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Media file 1: Erectile dysfunction. These images depict penile anatomy. Note the sinusoidal makeup of the corpora and thick fascia (ie, Buck fascia) that covers the corpora cavernosa. The major blood vessels to the corpora cavernosa enter through tributaries from the main vessels running along the dorsum of the penis
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Almost all antihypertensive medications have been implicated in erectile dysfunction.23 The mechanisms vary from central-acting sympatholytics, depression of libido as well as higher blood pressure requirement to achieve erection in atherosclerotic patients taking diuretics and vasodilators. The role of smoking in causing erectile dysfunction remains a source of controversy. A recent consensus group analysis failed to document a direct link to erectile dysfunction. However, smoking seems to amplify other risk factors, such as hypertension and coronary artery disease.24 Martin-Morales and colleagues25 have shown an increased risk of erectile dysfunction among smokers (odds ratio [OR] 2.5). Systemic diseases are also associated with erectile dysfunction. This is often multifactorial, as in diabetes and renal failure.26 Given the role of androgens in the physiology of erections, it is not surprising that many hypogonadal men do not experience erectile dysfunction per se. Low serum testosterone levels may be primary or secondary to another condition, such as hyperprolactinemia or hypothyroidism. Regardless of the mechanism, the result is primarily a loss of libido, although many hypogonadal men retain their ability to obtain erections.27
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TABLE 5 Multi-isoform inhibitors and secondary targets of selective inhibitors Although many inhibitors are called “selective”, this is really a relative term. The compounds are termed selective based on the fact that other isoforms are only inhibited at higher concentrations. Some compounds such as dipyridamole and zardaverine are selective for a limited number of isoforms. However, some of the inhibitors that target multiple isoforms may be useful because of this property. For example, dipyridamole is a component of the stroke treatment Aggrenox (aspirin/extended-release dipyridamole).
Metabolism (breakdown) of vardenafil can be slowed by aging, liver disease, and concurrent use of certain medications (such as erythromycin, ketoconazole (Nizoral), and protease inhibitors). Slowed breakdown allows vardenafil to accumulate in the body and potentially increase the risk for side effects. Therefore, in men over age 65, with liver dysfunction, or who are also taking medication(s) that can slow the breakdown of vardenafil, the doctor will initiate vardenafil at low doses to avoid its accumulation. For example:
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Since the mid-1980s, when the use of the prostate-specific antigen (PSA) screening test began to increase dramatically, the incidence of prostate cancer showed a concurrent steep rise. If early detection of prostate cancer truly saves lives, there should be a corresponding drop in the prostate cancer death rate. It hasnt happened. The prostate cancer death rate in the U.S. has not changed in 30 years. The vast majority of men with prostate cancer do not die of the disease because they have the slow-growing type that would never become lethal. Even if doctors could determine which cases of early-stage prostate cancer will be fatal (about 10-15%), there is no evidence that early detection will alter the outcome. About 2% who undergo prostatectomy die within 30 days of the operation.
The most significant improvements over placebo are at dosages of 4mg to 6mg. However it was clear in this same trial and others (9, 15, 16, 18), that increased dosages also increase the likelihood of the most common side effect of nausea. These side effects are reported to diminish with continued dosing. (15)
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