Vasculogenic and Postoperative Neurogenic Impotence

Mikkel Fode, Jens Sønksen, Susanne A. Quallich and Dana A. Ohl

Erectile dysfunction (ED) is defined as the “recurrent or persistent inability of the male to attain and maintain erection of the penis to permit satisfactory sexual intercourse,” according to the 1993 National Institutes of Health Consensus Development Panel on Impotence. It is important to take the patient’s satisfaction into consideration because expectations for sexual performance vary across a patient population. ED is considered to have an organic origin in 90% of cases, and the majority represent vasculogenic and/or neurogenic dysfunction. To understand ED it is necessary to first look at normal erectile and ejaculatory function.

Normal Erectile and Ejaculatory Function

In the flaccid penis, the sympathetic nervous system keeps the smooth muscle fibers of the corpora cavernosa contracted, thus limiting blood flow to the tissue and the volume of blood present in the penis. When sufficient sexual stimulation is present, the parasympathetic system becomes predominant and an erection is initiated through fibers arising from S2–S4. These fibers travel through the pelvic plexus to reach the cavernous nerves that enter the corpora cavernosa to release the neurotransmitters nitric oxide (NO) and acetylcholine (ACh). The course of the nerves makes them vulnerable to injury during pelvic surgery as they pass closely by the bladder, prostate, and the rectum. Both NO and ACh induce the production of cyclic guanosine monophosphate (cGMP) in the penile smooth muscle tissue, which leads to calcium flux and smooth muscle relaxation. As the smooth muscle surrounding the lacunar spaces of the corpora cavernosa relaxes, a 20- to 40-fold increase in blood flow into the tissue is realized.

The arterial blood supply to the penis is from the common iliac tree, via the internal iliac (hypogastric), internal pudendal, and common penile artery branches. The common penile artery divides into the dorsal penile artery and the deep penile artery. The dorsal artery supplies the skin and glans of the penis, and does not normally contribute blood to the erectile process. Unfortunately, this vessel has been used to measure blood flow to the penis with the archaic penile–brachial index test, giving misleading results. The other branch of the common penile artery is the deep penile artery (cavernosal artery, central penile artery) supplying the corpus cavernosum, and it is the true blood supply for the erectile process.

The penile arteries are small, being approximately 1 to 2 mm in diameter. As blood enters the lacunar spaces and the small blood vessels of the penis, a shear-stress mechanism is initiated in the endothelium, which then produces more NO. This reinforces the process and causes a maximal erection. It is mainly the endothelial NO that maintains blood flow after initiation by neural NO. The increased penile blood volume causes an increase in intracavernosal pressure, and this pressure in turn compresses the small venules leading blood away from the penis, resulting in blood trapping. This veno-occlusive mechanism is crucial in maintaining an erection.

As the erection is terminated, two basic mechanisms come into play. First, the basic sympathetic tone again becomes predominant, which means that smooth muscle tissue in the penis is contracted and blood flow to the penis is reduced. At the same time, cGMP is broken down in the penile tissue by phosphodiesterase 5 (PDE5). The breakdown of cGMP is a continual process occurring throughout the erection. With the reduced blood flow and the lack of neural supply of NO, breakdown now exceeds its production, and this contributes to the contraction of the smooth muscle of the corpora cavernosa. This means that the intracavernosal pressure falls and blood flow is directed away from the penis, which returns to the flaccid state.

With sexual stimulation, the coordination of different stimuli can result in climax and ejaculation. Before ejaculation, smooth muscle contractions transport semen from the epididymis through the vas deferens to the prostatic part of the urethra. This process is called seminal emission and is controlled by sympathetic fibers, which originate in the thoracolumbar part of the spinal cord and run by way of the least splanchnic nerve and the sympathetic chain to the inferior mesenteric ganglion. The postganglionic fibers reach the cavernous nerve through the hypogastric nerve and the pelvic plexus. The dorsal nerve of the penis constitutes the afferent limb of the ejaculatory reflex as it receives sensory input from the glans and carries the signal to the spinal cord at levels S2–S4. Here, somatic fibers traveling through the pudendal nerve are caused to fire, which causes rhythmic contractions of pelvic and periurethral muscles. This results in projectile ejaculation. During ejaculation, sympathetic fibers are responsible for closure of the bladder neck, which prevents retrograde ejaculation into the bladder.

Vasculogenic Erectile Dysfunction

If penile blood flow cannot be increased sufficiently to rapidly fill the penis, ED will result. Such a dysfunction is most often caused by atherosclerotic disease with possible endothelial dysfunction. There is a growing body of evidence linking ED to other cardiovascular disease (CVD) and to the metabolic syndrome. Thus ED and cardiovascular disease have been shown to share risk factors, and ED is widely considered a precursor of more serious vascular disease.

The debut of ED is generally noted to occur 2 to 5 years before other cardiovascular events become evident. This temporal relationship was first noted in the Prostate Cancer Prevention Trial in which men were examined yearly for up to 7 years for both ED and the occurrence of CVD. The prospective study showed that men with ED at study entry had a near-doubling of the rate of cardiovascular events including angina, myocardial infarction, and stroke. Men who had incident ED and who came to the hospital during the follow-up period also showed an increased risk of myocardial infarction or angina when compared to men with persistent normal erectile function. Subsequent studies have reported similar findings.

These observations have led to the view that ED represents the first manifestation of a generalized condition and can be used as a marker of future CVD. This means that the occurrence of ED might present an opportunity for early detection and prevention of further cardiovascular morbidity.

Correlation Between Erectile Dysfunction and Cardiovascular Disease

Estimates of the prevalence of ED vary widely depending on the definitions used and the age of the study subjects. The Massachusetts Male Aging Study of men ages 40 to 70 years found an overall prevalence of 52% of men suffering some degree of ED. After adjustment for age, a higher probability of ED was correlated with heart disease, hypertension, and diabetes, and it was inversely correlated with high-density lipoprotein (HDL) cholesterol. Smoking was found to increase the rate of complete ED in men with heart disease and hypertension. A European study by Corona and colleagues estimates the prevalence of moderate to severe ED to be 30% in men aged 40 to 79 years, and it confirmed cardiovascular disease, diabetes, and obesity to be predisposing factors. Likewise, Selvin and coauthors found that in a cross-sectional study of data from 2126 men that the prevalence of ED was increased in men with cardiovascular risk factors, such as hypertension, dyslipidemia, physical inactivity, and smoking. The rate was particularly high in men with a history of cardiovascular disease and in men with diabetes.

Data from the Integrated Healthcare Information Services National Managed Care Benchmark Database (IHCIS) (including 12,825 ED patients) has been used to perform a logistic regression analysis showing that ED patients have a twofold increase in the risk for myocardial infarction overall, with a risk that becomes more pronounced with increasing age. Another study has shown that ED is more common in people with silent coronary artery disease than in people without such disease (33.8% vs. 4.7%; p <.0001). Supporting these findings, a smaller study (N = 40) showed a significantly lower peak penile systolic velocity in ED patients with ischemic heart disease as diagnosed by a stress electrocardiogram (ECG) compared to ED patients with a normal stress test.

In addition to the basic correlation between ED and cardiovascular disease, several studies point to a correlation between the severities of the two conditions. Thus the COBRA (Association between Erectile Dysfunction and Coronary Artery Disease) study (N = 285) showed that ED prevalence was higher in CVD patients with multivessel coronary artery disease than in patients with one-vessel disease. Likewise, Gensini’s scores (a measure of the extent of the atherosclerotic burden) were significantly associated with presence and severity of ED.

A smaller study by Greenstein and coworkers (N = 40) also demonstrated a correlation between ED and the number of angiographically confirmed coronary vessels involved in CVD patients. Patients with one-vessel disease had better erectile function than men with two- or three-vessel disease. Age, diabetes, and hypertension were also correlated with ED in this study. Solomon and coauthors also studied ED in men undergoing coronary angiography (N = 132), and although this group did not find a significant correlation between the number of diseased arteries and the incidence of ED (p = .34), there was an inverse correlation between International Index of Erectile Function (IIEF) score and Gensini score.

A few different theories have been developed to explain the relationship between ED and CVD. Penile blood flow is reduced when the penile arteries are obstructed by artherosclerotic plaques, as in other arteries. However, differences in artery diameter can determine the functional deficit caused by plaque. The penile arteries are only about 1 to 2 mm in diameter. This means that the same degree of plaque burden has a greater effect on the penile artery cross-sectional diameter compared with larger arteries including the coronary (3–4 mm), carotid (5–7 mm), and femoral (6–8 mm) arteries. This might explain why ED tends to occur before other cardiovascular events.

ED and CVD have been linked to endothelial dysfunction because this leads to vasoconstriction and adhesion of platelets and leukocytes to the vascular wall, which all contribute to the development of atherosclerosis. The small artery size, as well as the dependence of the erectile mechanism on endothelial NO, might make the penile tissue very sensitive to endothelial dysfunction, again offering an explanation to the temporal relationship between ED and subsequent CVD. In support of this theory, impaired endothelium-dependent vasodilation (mediated by flow and by direct NO stimulation) has been shown in ED patients without other signs of CVD.

Atherosclerosis and endothelial dysfunction can also cause ED through structural damage within the cavernous tissue. This has been shown in animal models where ischemia has induced fibrosis and smooth muscle atrophy. Such damage would compromise blood trapping during the erectile process, allowing the blood to leave the penile tissue.

In addition to atherosclerosis and endothelial dysfunction, reduced testosterone levels might play a role in ED development in men with metabolic syndrome, and autonomic nerve dysfunction can contribute to the condition in diabetics.

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