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Early onset erectile dysfunction is usually not associated with abnormal cavernosal arterial Inflow


Endothelial dysfunction, a marker for atherosclerosis and hence arterial disease, has recently been proffered as the main offender within the vascular system to predict not only the future onset of erectile dysfunction (ED) but also as the main cause of the ED. To glean more insight into whether arterial disease is indeed operative during the early onset of ED, we reviewed the duplex ultrasound scans of 23 men with ED who were younger than 50 years of age. Depending on the criteria used for abnormal arterial responses, it was determined in this cohort of young men that there was only a 4–13% incidence of abnormal arterial responses. These observations suggest that the penile arterial system does not appear to be primarily involved in the etiology of the majority cases of ED that occur in young men.


It seems inevitable that most men, if they live long enough, will develop some form of erectile dysfunction (ED). The validity of this statement emanates from the data extracted from the Massachusetts Male Aging Study (MMAS) where 40% of men in their 40s had some form of ED, with this prevalence increasing by about 10% per decade such by the time a man is in his 60s or 70s, he has about a 60% or 70% chance, respectively, of having ED.1 Although men <40 years of age were not included in this MMAS survey, logic would dictate that the ED, at least in some of these men who presented with ED in their 40s, developed their condition sometime earlier than 40 years of age.

The initial and most common recognizable change in erectile function, which most men experience, is that they are unable to maintain or sustain their erection as long as they previously did. When sophisticated testing is performed in men with ED in order to ascertain the etiology of their ED, the majority of these men are found to have a physiological rather than a psychological reason for their ED.2

More specifically, it is the vascular system that is found to be at fault in most of these men with ED.3, 4, 5 The vascular system of the penis comprises both the arterial vessels, which deliver the blood to the corporal sinusoids, and the corporal smooth muscle mass that is responsible for trapping the blood emanating from the arterial system within the corporal sinusoids, thereby preventing the corporal blood from leaking out of the penis; that is, the process of veno-occlusion.3, 6 Data from studies conducted about three decades ago suggested that regardless of age, the most common problem with the vascular system of the penis in men with ED was not related to the arterial inflow but was due to cavernosal veno-occlusive dysfunction (CVOD) or venous leakage.5, 7, 8 As the veno-occlusive mechanism of the penis is totally dependent on the integrity of the corporal smooth muscle, the presence of CVOD in a patient tends to suggest some type of abnormality with this smooth muscle mass.3

Despite these early observations that CVOD or venous leakage is very common in men with ED regardless of their age, the last decade has seen a multitude of reports linking endothelial dysfunction, a marker of subsequent atherosclerosis and hence arterial disease, as the major cause of ED. These studies have even suggested that the onset of ED can presage the onset of atherosclerosis, specifically coronary artery disease9, 10 by about 3 years11 and, as a result, patients who present with ED should be considered having their cardiovascular system evaluated for the presence of subclinical coronary artery disease.12 If this presumptive association between endothelial dysfunction, arterial disease and ED is indeed correct, it would be expected that those men who present with ED at an early age should have some evidence of penile arterial dysfunction, specifically either abnormal cavernosal arterial dilatation and/or decreased cavernosal blood flow.13

In order to glean some preliminary insight into whether early onset ED may be associated with penile arterial dysfunction, we retrospectively reviewed the charts of the last 23 patients of ours who were between the ages of 18 and 49 and who had a duplex scan of the penis performed as part of an evaluation for their ED.

Materials and methods

The charts of all patients who were <50 years of age and who underwent a duplex scan of the penis during their routine evaluation for ED from January 2010 to July 2012 were retrospectively reviewed. Patients who were diagnosed with low testosterone or Peyronie’s disease, which was either found on physical exam or visualized to have this entity during their duplex scan, were excluded from this analysis, leaving 23 patients eligible for review. All 23 patients had their duplex scan performed because at our institution it is the standard practice of care for those patients who fail to respond appropriately to both oral phosphodiesterase inhibitors and then an intracorporeal injection of vasoactive substances during their work up for a complaint of ED.3, 14 However, not all patients with ED who were <50 years of age and failed to respond to both an oral PDE5 inhibitor as well as an intracorporeal injection had a duplex scan performed, and therefore these 23 patients represent a selected group.

The duplex ultrasound scan (Acuson 128XP, Siemens, Mountain View, CA, USA) was performed by one person (RS). Before giving an intracorporeal injection, the patient was placed in the supine position, and in the flaccid state both cavernosal arteries were identified and the anteroposterior diameter of each lumen was measured. An intra-cavernosal injection of the vasoactive medication was then administered and the patient was placed in the standing position for a period of 5–10 min in order to attain maximum tumescence. After this time period, the patient was then placed back in the supine position and the diameters of the cavernosal arteries were again measured. Color Doppler was then used to identify the course of the cavernosal arteries and for accurate placement of the Doppler cursor. A spectral Doppler was then performed and an attempt was made to perform the spectral Doppler at an angle <60°. Beam steering was used with the linear transducer in order to minimize the angle. Angle-corrected peak systolic velocities (PSV) were then obtained. Two to three samples were obtained for each cavernosal artery. In addition to peak velocities, acceleration time (the time from the initiation of systole to peak velocity) was measured as an indicator for arterial stenosis. The presence of any forward disastolic flow was empirically considered an indicator of possible venous leakage. The intracorporeal injection that each of the patients received was either composed of 30–45 mcg prostaglandin E1 only, or a combination of prostaglandin E1, papaverine, phentolamine, with and without atropine. Bilateral arterial inflow disease was defined by a PSV of 25 cm s−1, according to the recommendations of Lue et al.15 Fifteen of these 23 patients had also undergone a dynamic infusion cavernosometry (DIC) as has been previously described5 in which venous leakage in this current review of cases was determined to be present if the leak rate was found to be 17 cc min−1 to maintain the intracorporeal pressure slightly above the presumed mean arterial pressure (usually100 mm Hg).


The average age of the 23 patients in this case series was 33 years (Table 1), and all complained of ED for >6 months at the time of their clinical presentation. If arterial disease is to be defined as a PSV 25 cm s−1 in both cavernosal arteries,15 only 1 of these 23 patients (4%) met that cutoff and he was 46 years of age. One additional patient, 32 years of age, had one of the two cavernosal arteries with a PSV of 23 cm s−1 whereas the contralateral cavernosal artery registered 33 cm −1s. If arterial disease, however, is defined as a PSV of 35 cm s−1 in both cavernosal vessels, then 3 of the 23 (13%) meet this criterion of arteriolar disease.

Table 1 Clinical characteristics and findings of study population

Following the intracavernosal injection of a vasoactive substance, only 2 of the 23 patients failed to have a 50% dilatation of both of their cavernosal arteries. In one of these patients, there was normal flow in both vessels whereas in the other patient, the PSVs (cm s−1) were 30 and 27 in each of his cavernosal arteries. There were three other patients who demonstrated a 50% dilatation in one of their two cavernosal arteries and in all three of these patients, they had normal bilateral PSVs. All 23 patients, regardless of their PSV, had normal acceleration times.

Fifteen of the 23 patients underwent a DIC. Of these 15 patients, 9 demonstrated the presence of venous leakage although only one of these 9 with a positive DIC test had forward diastolic flow on duplex scan. Another one of these 9 patients who was 46 years of age had<25 cm s−1 of peak flow velocities in both cavernosal arteries, suggesting that his penile vasculopathy included both defective arterial inflow as well as the presence of CVOD.


This review of these 23 patients who were <50 years of age and who presented to our institution with ED within the last 2 years was undertaken because of the multitude of recent reports that seem to support the contention that endothelial dysfunction, known as a surrogate marker for arterial disease and hence a precursor for the development of atherosclerosis, is responsible for the majority of cases of ED.16 To us, these reports linking ED with endothelial dysfunction and hence arterial disease seemed to be at odds not only with previous observations that showed that it was CVOD,5, 7, 8 and not defective arterial inflow that was responsible for the majority of cases of ED, but also with what we were hearing at the bedside. When the majority of all our patients are asked to describe exactly what they actually experience when they first recognized that they were having problems with their erectile function, it is almost universal for them to state that it was difficulty in maintaining or sustaining their erection once the erection occurred. This inability to maintain an erection once the erection has occurred is clinically very suggestive of CVOD rather than an arterial inflow issue.

If we were to assume for argument’s sake that it was the arterial system and not CVOD that was the major culprit in the etiology of ED as has been promulgated by many, it stands to reason that when young men first develop ED, there should be some evidence that the arterial system may be impacted. The findings in our 23 patients with ED who were <50 years of age seem to contradict the assumption of those reports that state it is the arterial system that is at fault in the majority of patients who present with ED. Indeed, based on our duplex scan data, we could only identify poor arterial dilatation in 2 of these 23 patients and bilateral restriction in arterial flow, as defined by Lue et al.15 in 1 of 23 patients. These findings parallel in principle those of Lue et al.15 in which 87 men <40 years of age were reported to have by duplex scan ‘better’ arterial responses than those patients >60 years of age. The conclusion from these observations is that the arterial system does not seem to be severely impacted in young men who present with ED, and as such does not appear to be the primary cause of the ED in this age group.

The failure of each one of our 23 patients to respond to an intracorporeal injection of a vasoactive medication during their initial work-up suggested that a possible vascular etiology, that is, poor arterial inflow and/or poor veno-occlusion was most likely the cause of their ED. The fact that 6 of the 15 patients who then underwent DIC showed normal veno-occlusion suggests some of the patients may have had a non-vascular etiology as the cause of their ED. On the other hand, the fact that 9 of the 15 who had a DIC showed a significant venous leakage, suggests that if there is going to be a vascular component in this age group, it is most likely going to reside on the veno-occlusive side.

The observation that venous leakage may be the major cause of ED in both young and old men begs the question as to why this occurs.4 Our theory is that this decrease in the smooth muscle content that leads to venous leakage is simply an aging-related issue, which will ultimately occur in every man if they live long enough.17 However, the initiation of the decrease and the rapidity to which this decrease in corporal smooth muscle content occurs is most likely genetically predetermined for each individual. From both animal and human studies, it has been suggested that it only takes about a 15% decrease in the function of the smooth muscle content within the corpora before clinically significant venous leakage occurs.18 As an erection is a dynamic balance between arterial inflow and venous outflow, the individual with perfect arterial inflow will only become symptomatic from venous leakage if and when the content of the corporal smooth muscle reaches that 15% decline.18 On the other hand, the individual who develops a risk factor for arterial disease, for example, diabetes mellitus or hypertension, where there may now be a diminution in arterial inflow,19 the onset of clinically symptomatic venous leakage that is, the inability to maintain an erection, may occur earlier than before that 15% decrease in corporal smooth content is reached. This may be one of a possible number of reasons why men with certain risk factors for arterial disease, such as diabetes may develop symptomatic ED earlier than age-matched controls.

Another obvious question that arises from the observations in these 23 young men with ED is what does such a young individual experience during that time before reaching that 15% decline in his corporal smooth muscle content. We submit that what these men are experiencing is an aging-related increase in their refractory period. A man’s refractory period is most likely determined by the function of their corporal smooth muscle mass and data to support this concept emanates from two placebo-controlled, randomized studies where young men in their 30s with normal erectile function, as measured by the International Index of Erectile Function scores, were given oral sildenafil.20, 21 These men reported that although the drug did not enhance their ability to attain or maintain an erection, what it did do was decrease their refractory period. It is known that all the PDE5 inhibitors cause corporal smooth muscle relaxation so it is easy to assume that the decrease in the refractory period that these patients experienced was the result of the effect of the drug enhancing the relaxation of the corporal smooth muscle.

On the basis of the findings of this present case series, the current assumption that endothelial dysfunction is the major cause of ED requires some re-evaluation. It is known that most of the published ED studies have been populated with men >50 years of age, which is the time period when most men begin to develop various aging-related diseases, such as hypertension and/or diabetes mellitus. These latter two disorders are not only associated with the development of ED but they are also associated with the presence of atherosclerosis including coronary artery disease, as well as endothelial dysfunction. Therefore, the contamination of impotence studies with these hypertensive and diabetic patients will obviously tend to skew toward a strong association between endothelial dysfunction, the surrogate marker for arterial disease, and ED. As a result, these studies involving men >50 years of age may unwittingly mask the true role of the corporal smooth muscle mass in the onset of ED, which physiologically begins to occur much, much younger than 50 years of age.


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Correspondence to J Rajfer.

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Rajfer, J., Valeriano, J. & Sinow, R. Early onset erectile dysfunction is usually not associated with abnormal cavernosal arterial Inflow. Int J Impot Res 25, 217–220 (2013).

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  • cavernosal artery
  • duplex scan
  • erectile dysfunction
  • peak systolic velocity
  • venous leak

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