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.
Finally, prevalence rates will be affected by whether the study population is accrued from a single hospital/clinic setting or from a more general population of men with diabetes. For example, Siu et al.4 studied 500 Chinese diabetic men (of which 97% had type 2 disease) seen at a single medical clinic in Hong Kong during 1999 and found the overall prevalence of ED to be 63.6%. Contrast this to Fedele et al.,5 who studied 9,756 diabetic men accrued from 178 diabetes centers in Italy. Among the 8,373 men with type 2 diabetes, only 37% reported ED, considerably less than in the Chinese study.
Crucial to the understanding of the relationship between ED and CVD and the management of ED patients within the context of the (potential) CVD were the consecutive Princeton Consensus Recommendations (I: 2000, II: 2005, and III: 2012). The reader is strongly encouraged to refer to the most recent, third (2012) Princeton Consensus.30 Key notions in the assessment and management of the patient with organic ED are that (i) he should be considered at increased CVD risk until recommended checks suggest otherwise, and (ii) ED identifies increased CVD risk in the presence or absence of CVD symptoms or history.
According to Harvard Special Health Report Erectile Dysfunction, one study in the European Heart Journal looked at men newly diagnosed with heart disease, but without ED, who started treatment with the beta-blocker atenolol (Tenormin). Some of the study participants were told about the sexual side effect of the blood pressure drug, and ED was reported by almost one-third of the participants. In contrast, among those who were not told the drug's name or its side effects, only 3% said they experienced ED.
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.
Admitting to your doctor that you are having trouble achieving an erection can be difficult, but take comfort in the fact that they are not judging you and are there to improve your health and well-being. If you are just beginning a blood pressure treatment regimen and are beginning to experience erectile dysfunction, tell your doctor as soon as you can—they can solve the problem by simply changing the prescription.
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
Impotence, also known as erectile dysfunction or ED, is a very common problem, affecting up to half of 40-70 year old men in Australia.Treatment techniques for impotence have varied through the years, from external steel mechanical attachments, to static electricity attached to the penis and testicles, to simple aphrodisiacs such as oysters. Until as recently as 1970, erectile failure was almost always seen as being due to psychological causes and was usually treated with psychotherapy.Since then, the medical causes contributing to impotence have been recognised and the treatment of impotence has been revolutionised, providing a range of options which are far more acceptable and very much more successful.Treatment options for impotenceTreatment choices for erectile dysfunction include:medicines;self-injection therapy;devices such as vacuum pumps;penile implant surgery;hormone therapy; andcounselling.If you have erectile dysfunction, the treatment your doctor recommends will depend on the severity of symptoms and the underlying cause of your impotence.Your doctor will want to check that any conditions that could be contributing to or causing erectile dysfunction are being treated.Your doctor may also suggest that you make some lifestyle adjustments, such as:increasing the amount of physical activity you get;losing weight if you are overweight;reducing the amount of alcohol you drink;quitting smoking; andnot taking illicit drugs.These lifestyle recommendations can help improve impotence related to several causes and improve your health in general.Medicines for erectile dysfunctionThe first tablet available for erectile dysfunction, sildenafil (brand name Viagra), has been largely responsible for helping to bring the topic of erectile dysfunction out into the open. Similar medications — tadalafil (Cialis) and vardenafil ( Levitra) — are also available. These medicines all work in a similar way, although there is some difference in how long their effect lasts. Sildenafil, tadalafil and vardenafil belong to a group of medicines called phosphodiesterase type 5 (PDE5) inhibitors because they block the PDE5 enzyme.How do oral medicines help treat erectile dysfunction?PDE5 inhibitors help in the process of getting and keeping an erection by working on chemicals in the body that are involved in erections. These medicines work by stopping PDE5 from breaking down an erection-producing chemical called cyclic guanosine monophosphate (cGMP). cGMP helps to relax the smooth muscle cells in the penis's erectile tissue, allowing more blood to flow into the penis to cause an erection. When PDE5 is temporarily blocked by these medicines, it can’t break down the erection producing cGMP, so an erection can be achieved and maintained. PDE5 inhibitors can be used in the treatment of erectile dysfunction that is due to physical or psychological causes.Medications such as Viagra, Cialis and Levitra will work only if you are sexually stimulated. They are not aphrodisiacs and won’t increase your sex drive.Side effects of PDE5 inhibitorsSide effects of these medicines can include headaches, flushes, blocked nose, indigestion and dizziness.In rare situations, sildenafil and vardenafil can cause a distortion of vision or change in colour vision.Tadalafil has been associated with back pain.Who can take medicines for impotence?PDE5 inhibitors cannot be taken by all men, so your doctor will need to evaluate your suitability before prescribing either of these medications.Men taking nitrates (often used to treat angina) should never take phosphodiesterase type 5 (PDE5) inhibitors. PDE5 inhibitors should also not be taken with some medicines used to treat high blood pressure.PDE5 inhibitors may also not be suitable for men with certain heart conditions or low blood pressure. Check with your doctor to find out if this type of medication may be suitable for you.Self-injection therapySelf-injection therapy delivers a medicine called alprostadil (brand name Caverject), also known as prostaglandin E-1, to the erectile tissue of the penis. Prostaglandin E-1 occurs naturally in the body and helps increase the blood flow to the penis to cause an erection. Unlike the PDE5 inhibitors, alprostadil will cause an erection whether the penis is stimulated or not.Self-injection therapy is usually recommended if PDE5 inhibitor medicines are not suitable or have not been effective in the treatment of erectile dysfunction.How to use self-injection therapyAlprostadil is injected into either of the 2 cigar-shaped chambers of the penis known as the corpora cavernosa, which run along the length of the penis, one on either side. Your doctor or urologist (specialist in problems with male reproductive organs and the urinary tract) will give you instructions on how to do this.Alprostadil should produce an erection in 5 to 20 minutes and, generally, the erection will last for 30 to 60 minutes.You should not use alprostadil more than once in a 24-hour period, and you should use it no more than 3 times a week.Don’t try to use more than the recommended dose of alprostadil, as your erection may last longer than is medically safe.Who can use self-injection therapy?You should ask your doctor if alprostadil is suitable for you. Your doctor will also be able to tell you how much alprostadil to use, depending on your condition and whether or not you are taking any other medications, and also how to use alprostadil properly.People with certain illnesses, such as leukaemia and sickle cell anaemia, or who have a penile implant or Peyronie’s disease, where the penis may be scarred and produces erections that are not straight, should not use alprostadil.Men for whom sexual activity is not advised should not use alprostadil.Side effects of injection therapyThe most common side effects of alprostadil include pain in the penis or bruising in the penis at the site of injection. Fibrosis (the development of fibrous tissue) can also develop following injections into the penis.The most serious side effect is priapism (a persistent erection), which is a medical emergency. Your doctor will inform you of what to do if you have an erection that persists for 2 hours or more. It is very important that you follow your doctor’s instructions and inform them that you have experienced this side effect.Vacuum erection devicesVacuum erection devices work by creating a vacuum, which increases blood flow to the penis, producing an erection.The penis is lubricated and placed inside a hollow plastic chamber. Air is pumped out of the chamber, either manually or by a battery powered pump. This creates a vacuum which pulls blood into the penis to cause an erection. This takes about 5 minutes.Once the penis is erect, the man fits a rubber ring around the base of his penis to keep the blood trapped inside the penis when the cylinder is removed. After intercourse, the ring can be removed to return the penis to a limp state.Vacuum erection devices avoid surgery and can be used as often as required. However, they may be difficult to use, and many men and their partners feel they take much of the pleasure and spontaneity away from sexual activities. Vacuum pumps are not suitable for men who have problems with blood clotting, or blood disorders such as leukaemia.Penile implant surgery for impotencePenile implant surgery is not a common procedure but in some cases it may be the most appropriate treatment for erectile dysfunction.The procedure involves placing an implant inside the penis, along its length, so that it can become erect. The implant may be a pair of semi-rigid rods or a pair of inflatable cylinders.The inflatable implants allow the penis to look and feel limp (flaccid) or erect, depending on how much the cylinders are inflated. The cylinders in an inflatable implant are hollow, and the man gets an erection by squeezing a pump located in his scrotum to fill the cylinders with salt water (saline) stored in a reservoir implanted in his lower abdomen. A release valve drains the saline out of the cylinders and back into the reservoir.With the semi-rigid, malleable rod type of implant, the rods run along the length of the penis and can be bent upwards to produce an erect penis, or downwards when an erect penis is not required.Like all surgery, there are some risks, such as infection or bleeding. If you have had surgery and have severe pain, fever, swelling or excessive bleeding, you should contact your doctor as soon as possible.Vascular surgery for erectile dysfunctionIn cases where a man’s anatomy prevents blood flow into or out of the penis, vascular surgery may be an option. This treatment option is rarely recommended, and is usually only successful in younger men.If there is a blockage that prevents blood from flowing into the penis, a doctor may recommend an operation that bypasses the blocked blood vessels, using a length of vein or manufactured tubing, to allow more blood to flow into the penis and help produce an erection.If the problem is that blood leaks back out of the penis, this can be corrected by tying off the major veins that drain the penis, a procedure known as venous ligation.Hormone treatments for impotenceIn a small number of men, blood tests may show abnormally low levels of testosterone, the male sex hormone. In such cases your doctor might prescribe a course of testosterone injections or a testosterone implant. The supplements can help boost sex drive as well as increasing the ability to have erections. Testosterone gel or patches, applied daily to the skin, are another option.Complementary medicines for erectile dysfunctionThere is a lack of scientific evidence supporting the effectiveness of complementary therapies for the treatment of impotence.Always check with your doctor before taking any herbal medicines or supplements for impotence. These formulations may contain ingredients that can interact with other medicines or cause dangerous side effects.Counselling for men with impotenceErectile dysfunction often has physical causes, but sometimes there is a psychological basis for erection problems. Often this is a form of performance anxiety. A man may have had an episode of erectile dysfunction due to some passing cause like fatigue, stress, relationship difficulty or intoxication. This may have led to embarrassment or a feeling of failure. Even if the physical cause does not remain, future attempts to have sex may trigger memories of this embarrassment and acute anxiety that it will happen again. This anxiety itself is capable of causing erectile dysfunction, and so a man may get trapped in a self-reinforcing cycle of anxiety and erectile dysfunction. In these instances, seeing a GP, counsellor or psychologist can be very helpful.Stress, anxiety, depression and low self-esteem, in fact, almost all significant emotional problems, can have a major effect on sexuality. So do many chronic physical illnesses, even if they don't directly affect genital function. Counsellors and psychologists can assist with these and a wide range of other sexual and relationship problems and can also help female partners suffering from sexual problems. They are particularly skilled in helping patients to overcome guilt or anxiety relating to sexual abuse, and in helping couples to sort out relationship difficulties. Simple problems can be dealt with in a few visits, but more complex problems may require several months or even years of therapy.Your doctor may be able to recommend a psychologist or counsellor who specialises in sexual and relationship problems. Last Reviewed: 12 December 2016
The incidence of ED is 42.0–57.0 % in men with CAD and 33.8 % in those who have diabetes with silent ischaemia, compared with 4.7 % in men without silent ischaemia.6 The prevalence of ED is likely to be higher than the reported figures, because men generally do not seek medical advice for ED.6 Erection is thought to be a process that is regulated by hormones and neurovascular mechanisms in cerebral and peripheral levels.7
Prescription drugs called “oral phosphodiesterase-5 (PDE5) inhibitors” are considered the “first-line non-invasive treatment” options for patients with ED. These include the drugs that go by brand names: Sildenafil, Vardenafil or Tadalafil. They work by helping the smooth muscle cells lining the blood vessels that supply the penis with blood to work properly. This allows a man to maintain an erection more easily.
Crossref | PubMed | Scopus (47) | Google ScholarSee all References Because of this perceived increase in risk, many couples are concerned about resuming sexual activity in the setting of cardiac disease. A study that monitored male patients after coronary artery bypass grafting found that 17% of patients and 35% of their partners were afraid of resuming sexual activity.1x1Muller, JE. Sexual activity as a trigger for cardiovascular events: what is the risk?. Am J Cardiol. 1999; 84: 2N–5N
PubMed | Google ScholarSee all References A dose-related phenomenon with propranolol use was suggested by another study, which showed that patients receiving propranolol dosages exceeding 120 mg/d developed ED at a higher rate than patients who received lower dosages of the same medication.43x43Warren, SC and Warren, SG. Propranolol and sexual impotence [letter]. Ann Intern Med. 1977; 86: 112
Ginkgo biloba. Known primarily as a treatment for cognitive decline, ginkgo has also been used to treat erectile dysfunction -- especially cases caused by the use of certain antidepressant medications. But the evidence isn't very convincing. One 1998 study published in the Journal of Sex & Marital Therapy found that it did work. But a more rigorous study, published in Human Pharmacology in 2002, failed to replicate this finding. "Ginkgo has come out of fashion in the past few years," says Ronald Tamler, MD, assistant professor of medicine and codirector of the men's health program at Mount Sinai Medical Center in New York City. "That's because it doesn't do much. I can say that in my practice, I have not seen ginkgo work -- ever."
Erections also require neural input to redirect blood flow into the corpora cavernosae. Psychogenic erections secondary to sexual images or auditory stimuli relay sensual input to the spinal cord at T-11 to L-2. Neural impulses flow to the pelvic vascular bed, redirecting blood flow into the corpora cavernosae. Reflex erections secondary to tactile stimulus to the penis or genital area activate a reflex arc with sacral roots at S2 to S4. Nocturnal erections occur during rapid-eye-movement (REM) sleep and occur 3–4 times nightly. Depressed men rarely experience REM sleep and therefore do not have nocturnal or early-morning erections.
Penile erection is largely a vascular process, and the penile endothelium and smooth muscle tissue are very sensitive to functional and structural changes. Vasculogenic ED results from an impairment of endothelial dependent or independent smooth muscle relaxation (functional vascular ED, initial stages), occlusion of the cavernosal arteries by atherosclerosis (structural vascular ED, late stages), or a combination of these.3 Current data support a complex interplay between endothelial dysfunction, subclinical inflammation, and androgen deficiency (Figure 1). The relationship between ED and CAD at the clinical level is supported by this common pathophysiological basis. The ‘artery size’ hypothesis explains why patients with CAD frequently report ED before CAD detection.10 According to this hypothesis, for a given atherosclerotic burden, the smaller penile arteries suffer obstruction earlier than the larger coronary arteries (Figure 2). The same concept holds also true in the case of non-obstructing atherosclerosis: since the smaller penile artery have a greater endothelial surface and erection requires a large degree of vasodilation to occur when compared with arteries in other organs, the same degree of endothelial dysfunction will be symptomatic in these smaller vessels but subclinical in the larger ones (i.e. coronaries). In the same context, accelerated arterial ageing (as indicated by increased arterial stiffening that also affects large arteries of ED patients) may be a common background.11,12 Erectile dysfunction is associated with an incremental inflammatory and endothelial-pro-thrombotic activation.13 Interestingly, this activation is equal to that found in CAD patients with no ED, while when these two conditions are combined the burden is additive. Androgen deficiency may be also implicated in the common pathogenetic pathways of ED and CVD; however, this warrants further substantiation.2
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 initial step in evaluating ED is a thorough sexual history and physical exam. The history can help in distinguishing between the primary and psychogenic causes. It is important to explore the onset, progression, and duration of the problem. If a man gives a history of “no sexual problems until one night,” the problem is most likely related to performance anxiety, disaffection, or an emotional problem. Aside from these causes, only radical prostatectomy or other overt genital tract trauma causes a sudden loss of male sexual function.
In another study, 60 patients underwent stress exercise cardiovascular testing and Doppler ultrasonography for measurement of their cavernosal artery peak systolic velocity (PSV).17x17Kawanishi, Y, Lee, KS, Kimura, K et al. Screening of ischemic heart disease with cavernous artery blood flow in erectile dysfunctional patients. Int J Impot Res. 2001; 13: 100–103
Crossref | PubMed | Google ScholarSee all References The risk of myocardial infarction with sexual activity has been estimated to be less than 3% in high-risk patients with prior cardiovascular disease if they can exercise to more than 7 METs without symptoms.89x89Moss, AJ and Benhorin, J. Prognosis and management after a first myocardial infarction. N Engl J Med. 1990; 322: 743–753
The body’s source for nitric oxide production is the amino acid L-arginine, which is naturally found in many foods. The average American ingests about 3,000–5,000 mg of L-arginine per day, as it is an amino acid naturally contained in many foods. Meats of all varieties, nuts, and dairy products are rich in L-arginine, so the body is accustomed to intake levels of several thousand milligrams every day.
Cigarette smoking is an established risk factor in the development of atherosclerotic vascular changes and thus would be expected to play a role in the development of vasculogenic ED. The MMAS 9-year follow-up study found that the risk of developing moderate or complete ED in smokers was nearly doubled (odds ratio, 1.97) compared with that in matched nonsmokers.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
If the cause is believed to be organic but not hormonal, or if the patient defers psychological intervention, he can be offered the VCD or oral drug therapy. EDDM patients on organic nitrates or who have experienced or are concerned about potential adverse reaction to PDE-5 inhibitors are suitable candidates for the VCD. The VCD induces functional rigidity in 75% of patients with diabetes with autonomic neuropathy. Some patients or their partners may reject or discontinue the use of the VCD because it induces an unnatural erection, causes bruising and numbness of the penis, and or inhibits antegrade ejaculation.8
According to the Mayo Clinic, oral medications are usually the first-line treatment for ED. Those medications include Sildenafil (Viagra), vardenafil (Levitra, Staxyn), tadalafil (Cialis) and avanafil (Stendra). They operate by helping relax muscles in the penis by strengthening the effects of nitric oxide, a naturally occurring chemical in the body. The drugs increase blood flow to allow patients to get an erection.
A medical history focused on risk factors, such as cigarette smoking, hypertension, alcoholism, drug abuse, trauma, and endocrine problems including hypothyroidism, low testosterone levels, and hyperprolactinemia, is very important. Commonly used drugs that disrupt male sexual function are spironolactone (Aldactone), sympathetic blockers such as clonidine (Catapres), guanethidine (Islemin), methyldopa (Aldomet), thiazide diuretics, most antidepressants, ketoconazole (Nizoral), cimetidine (Tagamet), alcohol, methadone, heroin, and cocaine. Finally, assessment of psychiatric history will help identify emotional issues such as interpersonal conflict, performance anxiety, depression, or anxiety.
medicines called alpha-blockers such as Hytrin (terazosin HCl), Flomax (tamsulosin HCl), Cardura (doxazosin mesylate), Minipress (prazosin HCl), Uroxatral (alfuzosin HCl), Jalyn (dutasteride and tamsulosin HCl), or Rapaflo (silodosin). Alpha-blockers are sometimes prescribed for prostate problems or high blood pressure. In some patients, the use of Sildenafil with alpha-blockers can lead to a drop in blood pressure or to fainting
There are other treatment options for erectile dysfunction (ED). Alprostadil is a medication that improves blood flow to the penis and improves erections. It can be given either by injection (Caverject and other brands) at the base of the penis or by putting an alprostadil gel (brand name MUSE) directly into the urethra, using a thin tube and a little lubricant so it slides in easily. The medicine is absorbed from the lining of the urethra into the surrounding tissues. The shot is less appealing to most people, of course, but more effective.
Erectile dysfunction (ED), or impotence, is when a man has difficulty getting or maintaining a strong enough erection for sexual intercourse or other sexual activity. It can be caused by stress, anxiety or excessive alcohol consumption. But it can also be a symptom of an underlying condition such as atherosclerosis (narrowing of the arteries), diabetes or high blood pressure. Some medications can cause erectile dysfunction, for example beta-blockers and diuretics (commonly used to treat a variety of heart-related conditions such as high blood pressure and heart failure).
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 Sildenafil is absorbed rapidly, and peak plasma levels of 127 to 560 ng/mL are seen in a fasting state approximately 1 hour (range, 0.5-2 hours) after ingestion.3x3Zusman, RM, Morales, A, Glasser, DB, and Osterloh, IH. Overall cardiovascular profile of sildenafil citrate. Am J Cardiol. 1999; 83: 35C–44C
Erectile dysfunction (ED) is common in cardiac patients and shares the same risk factors--smoking, hypertension, hyperlipidaemia and diabetes mellitus. Sexual activity is not unduly stressful to the heart and, providing patients are properly assessed using established guidelines, sexual intercourse can be enjoyed without increased risk. The treatment of ED in patients with cardiovascular disease has been transformed by the introduction of the oral phosphodiesterase type 5 inhibitors, the first of which was sildenafil. Success in restoring erectile function is possible in up to 80% of patients (depending on the aetiology) with minimal adverse effects. A synergistic hypotensive effect with nitrates, and almost certainly nicorandil, is the only major contraindication. ED in asymptomatic patients may be a marker of silent vascular disease or increased vascular risk factors and should alert the physician to the need for cardiac risk screening. ED is common in patients with cardiovascular disease and should be routinely enquired about. ED is a distressing condition for the man and his partner, and severely impairs quality of life. Patients with cardiovascular disease and patients with diabetes represent the largest group of patients with ED, the majority of whom benefit from the drug therapies currently available. Addressing ED in patients with cardiovascular disease can lead to a substantial improvement in quality of life and success is not difficult to achieve.
Yohimbine: The main component of an African tree bark, yohimbine is probably one of the most problematic of all natural remedies for ED. Some research suggests that yohimbine can improve a type of sexual dysfunction that is linked with a drug used to treat depression. However, studies have linked yohimbine to a number of side effects, which can include anxiety, increased blood pressure, and a fast, irregular heartbeat. Like all natural remedies, yohimbine should only be used after advice and under supervision from a doctor.
Diabetes doubles or even triples the chance that you’ll have erectile dysfunction (ED) and that you could develop it a decade earlier than other men. In fact, the two conditions are so closely linked that some experts believe that for men younger than 45, impotence, or ED, could be an early warning sign of diabetes. The good news is that diabetes treatment, especially if you identify type 2 diabetes early, can also ease ED.
Abstract | PubMed | Scopus (136) | Google ScholarSee all References Attainment and maintenance of a firm erection requires good arterial inflow of blood and efficient trapping of venous outflow. Therefore, disease processes that affect the function of the arterial and venous systems would be expected to negatively affect erectile function. Unfortunately, cardiovascular disease is also prevalent in the male population and is especially evident with increasing age. The interplay of cardiovascular health and sexual function includes the risk of cardiac events precipitated by the physical exertion of sexual activity and by some medications, such as sildenafil, on the cardiovascular system. An estimated 500,000 patients survive a myocardial infarction each year in the United States, and an estimated 11 million patients have existing cardiovascular disease, making the issue of sexual function and cardiac disease relevant to many 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
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.
Following the breakthrough in ED treatment using PDE5-inhibitors, Western medicine has now moved on to a new frontier of regenerative medicine, with stem cell and gene therapy leading the way (25). There is a practical need for novel therapy as a significant portion of diabetic or post-prostatectomy ED patients do not respond to oral pharmacotherapy. To date, stem cells derived from different sites including adipose tissue-derived stem cells, bone marrow mesenchymal stem cells and muscle-derived stem cells have been investigated using animal models for ED, to study their effects on neural, vascular, endothelial or smooth muscle regeneration (25,26).