Erectile Dysfunction in the Cardiovascular Patient
Erectile Dysfunction in the Cardiovascular Patient
Penile erection is largely a vascular process, and the penile endothelium and smooth muscle tissue are very sensitive to functional and structural changes. Vasculogenic ED results from an impairment of endothelial dependent or independent smooth muscle relaxation (functional vascular ED, initial stages), occlusion of the cavernosal arteries by atherosclerosis (structural vascular ED, late stages), or a combination of these. Current data support a complex interplay between endothelial dysfunction, subclinical inflammation, and androgen deficiency (Figure 1). The relationship between ED and CAD at the clinical level is supported by this common pathophysiological basis. The 'artery size' hypothesis explains why patients with CAD frequently report ED before CAD detection.According to this hypothesis, for a given atherosclerotic burden, the smaller penile arteries suffer obstruction earlier than the larger coronary arteries (Figure 2). The same concept holds also true in the case of non-obstructing atherosclerosis: since the smaller penile artery have a greater endothelial surface and erection requires a large degree of vasodilation to occur when compared with arteries in other organs, the same degree of endothelial dysfunction will be symptomatic in these smaller vessels but subclinical in the larger ones (i.e. coronaries). In the same context, accelerated arterial ageing (as indicated by increased arterial stiffening that also affects large arteries of ED patients) may be a common background. Erectile dysfunction is associated with an incremental inflammatory and endothelial-pro-thrombotic activation. Interestingly, this activation is equal to that found in CAD patients with no ED, while when these two conditions are combined the burden is additive. Androgen deficiency may be also implicated in the common pathogenetic pathways of ED and CVD; however, this warrants further substantiation.
(Enlarge Image)
Figure 1.
Links between endothelial dysfunction, inflammation, testosterone deficiency, erectile dysfunction, and coronary artery disease. Modified with permission from Vlachopoulos et al.
(Enlarge Image)
Figure 2.
The 'artery size' hypothesis. Luminal narrowing due to atherosclerotic burden will manifest clinically earlier (A) in penile arteries than in (B) coronary arteries. TIA, transient ischaemic attack. Modified with permission from Montorsi et al.
Erectile Dysfunction and Cardiovascular Disease: Common Pathophysiology
Penile erection is largely a vascular process, and the penile endothelium and smooth muscle tissue are very sensitive to functional and structural changes. Vasculogenic ED results from an impairment of endothelial dependent or independent smooth muscle relaxation (functional vascular ED, initial stages), occlusion of the cavernosal arteries by atherosclerosis (structural vascular ED, late stages), or a combination of these. Current data support a complex interplay between endothelial dysfunction, subclinical inflammation, and androgen deficiency (Figure 1). The relationship between ED and CAD at the clinical level is supported by this common pathophysiological basis. The 'artery size' hypothesis explains why patients with CAD frequently report ED before CAD detection.According to this hypothesis, for a given atherosclerotic burden, the smaller penile arteries suffer obstruction earlier than the larger coronary arteries (Figure 2). The same concept holds also true in the case of non-obstructing atherosclerosis: since the smaller penile artery have a greater endothelial surface and erection requires a large degree of vasodilation to occur when compared with arteries in other organs, the same degree of endothelial dysfunction will be symptomatic in these smaller vessels but subclinical in the larger ones (i.e. coronaries). In the same context, accelerated arterial ageing (as indicated by increased arterial stiffening that also affects large arteries of ED patients) may be a common background. Erectile dysfunction is associated with an incremental inflammatory and endothelial-pro-thrombotic activation. Interestingly, this activation is equal to that found in CAD patients with no ED, while when these two conditions are combined the burden is additive. Androgen deficiency may be also implicated in the common pathogenetic pathways of ED and CVD; however, this warrants further substantiation.
(Enlarge Image)
Figure 1.
Links between endothelial dysfunction, inflammation, testosterone deficiency, erectile dysfunction, and coronary artery disease. Modified with permission from Vlachopoulos et al.
(Enlarge Image)
Figure 2.
The 'artery size' hypothesis. Luminal narrowing due to atherosclerotic burden will manifest clinically earlier (A) in penile arteries than in (B) coronary arteries. TIA, transient ischaemic attack. Modified with permission from Montorsi et al.