Erectile dysfunction (ED) is defined as the recurrent inability, of three months’ duration or longer, to attain or maintain an erection sufficient for satisfactory sexual performance.1,2 It is classified as either psychogenic or organic; organic ED will be addressed here. Up to 80% of cases of organic ED can be further categorized into vascular, neurogenic, anatomic, or hormonal subtypes,2,3 with many affected patients vulnerable to potentially serious comorbidities and risk factors.
In the early 1990s, the NIH reported that nearly 30 million US men were affected by ED.2 However, increased public awareness of the condition, beginning with the availability of effective oral medications in the late 1990s, may have led to increased numbers of reported cases—and of men seeking treatment.
COMMON CONDITION, COMMONLY UNTREATED
According to results from the 2001-2002 National Health and Nutrition Examination Survey,4,5 ED affects about 8% of US men: 4% of those in their 50s, 17% of those in their 60s, 47% of men older than 65, and 78% of men 75 or older. More than 27,000 men from Europe and North and South America (ages 20 to 75) were interviewed for the 2004 Men’s Attitudes to Life Events and Sexuality (MALES) study; findings included an overall prevalence for ED of 16%, and 22% among men from the United States.6 See information regarding self-reported ED prevalence in Table 1.7
An important finding from the MALES study was that only 58% of respondents with self-reported ED had sought medical treatment for the condition.6 Some men may be reluctant to broach the subject with a health care provider because they consider ED a purely sexual problem—whereas the etiology is most commonly vascular.8 Thus, it is important for health care providers to include the sexual history as a routine component in the wellness exam for all patients, and to be aware of the potential presentation in patients with organic ED, appropriate work-up, and physical examination.
Additionally, ED can be a wake-up call for men at risk for cardiovascular disease (CVD); ED occurs at a mean time of five years before a cardiovascular event.9 Therefore, in addition to counseling patients with ED regarding treatment and prevention strategies, clinicians should be prepared to identify and address the risk factors and medical comorbidities associated with ED.
The Mechanisms of Erection
When sexual stimulation occurs, parasympathetic activity increases production of the nucleotide cyclic guanosine monophosphate (cGMP), resulting in relaxation of cavernosal smooth muscle and an influx of blood into the penis. This filling action produces expansion of the sinusoidal spaces in the penis, compressing venous channels and thereby preventing outflow of blood to allow maintenance of a rigid erection.10,11
Nitric oxide is needed for vasodilation of the corpora cavernosa. Inhibition of the enzyme phosphodiesterase type 5 (PDE-5) allows increased production and accumulation of penile cGMP. This results in relaxation of the smooth-muscle cells and improved erectile function.1,10,11
PRESENTATION, HISTORY, AND TYPES OF ORGANIC ED
In the primary care setting, the opportunity to assess for and address erectile function generally presents itself at the patient’s annual wellness visit—but could easily go unmentioned if the health care provider does not initiate the discussion. Direct questioning during the review of systems may ease any anxiety for the patient and open up a dialogue regarding other problems or medical conditions. (See box, “How and What To Ask,”12)
Providers can also assess the patient’s risk factors for ED and its associated comorbid conditions (see Table 21,13,14). The patient’s medical history may hold important clues to a diagnosis of organic ED.
Because certain vasculopathies, including diabetes, are known to accelerate the process of endothelial dysfunction, inquiries should be made into the sexual history of men with these disorders, regardless of age.10 Marked hyperlipidemia, uncontrolled hypertension, atherosclerosis, and other manifestations of CVD can impair erectile as well as endothelial function, leading to vascular ED.
The potential for atherosclerosis in the penile arteries (which are significantly narrower than the carotid, coronary, or femoral arteries) should prompt the primary care provider to evaluate the patient’s risk for vascular disease and its sequelae in the heart as well.8 (Of note, in one study of metabolic syndrome and ED, ED was found to be a predictor for impaired elasticity in the large arteries, independent of cardiovascular risk factors.15) In addition to damaging the small blood vessels and the endothelium, diabetes and other components of the metabolic syndrome contribute to ED by affecting cavernous nerve terminals and smooth muscle.1,14
Lifestyle factors, such as overconsumption of alcohol, smoking, recreational drug use, obesity, and inactivity can contribute to decreased libido and ED.14 Cigarette smoking can cause vasoconstriction and penile venous leak, resulting in poor erectile quality or even loss of erection. While small amounts of alcohol can improve libido and erection due to its anti-anxiety and vasodilatory effects, “more is not better” in this case, as higher doses result in sedation and decreased libido. Chronic alcoholism results in hypogonadism and polyneuropathy.16