As a primary care doctor, my most important job is to tailor treatment for my patients while still making decisions based on the medical literature. So when patients tell me their treatment is causing undesired side effects—like ED—I work with them to create a plan to treat the condition while also finding a way to relieve those side effects. Fortunately, there are ways to deal with medically induced ED.
Erectile dysfunction is an accurate predictor of heart attacks and strokes in the future. Psychogenic components play a role in erectile dysfunction, but the most common and primary cause in most men is organic vascular insufficiency, meaning not enough blood gets to the penis. Erectile dysfunction usually occurs one to five years before a male manifests overt signs of cardiovascular disease. The first sign may be death.
SOURCES: Jackson, G. The Journal of Sexual Medicine, July 2005; vol 2: pp 513-516. Graham Jackson, MD, cardiologist, Cardiothoracic Centre, St. Thomas' Hospital, London. Richard Stein, MD, professor of clinical medicine, Albert Einstein College of Medicine; director of preventive cardiology, Beth Israel Hospital, New York City; spokesman, American Heart Association. Irwin Goldstein, MD, editor-in-chief, The Journal of Sexual Medicine.
It is recommended that testosterone be measured in patients with ED because low levels are a reliable measure of hypogonadism. Hypogonadism is not only a treatable cause of ED, but can also lead to reduced or lack of response to PDE5 inhibitors.73 Testosterone deficiency is also associated with increased cardiovascular and all-cause mortality.74 Levels >350 ng/dl do not usually require replacement, but in patients with testosterone <230 ng/dl, replacement can usually be beneficial.57 In patients with congestive heart failure, testosterone replacement can lead to fluid retention, so caution is advised. In these patients, the aim should be to keep testosterone levels in the middle range, i.e. 350–600 ng/dl.57
No matter what the cause of erectile dysfunction, it is likely to cause feelings of stress and other emotional reactions. It’s also not uncommon for erection problems to cause tension in a relationship, particularly if one or both partners withdraws emotionally and the problem is not talked about. And it’s possible for a man’s renewed ability to have intercourse after a period of no sexual activity to stir up relationship issues.
There are two kinds of penis implants. One kind is a rigid but flexible rod implanted in the penis. You bend it up for sex or down for daily living. The other kind is an inflatable implant. The device stores fluid in a reservoir under the skin of your abdomen or scrotum. You press on the reservoir to pump fluid into cylinders in the penis. That creates an erection. A valve drains the fluid out of the penis when you're done.
David F. Penson, MD, MPH, is an associate professor of urology and preventive medicine in the Keck School of Medicine at the University of Southern California, in Los Angeles. Hunter Wessells, MD, is an associate professor of urology at the University of Washington School of Medicine and chief of urology at Harborview Medical Center in Seattle, Wash.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References However, patients with hypertrophic obstructive cardiomyopathy and idiopathic hypertrophic subaortic stenosis are at increased risk of syncope and sudden death after exercise.51x51DeBusk, R, Drory, Y, Goldstein, I et al. Management of sexual dysfunction in patients with cardiovascular disease: recommendations of the Princeton Consensus Panel. Am J Cardiol. 2000; 86: 62F–68F
The authors observe that multiple factors may be involved. In addition to decreased exercise capacity, patients with chronic heart failure have blood vessel and circulation abnormalities that can reduce blood flow into the penis and interfere with the ability to maintain an erection. And erectile dysfunction can be caused or worsened by many of the medications that are commonly prescribed to treat chronic heart failure.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (124) | Google ScholarSee all References This was a doubleblind, single-dose crossover study involving 41 men with stable coronary artery disease characterized by reproducible stable exertional angina. After taking either 10 mg of vardenafil or placebo, these men underwent treadmill exercise tolerance testing to 5 to 10 METs. Compared with placebo, vardenafil use did not result in a change in exercise treadmill time or time to first awareness of angina but significantly increased the time to ischemic threshold. At peak exercise levels, vardenafil did not cause a change in either heart rate or blood pressure level. This study concluded that 10 mg of vardenafil did not impair the ability of men with stable coronary artery disease to exercise at levels consistent with the exertion associated with sexual intercourse.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Open-label trials showed a myocardial infarction rate of only 1.0 event per 1000 person-years of treatment with sildenafil.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Gazzaruso C, Solerte SB, Pujia A, Coppola A, Vezzoli M, Salvucci F, Valenti C, Giustina A, Garzaniti A. Erectile dysfunction as a predictor of cardiovascular events and death in diabetic patients with angiographically proven asymptomatic coronary artery disease: a potential protective role for statins and 5-phosphodiesterase inhibitors, J Am Coll Cardiol , 2008, vol. 51 (pg. 2040-2044)https://doi.org/10.1016/j.jacc.2007.10.069
Having ED means that all, most, or some of the time, the penis fails to become or stay hard enough for sexual intercourse. If, on rare occasions, you cannot get an erection, you do not have ED. You also do not have ED if you have a decrease in sexual desire, have premature ejaculation, or if you fail to ejaculate or reach orgasm. ED means that you can’t get or keep an erection.
Getting blood glucose under control is a good anti-ED tactic. Men with diabetes and poor blood glucose control are two to five times as likely to have ED as those with good control. One study in a group of men who had had type 1 diabetes for up to 15 years with minor complications found that intensive blood glucose control lowered the risk of ED compared with conventional treatment. A study in men with type 2 diabetes found that lowering A1C (average blood glucose in the past two to three months) below 7 percent and reducing blood pressure through a combination of medication, diet, and exercise improved sexual functioning.
Just because a product claims to be natural doesn't mean it's safe. Many herbal remedies and dietary supplements can cause side effects and dangerous interactions when taken with certain medications. Talk to your doctor before you try an alternative treatment for erectile dysfunction — especially if you're taking medications or you have a chronic health problem such as heart disease or diabetes.
Despite all the options and alternatives, sometimes there’s no suitable alternative to a prescription that contributes to ED. You might have an adverse reaction to an particular medication or an alternative is unavailable in your state, health insurance plan, or your budget. There are good reasons you were prescribed your original medication in the first place.
A sexually competent male must have a series of events occur and multiple mechanisms intact for normal erectile function. He must 1) have desire for his sexual partner (libido), 2) be able to divert blood from the iliac artery into the corpora cavernosae to achieve penile tumescence and rigidity (erection) adequate for penetration, 3) discharge sperm and prostatic/seminal fluid through his urethra (ejaculation), and 4) experience a sense of pleasure (orgasm). A man is considered to have ED if he cannot achieve or sustain an erection of sufficient rigidity for sexual intercourse. Most men, at one time or another during their life, experience periodic or isolated sexual failures. However, the term “impotent” is reserved for those men who experience erectile failure during attempted intercourse more than 75% of the time.
Penile Injection Medication: This is just what it sounds like. Injected at home directly into the penis, the medication alprostadil produces erection by relaxing certain muscles, increasing blood flow into the penis and restricting outflow. Although some sources report an 80 percent success rate, the therapy has disadvantages, such as risks of infection, pain, and scarring—fibrosis—in the penis, and it may also cause priapism. A popular version of this medication is Upjohn Corporation’s Caverject. The MUSE System, by VIVUS, involves the same medicine (a pellet of alprostadil) applied with an eye-dropper-like applicator, directly into the urethra.
This disparity is due not only to the setting in which the patients were accrued, but also to the manner in which they were questioned, because data in the Italian study were collected by the medical staff during subjects' visits for medical care, which might have also affected reporting rates. De Berardis et al.6 used a fairly generalizable cohort of 1,460 Italian men with type 2 diabetes accrued from 114 outpatient clinics and patient lists of 112 general practitioners. However, unlike the other Italian study, they used self-administered, validated questionnaires to assess the prevalence of ED among diabetic men. They found that 34% reported frequent erectile problems, and 24% reported moderate problems, for an overall prevalence of 58%. Depending on how one wishes to define “clinically significant” ED, this is probably a fairly accurate assessment.
The EDDM patient has a variety of firstline options. The risk factors for vascular disease are the risk factors for ED. First-line therapy begins with attempts to minimize or eliminate these factors. These include smoking cessation, regular exercise, tighter glycemic control by attention to dietary restrictions, addition of statin drugs to correct dyslipidemia, and moderation of alcohol ingestion. Although there is very limited evidence that these modifications will dramatically reverse ED, they certainly will sponsor improved general health.4
*** High-risk patients include those with unstable or refractory angina pectoris, uncontrolled hypertension, congestive heart failure (NYHA class IV), recent myocardial infarction without intervention (<2 weeks), high-risk arrhythmia (exercise-induced ventricular tachycardia, implanted internal cardioverter defibrillator with frequent shocks, and poorly controlled atrial fibrillation), obstructive hypertrophic cardiomyopathy with severe symptoms, and moderate to severe valve disease, particularly aortic stenosis.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (24) | Google ScholarSee all References Erectile function relies on the arterial blood supply from the internal pudendal arteries, which are branches of the hypogastric arterial system (Figure 1). Substantial increases in internal pudendal arterial flow result in pressures within the penis that are comparable to systemic arterial levels.12x12Rampin, O and Giuliano, F. Central control of the cardiovascular and erection systems: possible mechanisms and interactions. Am J Cardiol. 2000; 86: 19F–22F
Erectile dysfunction is common in the CVD patient. It is an important component of the quality of life and it also confers an independent risk for future CV events. The usual 3-year time frame between the onset of ED symptoms and a CV event offers an opportunity for risk mitigation. Thus, sexual function should be incorporated into CVD risk assessment for all men. Algorithms for the management of patient with ED have been proposed according to the risk for sexual activity and future CV events. A comprehensive approach to cardiovascular risk reduction (comprising of both lifestyle changes and pharmacological treatment) improves overall vascular health, including sexual function. Proper sexual counselling improves the quality of life and increases adherence to medication. Testosterone assessment may be useful for both diagnosis of ED, risk stratification and further management. There are issues to be addressed, such as whether PDE5 inhibition reduces CV risk. Management of ED requires a collaborative approach and the role of the cardiologist is pivotal.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (46) | Google ScholarSee all References Sedentary patients with a history of cardiac disease and patients with unstable angina or advanced congestive heart failure should undergo a full medical evaluation before resuming sexual activity.80x80Muller, JE. Triggering of cardiac events by sexual activity: findings from a case-crossover analysis. Am J Cardiol. 2000; 86: 14F–18F
Ginseng is the most common ingredient among top-selling supplements for men’s sexual health (36). The English word ginseng derives from the Chinese term renshen. Ren means “person” and shen means “plant root”. This plant has been named in this manner as its roots resemble the lower limbs of a human, Traditionally, ginseng has been used to restore and enhance the normal well-being of the body. The effects are due to ginseng’s reactions with the central nervous system, metabolism, immune function and cardiovascular system. The principal active compounds are triterpene saponins known as ginsenosides. Animal studies have suggested that specific ginsenosides may be responsible for ginseng-mediated effects on copulatory behavior (37). Ginsenoside induces smooth muscle relaxation by hyperpolarizing the smooth muscle membrane via activation of large-conductance KCa channels (38).
Crossref | PubMed | Scopus (697) | Google ScholarSee all References Subsequent in vitro electrical stimulation of these tissue samples showed decreased neurogenic and endothelium-dependent smooth muscle relaxation in the tissue from the patients with diabetes. These effects persisted even after controlling for smoking and hypertension. Other studies have shown a heightened smooth muscle tone in patients with diabetes mellitus.24x24Christ, GJ, Stone, B, and Melman, A. Age-dependent alterations in the efficacy of phenylephrine-induced contractions in vascular smooth muscle isolated from the corpus cavernosum of impotent men. Can J Physiol Pharmacol. 1991; 69: 909–913
For those patients who cannot take erectile dysfunction medications, the authors counsel that an exercise training regimen may be an appropriate substitute therapy to enhance sexual function and quality of life. The authors stress that clinicians should focus on the sexual activity history of chronic heart failure patients and not ignore it, since addressing this element can substantially improve their quality of life.
“I’m hoping this study will drive that (tie) a little bit harder and faster so that physicians will routinely be including ED when they’re screening patients for cardiovascular disease,” he said. “Doctors should ask the question and consider whether hardening of the arteries is occurring, ask about family history and signs or symptoms like chest pain with exertion, and spend the requisite amount of time to find out what’s going on.”
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.3 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.10 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.11,12 Erectile dysfunction is associated with an incremental inflammatory and endothelial-pro-thrombotic activation.13 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.2
Cardiovascular disease remains our nation’s biggest killer, responsible for about one-third of deaths in the U.S.1 Erectile dysfunction (ED) is typically the first clinical manifestation of cardiovascular disease, making it a helpful early marker for men who are likely to die of heart attacks. There is a strong relationship between erectile dysfunction and high blood pressure, high cholesterol, angina, stroke, heart attack and a premature death.2, 3