Erectile dysfunction (ED) is defined as the inability to attain or maintain a penile erection of sufficient quality to allow satisfactory sexual performance.
The prevalence of this condition increases with age with a 39% prevalence at the age of 40 years and a 67% prevalence at the age of 70 years. It has been estimated that the worldwide prevalence of erectile dysfunction will be 322 million cases by the year 2025.
Sexual function is a complex process involving both biologic and psychological factors.
Erections result from a combination of neurotransmission and vascular smooth muscle responses that culminate in increased arterial inflow and signaling between endothelial-lined cavernosal sinusoids and the underlying smooth-muscle cells.
Nitric oxide that is produced by the parasympathetic nonadrenergic,
noncholinergic neurons and endothelial cells triggers a molecular cascade that results in the relaxation of smooth-muscle cells Fig. 1 .
Fig. 1: Physiology of Penile Erection.
NO: Nitric Oxide.
PDE5:phosphodiesterase type 5.
cGMP: cyclic guanosine monophosphate.
The corpora cavernosa contain a network of smooth muscle cells and endothelial cells surrounded by an expansible tunica albuginea.
The sinusoid cavities are small in volume at rest as the smooth muscle cells are tonically contracted.
smooth muscle cells relax,
which allows the sinusoids to engorge with blood and causes the penis to become tumescent.
This process occludes venous return through passive compression of the subtunical venules,
resulting in an erection. If there is insufficient relaxation of smooth-muscle cells (lack of endogenous nitric oxide associated with endothelial disease),
a decreased sinusoid compliance,
an inadequate number of smooth-muscle cells (diabetes or neuropathy),
or tunical degeneration (Peyronie’s disease),
then insufficient compression of the subtunical veins results in erectile dysfunction Fig. 2 .
Fig. 2: Veno-oclusive mechanism in penile erection.
A- Normal flacid penis. Smooth muscle cells are contracted and the sinusoid spaces in corpus cavernosum are empty.
B- Normal erect penile anatomy. The increase of NO levels allows smooth muscle cells relaxation, sinusoid spaces are enlarged and compress the subtunical venous plexus.
C-Several mechanism of venogenic erectile dysfuntion.
References: McVary KT. Erectile Dysfunction. N Engl J Med 2007;357:2472-81.
There are many causes of erectile dysfunction Fig. 3,
and combined causes.
Organic causes are found in 80–90% of patients and include vasculogenic (arterial,
venous leak and mixed),
anatomic and endocrine causes.
Psychogenic disorders with ED are performance anxiety,
depression and inhibited sexual desire.
It is essential to identificate organic causes,
because they are potentially treatables.
The risk factors associated with ED includes advanced age,
diabetes and tobacco.
All of them leads to endothelial dysfunction,
which is a shared physiopathological mechanism involved in both cardiovascular diseases and erectile dysfunction Fig. 4
Fig. 4: Risk Factors in Erectile Dysfunction. Endothelial Dysfunction as a shared physiopathological mechanism between ED and cardiovascular diseases.
Erectile dysfunction is now being recognized as one of the earliest manifestations of endothelial dysfunction and peripheral vascular disease.
Several studies have demonstrated that ED presents about 39 months before cardiovascular diseases possibly because the smaller arteries reach critical narrowing and decreasing blood flow earlier than larger vessels Fig. 5.