TABLE 2
FROM:
Why do patients with heart failure suffer from erectile dysfunction? A critical review and suggestions on how to approach this problem
S Rastogi, J J Rodriguez, V Kapur and E R Schwarz
BACK TO ARTICLETable 2. Causes of ED in patients with heart failure
| Cause | Mechanism |
|---|---|
| Arterial insufficiency | Decreased blood flow to the corpus cavernosa due to arterial insufficiency secondary to atherosclerosis |
| Endothelial dysfunction | Inadequate vasodilatory response of the penile vessels and relaxation of trabecular smooth muscle due to a reduction in the availability of endothelium derived NO |
| ETs | Induce long-lasting contraction of corpus cavernosum and penile vessels. Also serve as modulators for other contractile agents, enhancing their contractile effect |
| Psychogenic (depression, performance anxiety) | Loss of libido, increased contraction of corpus cavernosum and penile vessels from increased sympathetic tone and/or impaired NO release |
| Cardiac capacity/exercise tolerance | Decreased sexual function due to decline in exercise capacity due to patient's inability to increase heart rate and stroke volume secondary to left ventricle dysfunction and neurohormonal changes associated with the pathophysiologic state of heart failure |
| Medication | |
| Beta-adrenergic receptor blockers | Exact mechanism unclear, decreased perfusion pressure from a direct (unknown) effect on penile smooth muscle or increased contraction of corporal smooth muscle and vessels from unopposed alpha-receptor stimulation |
| Digoxin | Corporal smooth muscle sodium-pump inhibition, which promotes contraction and impedes NO-induced relaxation |
| Spironolactone (aldosterone antagonist) | ED and decreased libido secondary to androgen suppression. Primarily a peripheral anti-androgen effect competing with testosterone and dihydrotestosterone (DHT) for androgen binding sites. Also, a weak inhibitor of testosterone biosynthesis |
| Thiazide diuretics | Mechanism unknown |
