Risk factors for organic erectile dysfunction (see Table 1, page 20) mainly stem from the fact that the erectile mechanism is a vasodilatory response dependent on smooth muscle function under neurogenic control. Aging, which has the strongest association with erectile dysfunction, probably exerts its effects mainly through impaired vasodilatory and venoocclusive mechanisms. Atheroma of the internal iliac arteries and their pudendal branches may be one factor, but age-related degeneration of intracorporeal smooth muscle mechanisms is probably more important. Venous leakage, another age-related phenomenon, may in itself be a manifestation of deterioration of intracorporeal smooth muscle function.
This disease is an important risk factor for erectile dysfunction. Damage to small blood vessels is the main etiology and, therefore, erectile dysfunction often occurs in association with diabetic retinopathy.
Diabetic peripheral autonomic neuropathy is a further contributory factor. Erectile dysfunction may develop as a result of the progressive loss of small unmyelinated so-called C fibers secondary to diabetes. Several groups have reported that diabetes is associated with loss of NO synthase from NANC nerve endings and endothelial cells in the corpora. This may explain the pathophysiological basis of the erectile dysfunction that so commonly accompanies diabetes.
This is frequently associated with erectile dysfunction. Approximately one-third of men beyond middle age have a diastolic blood pressure >90 mmHg. Hypertension causes damage to small blood vessels and this may adversely affect intracorporeal vasodilatory mechanisms. Moreover, many of the agents used to control hypertension, especially β-blockers and diuretics, are associated with the development of erectile dysfunction. It has been postulated that, because high intracorporeal pressures are required to produce penile rigidity, the reduction of blood pressure by any agent is likely to increase the incidence of erectile dysfunction. However, α-blockers, perhaps through the induction of intracorporeal vasodilatation, appear to enhance erection, while still lowering both systolic and diastolic blood pressures.
This disease often occurs in association with hypertension and is also a cause of damage to the peripheral vascular system.
Hypercholesterolemia and elevated serum triglyceride levels are both also associated with erectile dysfunction.
Although there have been few epidemiological studies to confirm this, it appears likely that heavy smoking is associated with erectile dysfunction because of its deleterious effects on blood vessels and its action leading to an increase of platelet stickiness.
Fibrosis developing in the corpora albuginea may result in permanent scarring and consequent deformity of erection. When the fibrosis is severe (
Figure 38), penetrative intercourse may be impossible. As a result of the loss of tunica elasticity, Peyronie’s disease may also be associated with venous leak-induced erectile dysfunction.
Various forms of pelvic surgery, particularly radical prostatectomy, cystoprostatectomy and abdominoperineal resection, are all strongly associated with subsequent erectile dysfunction.
Reactive or endogenous depression is strongly associated with erectile dysfunction: nearly 90% of severely depressed men report complete impotence. Treatment with antidepressants may sometimes improve the situation, although both monoamine oxidase inhibitors and tricyclic antidepressants may in themselves cause erectile dysfunction. Selective serotonin reuptake inhibitors, such as fluoxetine (Prozac®) may not only cause erectile dysfunction, but may also retard ejaculation.