By Brittany Thomas, M.D.
It has been estimated that more than 150 million men worldwide have some degree of erectile dysfunction. The prevalence of erectile dysfunction is approximately two fold higher in hypertensive patients compared to normotensive patients.
Due to the private nature of this problem, erectile dysfunction is often overlooked and left to the patient to initiate discussion. The consequences of unrecognized erectile dysfunction included medication non-adherence and decreased quality of life for the patient and the patientâ€™s partner.
Research suggests that erectile dysfunction is a risk predictor of cardiovascular disease. Physicians should therefore inquire about sexual dysfunction, understand the physiology, recognize medications that contribute to sexual dysfunction and risk stratify patients with erectile dysfunction.1
Normally, the cavernosal nerves synthesize and release nitric oxide (NO) onto the smooth muscle cells of both the corpora cavernosa and the penile arterial system. The NO causes relaxation of the smooth muscle within the media of the penile arterial vessels and cavernosal bodies. With aging, the smooth muscle cells are replaced by collagen fibers. These cells are not able to relax and store blood as well as previously.2
Â Vasculogenic ED results from an impairment of smooth muscle relaxation and occlusion of the cavernosal arteries by atherosclerosis or a combination of these. Hypertension plays a role in ED through various mechanisms, including prolonged exposure to elevated systemic blood pressure, endothelial dysfunction and circulation of vasoactive substances such as angiotensin II. These mechanisms lead to structural and functional alterations in the penile arteries.3
Â Relationship of ED and CV
ED is a risk predictor of cardiovascular disease. Approximately 40 percent of men who present with ED are shown to have occult cardiovascular disease. It has been shown that ED precedes the onset of symptomatic CAD by a mean of approximately 3 to 5 years. Men with ED appear to carry a 23 percent increased risk of cardiovascular death. Screening for erectile dysfunction may help to identify and improve the management of cardiovascular risk. 2-3
It is important to exclude other causes of erectile dysfunction before vasculogenic sexual dysfunction is diagnosed. The mainstay of treatment for ED is lifestyle modification. Moderate physical activity can reduce the risk of erectile dysfunction compared to a sedentary lifestyle. Caloric reduction, weight loss, alcohol reduction and smoking cessation may improve sexual function.
In terms of medical therapy, testosterone therapy may be helpful in men with testosterone deficiency. Regarding antihypertensives, thiazide-class diuretics have been shown to cause erectile dysfunction. Indapamide is rarely associated with an adverse effect on male sexual function.4
The incidence of sexual dysfunction linked to centrally acting antihypertensives such as clonidine has been estimated to be 20 percent.4 Most beta blockers have the potential adverse side effect of erectile dysfunction. The first-generation beta blockers such as propranolol are more likely than the second-generation beta blockers, like metoprolol, to cause erectile dysfunction. Nebivolol, a third-generation beta blocker, may even improve erectile dysfunction through nitric oxide production. ACE inhibitors and calcium channel blockers have a neutral effect on erectile function.
Angiotensin receptor blockers also have a positive effect on erectile function. Angiotensin receptor blockers block the vasoconstrictive action of angiotensin II. Angiotensin receptor blockers are considered a first-line treatment in hypertensive patients with erectile dysfunction.
Phosphodiesterase-5 (PDE5) inhibitors are effective medications used to treat erectile dysfunction. They are useful even for patients on multiple drug regimens unless contraindicated. They cannot be used with long- or short-acting nitrovasodilators due to hypotension. They should be used with caution in patients taking alpha blockers.
When conservative management fails, surgical penile prosthesis (inflatable or semi-rigid) should be considered. An implantable prosthesis has a high satisfaction rate but carries the risks of mechanical failure and infection.
Research regarding female sexual dysfunction (FSD) is limited. The underlying pathophysiology of hypertension contributing to female sexual dysfunction is similar to the role of hypertension in erectile dysfunction. Decreased blood flow from vascular remodeling and atherosclerosis causes clitoral and vaginal insufficiency. In addition, fibrosis of the clitoral smooth muscle and vaginal wall leads to impaired sexual stimulation. The ultimate result is vasculogenic FSD.
Sexual dysfunction was found in 42.1 percent of women with essential hypertension compared with 19.4 percent of normotensive women.5 The duration of hypertension, beta blockers and uncontrolled hypertension have been linked to sexual dysfunction in women. Hypertension is associated with decreased lubrication and orgasm and increased pain. 6
Although there is limited data on female sexual dysfunction, it is critical to recognize that there is an association with antihypertensive therapy. Changes in medication may improve quality of life and compliance with therapy.
In August 2015, the FDA approved flibanserin for premenopausal women with hypoactive sexual desire disorder. This medication does not target vasculogenic sexual dysfunction but may improve libido in those suffering from the disorder. Flibanserin is a centrally acting serotonin receptor 1A agonist and serotonin receptor 2A antagonist that results in transient decreases in serotonin and increases in dopamine and norepinephrine in certain regions of the brain.7 It has been associated with hypotension and dizziness and should not be taken with alcohol.
Sexual dysfunction is commonly associated with hypertension and antihypertensive medications in both men and women. It is time to start conversations with patients regarding this matter to improve quality of life, medication adherence and risk factor reduction.
- Duncan et al. Does hypertension and its pharmacotherapy affect the quality of sexual function in women? American Journal of Hypertension. 2000;13(6):640-647.
- Doumas M et al. Female sexual dysfunction in essential hypertension:
A common problem being uncovered.
Journal of Hypertension. 2006; 24(12):2387-2392.
- Al Khaja et al. Antihypertensive drugs and male sexual dysfunction: A review of Adult hypertension Guideline Recommendations. Journal of Cardiovascular Pharmacology and Therapeutics.
- Vlachopoulos C. et al. Erectile dysfunction in the cardiovascular patient. European Heart Journal. 2013;34 (27): 2034-2046.
- Clavijo RI, Miner MM, Rajfer J. Erectile Dysfunction and Essential Hypertension: The Same Aging-related Disorder? Reviews in Urology. 2014;16(4):167-171.
- Viigimaa M, Vlachopoulos C, Lazaridis A, Doumas M. Management of erectile dysfunction in hypertension: Tips and tricks. World Journal of Cardiology. 2014;6(9):908-915.
- Simon JA et al. Efficacy and safety of flibanserin in postmenopausal women with hypoactive sexual desire disorder: results of the SNOWDROP trial. 2014;21(6):633-40.