decreases, stops or even reverses the venous flow. This veno-occlusive mechanism maintains sinusoidal distension and rigid erection. A defect in these mechanisms ultimately leads to vasculogenic ED.
ED is either organic, psychogenic or both in origin. Organic causes are found in 80%–90% of patients, and include vasculogenic, neurogenic, anatomic and endocrine causes. Diabetes mellitus (DM), coronary artery disease and systemic hypertension are systemic problems that could affect penile erection and should be ruled-out clinically. Arteriogenic ED is either due to impaired cavernosal smooth muscle relaxation or arterial inflow stenosis, which invariably leads to compromised filling of the corpora bodies. In the case of corpora veno-occlusive dysfunction or venous leak, the required intracavernosal pressure is not sustainable. Either point of failure may results in vasculogenic ED. Atherosclerotic disease of the IIA or IPA may limit the increase in blood flow required to fill the CC and achieve an erection. The sole aim of colour Doppler evaluation in ED is to exclude vasculogenic causes which can be managed by medical and/or surgical means. Societal problems such as insurgency, high crime rates, drug addiction among youths are direct consequences of single parenthood as a result of divorce due to ED, and this can be prevented in part by this study, as most vascular causes are treatable.
Morphological abnormalities of the penis such as Peyronie's disease and penile fracture are also possible causes of ED. These are amenable to sonographic diagnosis. Arteriography with selective internal iliac angiography is the gold standard imaging modality used in the evaluation of arteriogenic ED. It is, however, invasive and prone to complications, hence the preference for the Doppler sonographic assessment, which is the thrust of this study.
In the study conducted by Benson and Vickers, the parameters that connote arteriogenic ED includes, a <60% increase in the diameter of CA and PSV <25 cm/s following cavernosal injection of pharmacologic agents such as papaverine, prostaglandin E1(PGE1), phentolamine or their combination (TRIMIX) to induce erection. TRIMIX (Papaverine 4.4 mg, phentolamine 0.15 mg and PG-E1 1.5 μg in a 0.25 ml) have been used to minimise the possibility of drug-induced priapism, which may occur in 2%–3% of the patients. When the arterial system is normal that is, CA-PSV ≥25 cm/s [Figure 1], the Doppler findings that suggest venogenic ED (venous leak) are persistent end-diastolic flow of CA >5 cm/s throughout all phases [Figure 2] and demonstration of persistent flow in the dorsal vein.,, The demonstration of diastolic flow reversal after an injection of pharmacologic agent is a reliable indicator of venous competence.,, This study was aimed at using sonography to establish the proportion of ED patients with vasculogenic abnormalities, which could be arteriogenic, venogenic or both. It was also aimed at establishing possible correlation between vasculogenic ED and structural morphological problems of the penis such as penile fracture or Peyronie's disease.
|Figure 1: Normal response to prostaglandin E1 of one of the patients showing normal peak systolic velocities recording of left cavernosal artery (50 cm/s) at 35 min with the spectral waveform showing holodiastolic flow reversal, features connoting normalcy (original image)|
Click here to view
|Figure 2: Veno-occlusive insufficiency. The spectral Doppler waveform of the right cavernosal artery at 50 min post-injection of prostaglandin E1 demonstrates high peak systolic velocity (35.27 cm/s), which excludes arterial insufficiency as a cause of erectile dysfunction in this patient. However, a persistent diastolic flow velocity of more than 6.05 cm/s is noted and is diagnostic of venous leak (original image)|
Click here to view
| Patients and Methods|| |
Approval for the study was obtained from the Health Research ethics committee of Federal Medical Centre, Abuja on the 20 June 2017 (PROTOCOL NUMBER: FMCABJ/HREC/2017/003). The study was conducted at the Department of Radiology Federal Medical Centre, Abuja, Nigeria. Thirty-five consecutive patients with clinical diagnosis of ED referred by urologist were evaluated using triplex Doppler sonography between July 2015 and January 2017. Those smoking cigarette among them were instructed to stop 72 h before the study as smoking causes penile vasospasm and increased sympathetic nervous system tone thus affecting penile erection. The procedure was explained in detail to the patients at booking and on the examination day. A drug (antihypertensive, anti-epileptic, etc.) and cardiac histories were also inquired before the study. After obtaining informed consent, they were evaluated with colour Doppler ultrasound scan (Mindray DC 7, 2014 China) using high-frequency (5.0–12.5 MHz) linear transducer in a quiet and comfortable room to ensure patients' privacy and cooperation. The study was performed with patients in supine position and penis in normal anatomical position. After application of ultrasound coupling gel to the ventral surface of the penis, longitudinal and transverse penile scans were done on both grey scale and colour Doppler studies before and after injection of PGE1 with the probe on the ventral surface of the penis. Pre-injection scan was to assess the echo pattern of the penis in the flaccid state for the presence of plaques, fibrosis or tunica albuginea defect/fracture. The diameter and peak systolic velocity (PSV) of the CAs were also assessed before intracavernosal injection.
About 10–20 μg of PGE1 was injected into one of the CC laterally at the distal two-third of the penis with a 30-gauge needle under aseptic condition. The variation in the doses of PGE1 was based on the patient's age; smaller doses were used for the younger ones while higher doses for the elderly. One-sided injection was also considered because the two CC are separated by a septum which has fenestrations that allow communication between the corpora bodies., The waveforms were obtained alternately using an angle of inclination equal or <60° when visualisation of CA was optimal. Immediately after intracavernosal injection (ICI), the longitudinal diameter of each CA, spectral waveform and PSVs of the CAs were documented each at 5 min intervals, from 5 to 30 min (5, 10, 15, 20, 25 and 30 min). The study was terminated at 30 min for most of the patients except for few that had persistent diastolic flow (venogenic ED/venous leak), who had their studies extended to about 50 min. Owing to the variation in the PSV of the CA at different locations across the penile shaft, PSV being higher proximally, CA was consistently interrogated for spectral waveform assessment and measurement at the junction of the proximal third and distal two-third of the penile shaft, where the artery bends. The PSV of CA was determined electronically with the software package of the ultrasound machine [Figure 1], [Figure 2], [Figure 3]. Bilateral CA diameters and PSVs were measured in both flaccid and post-ICI states [Figure 4] and [Figure 5]. The patients were kept in the observation room for 3 h after the procedure to check for the possibility of complications such as priapism, and the urologist was informed, but none had this complication. Furthermore, none of the patients had hematoma at the injection site, and no ecchymosis was observed in any of them.
|Figure 3: (a) Arteriogenic erectile dysfunction: recording of spectral Doppler waveform of the right cavernosal artery after injection of prostaglandin E1 demonstrates persistent low peak systolic velocity of the cavernosal artery (21.07 cm/s) (original image) (b) Arteriogenic erectile dysfunction: recording of spectral Doppler waveform of the left cavernosal artery of the same patient as in 3a after injection of prostaglandin E1 demonstrates persistent low peak systolic velocity of the cavernosal artery (22.06 cm/s) (original image)|
Click here to view
|Figure 4: Diameter of the right and left cavernosal arteries before intracavernosal injection of prostaglandin E1, measuring 0.1 cm on either side (original image)|
Click here to view
|Figure 5: Diameter of the cavernosal artery following intracavernosal injection of prostaglandin E1 of the same patient as in figure 4 showing 50% increase at 5 min post-injection. Note the distension of the cavernosal sinusoids at this time (original image)|
Click here to view
Approval for the study was obtained from the Health Research ethics committee of Federal Medical Centre, Abuja on the 20 June 2017 (PROTOCOL NUMBER: FMCABJ/HREC/2017/003). Anonymity was maintained on all the information obtained, and the patients had choice to deny consent or opt out of the study at any stage without necessarily affecting the quality of care obtained in the hospital.
The results were reported as mean ± (standard deviation). The collected data were analysed using Statistical Package for the Social Sciences (IBM SPSS) version 23 (United States). All test of significance were two-tailed, and P < 0.05 was considered statistically significant.
| Results|| |
Thirty-five consecutive patients with clinical diagnosis of ED between 30 and 66 years (mean age, 50.46 ± 9.22 years) presented for this study. Four were in their fourth decade; 13 each in fifth and sixth decades and only five were in seventh decade. The mean PSV of CA on the right and left sides, respectively, were 42.88 ± 18.79 cm/s and 41.96 ± 16.47 cm/s. Paired samples correlation and paired samples test showed no significant differences between the PSVs of the right and left CA [Table 1] and [Table 2]. Hence, the PSV of the right and left were analysed together. ED of organic origin was suspected clinically in four patients; one with DM and remaining three with Peyronie's disease.
|Table 1: Means and standard deviations of the right and left cavernosal arteries peak systolic velocities|
Click here to view
|Table 2: Paired samples test of right and left cavernosal arteries peak systolic velocities|
Click here to view
The measured PSV varied post-injection of PGE1 between 19.5 and 104.4 cm/s among the patients [Table 3] and between 19.5 and 24.7 cm/s among patients with arteriogenic ED [Table 4]. Abnormal response to PGE1(arteriogenic ED) was found in six (17%) of the patients [Figure 3]. No significant discrepancies were noted between right and left CA PSV among the entire patients (P = 0.481) and among the patients with arteriogenic ED (P = 0.656). The mean PSV of CA among the entire patients was 42.42 ± 17.55 cm/s [Table 3], while mean PSV among the patients with arteriogenic ED was 21.66 ± 1.40 cm/s [Table 5]. Persistent diastolic flow in CA after injection of PGE1 and dorsal vein peak velocity >5 cm/s, both being consistent with venogenic ED, were found in ten patients, which constitutes 29% of the patients [Figure 2]. No patient had combined arteriogenic and venogenic ED. Arteriogenic ED had no direct relationship with age [Table 5], but the PSV of the entire patients had a strong positive relationship with age, with P < 0.0001 [Table 6]. The graphical representation of the relationship between age and PSV of the patients is shown in [Figure 6]. The highest PSV of CA was found in patients <30 years of age, while the lowest PSV was found in patients above 65 years of age.
|Figure 6: Graphical representation of the relationship between age and peak systolic velocities of cavernosal artery (original image)|
Click here to view
|Table 3: Frequency distribution of the entire patients with the respective cavernosal arteries peak systolic velocities|
Click here to view
|Table 4: Mean peak systolic velocities of the right and left cavernosal artery among patients with arteriogenic erectile dysfunction descriptive statistics|
Click here to view
|Table 5: Relationship between age (years) and peak systolic velocities of cavernosal arteries (cm/s) among patients with arteriogenic erectile dysfunction (ANOVA)|
Click here to view
|Table 6: Relationship between age and peak systolic velocities of the cavernosal arteries (cm/s) among the entire participants (ANOVA)|
Click here to view
Grey scale sonography showed dense cavernosal calcifications with posterior acoustic shadows, features consistent with Peyronie's disease in seven patients [Figure 7]. None of the seven patients had arteriogenic or venogenic ED. The only patient with DM, aged 60 years had normal CA PSV (68.2 cm/s), and no persistent diastolic flow was observed. He, however, had CA wall and parenchymal calcifications. There was no case of penile fracture among the research participants. None of the patients had persistent painful erection (priapism) following intracavernosal injection of PGE1. The longest duration of erection was 2 h, found in one patient and later reverted back to flaccid state at home. There were no anatomical penile arterial variants seen among the research participants.
|Figure 7: Peyronie's disease: Grey scale ultrasound image of the corporal cavernosa showing a calcific focus with posterior acoustic shadow in the left corpora cavernosa before injection of prostaglandin E1 (original image)|
Click here to view
| Discussion|| |
Grey scale and colour Doppler sonographic penile evaluations are indicated in cases of ED to establish vasculogenic and morphological causes.,,, From previous studies, it was found that PSV of CA <25 cm/s post-ICI of active pharmacologic agent (s) is consistent with arteriogenic ED, while persistent end diastolic flow >5 cm/s of CA post-ICI and persistent dorsal vein flow are diagnostic of venogenic ED.,,,,,,,, Secondary diagnostic criteria of arteriogenic ED also exist and these include, asymmetry of >10 cm/s between PSV of right and left CA, focal stenosis in the CA and retrograde arterial flow. These secondary criteria are used when PSV of CA is borderline. CAdilatation >60% post-ICI of active pharmacologic agent (s) did not correlate with the results of angiography by many authors as it is difficult to accurately determine the diameter of the small vessel. Consequent to this, no correlation was made with changes in the diameter of CA in the present study, but PSV of CA was used instead.
Sixteen of the patients in the present study (46%) had ED of vasculogenic origin; 29% venogenic and 17% arteriogenic which affirmed the observation of Quam et al. where a good number of their patients had ED of vascular origin, hence the need for ultrasound in the evaluation of ED. Similarly, Sen et al. and Roy et al. in their respective studies observed that 22.5% and 29%, respectively, had arteriogenic ED while it was 17% in the index study. In the index study also, none of our patients had secondary criteria for diagnosis of arteriogenic ED. Majority of the patients in the index study ranged between 41 and 66 years, which constitutes 88.6%, while only four patients (11.4%) were <35 years of age. The mean age of patients with arteriogenic ED in the present study was 51.2 ± 12.0 years and the mean CA PSV of the patients was 21.7 ± 1.4 cm/s. Furthermore, the mean age of those with venogenic ED (venous leak) was 54.3 ± 7.8 years. A positive correlation was also established between patients' age and PSV of CA. The highest PSV of CA was found in patients <30 years with a mean PSV of 72.2 cm/s, while the lowest PSV (21.6 cm/s) was found in patients between 66 and 70 years of age. Only one patient aged 32 years had arteriogenic ED, and the youngest with venogenic ED was 44 years of age making it obvious from the findings that vasculogenic ED is age-related and has further reaffirms the previous submissions of other authors that ED is seen commonly in patients above 40 years of age.,,,,,
The advocacy, therefore, is that every patient with ED should have penile sonography before instituting any form of management. Establishing a specific cause is important, particularly in young men because of the frequency of correctable vascular abnormalities. Both arteriogenic and venogenic ED are managed medically and surgically, but the management protocols differ.,,, Differentiating them is, therefore, imperative and that was the thrust of this study. Medical treatment involves the use of oral phosphodiesterase-5 inhibitors (PDE5i). When oral ED therapy fails, intracavernosal injections, intraurethral suppositories, vacuum erection devices and penile prostheses may be implored. Vascular interventional treatment of atherosclerotic disease, zotarolimus-eluting peripheral stents of the IIA and IPA is a treatment option for arteriogenic ED in the presence of a proximal fixed obstruction to arterial flow. The fixed obstruction of either IIA, IPA or both usually lead to poor response to smooth muscle relaxation effects of PDE5i. But for veno-occlusive disease (venous leak), open surgical ligation of the deep dorsal vein and its collaterals is an option with variable success rates. Nearly 88.8% clinical success rate has also been reported with endovascular venous embolisation therapy with histoacryl-lipiodol.
Peyronie's disease is one of the leading causes of vasculogenic ED., Of the seven patients that had Peyronie's disease in the present study, none of them had arteriogenic or venogenic ED. This may be because the fibrotic plaques and calcific changes of the tunica albuginea, and CC were not sufficiently severe enough to affect the vascular supply of the corporal bodies. Furthermore, the only patient with DM in the index study had normal CA PSV of 68.2 cm/s and had no venous leak. Although he had CA wall calcification, the aetiology of ED in him may be psychogenic or autonomic in origin. None of the patients had anatomical penile arterial variants such as communications among the cavernosal, dorsal and spongiosal arteries, duplication of CA or cross communication between right and left CAs. Furthermore, shunt vessels which course from the CS into the corpus cavernosum is another variant and rarely, collaterals from the urethral arteries may also be seen., These were particularly sought for because they are known to affect the results of Duplex sonographic evaluation. Although these anatomical variations do not necessarily cause arteriogenic ED, they may cause inaccurate interpretation if they are not appreciated. For instance, PSV of CA may be significantly lower in men with a full-erection response if arterial collateral communications are present.,
False-positive venogenic ED was observed in the present study in anxious patients as anxiety during a penile ultrasound examination increases sympathetic drive which results in inadequate relaxation of sinusoidal smooth muscles and consequent failure of veno-occlusive mechanism. This was circumvented by calming down affected patients in a relaxed and isolated room where opposite gender were excused and the study extended to an hour so as to authenticate the features of venous leak. Additional intracavernosal injection of alpha-adrenergic agent such as phentolamine 2 mg was also considered as it blocks sympathetic drive and helps avoid the false-positive diagnosis of venous leak. This was not available but the initial method was effective.
| Conclusion|| |
Vasculogenic causes of ED have been established using duplex Doppler sonography among the patients that presented with ED. About 46% of them had vasculogenic ED; 17% arteriogenic and 29% venogenic. This has further added to the existing literature, the relevance of duplex Doppler sonographic evaluation of ED. It is, therefore, advocated that patients with ED should benefit from it before instituting therapy to avert treatment failure, relapse and unwarranted sequelae of some of the treatment protocols.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Golijanin D, Singer E, Davis R, Bhatt S, Seftel A, Dogra V, et al.
Doppler evaluation of erectile dysfunction – Part 1. Int J Impot Res 2007;19:37-42.
Clifford A, Toppo JN. Role of penile color Doppler in the evaluation of erectile dysfunction. Indian J Radiol Imaging 2006;16:891-6. [Full text]
Kim SH, Paick JS, Lee SE, Choi BI, Yeon KM, Han MC, et al.
Doppler sonography of deep cavernosal artery of the penis: Variation of peak systolic velocity according to sampling location. J Ultrasound Med 1994;13:591-4.
Pozniak AM, Lee TT. Doppler imaging of the penis. In: Allan P, Dubbins PA, McDicken WN, Pozniac AM, editors. Clinical Doppler Ultrasound. 2nd ed. Philadelphia, USA: Churchill Livingstone; 2006. p. 251-66.
Aboseif SR, Lue TF. Hemodynamics of penile erection. Urol Clin North Am 1988;15:1-7.
Lue TF. Erectile dysfunction. N
Engl J Med 2000;342:1802-13.
Kim ED, Owen RC, White GS, Elkelany OO, Rahnema CD. Endovascular treatment of vasculogenic erectile dysfunction. Asian J Androl 2015;17:40-3.
] [Full text]
Benson CB, Vickers MA. Sexual impotence caused by vascular disease: Diagnosis with duplex sonography. AJR Am J Roentgenol 1989;153:1149-53.
Paushter DM. Role of duplex sonography in the evaluation of sexual impotence. AJR Am J Roentgenol 1989;153:1161-3.
Quam JP, King BF, James EM, Lewis RW, Brakke DM, Ilstrup DM, et al.
Duplex and color Doppler sonographic evaluation of vasculogenic impotence. AJR Am J Roentgenol 1989;153:1141-7.
Biebel MJ, Burnett AL, Sadeghi-Nejad H. Male sexual function and smoking. Int Soc Sex Med 2016;4:366-75.
Meuleman EJ, Bemelmans BL, van Asten WN, Doesburg WH, Skotnicki SH, Debruyne FM, et al.
Assessment of penile blood flow by duplex ultrasonography in 44 men with normal erectile potency in different phases of erection. J Urol 1992;147:51-6.
Sen J, Godara R, Singh R, Airon RK. Colour Doppler sonography of flaccid penis in evaluation of erectile dysfunction. Asian J Surg 2007;30:122-5.
Roy C, Saussine C, Tuchmann C, Castel E, Lang H, Jacqmin D, et al.
Duplex Doppler sonography of the flaccid penis: Potential role in the evaluation of impotence. J Clin Ultrasound 2000;28:290-4.
Hatzimouratidis K, Eardley I, Giuliano F, Hatzichristou D, Moncada I, Salonia A, et al
. Guidelines on male sexual dysfunction: erectile dysfunction and Premature ejaculation. Eur Urol 2012;62: 543-52.
Rogers JH, Goldstein I, Kandzari DE, Köhler TS, Stinis CT, Wagner PJ, et al.
Zotarolimus-eluting peripheral stents for the treatment of erectile dysfunction in subjects with suboptimal response to phosphodiesterase-5 inhibitors. J Am Coll Cardiol 2012;60:2618-27.
Katzenwadel A, Popken G, Wetterauer U. Penile venous surgery for cavernosal venous leakage: Long-term results and retrospective studies. Urol Int 1993;50:71-6.
Aschenbach R, Steiner T, Kerl MJ, Zangos S, Basche S, Vogl TJ, et al.
Endovascular embolisation therapy in men with erectile impotence due to veno-occlusive dysfunction. Eur J Radiol 2013;82:504-7.
Patel DV, Halls J, Patel U. Investigation of erectile dysfunction. Br J Radiol 2012;85 Spec No 1:S69-78.
Mancini M, Bartolini M, Maggi M, Innocenti P, Forti G. The presence of arterial anatomical variations can affect the results of duplex sonographic evaluation of penile vessels in impotent patients. J Urol 1996;155:1919-23.
Jarow JP, Pugh VW, Routh WD, Dyer RB. Comparison of penile duplex ultrasonography to pudendal arteriography. Variant penile arterial anatomy affects interpretation of duplex ultrasonography. Invest Radiol 1993;28:806-10.
Aversa A, Rocchietti-March M, Caprio M, Giannini D, Isidori A, Fabbri A, et al.
Anxiety-induced failure in erectile response to intracorporeal prostaglandin-E1 in non-organic male impotence: A new diagnostic approach. Int J Androl 1996;19:307-13.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]