Men with a rare heart condition known as long QT syndrome should not take vardenafil since this may lead to abnormal heart rhythms. The QT interval is the time it takes for the heart's muscle to recover after it has contracted and is measured on an electrocardiogram (EKG). In addition, vardenafil is not recommended for men taking medications that can affect the QT interval such as quinidine, procainamide, amiodarone, and sotalol.
Other hormone levels: Measurement of other hormones beside testosterone (luteinizing hormone [LH], prolactin level, and cortisol level) may provide clues to other underlying causes of testosterone deficiency and erectile problems, such as pituitary disease or adrenal gland abnormalities. Doctors may check thyroid levels in some individuals as both hypothyroidism (low thyroid function) and hyperthyroidism (overactive thyroid function) can contribute to erectile dysfunction.

Another tip is to make sure you communicate with your partner what you like during the process of sex.  Many men are not communicative about what really turns them on.  If you are not aroused by what is going on, then you might experience ED.  Make sure you tell your partner what turns you on.  Communicating about intimacy should also lead to feeling more connected with your partner aiding in relaxing when you are sexual together.


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L-arginine, an amino acid that is naturally present in the body and helps make nitric oxide, supports a successful erection. Nitric oxide is responsible for making the blood vessels relax, which helps sustain an erection for men. A 1999 study, observed the effects of six weeks of high-dose (5 grams/day) orally administered nitric oxide (NO) donor L-arginine on men with organic ED. Thirty-one percent of those who took 5 grams/day of L-arginine experienced significant improvements in sexual function. Burns told Medical Daily, “l-arginine and deer antler velvet” have been the most popular go-to natural treatments for men.

The association between low testosterone and ED is not entirely clear. Although these 2 processes certainly overlap in some instances, they are distinct entities. Some 2-21% of men have both hypogonadism and ED; however, it is unclear to what degree treating the former will improve erectile function. [17] About 35-40% of men with low testosterone see an improvement in their erections with testosterone replacement; however, almost 65% of these men see no improvement. [15]

The most common treatment for erectile dysfunction is drugs known as phosphodiesterase-5 (PDE-5) inhibitors. These include tadalafil (Cialis), vardenafil (Levitra), and sildenafil citrate (Viagra). These are effective for about 75% of men with erectile dysfunction. They are tablets that are taken around an hour before sex, and last between 4 and 36 hours. Sexual stimulation is required before an erection will occur. The PDE-5 inhibitors cause dilation of blood vessels in the penis to allow erection to occur, and help it to stay rigid. Men using nitrate medication (e.g. GTN spray or sublingual tablets for angina) should not use PDE-5 inhibitors.
The laboratory results should be discussed with the patient and, if possible, with his sexual partner. This educational process allows a review of the basic aspects of the anatomy and physiology of the sexual response and an explanation of the possible etiology and associated risk factors (eg, smoking and the use of various medications). Treatment options and their benefits and risks should be discussed. This type of dialogue allows the patient and physician to cooperate in developing an optimal management strategy.
Normal erectile function depends on the release of NO and endothelial-dependent vasodilation of the penile arteries. The ‘artery size’ hypothesis, first described by Dr Montorsi, offers an explanation why men are more likely to develop ED before a myocardial infacrtion. It is believed that atherosclerosis affects all vascular beds equally but smaller arteries are more likely to become occluded than larger arteries.31 32 The penile arteries are 1–2 mm while the coronary arteries are 3–4 mm. Thus, the same degree of endothelial dysfunction and atherosclerosis is more likely to occlude blood flow in the penile arteries compared with the coronary arteries. The penile arteries therefore serve as a sensitive indicator for subsequent CVD. This theory is supported by the fact that ED occurs approximately 3 years prior to cardiac symptoms in virtually all patients with chronic coronary syndrome whereas patients with acute coronary syndrome have a much lower prevalence of sexual dysfunction.32
Zerman et al. performed penile implant surgery in 245 men with neurolgic impairment caused by spinal cord injury, CNS neoplasm, CNS infection, MS and SB (110). Mean follow-up time of 7.2 years was achieved in 195 patients, 50 patients were excluded for lost to follow-up or death from nonurological causes. Interestingly, 135 patients underwent penile implantation to assist with management of urinary incontinence and improve ability for condom/intermittent catheterization. Ninety-two patients patient underwent implantation for ED. Eighty two percent of patients were satisfied with implantation for ED, and 67% of partners were satisfied. Complications included infection (5%), perforation (0–18%), and technical dysfunction (7–33%). Perforation rates were high with the malleable device when it was placed through a subcoronal incision. After adopting an infrapubic approach the perforation rates dropped substantially.

The laboratory results should be discussed with the patient and, if possible, with his sexual partner. This educational process allows a review of the basic aspects of the anatomy and physiology of the sexual response and an explanation of the possible etiology and associated risk factors (eg, smoking and the use of various medications). Treatment options and their benefits and risks should be discussed. This type of dialogue allows the patient and physician to cooperate in developing an optimal management strategy.
Begot, I., Peixoto, T. C. A., Gonzaga, L. R. A., Bolzan, D. W., Papa, V., Carvalho, A. C. C., ... & Guizilini, S. (2015, March 1). A Home-Based Walking Program Improves Erectile Dysfunction in Men With an Acute Myocardial Infarction. The American Journal of Cardiology, 115(5), 5741-575. Retrieved from http://www.ajconline.org/article/S0002-9149(14)02270-X/abstract

3. Are there physical causes of erectile dysfunction? Erectile dysfunction may be a symptom of underlying medical conditions, which if not detected may cause further medical problems. A prior history of cigarette smoking, heart attacks, strokes, and poor circulation in the extremities (for example, intermittent claudication or cramping in your leg[s] when you walk) suggest atherosclerosis as the cause of the erectile dysfunction. Loss of sexual desire and drive, lack of sexual fantasies, gynecomastia (enlargement of breasts), and diminished facial hair suggest low testosterone levels. A prior history of pelvic surgery or radiation and trauma to the penis/pelvis/perineum can cause problems with the nerves and blood vessels. Symptoms of intermittent claudication of the lower extremities with exercise may suggest a vascular problem as a cause of the erectile dysfunction.
The association of CVD and ED was noted in 1997 as one analysed the results of the MMAS. In this landmark study, 1709 men aged 40–70 years were enrolled between 1987 and 1989. A follow-up some 10 years later revealed a striking relationship between ED and CVD. In this study, it became clear that the risk factors for ED were very similar to those of CVD, such as diabetes mellitus, smoking and dyslipidaemia.18
Sexual stimulation causes the release of neurotransmitters from cavernosal nerve endings and relaxation factors from endothelial cells lining the sinusoids. NOS produces NO from L-arginine, and this, in turn, produces other muscle-relaxing chemicals, such as cGMP and cyclic adenosine monophosphate (cAMP), which work via calcium channel and protein kinase mechanisms (see the image below). This results in the relaxation of smooth muscle in the arteries and arterioles that supply the erectile tissue, producing a dramatic increase in penile blood flow.
Several pathways have been described to explain how information travels from the hypothalamus to the sacral autonomic centers. One pathway travels from the dorsomedial hypothalamus through the dorsal and central gray matter, descends to the locus ceruleus, and projects ventrally in the mesencephalic reticular formation. Input from the brain is conveyed through the dorsal spinal columns to the thoracolumbar and sacral autonomic nuclei.
Male erectile problems often produce a significant emotional reaction based on the impact of erectile dysfunction on confidence, self-esteem, and morale in most men. This is described as a pattern of anxiety and stress that can further interfere with normal sexual function. Such "performance anxiety" needs to be recognized and addressed by a doctor.
How men can improve their sexual performance Many men want to know how to enhance their own and their partners’ sexual satisfaction. However, placing too much emphasis on performance can lead to anxiety. Certain lifestyle changes can help to reduce sexual anxiety, improve erectile dysfunction, and increase stamina. In this article, we describe 13 methods to try. Read now
"Sexual relations are not only an important part of people's wellbeing. From a clinical point of view, the inability of some men to perform sexually can also be linked to a range of other health problems, many of which can be debilitating or potentially fatal," says Professor Gary Wittert, Head of the Discipline of Medicine at the University of Adelaide and Director of the University's Freemasons Foundation Centre for Men's Health.
Erectile dysfunation medications may not be suitable for you if you have been told not to have sex, not to engage in sexual activity/actions that widen your blood vessels, have low blood pressure (hypotension), have recently had a stroke, have unstable angina, have had a heart attack or have a history of non-arteritic anterior ischaemic optic neuropathy. Men with cardiovascular disease/anatomical issue with their penis/priapism/taking long-lasting alpha-blockers should use with caution and discuss with a doctor first. Do not mix with drugs/medications containing nitrates.
For many of the 30 million Americans affected by erectile dysfunction, Viagra, Levitra, and Cialis are the first line of ED treatment — and they’re successful for about 80 percent of men. These drugs, called phosphodiesterase-5 inhibitors, are approved by the U.S. Food and Drug Administration (FDA) and work by increasing blood flow to an erection. Common side effects include nasal congestion and headache. Note: If you take nitroglycerin pills for heart disease, you won’t be able to take ED pills, as they can cause a dangerous drop in blood pressure.
Traditionally, erectile impotence (the classical definition of impotence) is the failure to achieve penile erection during intercourse. It may have either physical or psychological causes. Alcoholism, endocrine disease, and neurological disorders are typical physical causes. Psychological causes include anxiety over performance, hostility or other negative feelings toward the sexual partner, and stress, anxiety, depression, or other emotional conflicts outside of the relationship. Erectile impotence occasionally occurs with age and, although attributed by the individual to the aging process itself, it is usually secondary to disorders of aging, such as faulty blood circulation or prostate disease. In cases of impotence caused by blood vessel dysfunction, an insufficient supply of blood flows into the penis, or the blood diffuses out into adjacent tissues.
Surgery to repair arteries (penile arterial reconstructive surgery) can reduce impotence caused by obstructions that block the flow of blood to the penis. The best candidates for such surgery are young men with discrete blockage of an artery because of a physical injury to the pubic area or a fracture of the pelvis. The procedure is less successful in older men with widespread blockage of arteries.
Induction of erection occurs after stimulation of the cavernous and pelvic nerve plexus. Conversely, stimulation of the sympathetic trunk leads to detumescence. The reflex erectile response requires that the sacral reflex arc remain intact. Tactile and sensory signals are received by the somatic sensory pathways and integrate with parasympathetic nuclei within the sacral spinal cord (S2-4) leading to induction of erection via cholinergic signaling. These reflexogenic erections remain intact with upper motor neuron injuries. Psychogenic erections do not require that the sacral reflex arc remain intact. In a cat models, spinal cord removal below L4/L5 led to absence of a reflexogenic erection but stimulation of the medial preoptic area (MPOA) or placement near a female cat in heat led to erection (5,6). Psychogenic erections occur via induction of central pathways traveling from the brain through the sympathetic chain. Non-penile sensory pathways induced by sight, sound, touch and smell travel through the MPOA to the erection centers within the cord T11-L2, and S2-S4 to induce erections (7). When a sacral lower motor neuron injury is present in men, below T12 these types of erections are more likely to occur (8). Spinal cord lesions above T9 are not associated with psychogenic erections (9). Rigidity of erections is less with psychogenic erections because the thoracolumbar sympathetic outflow may contain a decreased concentration of neurons compared to the parasympathetic outflow from the sacral spinal cord.
Then you have to be able to make the right diagnosis. What is the basis for their erectile dysfunction? Is it psychogenic? Is it some sort of neurological or blood vessel or hormonal issue? So you have to make a diagnosis. You have to be able to make an assessment. And then only after those things are done, then you start to think about medications.
VIP is a neurotransmitter with regulatory actions on blood flow, secretion and muscle tone with intracorporal adenylate cyclase activation and smooth muscle relaxation. VIP has been shown to elevate cAMP intracellular concentrations without affecting cGMP levels. However, when VIP is given alone it may not induce erection and requires combination with phentolamine or papaverine for it to be effective (88). Common associated adverse effects were facial flushing and headache. VIP in combination with phentolamine is currently being used in the UK and Europe and is seeking regulatory approval for use in the United States.
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In 1983, Brindley injected the corpora of several SCI men with phentolamine (85). Two out of the three men had a sufficient erection produced. Since then multiple reports on the efficacy of intracavernosal therapy have been published using, phentolamine, papaverine, prostaglandin, vasoactive intestinal peptide (VIP), and these medications in combination (86-90). These medications have been found to be extremely effective for neurogenic ED due to their ability act locally and essentially bypassing neuronal pathways. Local therapies are usually considered second-line after PDE5i fail to elicit a desired response which can occur in about 25–30% of men with ED, in general (91). Furthermore, the locally delivered medications can be quite dangerous if not used appropriately as priapism and significant pain with injections can occur. These specific occurrences have been suggested as a reason for high discontinuation rates with intracavernosal therapy (92).
The mechanisms by which testosterone plays a role in erectile function are not completely understood. A study evaluating the effect of testosterone on erections in surgically castrated rabbits and control animals, in which the rabbits’ intracavernosal pressures were compared after cavernosal nerve stimulation, determined that castrated rabbits had much lower pressures after stimulation than control rabbits did. [21] Notably, the pressures increased when castrated rabbits received exogenous testosterone replacement.
The Massachusetts Male Aging Study (MMAS) documented an inverse correlation between ED risk and high-density lipoprotein (HDL) cholesterol levels but did not identify any effect from elevated total cholesterol levels. [15] Another study involving male subjects aged 45-54 years found a correlation with abnormal HDL cholesterol levels but also found a correlation with elevated total cholesterol levels. The MMAS included a preponderance of older men.
VED involved placing the penis in a clear plastic tube where negative pressure created by the vacuum pump leads to penile engorgement and tumescence. Usually a constriction ring can be placed on the base of penis following penile engorgement. Some men complain of bruising, a “cold” penis and pain associated with the constriction ring; however, in some men with NED sensation may not be intact mitigating the side effects of VEDs. VEDs have reported effectiveness up to 90% in certain ED populations and it remains a non-invasive means to achieve and erection.
The percentage of men who engage in some form of sexual activity decreases from 73% for men aged 57–64 years to 26% for men aged 75–85 years.3 For some men, this constitutes a problem, but for others it does not. The aetiology for this decline in sexual activity is multifactorial and is in part due to the fact that most of the female partners undergo menopause at 52 years of age with a significant decline in their libido and desire to engage in sexual activity. A study by Lindau and colleagues3 that examined sexuality in older Americans showed that 50% of the men in a probability sample of more than 3000 US adults reported at least one bothersome sexual problem and 33% had at least two such problems.3 This article will review the normal changes that occur with ageing, factors that influence these changes, individual variations and perspectives, and the available treatment options for ED and androgen deficiency.

A physical examination is necessary. The doctor will pay particular attention to the genitals and nervous, vascular, and urinary systems. Your blood pressure will be checked because several studies have demonstrated a connection between high blood pressure and erectile dysfunction. The physical examination will confirm information you gave the doctor in your medical history and may help reveal unsuspected disorders such as diabetes, vascular disease, penile plaques (scar tissue or firm lumps under the skin of the penis), testicular problems, low male hormone production, injury, or disease to the nerves of the penis and various prostate disorders.


Sexual dysfunction and ED become more common as men age. The percentage of complete ED increases from 5% to 15% as age increases from 40 to 70 years. But this does not mean growing older is the end of your sex life. ED can be treated at any age. Also, ED may be more common in Hispanic men and in those with a history of diabetes, obesity, smoking, and hypertension. Research shows that African-American men sought medical care for ED twice the rate of other racial groups.
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