Some blood pressure medicines can also cause erectile dysfunction. Thiazide diuretics and beta-blockers are most likely to cause problems, but this is not a common effect of these medicines and will not happen to everyone. If you are taking either of these medicines and are worried about erectile dysfunction, your GP may be able to change your medicines.

Since erectile dysfunction presents such an intimate relationship with CV parameters, it is easily deducted that it could constitute a powerful tool for detecting asymptomatic CV disease. Consequently, recognition of sexual dysfunction in a hypertensive individual should prompt further diagnostic procedures and therapeutic interventions in order to disclose its silent cardiovascular risk and improve patient’s quality of life and life expectancy.

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.


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Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Sildenafil has a 4000-fold increased selectivity for PDE-5 over PDE-3, has negligible effects on heart rate, and has only a modest effect on blood pressure level in healthy persons, with an average systolic pressure decrease of 10 mm Hg with a single dose of 100 mg.3x3Zusman, RM, Morales, A, Glasser, DB, and Osterloh, IH. Overall cardiovascular profile of sildenafil citrate. Am J Cardiol. 1999; 83: 35C–44C


Poor sleep patterns can be a contributing factor for erectile dysfunction, Mucher says. One review published in the journal Brain Research emphasized the intricate relationship between the level of sex hormones like testosterone, sexual function, and sleep, noting that testosterone levels increase with improved sleep, and lower levels are associated with sexual dysfunction. Hormone secretion is controlled by the body’s internal clock, and sleep patterns likely help the body determine when to release certain hormones. 
Counselling or sex therapy (58% of people find this works for them) –mind-related causes of erectile dysfunction can affect anyone. They are more likely if you experience erectile dysfunction at a younger age. Talking to a counsellor or therapist can help some people overcome erectile dysfunction related to these problems, possibly for good. They can also help you if your erectile dysfunction is causing you stress, as this can make matters worse.
The Massachusetts Male Aging Study of 1,290 men, aged 40–70 years, has documented the extraordinarily high prevalence of erectile dysfunction among aging men: 50% of men at 50 years of age, and 70% by age 70 have erectile dysfunction.2 Furthermore, a recent Italian study of men with severe heart disease has uncovered an astounding 93% with erectile dysfunction 24 months before their heart attack or onset of heart disease symptoms.3
Some research even suggests the effect of blood pressure drugs may be more psychological than physical. When ED occurs after a man begins to take a new medication, it's possible that anxiety about his health, rather than the medication, may trigger the problem. And being aware of possible side effects may make a man more likely to recognize them as abnormal.
Since their introduction in the therapeutic field, more than a decade ago, PDE-5 inhibitors have revolutionized the treatment of sexual dysfunction. By blocking the activity of PDE-5 isoenzyme, localized throughout the smooth muscle cells of the vasculature (genital vessels included), PDE-5 inhibitors increase the levels of cyclic guanosine monophosphate thus exerting vasodilating properties and facilitating penile erection[40-42]. Due to these properties, sildenafil was the first drug of its class to receive wide acceptance. Its short half-life, food interactions and the associated visual disturbances however, paved the way for the development of newer PDE-5 inhibitors. As such vardenafil with its more rapid onset of action, and tadalafil with its longer half-life and the lack of food interactions or side effects, have offered significant alternatives to sildenafil[43-50].
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References, 56x56Wallis, RM, Corbin, JD, Francis, SH, and Ellis, P. Tissue distribution of phosphodiesterase families and the effects of sildenafil on tissue cyclic nucleotides, platelet function, and the contractile responses of trabeculae carneae and aortic rings in vitro. Am J Cardiol. 1999; 83: 3C–12C
Vasculogenic sexual dysfunction is the main cause of sexual dysfunction in untreated hypertensive patients. However, due to the complex etiologic and pathophysiologic nature of sexual dysfunction, exclusion of concomitant diseases and drugs should be the initial step when approaching a hypertensive patient with this clinical condition that is not receiving any antihypertensive medication. Consequently, a significant amount of neurological, psychiatric, urologic and endocrine disorders should be ruled out before vasculogenic sexual dysfunction is diagnosed.
Crossref | PubMed | Scopus (53) | Google ScholarSee all References This study found that, although hypertensive patients had more coronary artery disease, no direct evidence supported an association between hypertension and arteriogenic impotence, as measured by the PBI, peak systolic velocity, and resistive index, in patients with mild to moderate hypertension.
The vascular endothelium has an important role in angiogenesis and vascular repair by producing regulatory substances, including NO, prostaglandin, endothelins, prostacyclin and angiotensin II. These regulatory factors regulate the blood flow to the penis by controlling smooth muscle contractility and subsequent vasoconstriction and vasodilatation. Generally, in erectile tissue, increased blood flow through the cavernosal artery increases shear stress and produces NO, which further relaxes the vascular smooth muscles and increases blood flow in the corpora cavernosa.54 These events cause penile erection. However, in ED, endothelial NO synthesis is reduced and there is increased endothelial cell death (Figure 2).55
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
Diuretics: Diuretics are also referred to as water pills. They can make the flow of blood to your penis less intense. This makes getting an erection difficult. Diuretics are also known to lower zinc levels, which can decrease the amount of testosterone your body makes. In turn, this can decrease your sex drive. It may also affect your muscle contraction.
This may seem like a lot to manage at a glance, however, just focus on one step at a time. If it is more exercise you want to start with, park your car further away from the front door at work so you have to walk a little more every day. Or go out on a walk to make your phone calls.  If you need to eat better,  try low-fat meat and chicken for lunch. Just keep it simple and don’t try to do it all at once.
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
Bohm M,  Baumhakel M,  Teo K,  Sleight P,  Probstfield J,  Gao P,  Mann JF,  Diaz R,  Dagenais GR,  Jennings GL,  Liu L,  Jansky P,  Yusuf S. ONTARGET/TRANSCEND Erectile Dysfunction Substudy InvestigatorsErectile 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, vol. 121 (pg. 1439-1446)https://doi.org/10.1161/CIRCULATIONAHA.109.864199
The natural history of ED in people with diabetes is normally gradual and does not occur overnight. Both vascular and neurological mechanisms are most commonly involved in people with diabetes. Atherosclerosis in the penile and pudendal arteries limits the blood flow into the corpus cavernosum. Because of the loss of compliance in the cavernous trabeculae, the venous flow is also lost. This loss of flow results in the inability of the corpora cavernosae to expand and compress the outflow vessels.

Higher consumption of fiber-rich vegetables, fruits and beans helps to keep blood pressure in the favorable range.10 Beans, nuts and seeds have unique cholesterol-lowering capabilities.11-13 Berries and the flavonoids they contain have a blood pressure-lowering effect, plus berries and pomegranate have potent antioxidant and anti-inflammatory effects that protect against the development of heart disease.14-18


If you can't take one of these oral medications, your physician may have you try Caverject (alprostadil for injection), a hormone that you inject into your penis using a fine needle, or Muse (alprostadil urogenital), a tiny suppository that you insert into the tip of the penis. Both of these will bring on an erection within five to 15 minutes without sexual stimulation.
Poor sleep patterns can be a contributing factor for erectile dysfunction, Mucher says. One review published in the journal Brain Research emphasized the intricate relationship between the level of sex hormones like testosterone, sexual function, and sleep, noting that testosterone levels increase with improved sleep, and lower levels are associated with sexual dysfunction. Hormone secretion is controlled by the body’s internal clock, and sleep patterns likely help the body determine when to release certain hormones. 
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.
Arginine. The amino acid L-arginine, which occurs naturally in food, boosts the body's production of nitric oxide, a compound that facilitates erections by dilating blood vessels in the penis. Studies examining L-arginine's effectiveness against impotence have yielded mixed results. A 1999 trial published in the online journal BJU International found that high doses of L-arginine can help improve sexual function, but only in men with abnormal nitric oxide metabolism, such as that associated with cardiovascular disease. In another study, published in 2003 in the Journal of Sex & Marital Therapy, Bulgarian scientists reported that ED sufferers who took L-arginine along with the pine extract pycnogenol saw major improvements in sexual function with no side effects. Arginine can be helpful, says Geo Espinosa, ND, director of the Integrative Urological Center at NYU Langone Medical Center. Espinosa says that men with known cardiovascular problems should take it only with a doctor's supervision; L-arginine can interact with some medications.
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.
A nutrient-dense, plant-rich (Nutritarian) diet is a huge defense. When men eat for optimal health, they protect their heart, prostate, brain, and, in effect, the entire body. A nutrient-dense, plant-rich (Nutritarian) diet floods the body with protective nutrients, and supports a healthy weight. It not only normalizes risk factors for heart disease and diabetes, but also offers a substantial level of protection against common cancers.

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


Hyperlipidemia has been implicated in the development of ED by several different mechanisms. Hyperlipidemia is associated with development of atherosclerotic blood vessel disease, thus contributing to vasculogenic impotence. Penile vascular changes have been noted in impotent patients with elevated serum lipids.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
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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.
PubMed | Google ScholarSee all References As with sildenafil, use of nitrate or NO-donor medications is contraindicated while taking tadalafil because of the potential for marked hypotensive interactions.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446

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 (72) | Google ScholarSee all References This study found that the mean PSV was a better predictor of the presence of cardiovascular disease than stratification by standard cardiac risk factors such as diabetes mellitus, hypertension, obesity, and smoking. The researchers recommended that persons with no history of prior perineal trauma and with a PSV lower than 35 mL/s should undergo exercise testing before receiving treatment of ED because these patients had a 42% risk of having ischemic heart disease. However, other investigators questioned the utility of using penile arterial flow to predict the presence of ischemic heart disease.18x18Chiu, AW, Chen, KK, Chen, MT, Chang, LS, and Chang, MS. Penile brachial index in impotent patients with coronary artery disease. Eur Urol. 1991; 19: 213–216
Owing to its delicate nature, discussion about the sexual life of the patient is effective not on a circumstantial visit to the doctor, but on the basis of confidence between the patient and the physician, as is usually the case with the cardiologist. Thus, the cardiologist is given a unique opportunity to identify ED and thus ‘recharacterize’ the risk of the patient. In addition, since normal sexual activity is important to most men with CVD, irrespective of age, the cardiologist can clarify issues that relate to such activity after a cardiac event or to a specific cardiac condition (e.g. heart failure). Often, such issues are hampered by misconceptions from the side of the patient. Therefore, while less than half of the patients receive information about resuming sexual activity after a cardiac event, proper counselling increases their likelihood to resume their previous level of sexual activity by 50%.50 Furthermore, the cardiologist can increase adherence to the medication by clarifying that it is uncommonly the true cause of ED. Finally, proper counselling is required to ensure safety of concomitant PDE5 inhibitors medication, the use of which has the additional advantage to increase compliance to CVD mediation, especially in hypertension. It should be noted that while patients are often reluctant to bring up the issue of sexual health, they are relieved and respond positively when their cardiologist has done so. It should also be emphasized that, frequently, sexual counselling is more effective when done together with their partner.
If you have several atherosclerotic risk factors or symptoms of heart disease, your doctor might do additional tests to look for atherosclerosis in the coronary arteries. A stress test involves monitoring the heart with an electrocardiogram or images before and after exercise. An angiogram, or cardiac catheterization, involves entering a blood vessel in the leg or wrist to pass instruments into the heart to directly visualize the coronary arteries. During this procedure, atherosclerosis can be treated by inflating a balloon or placing a metal stent in the coronary blood vessel to keep it open. If you and your doctor begin a treatment plan to prevent atherosclerosis at the first sign of ED, then you may significantly delay or prevent the need for these more invasive procedures.
While additional investigation is usually necessary, the medical and sexual history is essential and frequently the most revealing aspect of the ED assessment process. Questionnaires are an integral part of the history. The International Index of Erectile Function (IIEF), a 15-item, self-evaluation questionnaire is a validated instrument for assessing erectile function, orgasmic function, desire and satisfaction after sexual relations.8 An abridged version of the IIEF is a 5-item questionnaire the Sexual Health Inventory for Men (SHIM) or IIEF-5 (Table 2). Responses to the five questions range from 1 (worst) to 5 (best). Questions 2 to 4 may be graded 0 (if there is no sexual activity, or no sexual intercourse attempt) and the final score ranges from 1 to 25 points; a descending score indicates worsening of erectile function, with values ≤21 being diagnostic of ED.8 Importantly, validated questionnaires correlate with the extend of CAD9 and improve the predictive value of ED for total cardiovascular events compared with a single-question ED diagnosis.5 It cannot be overemphasized that the SHIM can be effectively used not only by andrologists and urologists but by a wide array of medical specialists, such as cardiologists, diabetologists, primary care physicians, etc.
Whereas management of sexual dysfunction in previously untreated hypertensive patients can be a challenging procedure, confronting the same clinical condition in individuals under antihypertensive regime can be even more demanding. In such cases there will always be a question hovering over physicians head. Is hypertension per se, antihypertensive medication or both, the causative factors provoking sexual dysfunction[15]?
In Western medicine approach, health and disease are clearly divided entities. The emphasis is on protection of the individual body from disease or how to replace the body’s lost functions. Antibiotic therapy is used to combat harmful bacteria during infections, exogenous synthetic hormones are used to replace hormone-deficient individuals and artificial prostheses are applied when an organ loses its functions. This is very different from the holistic Eastern approach where the treatment entity is taken as a whole, and the objective is to seek harmony between different bodily systems.
Most importantly, herbal supplements are not well regulated in the United States.  Studies have shown that 40-50% of herbal supplements do not even contain the supposed main ingredient, and many contain substances that are not listed which may have dangerous side effects2.  Another study found that over two thirds of the products tested had substituted other plant species for the plants listed on the label, and a third of products also contained other fillers or contaminants3.  A study by the New York State Attorney General of herbal products sold at GNC, Target, Walgreens, and Walmart found that four out of every five products didn’t contain the ingredient they claimed!  Fourteen US states and territories have petitioned Congress to regulate the herbal supplements industry.
Apart from their beneficial effect in erectile dysfunction and their safe profile in antihypertensive medication, PDE-5 inhibitors have even more advantages to demonstrate. Several lines of evidence has proven that patients receiving PDE-5 inhibitors are more likely to initiate an antihypertensive regime and more willing to add a new agent to their existing treatment, a fact that raises significantly patient’s adherence and as a matter of fact control of high blood pressure and quality of life[63,64]. Moreover, a handful of clinical data has demonstrated the considerable vasodilating and anti-proliferative properties of PDE-5 inhibitors in the pulmonary vasculature, establishing them as a first-line treatment in patients with pulmonary arterial hypertension[65,66]. The same properties have been considered as potentially responsible for improving microcirculation in patients with secondary Raynaud phenomenon and ameliorating cardiopulmonary exercise performance in patients with heart failure[67,68]. In addition, the therapeutic implementation of PDE-5 inhibitors has expanded in the field of benign prostate hyperplasia-lower urinary tract symptoms (BPH-LUTS). The common pathophysiologic substrate between erectile dysfunction and BPH-LUTS has rendered PDE-5 inhibitors an effective treatment which significantly improves measures of both conditions while at the same time exhibits high efficacy and safety. The beneficial effect is much more pronounced when taking into consideration the fact that a-blockers, the mainstay of therapy for benign prostate hyperplasia frequently provoke sexual side effects, erectile dysfunction included[69].
Another risk factor is that men with type 2 diabetes may produce less than normal amounts of testosterone, a condition called hypogonadism. A 2007 study found that one-third of men with type 2 diabetes had low testosterone levels. Those men were also more likely to have ED, though the link may have to do with weight, not diabetes per se. Being overweight or obese is a risk factor for hypogonadism.
There are so many potential reasons a man might develop erectile dysfunction (ED), it's nearly impossible to generalize the best ways to treat it. What works for one man may not work for another simply because they are having problems for different reasons. That said, it may encouraging to hear that there are a variety of options that may be considered, from psychological counseling to lifestyle changes, medications to treatments and devices.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (395) | Google ScholarSee all References The maximum decrease in blood pressure level was noted at 1 hour after the oral dose was taken and was correlated with peak plasma levels. The blood pressure level in these patients returned to baseline within 4 hours.56x56Wallis, RM, Corbin, JD, Francis, SH, and Ellis, P. Tissue distribution of phosphodiesterase families and the effects of sildenafil on tissue cyclic nucleotides, platelet function, and the contractile responses of trabeculae carneae and aortic rings in vitro. Am J Cardiol. 1999; 83: 3C–12C
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).
Consider this:  penicillin, the first successful antibiotic, was derived from molds that inhibit bacterial growth.  Scientists had to figure out why the molds slowed bacteria, and refine the active ingredients.  Using herbal supplements is somewhat like putting mold on a wound.  It might help, a little, but it’s certainly not going to help as much as using penicillin.
In particular, patients are classified into three categories (low, intermediate, high) depending on their CV risk profile. Individuals with controlled hypertension belong to the low-risk group where sexual dysfunction can be safely managed with the approved medical therapies regardless of the number or class (with the exception of b-blockers and diuretics) of agents of the patient’s antihypertensive regime. Moreover, patients of this group can safely initiate or reinstitute sexual activity without any need for additional cardiovascular evaluation.
As ED has become more prevalent among the U.S. population, entrepreneurs have set out to serve this patient population by introducing a variety of non-invasive devices to help correct the condition. There’s the penis pump, which includes a plastic tube that fits over the penis and a hand or battery-powered pump attached to the tube, and a band that circles the base of the penis when it becomes erect.
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
Testosterone therapy (TTh) should be reserved for patients who (i) are symptomatic (ED or reduced libido) of testosterone deficiency45 and (ii) they have biochemical evidence of low testosterone (TT <8 nmol/L or 2.3 ng/mL). In men with borderline TT (8–12 nmol/L or 2.3–3.5 ng/mL), a TTh trial (for 3–6 months and continuation if effective) may be envisaged. While adding a PDE5 inhibitor can be considered in men who have not improved with TTh, the usual clinical scenario is to add TTh in patients who have not responded to PDE5 inhibitors. Improvement is dependent on the testosterone levels with better results being obtained at lower levels of TT.45 Despite evidence of benefit in patients with pre-existing cardiovascular conditions (angina or heart failure), it should be emphasized that TTh is not a medication with cardiovascular indications.
A penile prosthesis is another treatment option for men with erectile dysfunction. These devices are either malleable (bendable) or inflatable. The simplest type of prosthesis consists of a pair of malleable rods surgically implanted within the erection chambers of the penis. With this type of implant the penis is always semi-rigid and merely needs to be lifted or adjusted into the erect position to initiate sex. Today, many men choose a hydraulic, inflatable prosthesis, which allows a man to have an erection whenever he chooses and is much easier to conceal. It is also more natural.
At the same time, people with diabetes are susceptible to a type of blood vessel damage known as endothelial dysfunction. A recent study found that men with ED are at a greater risk of heart disease, which is also associated with endothelial dysfunction. If blood vessels aren't in good working order, the penis may not get enough blood for an erection.
Surgical implantation of a penile prosthesis, either the inflatable (2- and 3-piece) or the malleable device, is a feasible technique that offers a third-line treatment and a more permanent solution to the problem of erectile dysfunction. Interestingly, prosthesis implantation receives a significantly high satisfaction rate as evidenced by the proportionate scores in sexual satisfaction scales. Mechanical failure and infection are the two major disadvantages of those prosthetic implants however, their great efficacy, safety and satisfaction rate in general render them an attractive solution when conservative treatment fails[70-74].
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.
The research is based on a Swedish national database of health records that includes all hospitals in Sweden. Researchers analyzed the records of men age 80 years or younger who were hospitalized for a first heart attack between 2007 and 2013. Tracking the men for an average of 3.3 years following this first heart attack, they compared outcomes among those who subsequently filled a prescription for a PDE5 inhibitor or alprostadil to those who did not. Overall just over 7 percent of men were prescribed an erectile dysfunction drug, 92 percent of whom were prescribed a PDE5 inhibitor and 8 percent of whom were prescribed alprostadil.
Abstract | Full Text PDF | PubMed | Scopus (105) | Google ScholarSee all References Aspirin and β-blocker use have been suggested to decrease the risk of cardiovascular events with sexual activity, although their benefit has not been proved definitively.79x79Kimmel, SE. Sex and myocardial infarction: an epidemiologic perspective. Am J Cardiol. 2000; 86: 10F–13F
Abstract | Full Text | Full Text PDF | PubMed | Scopus (37) | Google ScholarSee all References It has been postulated that regular exercise can decrease or possibly eliminate the small risk of myocardial infarction associated with sexual intercourse in most patients.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
PubMed | Google ScholarSee all References Postulated mechanisms of effect on sexual function with these centrally acting medications have included increased prolactin levels and a direct effect on α2-adrenergic receptors in the central nervous system.36x36Wein, AJ and Van Arsdalen, KN. Drug-induced male sexual dysfunction. Urol Clin North Am. 1988; 15: 23–31
Vacuum therapy devices have a few disadvantages. One must interrupt foreplay to use them. You must use the correct-size tension ring and remove it, to prevent penile bruising, after sustaining the erection for 30 minutes. Initial use may produce some soreness. Such devices may be unsuitable for men with certain bleeding disorders. In general, vacuum constriction devices are successful in management of long-term ED.
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