Erectile dysfunction becomes more common with age. However, the condition is even more common among men who have diabetes. Over time, diabetes can damage the blood vessels and nerves that control erections. In addition, some of the other conditions that often occur with diabetes, such as coronary artery disease, can also contribute to the development of erectile dysfunction.

The study, which retrospectively tracked more than 43,000 men for an average of 3.3 years, found that men prescribed phosphodiesterase-5 (PDE5) inhibitors—the type of erectile dysfunction drug sold under the names Viagra, Levitra, Cialis and others—after their first heart attack were 38 percent less likely to die from any cause. No survival benefit was seen among men taking alprostadil, another type of erectile dysfunction drug that works through a different mechanism.
Montorsi F,  Briganti A,  Salonia A,  Rigatti P,  Margonato A,  Macchi A,  Galli S,  Ravagnani PM,  Montorsi P. Erectile dysfunction prevalence, time of onset and association with risk factors in 300 consecutive patients with acute chest pain and angiographically documented coronary artery disease, Eur Urol , 2003, vol. 44 (pg. 360-364)https://doi.org/10.1016/S0302-2838(03)00305-1
Crossref | Google ScholarSee all References Different classes of β-blockers have been postulated to have differential effects on erectile function, with the nonselective β-blockers (eg, propranolol) having more deleterious effects than the more cardioselective medications (eg, atenolol, metoprolol).42x42Weiss, RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician. 1991; 44: 2075–2082
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.
Relaxation of erectile tissue requires nitric oxide from nonadrenergic-noncholinergic neurons and the endothelium.21 Penile tissue from diabetic men with ED demonstrates impaired neurogenic and endothelium-mediated relaxation of smooth muscle,22 increased accumulation of advanced glycation end products (AGEs),23 and upregulation arginase, a competitor with nitric oxide synthase for its substrate L-arginine.24 Normal responses to direct smooth muscle relaxants in most of these studies implies that the impairments are due to decreased synthesis, release, or activity of nitric oxide. The fundamental mechanisms mediating these changes are thought to be the same as for other diabetic complications: increased polyol pathway flux, intracellular accumulation of AGEs, activation of protein kinase C, and increased flux through the hexosamine pathway.25
Few simple laboratory tests can help identify obvious causes of organic ED. Initial labs should include HbA1c, free testosterone, thyroid function tests, and prolactin levels. However, patients who do not respond to pharmacological therapy or who may be candidates for surgical treatment may require more in-depth testing, including nocturnal penile tumescence testing, duplex Doppler imaging, somatosensory evoked potentials, or pudendal artery angiography.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (30) | Google ScholarSee all References Increased cGMP levels cause intracellular calcium levels to decrease, resulting in relaxation of the corporeal smooth muscle, active dilatation of the penile arteries, arterioles, and sinusoids, and finally, increased arterial inflow and passive compression of penile venous outflow.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N

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.
A number of nonprescription products claim to be herbal forms of Viagra. Some of these products contain unknown amounts of ingredients similar to those in prescription medications, which can cause dangerous side effects. Some actually contain the real drug, which should be given by prescription only. Although the Food and Drug Administration has banned many of these products, some potentially dangerous erectile dysfunction remedies remain on the market.
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.

There are currently two models of the inflatable penile prosthesis (IPP), namely, the two-piece IPP vs. the three-piece IPP. The three-piece IPP consists of a pair of corporal cylinders, a scrotal pump and an abdominal reservoir filled with saline. Owing to the presence of the reservoir, the corporal cylinders can be completely deflated to give the patient the physiological flaccid state when not in use, and likewise a maximally turgid state when inflated (21). The two-piece IPP lacks an abdominal reservoir and is often offered in patients with whom placement of reservoir is challenging or not possible such as following radical cysto-prostatectomy with orthotopic ileal neobladder creation, or patients who had previous open book fracture of the pelvis with metal implants. The concept of ectopic reservoir placement has allowed many of these men the option for three-piece IPP placement (22). Technological advances have improved mechanical reliability, reduced prosthesis infection risk and offered excellent patient and partner satisfaction rate (23).
Abstract | Full Text | Full Text PDF | PubMed | Scopus (46) | Google ScholarSee all References Sedentary patients with a history of cardiac disease and patients with unstable angina or advanced congestive heart failure should undergo a full medical evaluation before resuming sexual activity.80x80Muller, JE. Triggering of cardiac events by sexual activity: findings from a case-crossover analysis. Am J Cardiol. 2000; 86: 14F–18F

Crossref | PubMed | Scopus (165) | Google ScholarSee all References Typically, the response to sexual activity is no more than an increase in heart rate to 130 beats/min and an increase in systolic blood pressure level to 170 mm Hg.51x51DeBusk, R, Drory, Y, Goldstein, I et al. Management of sexual dysfunction in patients with cardiovascular disease: recommendations of the Princeton Consensus Panel. Am J Cardiol. 2000; 86: 62F–68F


I have cared for hundreds of men with erectile dysfunction that have reversed their condition with a Nutritarian diet and the judicious use of dietary supplements. I have cared for hundreds of heart patients with angina and advanced heart disease, who have turned their backs on invasive cardiac procedures, recovered from angina and opened up the closed blood vessels in their diseased hearts. Out of thousands of men with advanced heart and erectile problems who have followed my nutritional advice, I have never had a patient suffer a heart attack or cardiac related death.

Table 3 is a suggested algorithm for the assessment of patients and their further categorization and handling. There are parts of investigation that are common for patients both with and without CVD, while additional elements of investigation are helpful in categorizing the patient without CVD to the appropriate risk category. Determination of exercise ability and stress testing is crucial to the assessment (see also below ‘Exercise ability: the risk of sexual activity’). Patients without established CVD or diabetes should be evaluated for their risk of future events according to risk scores (SCORE or Framingham). Patients with established CVD or diabetes are by default considered at increased risk. Patients with adequate exercise ability or a negative stress test can initiate or resume sexual activity and begin treatment for ED. In patients with a positive stress test or in high-risk patients, sexual activity should be deferred until the cardiac condition has been treated and stabilized. In all cases, patient follow-up and reassessment is recommended.
If you take a diuretic, you should stay on it until high blood pressure is under control. If erection problems persist, or blood pressure goes back up, then your doctor might switch to a drug that's less likely to cause erectile dysfunction. Or, a combination of medications might work better to control high blood pressure and lower the risk of erectile dysfunction.
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.
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
The pilot study by Vardi et al. (18) showed that LIESWT was effective in treating men with ED, suggesting a physiologic impact of LIESWT on cavernosal hemodynamics. The LIESWT is an effective penile rehabilitation tool that improves erectile function and potentially reverses underlying ED. Recent meta-analysis (19) of 14 studies showed that LiESWT could significantly improve the International Index of Erectile Function (IIEF) [mean difference: 2.00; 95% confidence interval (CI), 0.99–3.00; P<0.0001] and Erection Hardness Score (EHS) (risk difference: 0.16; 95% CI, 0.04–0.29; P=0.01). In addition, the therapeutic efficacy was noted to last for at least 3 months. LiESWT has been cited to a potential cure for ED, unlike other well established non-surgical methods of treatment (i.e., PDE5i, ICI and VED) being on demand treatments.

Sexual dysfunction refers to a problem during any phase of the sexual response cycle that prevents the individual or couple from experiencing satisfaction from the sexual activity. The sexual response cycle has four phases: excitement, plateau, orgasm, and resolution. Sexual dysfunction can be caused by physical and emotional factors, or a combination of both. The side effects of some medications also can lead to sexual dysfunction.


A number of drugs are known to cause ED in patients with DM (Table 1). For example, many EDDM patients are on antihypertensive medications. Replacement of thiazides or beta-blockers with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may be sufficient to regain erectile ability.5 Furthermore, discontinuation of selective serotonin reuptake inhibitors, if these drugs are not essential for patient well-being, may be therapeutic. Careful monitoring following drug discontinuation will help to determine if ED is due to the medication or other underlying disorders. The benefits of continued drug therapy with these drugs should always be weighed against the likelihood of causing ED and impacting on the patient's QOL.
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.
Severe testosterone deficiency, known as “hypogonadism,” is present in approximately 2–35% of men with erectile dysfunction.19 However, lesser degrees of deficiency are common, perhaps present in the majority, depending on the definition of “low” applied, the method of measurement, and the parameter being used to define testosterone (total, free, or bioavailable) deficiency.19,20 Most authorities agree that a total testosterone level below 300 ng/dL is clearly low, and that 300–400 ng/dL is low to low-to-normal. Most studies using testosterone replacement for erectile dysfunction have attempted to achieve blood levels of 450–850 ng/dL.
Heart disease describes a range of conditions that affect your heart. Diseases under the heart disease umbrella include blood vessel diseases, such as coronary artery disease; heart rhythm problems (arrhythmias); and heart defects you’re born with (congenital heart defects), among others.The term “heart disease” is often used interchangeably with the term “cardiovascular disease.” Cardiovascular disease generally refers to conditions that involve narrowed or blocked blood vessels that can lead to a heart attack, chest pain (angina) or stroke. Other heart conditions such as those that affect your heart’s muscle, valves or rhythm, also are considered forms of heart disease.
Due to their vasorelaxing effect, administration of PDE-5 inhibitors in hypertensive individuals was initially confronted with great suspicion. A wealth of clinical data however has proven that PDE-5 inhibitors are associated with few side effects and provoke a small and insignificant reduction in blood pressure with minimal heart rate alterations in both normotensive and hypertensive patients as well. As a matter of fact, they can be safely and effectively administered to hypertensive individuals even when they are already taking multiple antihypertensive agents[51-56]. The sole exception to the rule is co-administration with organic nitrates, which is an absolute contraindication due to profound and possibly hazardous hypotension effect[57,58]. Moreover, precaution should be taken when PDE-5 inhibitors are combined with a-blockers where, due to possible orthostatic hypotension effect, lower starting doses should be implemented in the therapeutic regime[59-62].
Artery size also explains the onset of ED before occurrence of CAD. Coronary arteries are 3–4 mm in diameter, while the penile artery is 1–2 mm in diameter.17 Endothelial dysfunction and plaque burden in the small arteries may cause symptoms of ED before they affect blood flow in large arteries. Also, an asymptomatic lipid-rich plaque in the coronary arteries carries the risk of rupture that leads to acute coronary syndrome or death, so ED may be predictive of these serious events without warning cardiac symptoms.17
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.
With atherosclerosis, the blood vessels are not able to dilate properly, which is called endothelial dysfunction (see the Figure). Cholesterol builds up in the blood vessel walls and forms plaques, which make the vessels narrow and slow down blood flow. When a plaque becomes very advanced, it can completely stop blood from passing through, which is what happens in a heart attack. Atherosclerosis affects not only the blood vessels supplying the heart (coronary arteries), but also blood vessels throughout the entire body. Atherosclerosis causes angina (chest pain that is often exertional), heart attacks, strokes, claudication (pain in the legs with walking), and ED. Atherosclerosis affects different people in different places, but it often affects the penis first, then the heart and brain, and the legs last. Because the first stage of atherosclerosis, endothelial dysfunction, usually affects the penis first, ED can be a warning sign that a heart attack or a stroke may follow, often in the next 3 to 5 years. This warning sign can be a good thing if it alerts you and your doctor that you have atherosclerosis, because then you can take steps to treat the atherosclerosis and prevent a heart attack or stroke.
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.

For patients who failed oral medical therapy or unable to tolerate the side effects, intracavernosal injection of vasoactive agents can often provide effective alternative. Various vasoactive agents such as alprostadil, papaverine or phentolamine have been used either as single agent or combination agents to potentiate the NO release and cavernosal smooth muscle vasodilation. However, intracavernosal injection therapy has high attrition rate and can be associated pain especially with alprostadil injection (2). The practice of isolating compounds and understanding its pharmacological attributes before using it as a drug therapy has been a strength of Western medicine.
Taking one of these tablets will not automatically produce an erection. Sexual stimulation is needed first to cause the release of nitric oxide from your penile nerves. These medications amplify that signal, allowing some men to function normally. Oral erectile dysfunction medications are not aphrodisiacs, will not cause excitement and are not needed in men who get normal erections.

Getting blood glucose under control is a good anti-ED tactic. Men with diabetes and poor blood glucose control are two to five times as likely to have ED as those with good control. One study in a group of men who had had type 1 diabetes for up to 15 years with minor complications found that intensive blood glucose control lowered the risk of ED compared with conventional treatment. A study in men with type 2 diabetes found that lowering A1C (average blood glucose in the past two to three months) below 7 percent and reducing blood pressure through a combination of medication, diet, and exercise improved sexual functioning.
Physical and emotional stress — whether over-exercising, under-sleeping or just dealing with everyday stressors like work and a busy schedule — causes an increase in “stress hormones,” including cortisol and adrenaline. Stress can lower desire for sex. This is because stress can contribute to fatigue or preoccupation with other tasks. It can also significantly affect blood flow by increasing inflammation.
Powerful clinical and scientific experience suggests a close link between erectile dysfunction and heart disease. Studies like the Health Professionals Follow-up Study have revealed the risk factors for erectile dysfunction to be very similar to those for heart disease. Hypertension, smoking, diabetes, high cholesterol, obesity, and physical inactivity all strongly predict sexual dysfunction in men, as they do heart disease.1
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.
4. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Erectile dysfunction (updated Nov 2015). https://www.niddk.nih.gov/health-information/health-topics/urologic-disease/erectile-dysfunction/Pages/facts.aspx (accessed Nov 2016). myDr myDr provides comprehensive Australian health and medical information, images and tools covering symptoms, diseases, tests, medicines and treatments, and nutrition and fitness.Related ArticlesImpotence causesFind out the physical and psychological causes of impotence, also called erectile dysfunction or ED.Erectile dysfunction: visiting your doctorFind out what questions a doctor may ask when discussing erectile dysfunction (ED, or impotence8 Surprising causes of erectile dysfunctionOccasional erectile dysfunction is not uncommon, but if it's persistent, erectile dysfunction caAdvertisement
Abstract | Full Text PDF | PubMed | Scopus (19) | Google ScholarSee all References However, there has been disagreement regarding the effects of diuretics on erectile function; many studies found that only rarely have these medications been implicated convincingly as the cause of a patient's ED.36x36Wein, AJ and Van Arsdalen, KN. Drug-induced male sexual dysfunction. Urol Clin North Am. 1988; 15: 23–31

The prevalence of erectile dysfunction is approximately 2-fold higher in hypertensive patients compared to normotensive individuals. However, erectile dysfunction remains under-reported, under-recognized, and under-treated in hypertensive patients. Hypertension per se and antihypertensive drug therapy may contribute to the development of erectile dysfunction in patients with arterial hypertension. The management of erectile dysfunction in hypertensive patients is tricky and should take into account the different effects of antihypertensive drug categories on erectile function. Lifestyle modification should be the mainstay of treating erectile dysfunction in patients with untreated hypertension. Switching antihypertensive therapy should be considered in treated hypertensive patients, unless administered drugs are absolutely indicated for the individual patient. Otherwise, PDE-5 inhibitors should be used, since they are both effective and safe in hypertensive patients. Finally, erectile dysfunction offers the opportunity to recognize asymptomatic cardiovascular disease and better characterize the relevant risk with obvious benefits for cardiovascular disease prevention.


Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References The risk after sexual activity in these patients is unknown, although vasodilators should be avoided because they may increase the intraventricular gradient.51x51DeBusk, R, Drory, Y, Goldstein, I et al. Management of sexual dysfunction in patients with cardiovascular disease: recommendations of the Princeton Consensus Panel. Am J Cardiol. 2000; 86: 62F–68F
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
The views expressed in this article intend to highlight alternative studies and induce conversation. They are the views of the author and do not necessarily represent the views of hims, and are for informational purposes only, even if and to the extent that this article features the advice of physicians and medical practitioners. This article is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment, and should never be relied upon for specific medical advice.
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.
Crossref | PubMed | Scopus (165) | Google ScholarSee all References Typically, the response to sexual activity is no more than an increase in heart rate to 130 beats/min and an increase in systolic blood pressure level to 170 mm Hg.51x51DeBusk, R, Drory, Y, Goldstein, I et al. Management of sexual dysfunction in patients with cardiovascular disease: recommendations of the Princeton Consensus Panel. Am J Cardiol. 2000; 86: 62F–68F
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."
The same device is considered a vacuum erectile device (VED), when it is used to increase inflow of the blood to the penis without a constriction band. Regular use of VED in post-prostatectomy patient increases penile oxygenation and is accepted as a valid option in penile rehabilitation. Recent study reported transient increase in oxygenation to the glans penis and corporal bodies were detected by oximetry after VED was applied, providing proof for possible role for VED to counter the early penile hypoxia, cavernosal fibrosis and long-term ED after radical prostatectomy (9).
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.
Crossref | PubMed | Scopus (165) | Google ScholarSee all References Typically, the response to sexual activity is no more than an increase in heart rate to 130 beats/min and an increase in systolic blood pressure level to 170 mm Hg.51x51DeBusk, R, Drory, Y, Goldstein, I et al. Management of sexual dysfunction in patients with cardiovascular disease: recommendations of the Princeton Consensus Panel. Am J Cardiol. 2000; 86: 62F–68F
Artery size also explains the onset of ED before occurrence of CAD. Coronary arteries are 3–4 mm in diameter, while the penile artery is 1–2 mm in diameter.17 Endothelial dysfunction and plaque burden in the small arteries may cause symptoms of ED before they affect blood flow in large arteries. Also, an asymptomatic lipid-rich plaque in the coronary arteries carries the risk of rupture that leads to acute coronary syndrome or death, so ED may be predictive of these serious events without warning cardiac symptoms.17
Abstract | PubMed | Scopus (136) | Google ScholarSee all References In a prospective review of 3250 men aged 26 to 83 years without ED at their first examination, total cholesterol and high-density lipoprotein (HDL) cholesterol levels were found to be strongly predictive of onset of ED after controlling for age, diabetes mellitus, stress level, cardiovascular disease, and prostate disease.25x25Wei, M, Macera, CA, Davis, DR, Hornung, CA, Nankin, HR, and Blair, SN. Total cholesterol and high density lipoprotein cholesterol as important predictors of erectile dysfunction. Am J Epidemiol. 1994; 140: 930–937
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
Previous studies reported that there is a strong chance of future cardiac events when ED occurs in younger men compared with older men.11 Another study suggested that there is consistent association across age groups.12 A study of men with diabetes found that ED acts as an indicator of cardiovascular events after adjusting for other illnesses, psychological aspects and the usual cardiovascular risk factors.13 Another large-scale study comprising 25,650 men with pre-existing ED suggested that these men had a 75 % increased risk of peripheral vascular disease.14 Moreover, some studies demonstrated a relationship between ED score and number of diseased coronary arteries and plaque burden in coronary arteries.2,15

80. Montorsi F, Briganti A, Salonia A, Rigatti P, Margonato A, Macchi A, Galli S, Ravagnani PM, Montorsi P. Erectile dysfunction prevalence, time of onset and association with risk factors in 300 consecutive patients with acute chest pain and angiographically documented coronary artery disease. Eur Urol. 2003;44:360–364; discussion 364-365. [PubMed]

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.
For those patients who cannot take erectile dysfunction medications, the authors counsel that an exercise training regimen may be an appropriate substitute therapy to enhance sexual function and quality of life. The authors stress that clinicians should focus on the sexual activity history of chronic heart failure patients and not ignore it, since addressing this element can substantially improve their quality of life.
Since time immemorial, TCM has been adopted by many cultures and is widely practiced in Asian countries despite paucity of level 1 clinical evidence and limited published safety records. TCM is more congruent with Asian values, beliefs and philosophical orientation to health, simple administration, readily available and ease of access or procurement, and general belief that TCM is safer. While Asian males are clearly different from their Western counterparts with respect to biology, culture and beliefs, the practice of TCM appears to be adopted by many Western nations lately. Many men seek TCM to avoid embarrassing visits to physicians and potential side effects of pharmaceutical drugs, or after becoming frustrated with the outcome of modern medicine. Patients are choosing to take more responsibility for their health by exploring a variety of non-pharmaceutical drugs and wellness practices. Furthermore, TCM such as herbal medicine does not address a specific organ system only and is meant to restore and realign the vital energy within the body, which is responsible for ageing, clinical diseases and the deterioration of bodily function; while in Western medicine, each pill is intended for a specific organ/system and that a patient may need a collection of pills to treat multiple comorbidities, rendering modern medicine less attractive to TCM.
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.
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.

Crossref | PubMed | Scopus (539) | Google ScholarSee all References Possible etiologies for ED secondary to hypertension include vascular damage due to hypertensive changes as well as hormonal abnormalities such as elevated prolactin levels.30x30Jaffe, A, Chen, Y, Kisch, ES, Fischel, B, Alon, M, and Stern, N. Erectile dysfunction in hypertensive subjects: assessment of potential determinants. Hypertension. 1996; 28: 859–862
ED can be caused by many things. The most common causes in men with diabetes are problems related to blood vessel– and nerve-related complications. Sometimes, though rarely, ED can be caused by a hormonal imbalance. Depression can also cause ED, as can stress and excessive worrying about sexual performance. Certain medications can cause temporary ED.
Gazzaruso C,  Solerte SB,  Pujia A,  Coppola A,  Vezzoli M,  Salvucci F,  Valenti C,  Giustina A,  Garzaniti A. Erectile dysfunction as a predictor of cardiovascular events and death in diabetic patients with angiographically proven asymptomatic coronary artery disease: a potential protective role for statins and 5-phosphodiesterase inhibitors, J Am Coll Cardiol , 2008, vol. 51 (pg. 2040-2044)https://doi.org/10.1016/j.jacc.2007.10.069

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
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