Which Of The Following Statements Is True About Erectile Dysfunction - T-Tees - Your Answers Await, Life's Questions Unraveled

Etiology

The cause of ED is often multifactorial. Distinguish whether the condition has an underlying psychological cause or an organic etiology. Depression, performance anxiety, and other sexual disorders can be strong contributing factors even when organic causes also exist. Aging is an essential factor contributing to ED. As patients age, cardiovascular diseases, hypertension, and other co-morbidities play an increasingly significant role in this condition. Diabetes mellitus and metabolic syndrome can affect several organ systems, resulting in the accelerated deterioration of erectile function, and can disrupt the mechanisms underpinning erections on a molecular level.[8][9]

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Other causes of ED include neurological diseases (such as multiple sclerosis), hormonal causes (hypogonadism, thyroid), traumatic (eg, pelvic fractures, spinal cord injuries), hyperlipidemia, stroke, sleep apnea, COPD, glaucoma, multiple sclerosis, sequela of priapism, depression, prostatic hyperplasia with lower urinary symptoms (BPH with LUTS), iatrogenic (eg, post transurethral resection of the prostate) and a variety of medications (antidepressants, antihypertensives, antipsychotics, opioids, and recreational drugs).[10][11][12][13][14][15][16][17][18]

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Cardiovascular Disease and Erectile Dysfunction

Cardiovascular disease is a very significant risk factor for ED. Almost 50% of men with known coronary artery disease proven by cardiac catheterization have significant ED.[19] Part of the reason for this is that the coronary arteries and the penile cavernosal arteries are similar in size and tend to develop atherosclerotic problems similarly. Since the cavernosal arteries are small, they can develop blockages from atherosclerotic plaques earlier, resulting in vasculogenic ED years before the clinical appearance of coronary artery disease. Both cardiovascular disease and ED involve endothelial cell dysfunction in their pathophysiology.[20]

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Patients will often demonstrate subclinical atherosclerosis long before any overt ED by as much as 10 years. The cavernosal arteries being of smaller diameter means that vasculogenic ED often precedes coronary artery disease, myocardial infarctions, and strokes by up to 5 years.[3][21] Younger men who present with unexplained ED appear to have a very significant increase, up to 50-fold, of their cardiovascular risk in later life compared to an age-matched control group.[4][22] Inform patients that ED is a significant indicator of underlying heart disease and refer them for further cardiovascular risk screening and treatment.[3][4][5][6][7][22]

The Prostate Cancer Prevention Trial database showed that having ED increased a patient’s cardiovascular risk roughly equivalent to the risk of smoking or having a family history of myocardial infarctions.[23] A meta-analysis of 14 studies totaling over 90,000 men with ED found that these patients had 44% more cardiovascular events, 62% more myocardial infarctions, 39% more strokes, and a 25% increased risk of death compared to patients presenting without ED.[24]

ED has useful independent predictive value for future cardiovascular events; therefore, screen all patients with ED for cardiovascular risks.[21] If cardiovascular risk is intermediate, perform non-invasive testing for subclinical atherosclerosis and an exercise stress test, but if the patient has a high risk, recommend a formal cardiology referral.[4][25][26][27]

Besides cardiovascular disease, there are strong correlations between ED, hypertension, hyperlipidemia, diabetes, hypogonadism, obesity, smoking, alcoholism, benign prostatic hyperplasia (BPH) with lower urinary symptoms (LUTS), depression, and premature ejaculation.

Prescription medications are thought to cause one-quarter of all cases of ED. Of the 12 most commonly prescribed medications in the US, 8 list erectile dysfunction as a possible side effect.[35][50] These drugs would include most antidepressants (especially selective serotonin reuptake inhibitors), cimetidine, ketoconazole, spironolactone, sympathetic blockers (methyldopa, clonidine, and guanethidine), thiazide diuretics, and other antihypertensives. (Angiotensin-converting enzyme [ACE] inhibitors and calcium channel blockers are the least likely to cause ED.) Beta-blockers are only a minor contributor to ED, while alpha-blockers improve erectile function.[51][52]

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Of the prostate cancer patients who undergo radical prostatectomy surgery, 85% can expect ED post-operatively, compared to an ED rate of only 25% for men who received definitive radiation therapy.[53][54] (This data refers to patients who did not have ED prior to their prostate cancer treatment.) Interestingly, the use of robotic surgery for radical prostatectomies has not changed the post-operative incidence of ED.

The role of bicycle riding in ED is controversial. Traditional racing bicycle seats place considerable pressure directly on the perineal nerves as well as the pudendal and cavernosal arteries, which suggests it could be a potential problem for cyclists.[55][56] A 2020 meta-analysis of 3330 cyclists compared to 1524 non-cycling controls indicated a significantly increased risk of ED in cyclists.[57]

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