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
Crossref | PubMed | Scopus (539) | Google ScholarSee all References The MMAS found the total prevalence of minimal to severe ED to be 52% and estimated that more than 617,000 new cases were expected to occur annually in the United States.4x4Feldman, HA, Goldstein, I, Hatzichristou, DG, Krane, RJ, and McKinlay, JB. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol. 1994; 151: 54–61
Diabetes care providers, while becoming more aware of the high prevalence of ED in men with diabetes, may not appreciate the importance of maintaining erectile function to their patients. A recent study by Rance et al.40 underscores the fact that diabetic men, regardless of whether they actually have ED, believe that ED has a major impact on quality of life and that it is as important to treat as many other conditions associated with diabetes. In an effort to determine the relative importance of treatment for ED compared to other diabetic complications, they gave 192 consecutive diabetic men and 51 control patients seen at two hospitals a standardized questionnaire that assessed the relative importance of a number of diabetic complications and the patients' willingness to pay per month to avoid a particular complication.
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
PubMed | Google ScholarSee all References In a double-blind, placebo-controlled study, sildenafil was effective in patients with diabetes mellitus.58x58Rendell, MS, Rajfer, J, Wicker, PA, Smith, MD, and Sildenafil Diabetes Study Group. Sildenafil for treatment of erectile dysfunction in men with diabetes: a randomized controlled trial. JAMA. 1999; 281: 421–426
Abstract | Full Text | Full Text PDF | PubMed | Scopus (164) | Google ScholarSee all References Several double-blind, placebo-controlled studies have shown vardenafil to be more effective than placebo in the treatment of ED secondary to a wide range of other etiologies as well.71x71Hellstrom, WJ, Gittelman, M, Karlin, G..., and Vardenafil Study Group. Sustained efficacy and tolerability of vardenafil, a highly potent selective phosphodiesterase type 5 inhibitor, in men with erectile dysfunction: results of a randomized, double-blind, 26-week placebo-controlled pivotal trial. Urology. 2003; 61: 8–14
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.
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

Crossref | PubMed | Google ScholarSee all References Patients with vascular risk factors (diabetes mellitus, hypertension, heart disease, and hyperlipidemia) had significantly decreased peak systolic velocities and increased end-diastolic velocities. Patients with diabetes mellitus had increased end-diastolic velocities and decreased resistive indices, indicating a disorder of venous trapping during erections. Another study examined corpora cavernosal tissue removed at penile prosthesis placement in 21 diabetic men and 42 nondiabetic controls.23x23Saenz de Tejada, I, Goldstein, I, Azadzoi, K, Krane, RJ, and Cohen, RA. Impaired neurogenic and endothelium-mediated relaxation of penile smooth muscle from diabetic men with impotence. N Engl J Med. 1989; 320: 1025–1030
If you have been diagnosed with heart disease or have already had a heart attack and are experiencing erectile dysfunction, it is critical that you discuss erectile dysfunction medication with your physician before considering taking it. Popular erectile dysfunction medications such as Viagra (sildenafil), Cialis (tadalafil) and Levitra (vardenafil) can interact with a range of cardiovascular disease medications. Interactions are possible with blood pressure medications; blood thinners such as Coumadin (warfarin), nitrates for the treatment of chest pain, and antiarrhythmia medication for the treatment of irregular heart rhythms.
The impact of third-generation cardioselective beta-blockers such as carvedilol and nebivolol has also been investigated. Fogari et al. investigated the effect of carvedilol on erectile function in a double-blind crossover study involving 160 men newly diagnosed with hypertension and found chronic worsening of sexual function in those treated with carvedilol compared with valsartan and placebo.24

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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
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
Abstract | Full Text | Full Text PDF | PubMed | Scopus (53) | Google ScholarSee all References Early work in this field, performed by Masters and Johnson in 1966, involved evaluation of young patients in a laboratory setting and found that heart rates and systolic blood pressure levels during sexual activity approached levels seen during maximal exercise.84x84Stein, RA. Cardiovascular response to sexual activity. Am J Cardiol. 2000; 86: 27F–29F
The impact of third-generation cardioselective beta-blockers such as carvedilol and nebivolol has also been investigated. Fogari et al. investigated the effect of carvedilol on erectile function in a double-blind crossover study involving 160 men newly diagnosed with hypertension and found chronic worsening of sexual function in those treated with carvedilol compared with valsartan and placebo.24
Organic nitrates are drugs that widen arteries by increasing their supply of nitric oxide; that's how they open the partially blocked coronary arteries in patients with angina. But because nitrates and ED pills both act on nitric oxide, the drugs don't mix; healthy volunteers given Viagra followed an hour later by nitroglycerin see their blood pressures drop by 25–51 mm Hg, a potentially dangerous amount. All experts agree that men who are taking nitrates cannot use ED pills; this includes all preparations of nitroglycerin (short-acting, under-the-tongue tablets or sprays), long-acting nitrates (isosorbide dinitrate or Isordil, Sorbitrate, and others, and isosorbide mononitrate, Imdur, ISMO, and others), nitroglycerin patches and pastes, and amyl nitrite or amyl nitrate (so-called poppers, which some men use for sexual stimulation).
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.

What comes after an ED diagnosis in diabetic patients? Often, Dr. Eid will instantly refer these men to a cardiologist. “If a patient has diabetes and is newly diagnosed, a significant portion of these men are going to develop coronary artery disease in the next 2-3 years,” he said. “One of the things we do is recommend is that they see a cardiologist and perhaps have a stress test or some sort of evaluation.”


Abstract | Full Text | Full Text PDF | PubMed | Scopus (272) | Google ScholarSee all References Between 1987 and 1989, the Massachusetts Male Aging Study (MMAS), a community-based random sample observational study of 1709 men, used self-administered sexual activity questionnaires to gather information about noninstitutionalized men aged 40 to 70 years in cities near Boston.4x4Feldman, HA, Goldstein, I, Hatzichristou, DG, Krane, RJ, and McKinlay, JB. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol. 1994; 151: 54–61
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.
Cardiovascular disease remains our nation’s biggest killer, responsible for about one-third of deaths in the U.S.1 Erectile dysfunction (ED) is typically the first clinical manifestation of cardiovascular disease, making it a helpful early marker for men who are likely to die of heart attacks. There is a strong relationship between erectile dysfunction and high blood pressure, high cholesterol, angina, stroke, heart attack and a premature death.2, 3

Recent revised labeling for sildenafil states that there is a lack of controlled data for its use in patients with resting hypotension (<90/50 mm Hg) or hypertension (>170/110 mm Hg); a history of myocardial infarction, cerebrovascular accident, or life-threatening arrhythmia within the past 6 months; coronary artery disease or cardiac failure causing unstable angina; or retinitis pigmentosa and possible genetic disorders of retinal PDEs.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N


Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Theoretically, the risk of a cardiac event during sexual activity should be increased. Sexual activity is associated with an elevated heart rate, blood pressure level, and myocardial oxygen demand, and this increase in hemodynamic stress may result in myocardial ischemia.79x79Kimmel, SE. Sex and myocardial infarction: an epidemiologic perspective. Am J Cardiol. 2000; 86: 10F–13F
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.
A similar situation develops in the fragile penile circulation. Any disturbance in nitric oxide production lowers the capacity to dilate penile arteries, impairing penile engorgement for erection. Release of nitric oxide is readily sabotaged by many conditions, including elevated levels of cholesterol, high blood pressure, increased triglycerides, smoking, metabolic syndrome and diabetes, and excessive consumption of dietary saturated fat.9 If an artery’s inner wall can’t produce nitric oxide, an abnormal constriction of the arteries to the penis follows, effectively choking off blood flow.
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].

Testosterone cypionate and testosterone enanthate injections are used for replacement therapy in patients with low testosterone. Other formulations, such as gels and patches, are recommended in older patients with chronic conditions.57 Serum prostate specific antigen should be measured before starting testosterone replacement, then 3–6 months after starting the treatment, followed by annual measurement.74


Currently, the preferred treatment for erectile dysfunction includes sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis). However, numerous experts have raised concerns about the use of these drugs in patients with chronic heart failure who also take nitrates (or other medications that relax and widen blood vessels). This drug combination has been shown to be dangerous, because it can increase the risk for a life-threatening drop in blood pressure.
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.
Myocardial ischaemia is caused by the reduction of coronary blood flow as a result of fixed or dynamic epicardial coronary artery stenosis, abnormal constriction or deficient relaxation of coronary microcirculation, or because of reduced oxygen-carrying capacity of the blood.56 Atherosclerosis is the major cause of myocardial ischaemia. Plaque that develops in atherosclerosis can rupture causing platelet aggregation and subsequent thrombus formation, which leads to MI. The other mechanisms of myocardial ischaemia are encountered far less than atherosclerosis. Endothelial dysfunction has an important role in the progression of atherosclerosis. Endothelial dysfunction enhances the intimal proliferation and malregulation that results in plaque destabilisation in the arteries.6 This process, coupled with paradoxical vasoconstriction, can result in major cardiovascular events such as MI.32
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

Erectile dysfunction carries an independent risk for cardiovascular events. A considerable number of studies have examined the ability of ED to predict the risk of future fatal and non-fatal cardiovascular events (myocardial infarction, stroke, revascularization) and total mortality in the general population and in high CV risk patients, in diabetics and in heart failure patients.5,19–22 In a meta-analysis of 14 prospective cohort studies involving 92 757 men followed for a mean period of 6.1 years (Figure 4), ED increased significantly and independently of traditional risk factors the risk of CV events, CV mortality, myocardial infarction, cerebrovascular events, and all-cause mortality by 44, 19, 62, 39, and 25% respectively.5 This predictive ability also extends in men with known CVD: ED increased the risk of all-cause mortality by 90%.5 Of importance, the predictive ability of ED is higher in younger ED patients5 despite the fact that probability of ED increases with age, most likely identifying a group of patients with early and aggressive vascular disease.23 Clinical implementation of ED as a biomarker relies on whether its addition on classical risk scores such as the Systematic COronary Risk Evaluation (SCORE) or the Framingham correctly reclassifies a meaningful percentage of patients into a higher or lower risk category. To this end, data are limited. Yet, in a population-based study of men 40–70 years of age, the addition of the ED status to the Framingham risk score resulted in a reclassification of 6.4% of low-risk patients to intermediate risk.19


Beta-blockers: A popular blood pressure medication that affects part of the nervous system in an attempt to slow and regulate heartbeats, helping reduce blood pressure. Unfortunately, this same part of the nervous system is also responsible for causing erections, and when beta blockers are used, it indirectly reduces the amount of blood flow to the penis.
Men with diabetes are at a higher risk of erectile dysfunction or impotence, especially if their diabetes is not well controlled. Erectile dysfunction means you cannot have an erection that is sufficient to perform sexual intercourse. Many men experience short-term episodes of erectile dysfunction but, for about one in 10 men, the problem may continue.
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.
In a 2005 study, three months of twice-daily sets of kegel exercises combined with biofeedback and advice on lifestyle changes, such as quitting smoking, losing weight, and limiting alcohol, worked far better than just giving the participants advice. “Wearing tight pants will affect impotence along with some other medical conditions like diabetes and heart disease,” which can also affect a man’s degree of impotence, Dr. Jennifer Burns, specializing in family practice with an emphasis on gastrointestinal health at the BienEtre Center, told Medical Daily.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Avoiding sexual activity between 6 AM and noon may be recommended to higher-risk patients because this is the time of peak incidence of most arrhythmias, myocardial ischemia, sudden cardiac death, and cerebrovascular accidents.1x1Muller, JE. Sexual activity as a trigger for cardiovascular events: what is the risk?. Am J Cardiol. 1999; 84: 2N–5N
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."
Experimental hyperglycemia may also affect cavernosal smooth muscle cell contractile responses. In experimental diabetes, penile smooth muscle has augmented force responses to vaconstrictors, possibly mediated by changes in expression of protein kinase C and the RhoA-Rho kinase Ca2+-sensitization pathway.32 These changes may promote flaccidity and alter the relaxation responses to nitric oxide. End-stage penile dysfunction may occur as a result of diabetes, with progressive loss of normal cavernosal endothelium and smooth muscle cells from the corpus cavernosum.33 Replacement by fibrotic tissue may lead to complete erectile failure.34
Experimental in vivo studies have implicated central and peripheral neuropathy, impaired neurotransmission, and endothelial dysfunction in the pathogenesis of diabetic ED.26,27 Copulatory behavior and penile reflexes are uniformly impaired 4–12 months after the onset of diabetes in the BB rat.26,27 McVary et al.26 found that peripheral neuropathy accounts for only part of the dysfunctional findings, and that spinal sexual reflexes were also severely impaired.
Hypertension can affect endothelial function in many ways. It can reduce endothelium-dependent vasodilatation by increasing the vasoconstrictor tone as a result of increased peripheral sympathetic activity.41–43 Another mechanism is hypertension-induced increase in cyclooxygenase activity that leads to an increase in reactive oxygen species; these in turn damage endothelial cells and disrupt their function.44–46 In some cases, endothelial NO synthase (eNOS) gene variations may relate to hypertension-associated endothelial dysfunction.6
PubMed | Google ScholarSee all References The risk of ED was 1.83 times higher in men with a total cholesterol level greater than 240 mg/dL as opposed to less than 180 mg/dL. Also, an HDL cholesterol level greater than 60 mg/dL was found to be protective against the development of ED. In the MMAS, HDL cholesterol levels were noted to have an inverse relationship with the presence of ED.4x4Feldman, HA, Goldstein, I, Hatzichristou, DG, Krane, RJ, and McKinlay, JB. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol. 1994; 151: 54–61
These medications don’t work for everyone but they are easy to use and work for around 60% of people who try them. They work by making it easier to get an erection by reducing the effect of (inhibiting) the chemical PDE-5. This chemical is used in the body to make sure there isn’t too much blood in the penis during an erection, but if you have erectile dysfunction then this chemical ends up over-compensating.
If you have symptoms of ED, it’s important to check with your doctor before trying any treatments on your own. This is because ED can be a sign of other health problems. For instance, heart disease or high cholesterol could cause ED symptoms. With a diagnosis, your doctor could recommend a number of steps that would likely improve both your heart health and your ED. These steps include lowering your cholesterol, reducing your weight, or taking medications to unclog your blood vessels.
Although ED is a common complication of diabetes, its effect on quality of life is not well understood. Recent work for the Exploratory Comprehensive Evaluation of Erectile Dysfunction (ExCEED) database demonstrates that in the general population of patients presenting to their urologist, ED negatively affects both general and disease-specific health-related quality of life (HRQOL).35 While this study provides insight into the detrimental affect of ED on quality of life, the cohort is somewhat selected, in that all of the patients were seen in sexual dysfunction clinics and therefore may have been more likely to be bothered by their condition and to report worse quality of life.
The diagnosis of ED in a patient may affect its management in two ways.30 The first relates to the fact that the ED patient, irrespective of whether he has or has not established CVD, is ‘reclassified’ into a higher risk category for future CV events. Management in this case is altered in the sense that more aggressive treatment of risk factors, as well as a close follow-up, is warranted. Implementation of biomarkers in this setting is desirable.
Both erectile dysfunction and heart disease have been linked with impaired activity of nitric oxide, the body’s most powerful vasodilator. An endogenous (produced by the body) compound called asymmetric dimethylarginine is an L-arginine analog, which interferes with the production of nitric oxide and may increase the risk for erectile dysfunction and heart disease.
PubMed | Google ScholarSee all References This prolonged excretion half-life produces enhanced erections up to 36 hours after oral dosing, thereby potentially allowing for more spontaneous engagement of intercourse. The efficacy of tadalafil in the treatment of ED has been proved in randomized double-blind, placebo-controlled trials.78x78Porst, H, Padma-Nathan, H, Giuliano, F, Anglin, G, Varanese, L, and Rosen, R. Efficacy of tadalafil for the treatment of erectile dysfunction at 24 and 36 hours after dosing: a randomized controlled trial. Urology. 2003; 62: 121–125
Towards this direction, several sufficiently powered studies have demonstrated a higher incidence of erectile dysfunction in patients with coronary artery disease, either asymptomatic or overt. At the same time, patients with erectile dysfunction are more prone to have established coronary artery stenosis of more than 50% and consequently evident CV disease[75]. This is in conformity with the “artery size hypothesis” according to which smaller arteries (e.g., penile arteries) are the first to undergo a vascular lesion prior to the larger ones (e.g., coronary arteries). Moreover, in such patients erectile dysfunction is connected to the number of occluded vessels and more interestingly occurs over three years before coronary artery disease becomes apparent[76-80].
The diagnosis of ED in a patient may affect its management in two ways.30 The first relates to the fact that the ED patient, irrespective of whether he has or has not established CVD, is ‘reclassified’ into a higher risk category for future CV events. Management in this case is altered in the sense that more aggressive treatment of risk factors, as well as a close follow-up, is warranted. Implementation of biomarkers in this setting is desirable.
Medications used in the treatment of cardiovascular disease, especially antihypertensive medications, have been implicated frequently in the development of sexual dysfunction. A study of 5485 patients in the Hypertension Detection and Follow-up Program found that, during a 5-year period, 8.3% of male hypertensive patients stopped taking their antihypertensive medications secondary to sexual adverse effects.35x35Curb, JD, Borhani, NO, Blaszkowski, TP, Zimbaldi, N, Fotiu, S, and Williams, W. Long-term surveillance for adverse effects of antihypertensive drugs. JAMA. 1985; 253: 3263–3268
Erectile dysfunction can occur as a side effect of medication taken for another health condition. Common culprits are high blood pressure meds, antidepressants, some diuretics, beta-blockers, heart medication, cholesterol meds, antipsychotic drugs, hormone drugs, corticosteroids, chemotherapy, and medication for male pattern baldness, among others.
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.
Erectile dysfunction (ED) is commonly called impotence. It’s a condition in which a man can’t achieve or maintain an erection during sexual performance. Symptoms may also include reduced sexual desire or libido. Your doctor is likely to diagnose you with ED if the condition lasts for more than a few weeks or months. ED affects as many as 30 million men in the United States.
Until recently, erectile dysfunction (ED) was one of the most neglected complications of diabetes. In the past, physicians and patients were led to believe that declining sexual function was an inevitable consequence of advancing age or was brought on by emotional problems. This misconception, combined with men’s natural reluctance to discuss their sexual problems and physicians’ inexperience and unease with sexual issues, resulted in failure to directly address this problem with the majority of patients experiencing it.
More than 11 million people in the United States have cardiovascular disease, and each year, about 500,000 survive a myocardial infarction. These patients often seek counseling on their relative risk of resuming sexual activity. In the past, it was often assumed that if a patient could climb 2 flights of stairs without symptoms, it was safe for the patient to engage in sexual activity.82x82Hellerstein, HK and Friedman, EH. Sexual activity and the postcoronary patient. Arch Intern Med. 1970; 125: 987–999
Despite physician’s inexperience and patient’s reluctance to disclose sexual dysfunction problems, attempts to estimate the magnitude of this clinical condition have predicted that over 150 million men worldwide experience some degree of erectile dysfunction. Several studies have demonstrated a wide range regarding the prevalence of erectile dysfunction, which is even higher in patients with essential hypertension where the relative risk is approximately two times higher than in normotensive individuals[6-11]. The etiology can be found in the structural and functional abnormalities of the penile arteries induced by high blood pressure. Smooth muscle hypertrophy, stenotic lesions due to atherosclerosis and impaired blood flow are among the prominent structural alterations whereas endothelial dysfunction and the defective nitric oxide-induced vasodilatory mechanism belong to the main functional abnormalities induced by increased blood pressure[12,13]. As a matter of fact, sexual dysfunction is encountered more frequently that it is indeed believed underlining the need for a more proper and concrete assessment.
The following products are considered to be alternative treatments or natural remedies for Erectile Dysfunction. Their efficacy may not have been scientifically tested to the same degree as the drugs listed in the table above. However there may be historical, cultural or anecdotal evidence linking their use to the treatment of Erectile Dysfunction.
Yes, and there’s the rub. High blood pressure, especially if untreated, can lead to erectile dysfunction (ED). So can medications your doctor prescribes to bring down your high blood pressure. Fortunately, not all meds cause ED. Thiazides, diuretics or “water pills,” are common ED culprits. So are beta blockers. These effective heart meds slow your system down, and also affect blood flow where you need it -- in your penis -- at the right time. Alpha blockers, another class of medications that lower high blood pressure, are less likely to cause ED. So talk with your good doc about medication choices and side effects, so you can choose the right med for you.
The initial event for normal erectile function is sexual stimulation. Subsequent to processing in the central nervous system neural impulses are conveyed along the spinal cord, exiting through the pelvic parasympathetic preganglionic nerves. These pelvic nerves form the pelvic plexus and send their message through first messenger, acetyl choline, to the cavernosal nerves. The cavernosal nerves enter erectile bodies (corpora cavernosa) (Figure 1). Here, their nerve endings release a second messenger, nitric oxide. Nitric oxide activates the enzyme guanylyl cyclase, which lyses guanosine triphosphate (GTP) to produce a third messenger, the intracellular cyclic guanosine monophosphate (cGMP). Ultimately, the result is a decrease of intracellular calcium and an opening of potassium channels with the resultant relaxation of vascular smooth muscle in the arteries, aterioles, and sinusoids of the corpora cavernosa. The sinusoids open and rapidly fill with blood. Finally, the distended sinusoids compress their drainage pathways (venules) against the fibroelastic covering of the cavernosal bodies (tunica albuginea) and trap the blood in cavernosal bodies. The combination of an increased inflow of blood into the penis and coincident markedly diminished outflow results in rapidly increasing intracavernosal pressure that ultimately approximates systolic pressure. At this pressure the penis has sufficient axial rigidity to permit vaginal penetration.
Penile prosthesis implant remains the most effective and permanent treatment for ED. Penile prosthesis implants can be broadly divided into malleable and inflatable prostheses (20). Malleable penile prosthesis, also known as semi-rigid prosthesis, does not allow for (physiological) flaccid state of the penis. The patient can bend the prosthesis upwards for sexual intercourse and downwards for concealment. Although the angle of prosthesis concealment has improved with recent devices, however due to the constant rigid state of the penis, they are still less comfortable compared to their inflatable counterparts, are more likely to cause social embarrassment and associated with higher risk of implant erosions (21). However, malleable prosthesis still has its place for the treatment of ED as these implants are easier to handle, easier to place and would benefit patients with impaired manual dexterity.
ED is a common disease affecting men with IHD. Endothelial dysfunction is the link between ED and IHD and both diseases share the same aetiology, risk factors and pathogenesis. Aggressive control of these risk factors – along with lifestyle modification – is recommended to improve symptoms of ED and reduce cardiovascular risk. PDE5 inhibitors remain the first-choice treatment for ED in IHD patients and they have been shown to be safe and effective. However, PDE5 inhibitors can potentiate the hypotensive effect of nitrates so concomitant administration of sildenafil and nitrates is contraindicated. Gene and stem cell therapy are being investigated as a future therapies for ED.
Erections are extremely complicated and surprisingly fragile. Erections involve chemical signals, nerve impulses, complicated blood pressure changes, and overall fitness in systems ranging from your heart and hormones to your mood. When medication changes how one of these factors works—like blood pressure drops or depression medication—ED is a common side effect. The problem with these completely predictable medically induced side effects is how people react.
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
A considerable number of patients with ED can have psychogenic factors as the only cause, or in combination with organic causes of ED. Depression, low self-esteem and social stresses are among the psychogenic factors that can lead to ED. Depression is an independent risk factor for both ED and IHD; these three disease conditions are interlinked.51 Psychogenic ED can be managed by multiple psychological interventions such as cognitive behavioural therapy, couples counselling and guided sexual stimulation techniques.52
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

When it comes to scientific development, in Western medicine, an analytic approach is often used to identify and resolve medical challenges. A hypothesis is first derived through general observations of a phenomenon. A research plan is then carefully designed and data collected. Once sufficient data is collected, critical statistical evaluations are done and conclusions are drawn (4). Every aspects of a disease entity are studied from macroscopic to microscopic views, down to the cellular and molecular levels. The deep understanding of the role of cGMP-specific phosphodiesterase type 5 enzymes in ED and the use of phosphodiesterase-5 inhibitors in treatment of ED exemplifies the success of this approach.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (53) | Google ScholarSee all References Coital position has not been shown to play a role in increased cardiovascular risk; similar peak heart rates and blood pressure levels are evident with either the man or the woman in the superior position during intercourse.90x90Nemec, ED, Mansfield, L, and Kennedy, JW. Heart rate and blood pressure responses during sexual activity in normal males. Am Heart J. 1976; 92: 274–277

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