Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Erectile dysfunction secondary to cardiovascular disease often responds well to the standard ED treatments developed over the past few decades. Penile prosthesis implantation was developed in the 1970s, followed by intracavernosal injections of vasoactive agents, including papaverine, phentolamine, and prostaglandin E1, introduced in the 1980s.11x11Nehra, A. Intracavernosal therapy: when oral agents fail. Curr Urol Rep. 2001; 2: 468–472
Erectile dysfunction (ED) is highly prevalent affecting at least 50 % of men with diabetes mellitus (DM). DM may cause ED through a number of pathophysiological pathways. These include neuropathy, endothelial dysfunction, cavernosal smooth muscle structural/functional changes, and hormonal changes. Lifestyle changes, diabetes control, and treatment of hypogonadism are important as the first step in ED management since there is no curative treatment for ED. Phosphodiesterase type 5 inhibitors (PDE5i) are the first-line treatment option. Intracavernous administration of vasoactive drugs is commonly used as a second-line medical treatment when PDE5i have failed. Alprostadil is the most widely used drug in this second-line setting. The combination of papaverine, phentolamine, and alprostadil represents the most efficacious intracavernous pharmacologic treatment option that may save non-responders to alprostadil. Penile prosthesis implantation can be considered in treatment refractory cases, with excellent functional and safety results in the properly informed patients.
Crossref | PubMed | Scopus (528) | Google ScholarSee all References Sildenafil also has good efficacy in patients with ischemic heart disease, as shown by a retrospective subanalysis of data from 11 double-blind, placebo-controlled studies involving 3672 patients with ED and ischemic heart disease who were not taking nitrates.59x59Kloner, RA. Cardiovascular risk and sildenafil. Am J Cardiol. 2000; 86: 57F–61F
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.
Severe testosterone deficiency, known as “hypogonadism,” is present in approximately 2–35% of men with erectile dysfunction.19 However, lesser degrees of deficiency are common, perhaps present in the majority, depending on the definition of “low” applied, the method of measurement, and the parameter being used to define testosterone (total, free, or bioavailable) deficiency.19,20 Most authorities agree that a total testosterone level below 300 ng/dL is clearly low, and that 300–400 ng/dL is low to low-to-normal. Most studies using testosterone replacement for erectile dysfunction have attempted to achieve blood levels of 450–850 ng/dL.
The great majority of ED cases in diabetic men have a physical cause, such as neuropathy or circulatory problems. In some cases, however, the cause of ED is psychological, including depression, guilt, or anxiety. With a thorough exam, the doctor should be able to determine whether the ED is psychological or physical in nature. If the cause is psychological, your doctor may refer you to a psychiatrist, psychologist, sex therapist, or marital counselor. Do not view such a diagnosis as an insult. Most psychologically-based ED is easily and successfully treated.
Heart disease describes a range of conditions that affect your heart. Diseases under the heart disease umbrella include blood vessel diseases, such as coronary artery disease; heart rhythm problems (arrhythmias); and heart defects you’re born with (congenital heart defects), among others.The term “heart disease” is often used interchangeably with the term “cardiovascular disease.” Cardiovascular disease generally refers to conditions that involve narrowed or blocked blood vessels that can lead to a heart attack, chest pain (angina) or stroke. Other heart conditions such as those that affect your heart’s muscle, valves or rhythm, also are considered forms of heart disease.
The primary complication of the surgical implantation is postoperative infection, which occurs in about 8% of cases involving diabetes. This infection can be difficult to treat and may require the removal of the device, although this occurs <3% of the time. The infection can also cause penile erosion, reduced penile sensation, and auto-inflation. Glycemic control should be optimized several weeks before surgery. Once a patient has surgery, none of the oral agents or vacuum devices will work because of the destroyed penile architecture.
Treatments might be slightly different for different people, depending on their risk factors, but in general all treatment plans have similar elements: diet, exercise, and medications, if necessary (see the Table). Diet and exercise are the cornerstones of the treatment of atherosclerosis. Every diet should include low salt (especially for high blood pressure), low fat and cholesterol (especially for high cholesterol), and limited total calories (especially for patients who are overweight). People with diabetes mellitus should limit their intake of sugars and carbohydrates. Exercise helps to limit atherosclerosis. The more exercise, the better, but every little bit helps. The general recommendation is 30 minutes a day 5 days a week. Check with your doctor to be sure that an exercise program is safe for you. Cigarettes cause a variety of health problems, including atherosclerosis, so cigarette smoking should be stopped. If diet and exercise are not enough to control your atherosclerotic risk factors, then your doctor will prescribe medications. Heart attacks are prevented by controlling atherosclerotic risk factors, which means diet, exercise, and medications if necessary.
An equally valuable observation though, is the fact that sexual dysfunction could indeed indicate asymptomatic CV disease. A solid amount of evidence accumulated over the last years has pointed out towards that trend moving, hesitatingly though, sexual dysfunction in the surface of scientific interest. As such, commonly under-reported, under-recognized and under-treated, sexual dysfunction could indeed play its role in cardiovascular risk assessment and stratification.

Abstract | Full Text PDF | PubMed | Scopus (1528) | Google ScholarSee all References After sexual intercourse, this risk increases approximately 2-fold, to 2 chances per million per hour, but only for the 2 hours after intercourse. For low-risk patients with no history of cardiovascular disease and an annual myocardial infarction risk of 1% per year, the risk increases to 1.01% with weekly sexual activity.8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409


If you take a diuretic, you should stay on it until high blood pressure is under control. If erection problems persist, or blood pressure goes back up, then your doctor might switch to a drug that's less likely to cause erectile dysfunction. Or, a combination of medications might work better to control high blood pressure and lower the risk of erectile dysfunction.
Clinical practice in TCM has been an exemplary case of customized treatment with holism epitomizes the essence of TCM. TCM encompasses these aspects, taking a holistic approach to patient’s problem and these methods combine body, mind and spirit, and healings are achieved via the concept of energy rather than matter, as in modern medicine. Compared to the complexity of modern science, which is the basis of Western medicine, this concept is easily understood and comprehended, and is readily accepted because of its holistic approach.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (56) | Google ScholarSee all References Of 1774 patients with a history of myocardial infarction, only 2 who had experienced a myocardial infarction after sexual intercourse were able to exercise to at least 6 METs without symptoms.8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409
Abstract | Full Text PDF | PubMed | Scopus (49) | Google ScholarSee all References Also, cigar smoking and passive exposure to cigarette smoke have been shown to significantly predict onset of ED.5x5Feldman, HA, Johannes, CB, Derby, CA et al. Erectile dysfunction and coronary risk factors: prospective results from the Massachusetts Male Aging Study. Prev Med. 2000; 30: 328–338
It's an all too common problem: Roughly half of men with diabetes—and up to 25 percent of men overall—experience erectile dysfunction (ED) at some point in their lives. And it's a complicated problem, too, with diverse physical origins and complex emotional ramifications. Yet diabetes-related ED needn't be a no-sex sentence for men. There are ways to avoid this disorder and to treat it at any age. While much of the research on ED is still in its infancy, here is what science has to say so far.
Quassinoids isolated from Tongkat Ali have been reputed to be anti-tumor, anti-malarial, anti-amoebic and anti-inflammatory. Its leaves are used for washing itches, its fruits for the treatment of dysentery, its bark used as a vermifuge, the taproots used for treatment of hypertension and the root bark for treatment of diarrhea and fever. The roots extracts are used for sexual dysfunction, aging, malaria, cancer, diabetes, anxiety, aches, constipation, exercise recovery, fever, increased energy, increased strength, leukemia, osteoporosis, stress and syphilis. Animal studies done on middle age sex rats showed enhancement of the sexual qualities in terms of hesitation time among middle aged rats (46).
Viagra, Cialis, Levita, and Staxyn all work in a similar fashion and make it physically possible to get an erection when aroused. However, men whose blood pressure is poorly controlled and who take alpha-blockers for high blood pressure treatment should not take any of these treatments for erectile dysfunction as it may reduce blood pressure to critically low levels, causing fainting or sudden death. Also, you may be prohibited to use these drugs if you demonstrate any of the following:
ED almost always has an organic or mixed etiology in diabetic men. This often results in diabetic men reporting more severe ED when they present for treatment of this condition. It is not surprising, therefore, to learn that diabetic men's responses to standard therapy for ED differ from those of the general population of men with ED.38 We, therefore, will now briefly review the literature regarding effectiveness of various ED therapies specifically in diabetic men.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References However, some researchers have questioned whether the strain of sexual activity can be compared accurately with standard types of physical activity and whether sexual activity is more closely related to episodes of anger or fear.85x85DeBusk, RF. Evaluating the cardiovascular tolerance for sex. Am J Cardiol. 2000; 86: 51F–56F
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.
Sexual intercourse is an infrequent cause of myocardial infarction. In a study of 1774 patients after myocardial infarction, only 1.5% of these events occurred within 2 hours of sexual intercourse, and sexual activity was considered a direct contributing factor in 0.9%.8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409
The physical exam should focus on femoral and peripheral pulses, femoral bruits (vascular abnormalities), visual field defects (prolactinoma or pituitary mass), breast exam (hyperprolactinemia), penile strictures (Peyronie’s disease), testicle atrophy (testosterone deficiency), and asymmetry or masses (hypogonadism). A rectal exam allows for assessment of both the prostate and sphincter tone, abnormalities that are associated with autonomic dysfunction. Sacral and perineal neurological exam will help in assessing autonomic function.
Three FDA-approved oral medications, sildenafil, tadalafil, and vardenafil are available. These drugs are phosphodiesterase type 5 (PDE-5) inhibitors that can prolong levels of cGMP in tissue allowing improved smooth muscle relaxation, thus facilitating an erection. PDE-5 inhibitor drugs are effective in 56-63% of diabetic men with ED. More stringent glycemic control can improve these results. Men with testosterone deficiency may benefit from a combination of oral ED medication and testosterone supplementation.
The discovery in 1992 of the second messenger of cavernosal smooth muscle relaxation was the critical step that led to the era of nonhormonal oral drug therapy for ED. In 1998, the multicenter trial of sildenafil in the treatment of ED was published in the New England Journal of Medicine, and the era of the phosphodiesterase type 5 (PDE-5) inhibitor began.1 For 5 years, sildenafil was the primary therapy for men with EDDM. Recently, 2 new PDE-5 inhibitors, vardenafil and tadalafil, were introduced.
Chronic heart failure often develops after other cardiac problems have damaged or weakened the heart, leaving it too weak or too stiff to fill and pump efficiently. Many underlying heart conditions can lead to heart failure. It can develop quickly after damage caused by a heart attack, or it can develop gradually after years of high blood pressure or coronary artery disease.

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)

Montorsi P,  Ravagnani PM,  Galli S,  Rotatori F,  Veglia F,  Briganti A,  Salonia A,  Dehò F,  Rigatti P,  Montorsi F,  Fiorentini C. Association between erectile dysfunction and coronary artery disease. Role of coronary clinical presentation and extent of coronary vessels involvement: the COBRA trial, Eur Heart J , 2006, vol. 27 (pg. 2632-2639)https://doi.org/10.1093/eurheartj/ehl142
The number of men reporting improvement was at 88% during the study. The number of men involved in the study who reported impotence dropped from 75.3 % to 11.8%. The results of this study raise hope for men who have quit taking other blood pressure medications because they interfered with sexual function. Sexual dysfunction was defined for the study as decreased libido, impotence and poor sexual satisfaction.
ED is generally associated with significant changes in established cardiovascular risk factors. Atherosclerosis is the main cause of ED development in both the general population and patients with diabetes. However, the prevalence of ED is greater in patients with diabetes than in the general population.8 ED has been shown to occur at rates as high as 50 % in patients with CAD.9 A meta-analysis of 12 prospective cohort studies has provided evidence that ED is a predictor of IHD associated with an increased risk of CVD, stroke and all-cause mortality.10
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).
Guidelines recommend that phosphodiesterase type 5 (PDE5) inhibitors are the first-line drug for the treatment of ED (Table 1). Sildenafil citrate was the first oral drug approved for ED in the US.59 The newer PDE5 inhibitors include vardenafil, tadalafil and avanafil. The inhibition of PDE5 enhances cyclic guanosine monophosphate (cGMP)-NO-mediated vasodilatation by preventing PDE5 catabolism of cGMP and so delaying detumescence. PDE5 inhibitors increase the number and duration of erections, as well as the percentage of successful sexual intercourse.60

With great interest we have read the recently published review by Vlachopoulos et al, a very detailed and extensive overview of erectile dysfunction in the cardiovascular patients. Guidelines for the management of erectile dysfunction with heart failure were noted, as well as advice about dealing with erectile dysfunction (ED) in patients with cardiovascular disease (CVD). However, many others have written similar reviews and guideline concerning the care for ED as well as (female) sexual dysfunction in CAD in the past years (1-4), cardiologists should be familiar with this matter by now. The problem is the actual translation of this knowledge into actions in cardiologists' daily clinical practice. Our research group performed a survey among Dutch cardiologists, aiming to evaluate their inquiry about erectile function in day-to-day practice, to detect their attitude towards this discussion and their perceived barriers for addressing sexual activity. Results from this survey indicated that cardiologists (n=414) did not routinely discuss erectile dysfunction: 48.7% indicated to discuss sexual function 'sometimes' and only 16.9% said to discuss the subject regularly. Of respondents, 41.5% marked that care for patients' sexual quality of life is not their responsibility. Nevertheless, 42% indicated that they would benefit from training to obtain knowledge about treatment of erectile and sexual dysfunction in cardiologic patients. Barriers not to inquire about sexual activity included 'the patient does not ask about it' (53.7%), 'I do not have an angle or motive to start about it'(45.9%), as well as time constraints (42.9%) and lack of training in dealing with sexual dysfunction (35.2%). The more experienced the cardiologist was the less he/she stated the need for training or for a referral directory(5). Since all cardiologists should, meanwhile, know that ED is part of their responsibility, as it is a sentinel marker of CVD(6). It is now case to pay attention to the implementation of the care for erectile and other sexual dysfunction in the cardiology practice. Our study suggests that physicians' experience in the field plays an important role in discussing sexual activity and that sexual healthcare can be improved with more education about the subject. Furthermore a directory of the available healthcare professionals for the referral of patients with sexual dysfunction was indicated as mandatory. We suggest that attention of cardiologists should not only be focused on writing about ED and CVD, attention should be diverted to the actual implementation of care for patients with ED as well, in order to improve patient-centered healthcare in cardiology.
PubMed | Google ScholarSee all References They evaluated 40 patients with coronary artery disease who underwent coronary artery catheterization and whose penile brachial index (PBI) was measured by Doppler ultrasonography. Although a positive correlation was noted between the PBI and the severity of coronary artery obstruction, the relationship was not strong. Also, the degree of PBI abnormality did not effectively stratify the patients according to the severity of their coronary artery blockage. This study concluded that the PBI used alone would not be an effective predictor of ischemic heart disease.
Figure. Progression of atherosclerosis. Endothelial dysfunction occurs early in atherosclerosis and prevents blood vessels from dilating properly. When the blood vessels that supply the penis are not able to dilate during sexual stimulation because of endothelial dysfunction, the penis cannot fill with blood, and the man develops erectile dysfunction. As atherosclerosis progresses, plaques build up in blood vessels and blood flow is slowed, further worsening erectile function. A heart attack occurs when an atherosclerotic plaque in a coronary artery ruptures, a blood clot forms over the plaque, and blood flow to the heart muscle is completely blocked. Atherosclerotic risk factors (black arrows) worsen cardiovascular health; modification of these risk factors (red arrows) improves cardiovascular health.

Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Since then, several other oral PDE-5 inhibitors have been developed, including vardenafil and tadalafil, which generated considerable interest in both the scientific and lay communities. There was also much concern about their safety, especially in men with cardiovascular disease. Compared with the 2 newer PDE-5 inhibitors vardenafil and tadalafil, sildenafil has been available for a much longer time; therefore, the vast majority of published cardiovascular safety studies have been performed on this medication. Recommended starting and maximum doses of oral PDE-5 inhibitors are shown in Table 1.
Crossref | PubMed | Google ScholarSee all References Risk factors for cardiovascular disease include diabetes mellitus, obesity, physical inactivity, hyperlipidemia, tobacco use, and hypertension. Often, the relative risk of each of these factors in the development of ED is difficult to assess because many patients with ED and cardiovascular disease have more than 1 risk factor. Another important consideration is the effect of cardiac disease itself on erectile function. A history of a prior myocardial infarction was not found to be a significant independent risk factor for ED in a study comparing sexual function in 50 patients who had a prior myocardial infarction with a control group of 50 patients.14x14Dhabuwala, CB, Kumar, A, and Pierce, JM. Myocardial infarction and its influence on male sexual function. Arch Sex Behav. 1986; 15: 499–504
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References The risk after sexual activity in these patients is unknown, although vasodilators should be avoided because they may increase the intraventricular gradient.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
A significant proportion (ranging from ∼60 to 90%) of heart failure patients report ED and marked decrease in sexual interest, with ultimately one-quarter reporting cessation of sexual activity altogether.48 Erectile dysfunction contributes further to the poor quality of life and aggravates depression. Of interest, many heart failure patients place a greater importance on improving the quality of life (including sexual activity) than on improving survival. Sexual function correlates with the symptomatic status (i.e. NYHA functional class and 6-minute walk test).48 In the Evaluation of Role of Sexual Dysfunction in the Saarland (EROSS) Program, left ventricular dysfunction was a risk factor for ED independent of heart failure symptoms. While heart failure and ED share common pre-disposing risk factors, heart failure by itself can cause ED or affect engagement to sexual activity. Neurohumoral activation, medication (thiazides), limited exercise capacity, and depression are responsible.49
Abstract | Full Text PDF | PubMed | Scopus (19) | Google ScholarSee all References However, there has been disagreement regarding the effects of diuretics on erectile function; many studies found that only rarely have these medications been implicated convincingly as the cause of a patient's ED.36x36Wein, AJ and Van Arsdalen, KN. Drug-induced male sexual dysfunction. Urol Clin North Am. 1988; 15: 23–31

Characteristics that imply a higher risk is severe ED (SHIM 1–7) and ED duration >3 years.15,30 Vascular and circulating biomarkers may help to characterize further the patient with ED.23 Of the wide array of biomarkers that have been proposed for the assessment of cardiovascular risk in asymptomatic adults,34,35 some have been studied specifically in the context of ED.23Table 4 offers a critical evaluation of these biomarkers. Such tests should be considered as potentially helpful and thus recommended where available, but not mandatory.30 Despite its potent predictive ability recently shown,36 exposure to radiation with coronary artery calcium scoring should be carefully weighed. Although not specific for ED, it might be reasonable to evaluate biomarkers that have been proposed for the intermediate-risk patient such as uric acid, glycated haemoglobin, microalbuminuria, and lipoprotein-associated phospholipase A2.30


Crossref | PubMed | Scopus (539) | Google ScholarSee all References Possible etiologies for ED secondary to hypertension include vascular damage due to hypertensive changes as well as hormonal abnormalities such as elevated prolactin levels.30x30Jaffe, A, Chen, Y, Kisch, ES, Fischel, B, Alon, M, and Stern, N. Erectile dysfunction in hypertensive subjects: assessment of potential determinants. Hypertension. 1996; 28: 859–862
Abstract | Full Text PDF | PubMed | Scopus (29) | Google ScholarSee all References After controlling for diabetes mellitus, tobacco use, and hyperlipidemia, hypertension was not found to be an independent predictor of vasculogenic ED in 440 impotent men as measured by the PBI.7x7Virag, R, Bouilly, P, and Frydman, D. Is impotence an arterial disorder? a study of arterial risk factors in 440 impotent men. Lancet. 1985; 1: 181–184
Crossref | PubMed | Scopus (25) | Google ScholarSee all References In comparison, a randomized placebo-controlled trial of 65 patients given either placebo or 95 mg/d of sustained-release metoprolol for 4 months after percutaneous coronary angioplasty found no significant difference in sexual function between the 2 groups.44x44Franzen, D, Metha, A, Seifert, N, Braun, M, and Hopp, HW. Effects of beta-blockers on sexual performance in men with coronary heart disease: a prospective, randomized and double blinded study. Int J Impot Res. 2001; 13: 348–351
There are a number of reasons a man may not achieve the desired result from an oral erectile dysfunction drug. In some cases, a man may experience drug side effects severe enough to outweigh any potential benefit of taking the drug. Possible side effects of these drugs include headache, facial flushing, nasal congestion, and transient abnormal vision. (In October 2007, the FDA added a warning about sudden hearing loss to the package labels of oral erectile dysfunction drugs. While it’s not absolutely clear that the drugs can cause sudden hearing loss, a number of cases have been reported in men within hours or days of taking one of the drugs.)
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