There have been some studies to suggest that a placebo effect that improves ED may work for some men. One study found that men taking an oral placebo pill showed as much improvement in ED symptoms as men who took actual medication to improve ED. Conversely, men who were given therapeutic suggestions to improve ED did not see signs of symptom improvement.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (395) | Google ScholarSee all References Sildenafil has no effect on bleeding time or prothrombin time when used either alone or in patients taking aspirin or warfarin.61x61Nehra, A, Colreavy, F, Khandheria, BK, and Chandrasekaran, K. Sildenafil citrate, a selective phosphodiesterase type 5 inhibitor: urologic and cardiovascular implications. World J Urol. 2001; 19: 40–45
As you get older, your risk of both ED and heart disease increases. But the connection between these conditions is stronger among younger men, according to the Mayo Clinic. If you experience ED under the age of 50, it’s more likely to be a sign of underlying heart problems. If you experience it after the age of 70, it’s much less likely to be linked to heart disease.
The recommended dosage of sildenafil is 50 mg/day, usually taken 1 hour before sexual activity. This dose may be increased to 100 mg or decreased to 25 mg based on side effects.6 PDE5 inhibitors also have a beneficial effect in the treatment of heart failure with reduced ejection fraction as well as pre- and post-capillary pulmonary hypertension. The use of PDE5 inhibitors in the treatment of right heart failure and left ventricular failure associated with combined pre- and post-capillary pulmonary hypertension has been well studied.71,72
Ischaemic heart disease (IHD), also known as coronary artery disease (CAD), is a predominant manifestation of cardiovascular disease (CVD). CVD is the leading cause of morbidity and mortality, accounting for 17.3 million deaths globally every year; this figure is expected to grow to 23.6 million by the year 2030. Eighty per cent of these deaths occur in lower- and middle-income countries.5 ED and IHD are highly prevalent and occur concomitantly because they share the same risk factors, including diabetes, hypertension, hyperlipidaemia, obesity and smoking.
Treatment of ED which was previously confined to invasive procedures, cavernosal injections or to rather ineffective oral medications was revolutionized in 1999 with the introduction of the orally administered PDE5 inhibitor sildenafil. Phosphodiesterase type 5 inhibitors are the first-line therapy for ED of organic aetiology unless there is a specific contraindication to their use. This class of agents is widely used because of its effectiveness and safety.38 Interactions with cardiovascular drugs have been minimal with the exception of nitrates and other nitric oxide (NO) donors (such as nicorandil), where co-administration may result in severe vasodilation and hypotension. However, nitrates are often overused in clinical practice; therefore, the option of their discontinuation should be considered. A strong body of clinical data shows that all three agents (sildenafil, tadalafil, and vardenafil) do not increase the risk of non-fatal myocardial infarction, stroke, or cardiovascular deaths. These drugs do not exacerbate ischaemia or worsen exercise tolerance in patients with known CAD who achieve levels of exercise comparable or greater than that achieved during sexual intercourse.38,39 Phosphodiesterase type 5 is expressed throughout the human body, including the pulmonary and systemic vasculature and hypertrophied myocardium. While currently their only additional indication, beyond ED, is idiopathic pulmonary hypertension (for sildenafil and tadalafil), they show potential to be of benefit in several other conditions, such as CAD and systolic heart failure.39 Mechanisms of benefit of PDE5 inhibitors include pulmonary and systemic vasodilation, increased myocardial contractility, reduced large artery stiffness and wave reflections, improved endothelial function, and reduced apoptosis, fibrosis and hypertrophy through mechanisms involving NO, cyclic guanosine monophosphate, protein kinase G and Rho kinase.39 A very important issue is whether treatment of ED per se (and not of its risk factors and comorbidities) will have an impact on cardiovascular risk. While this applies to all therapeutic modalities of ED, it is particularly pertinent for PDE5 inhibitors, since they represent the mainstay of ED therapy. Data are limited to date. Gazzaruso et al.21 showed a trend of PDE5 inhibitors to reduce cardiovascular morbidity and mortality in diabetic patients with silent CAD and ED, while Frantzen et al.40 showed that 2 years after the introduction of sildenafil, the relative risk of the incidence of CVD among men with ED compared with healthy men significantly decreased from 1.7 to 1.1.
Patients who use this therapy should be trained under the guidance of a urologist, and sterile technique must be used. The drugs must be injected into the shaft of the penis and into one of the penile erectile bodies (corpus cavernosum) 10–15 min before intercourse. Most patients do not complain of pain upon injection. Sexual stimulation is not required, and resulting erections may last for hours. Side effects include penile pain and priapism. The cost is about $12–20 per injection.
A thorough history (including cardiovascular symptoms, age, presence of risk factors and comorbid conditions such as obesity, hypertension, dyslipidaemia, pre-diabetes, CAD, peripheral artery disease, symptoms suggestive of sleep apnoea, family history of premature atherothrombotic CVD and lifestyle factors), assessment of ED severity (according to SHIM) and duration, and physical examination (for both heart and peripheral circulation pathology) are mandatory first-line elements of investigation. A resting electrocardiogram, measurement of fasting plasma glucose, and estimation of glomerular filtration rate are desirable tests that may be used to further characterize cardiovascular status and risk and to identify men who require additional cardiologic workup. Owing to the accumulating evidence supporting the link with CVD, the measurement of testosterone is recommended in all men with a diagnosis of organic ED, especially in those for whom phosphodiesterase type 5 (PDE5) inhibitor therapy failed.
Oral medicines: The best known ED medications are the Big Three: Viagra (sildenafil citrate, made by Pfizer, Inc.), Levitra (vardenafil HCl, made by Bayer and GlaxoSmithKline), and Cialis (tadalafil, made by Eli Lilly). The three are chemically very similar, and all have proven very effective. Because they are effective, convenient, and relatively inexpensive (about nine dollars per pill), these medicines have become the treatment of choice for most men experiencing ED.
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 (25) | Google ScholarSee all References Patients with prior cardiac events should be encouraged to enroll in cardiac rehabilitation programs before restarting sexual activity.80x80Muller, JE. Triggering of cardiac events by sexual activity: findings from a case-crossover analysis. Am J Cardiol. 2000; 86: 14F–18F
The Epimedium plant is a flowering perennial found throughout Asia and parts of the Mediterranean. Horny Goat Weed’s active ingredient is icariin, a falvonol glycoside and reputed to improve cardiovascular function, hormone regulation, modulation of immunological function and antitumor activity (44). Icariin has also been shown to have a PDE5i effect. Animal studies have been carried out showing improvements in penile hemodynamic parameters. There is one report of tachyarrhythmia and hypomania with the use of this herb (45).
Abstract | Full Text | Full Text PDF | PubMed | Scopus (30) | Google ScholarSee all References Erections result from relaxation of the corpora cavernosa, which is mediated either by increasing intracellular cyclic guanosine monophosphate (cGMP) or cyclic adenosine monophosphate or by inhibition of their degradation. Increased parasympathetic tone results in a decrease in norepinephrine release and an increase in the release of acetylcholine; subsequently, NO synthase activity increases, which releases NO from both endothelial cells and nonadrenergic, noncholinergic neurons.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Despite the existing controversies, available data so far imply the old generation b-blockers (e.g., propranolol) as the major culprits for sexual dysfunction with the newer ones (carvedilol, celiprolol) to exert a less pronounced negative effect[21-24]. A luminous exception to the rule, nebivolol, is a newer agent of its class which significantly ameliorates erectile dysfunction through increased nitric oxide generation, an effect consistently demonstrated in recent studies[25,26]. Diuretics, even on adjunct therapy, constitute another antihypertensive agent negatively associated with sexual function[27-29]. On the other hand, calcium antagonists and angiotensin converting enzyme inhibitors seem to demonstrate a neutral effect[30-32]. Interestingly, angiotensin receptor blockers (ARBs) by blocking the vasoconstrictive action of angiotensin II seem to positively affect erectile function and are thus regarded as a first-line treatment in hypertensive patients with erectile dysfunction[22,25,33-35].
One study the authors reviewed measured these changes in middle-aged men with and without coronary artery disease. This study found that the peak heart rate during intercourse was lower than heart rates measured during the patients' normal daily activities. The study participants' peak oxygen consumption levels during intercourse were moderate -- comparable to their oxygen consumption levels during moderate activities such as walking on level ground at 3 to 4 miles per hour, climbing stairs slowly or doing general housework such as vacuuming.
There are currently two models of the inflatable penile prosthesis (IPP), namely, the two-piece IPP vs. the three-piece IPP. The three-piece IPP consists of a pair of corporal cylinders, a scrotal pump and an abdominal reservoir filled with saline. Owing to the presence of the reservoir, the corporal cylinders can be completely deflated to give the patient the physiological flaccid state when not in use, and likewise a maximally turgid state when inflated (21). The two-piece IPP lacks an abdominal reservoir and is often offered in patients with whom placement of reservoir is challenging or not possible such as following radical cysto-prostatectomy with orthotopic ileal neobladder creation, or patients who had previous open book fracture of the pelvis with metal implants. The concept of ectopic reservoir placement has allowed many of these men the option for three-piece IPP placement (22). Technological advances have improved mechanical reliability, reduced prosthesis infection risk and offered excellent patient and partner satisfaction rate (23).
88. Böhm M, Baumhäkel M, Teo K, Sleight P, Probstfield J, Gao P, Mann JF, Diaz R, Dagenais GR, Jennings GL, et al. Erectile dysfunction predicts cardiovascular events in high-risk patients receiving telmisartan, ramipril, or both: The ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial/Telmisartan Randomized AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease (ONTARGET/TRANSCEND) Trials. Circulation. 2010;121:1439–1446. [PubMed]
Most studies into the effect of beta-blockers on ED point to negative effects of first- and second-generation beta-blockers, while beta-blockers with vasodilating effects can improve erectile function. Alpha-blockers, calcium channel blockers, and angiotensin-converting enzyme inhibitors seem to have a neutral effect on erectile function. Multiple previous studies have demonstrated a beneficial effect of angiotensin receptor blockers on erectile function and they should probably be the favoured antihypertensive agents in patients with ED.29
According to the Cleveland Clinic, “because erectile dysfunction is caused by a complex set of psychosocial, neurologic, and vascular factors, a specific cause in a patient may remain ambiguous.” The root causes are often related to a blockage or dysfunction of blood vessels. For example, ED can be due to conditions like atherosclerosis or diabetes, hormonal imbalances or problems related to mental health. It’s been found that common causes typically include one or more of the following factors: (2)
Now that we better appreciate the complex sequence of events necessary for erections to occur, it’s no surprise that testosterone alone yields less than perfect results. Erectile dysfunction represents more than just low testosterone, which is just one facet of the spectrum of dysfunctional phenomena that cause sexual dysfunction. Nonetheless, when testosterone is combined with popular drugs like Viagra®, success is enhanced to an even greater degree—orgasmic function improves, along with erectile capacity and libido.20 Testosterone also activates penile nitric oxide; ultrasound studies have demonstrated a 27% increase in arterial blood flow into the penis with testosterone supplementation.23
Because ED has several causes, sorting out exactly what is causing your problem may take some time. First, make sure your doctor knows about all the medicines you are using, including over-the-counter or herbal products. Drugs frequently used to treat high blood pressure, anxiety, depression, and peptic ulcers can all cause ED. But don’t stop taking any of your medications without first talking to your doctor.
airdone/ShutterstockErectile dysfunction (ED) is a serious issue for men, which helps explain all the prescription drugs, over-the-counter treatments, and herbal concoctions that claim to cure ED. (In fact, it’s one of the top nine health risks men need to watch out for.) But before any guy decides to take matters into his own hands, he should talk to his doctor about a heart checkup: A new study published in the journal Vascular Medicine suggests ED can signal cardiovascular concerns.
People sometimes refer to ED as "impotence," although the two aren't really the same condition. ED is the physical inability to develop or maintain an erection that is rigid enough for sex. Impotence is a broader term. While one cause of it is ED, impotence may also involve a lack of sexual desire, an inability to ejaculate, or problems with orgasm.
Yet another common erectile dysfunction treatment that can be used in combination with oral drugs is a vacuum pump. This device consists of a plastic cylinder, a pump, a set of constriction bands, and a water-soluble lubricant. The lubricant is applied to the base of the penis to help form an airtight seal. The cylinder is placed over the flaccid penis and held tight against the pelvis. The pump is used to create a vacuum within the cylinder, drawing blood into the penis. Once the penis is engorged with blood, a constriction band is rolled off the cylinder to near the base of the penis. The constriction band is helpful for men with venous leakage, in which blood flows out of the penis as fast as it flows in. However, it should be left on for no more than 30 minutes at a time.