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.
After getting a diagnosis of ED, most patients can begin treatment right away, but treatment may be delayed for some patients until the health of the heart is more fully assessed or improved. The most common treatment for ED is a pill (phosphodiesterase-5 inhibitor; PDE5-I): Viagra (sildenafil), Cialis (tadalafil), or Levitra (vardenafil). Each of these pills improves erections when taken before sexual activity; alternatively, a low dose of Cialis can be taken once a day. These medicines work by allowing the blood vessels that supply blood to the penis to dilate better during sexual stimulation. The PDE5-Is decrease blood pressure a little bit, but they are safe with most other medications and with other blood pressure pills. The PDE5-Is are not safe with nitrate medications like nitroglycerin, Nitrostat, Nitro Paste, Imdur, isosorbide mononitrate, and Isordil. Mixing a PDE5-I with a nitrate medication could result in severely low blood pressure and even death. Inform all medical professionals (including the ambulance or emergency department) about your most recent ED pill ingestion so that nitrates can be avoided. If you have high blood pressure or benign prostatic hypertrophy (enlarged prostate) and take medicines called α-blockers, your doctor may need to start you on the lowest dose of the PDE5-I.
Diabetes occurs when you have too much sugar circulating in your bloodstream. There are two main types of diabetes: type 1 diabetes, which affects less than 10 percent of those who have diabetes, and type 2 diabetes, which accounts for over 90 percent of diabetes cases. Type 2 diabetes often develops as a result of being overweight or inactive. Approximately 30 million Americans have diabetes, and about half of them are men.

Just because a product claims to be natural doesn't mean it's safe. Many herbal remedies and dietary supplements can cause side effects and dangerous interactions when taken with certain medications. Talk to your doctor before you try an alternative treatment for erectile dysfunction — especially if you're taking medications or you have a chronic health problem such as heart disease or diabetes.
The safety of PDE5 inhibitors in patients with IHD has been shown in multiple trials. Arruda-Olson et al. investigated the safety of sildenafil during exercise stress tests in patients with IHD to ascertain whether the drug induces or exacerbates myocardial ischaemia. This was a prospective, randomised crossover study that demonstrated safety of sildenafil when given 1 hour before an exercise stress test.69 Another study that investigated 120 trials of sildenafil revealed that the rates of MI and cardiovascular death with sildenafil are as low as with placebo.70

A thorough history (including cardiovascular symptoms, age, presence of risk factors and comorbid conditions such as obesity, hypertension, dyslipidaemia, pre-diabetes, CAD, peripheral artery disease, symptoms suggestive of sleep apnoea, family history of premature atherothrombotic CVD and lifestyle factors), assessment of ED severity (according to SHIM) and duration, and physical examination (for both heart and peripheral circulation pathology) are mandatory first-line elements of investigation. A resting electrocardiogram, measurement of fasting plasma glucose, and estimation of glomerular filtration rate are desirable tests that may be used to further characterize cardiovascular status and risk and to identify men who require additional cardiologic workup. Owing to the accumulating evidence supporting the link with CVD, the measurement of testosterone is recommended in all men with a diagnosis of organic ED, especially in those for whom phosphodiesterase type 5 (PDE5) inhibitor therapy failed.
Having chronically high blood pressure can affect overall satisfaction with sex and affect men’s ability to achieve a firm erection. Due to constant vessel damage as a result of high blood pressure, linings of the arteries begin to harden and narrow, a process called atherosclerosis. Because blood flow is limited to the affected regions of the body, arterial blood circulation to various organs—including the heart muscles, brain, and even the groin—can be compromised, with myocardial infarctions, strokes, and erectile difficulty being common in hypertensive patients. Studies show that approximately 30 percent of hypertensive patients reported having erectile dysfunction, and approximately 49 percent of men aged 40 to 79 had both high blood pressure and ED.

Owing to its delicate nature, discussion about the sexual life of the patient is effective not on a circumstantial visit to the doctor, but on the basis of confidence between the patient and the physician, as is usually the case with the cardiologist. Thus, the cardiologist is given a unique opportunity to identify ED and thus ‘recharacterize’ the risk of the patient. In addition, since normal sexual activity is important to most men with CVD, irrespective of age, the cardiologist can clarify issues that relate to such activity after a cardiac event or to a specific cardiac condition (e.g. heart failure). Often, such issues are hampered by misconceptions from the side of the patient. Therefore, while less than half of the patients receive information about resuming sexual activity after a cardiac event, proper counselling increases their likelihood to resume their previous level of sexual activity by 50%.50 Furthermore, the cardiologist can increase adherence to the medication by clarifying that it is uncommonly the true cause of ED. Finally, proper counselling is required to ensure safety of concomitant PDE5 inhibitors medication, the use of which has the additional advantage to increase compliance to CVD mediation, especially in hypertension. It should be noted that while patients are often reluctant to bring up the issue of sexual health, they are relieved and respond positively when their cardiologist has done so. It should also be emphasized that, frequently, sexual counselling is more effective when done together with their partner.
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
When your blood pressure is high for an extended time, it can damage the lining of your arteries and interfere with your blood flow. This appears to affect your ability to get and maintain an erection. A 2012 study published in the journal Current Opinion in Nephrology and Hypertension found that approximately 30 percent of men with hypertension complain of ED.
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.

Core tip: 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. 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, phosphodiesterase-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 with obvious benefits for cardiovascular event prevention.

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The most important way to protect your heart is to eat a Nutritarian diet and that means eating your G-BOMBS: greens, beans, onions, mushrooms, berries and seeds. Natural plant foods have numerous cardio-protective effects. For example, greens activate the Nrf2 system, which turns on natural detoxification mechanisms and protects blood vessels against inflammatory processes that lead to atherosclerotic plaque buildup.9
A component of the increased risk conferred by ED could be testosterone deficiency.24 Low testosterone leads to increased levels of total and LDL cholesterol, as well as to increased production of pro-inflammatory markers and mediators.25 Endothelial dysfunction and increased arterial wall thickness, stiffening, and calcification also ensue. On this basis it has been hypothesized that chronically lowered testosterone may increase CVD risk. Indeed, androgen deficiency has emerged as a predictor of CV events, as well as of all-cause and CV mortality, both in the general population and in patients with CV risk factors, with hypertension, with established CVD, and with ED.26 Viewed from the opposite angle, higher serum testosterone showed a protective role for CV events in elderly men.27 A 2010 meta-analysis limited to studies in middle-aged men found no association between total testosterone (TT) levels and CVD risk.28 However, a more recent meta-analysis involving a larger number of studies identified significant associations between androgen deficiency and increased risk of CVD and CVD mortality.29 It should be stressed, however, that the nature of these studies cannot prove causality. The possibility that low testosterone may be an epiphenomenon, marking poor general health rather than modulating CVD risk per se has to be explored.
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You may reduce your risk of ED by improving your heart health. Healthy lifestyle choices often encourage you to stop smoking, lose weight and increase physical activity. If ED persists, oral medications are a common first therapy for ED. If oral medications don’t work for you, the penile implant may be an option. The implant is concealed inside the body. It offers support for an erection whenever and wherever desired.
The use of penile support device such as penile cast worn externally during intercourse has been tried to provide length and rigidity to the penile shaft (24). Each device can be customised to the patient’s penile size and provided an option for patients who are seeking non-pharmaceutical/non-invasive treatment, or have end-organ failure who may not be candidates for, or unable to afford, penile prosthesis implant.
Abstract | Full Text PDF | PubMed | Scopus (1528) | Google ScholarSee all References After sexual intercourse, this risk increases approximately 2-fold, to 2 chances per million per hour, but only for the 2 hours after intercourse. For low-risk patients with no history of cardiovascular disease and an annual myocardial infarction risk of 1% per year, the risk increases to 1.01% with weekly sexual activity.8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409

Lindau ST,  Abramsohn E,  Gosch K,  Wroblewski K,  Spatz ES,  Chan PS,  Spertus J,  Krumholz HM. Patterns and loss of sexual activity in the year following hospitalization for acute myocardial infarction (a United States National Multisite Observational Study), Am J Cardiol , 2012, vol. 109 (pg. 1439-1444)https://doi.org/10.1016/j.amjcard.2012.01.355
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].
Just because a product claims to be natural doesn't mean it's safe. Many herbal remedies and dietary supplements can cause side effects and dangerous interactions when taken with certain medications. Talk to your doctor before you try an alternative treatment for erectile dysfunction — especially if you're taking medications or you have a chronic health problem such as heart disease or diabetes.
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 | Scopus (174) | Google ScholarSee all References All these men had ED and twice underwent symptom-limited supine bicycle exercise echocardiography 1 hour after taking either sildenafil (50 mg or 100 mg) or placebo. This study found no significant changes in resting heart rate, diastolic blood pressure level, or wall motion score index, and the exercise capacity of the 2 groups was similar. Both groups had similar numbers of patients who experienced dyspnea and/or chest pain, had a positive exercise echocardiographic test, and had exercise-induced wall motion abnormalities. Sildenafil caused a mean decrease of 7 mm Hg in the resting systolic blood pressure level compared with the placebo group. In conclusion, this study showed that in patients with stable coronary artery disease, sildenafil caused no change in symptoms, exercise endurance, or presence/extent of exercise-induced ischemia as measured by exercise echocardiography.

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.


A study conducted by Prince Henry’s Institute in Melbourne Australia published in the Medical Journal of Australia found that men over 20 years of age with erectile dysfunction (ED) have twice the risk of cardiovascular incidents than those of men with normal sexual health. It was also found out that 2% of men aged 55 and older experienced major stroke and cardiac arrest after the initial episode of ED, within a year; 11% experienced something within five years.  Experts from Prince Henry’s Institute warned men with these failures to seek advice on erectile dysfunction and high blood pressure. This may indicate a missing vital warning sign of impending heart disease. Why is this happening? Do men with ED predispose themselves to have cardiovascular diseases and strokes or just the other way around?
Erectile dysfunction is common in the patient with cardiovascular disease. It is an important component of the quality of life and it also confers an independent risk for future cardiovascular events. The usual 3-year time period between the onset of erectile dysfunction symptoms and a cardiovascular event offers an opportunity for risk mitigation. Thus, sexual function should be incorporated into cardiovascular disease risk assessment for all men. A comprehensive approach to cardiovascular risk reduction (comprising of both lifestyle changes and pharmacological treatment) improves overall vascular health, including sexual function. Proper sexual counselling improves the quality of life and increases adherence to medication. This review explores the critical connection between erectile dysfunction and cardiovascular disease and evaluates how this relationship may influence clinical practice. Algorithms for the management of patient with erectile dysfunction according to the risk for sexual activity and future cardiovascular events are proposed.
 Other treatment options such as penile self-injection therapy, external vacuum pumps and the medicated urethral system for erection are on rare occasions an effective long-term treatment. A very small percentage of men will continue with these treatments as evidenced by a very high drop out rate and a very low refill rate for these treatments. These procedures require extensive planning which interfere with sexual spontaneity and are really not a realistic long-term treatment for young patients with permanent ED. 
Crossref | PubMed | Scopus (174) | Google ScholarSee all References All these men had ED and twice underwent symptom-limited supine bicycle exercise echocardiography 1 hour after taking either sildenafil (50 mg or 100 mg) or placebo. This study found no significant changes in resting heart rate, diastolic blood pressure level, or wall motion score index, and the exercise capacity of the 2 groups was similar. Both groups had similar numbers of patients who experienced dyspnea and/or chest pain, had a positive exercise echocardiographic test, and had exercise-induced wall motion abnormalities. Sildenafil caused a mean decrease of 7 mm Hg in the resting systolic blood pressure level compared with the placebo group. In conclusion, this study showed that in patients with stable coronary artery disease, sildenafil caused no change in symptoms, exercise endurance, or presence/extent of exercise-induced ischemia as measured by exercise echocardiography.
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
Abstract | PubMed | Scopus (136) | Google ScholarSee all References Another study evaluated 32 hypertensive men with ED and 78 normotensive men with ED with regard to age, body mass index, hormonal profile, penile arterial flow, risk factors for arterial disease, psychiatric disease, and neurologic disease measured by pudendal nerve conduction studies.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

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 (95) | Google ScholarSee all References Nitrates have only modest antianginal effects and offer no prognostic benefit for mild recurrent angina or unstable angina. Therefore, such anginal symptoms occurring after sildenafil use should be treated with other nonnitrate antianginal agents such as β-blockers.15x15Taylor, HA Jr. Sexual activity and the cardiovascular patient: guidelines. Am J Cardiol. 1999; 84: 6N–10N
After analyzing 28 previous studies on the link between ED and heart disease, the researchers found a connection between erectile dysfunction and poor endothelial function. “Blood vessels are unable to fully dilate and allow blood to flow through,” explains Medicalnewstoday.com. “Endothelial dysfunction is an early sign of atherosclerosis, a condition in which plaque builds up in the arteries, raising the risk of heart attack and stroke.” The researchers also determined that there was a thickening of one of the inner two layers of the carotid artery—another heart-disease indicator.
The use of shock wave therapy has revolutionized the treatment of many aspects of medicine. High intensity extracorporeal shockwave therapy has been used for the treatment of nephro-urolithiasis while medium intensity shockwave therapy is used by orthopaedic surgeons to treat joint pain as well as tendinitis. Low intensity shockwaves therapy was first noted to improve ischaemia-induced myocardial dysfunction in animal studies when low intensity shockwaves were applied to porcine myocardium (13). Shockwaves induces a localized stress on cell membranes in the same way that shear stress affects endothelial cell membranes (14) and this triggers the release of angiogenic factors, such as increased NO production through increased activity of endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS), platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) (15). These shockwaves also cause membrane hyperpolarization (16), activation of the Ras signaling pathway, non-enzymatic synthesis of NO and induction of stress fibers and intercellular gaps (17).
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.
Crossref | PubMed | Scopus (174) | Google ScholarSee all References All these men had ED and twice underwent symptom-limited supine bicycle exercise echocardiography 1 hour after taking either sildenafil (50 mg or 100 mg) or placebo. This study found no significant changes in resting heart rate, diastolic blood pressure level, or wall motion score index, and the exercise capacity of the 2 groups was similar. Both groups had similar numbers of patients who experienced dyspnea and/or chest pain, had a positive exercise echocardiographic test, and had exercise-induced wall motion abnormalities. Sildenafil caused a mean decrease of 7 mm Hg in the resting systolic blood pressure level compared with the placebo group. In conclusion, this study showed that in patients with stable coronary artery disease, sildenafil caused no change in symptoms, exercise endurance, or presence/extent of exercise-induced ischemia as measured by exercise echocardiography.
Ischaemic heart disease (IHD), also known as coronary artery disease (CAD), is a predominant manifestation of cardiovascular disease (CVD). CVD is the leading cause of morbidity and mortality, accounting for 17.3 million deaths globally every year; this figure is expected to grow to 23.6 million by the year 2030. Eighty per cent of these deaths occur in lower- and middle-income countries.5 ED and IHD are highly prevalent and occur concomitantly because they share the same risk factors, including diabetes, hypertension, hyperlipidaemia, obesity and smoking.
Deer velvet is a covering found on the growing bone and cartilage of deer’s antlers. In Eastern medicine, deer velvet is sought after for its Chinese medicinal properties which include boosting one’s endurance and improving one’s immunity. People have also used deer velvet as an aphrodisiac or to treat ED. The randomized double-blind placebo-controlled study on deer velvet by Conaglen et al. (31), no benefit but this study was underpowered involving healthy participants with no sexual dysfunction.
Despite its limitations in detecting CVD without significant stenosis, EST (with or without imaging) can further define the cardiovascular risk in patients with ED and no overt CAD and may be particularly helpful for identifying silent CAD in patients with diabetes. Chemical stress tests are appropriate for patients who cannot complete an EST or in whom ECG is non-interpretable. In patients with established CVD, an interpretable EST is mandatory in the indeterminate risk category and is at the discretion of the cardiologist in the low risk category (Table 3B), since it determines exercise ability and estimates cardiovascular risk associated with sexual activity.
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.
Physical and sexual activity can trigger acute cardiac events. In a recent meta-analysis, a significant association between acute cardiac events and episodic physical (relative risk 3.45 for myocardial infarction and 4.98 for sudden cardiac death) and sexual activity (relative risk 2.7 for myocardial infarction) was demonstrated.32 This association was attenuated among individuals with high levels of habitual physical activity (for every additional time per week the relative risk for myocardial infarction decreased by ∼45%, and the relative risk for sudden cardiac death decreased by 30%). The physical demands of sexual activity have been identified as follows. Studies conducted primarily in young married men showed that sexual activity with a person's usual partner is comparable with mild-to-moderate physical activity in the range of 3–4 metabolic equivalents of the task (METS).30,33 The heart rate rarely exceeds 130 b.p.m. and systolic blood pressure rarely exceeds 170 mmHg in normotensive individuals. Accordingly, demands during sexual activity correspond to walking 1.5 km (or 1 mile) on the flat in 20 min or briskly climbing two flights of stairs in 10 s. Generalization, however, may not characterize all individuals (especially those who are older, are less physically fit, or have CVD) or sexual activity circumstances (e.g. extramarital, unfamiliar setting, excessive food and alcohol consumption). Therefore, completing 4 min of the standard Bruce treadmill protocol (5–6 METS) without symptoms, ST segment changes, arrhythmias, or a fall in systolic BP identifies the safety of sexual activity.30,33
The choice is yours. You do not have to die of a heart attack, and you do not have to have erectile dysfunction. Both are the result of dietary choices, and you can make a choice right now to protect your life. Do you want to die of a heart attack or don’t you? If you don’t, then are you willing to do what it takes to reduce your risk almost 100 percent? I don’t know about you, but for me, just dropping my risk 20 to 40 percent with medical care is not enough. I want maximum protection.
If your physician advises you that the risks of taking an erectile dysfunction medication are too high, he or she can advise you of other treatment options that can enable you to resume sexual activity without risks of complications. These might also include screening to try to determine if your erectile dysfunction has a physiological basis in need of medical intervention, can be corrected through lifestyle changes or if it may have psychological roots. After all, a heart attack or diagnosis of heart disease can lead to depression, which can also affect libido. Talk with your doctor to establish a safe, effective plan for resuming intimacy after your heart disease diagnosis.
Testosterone therapy (TTh) should be reserved for patients who (i) are symptomatic (ED or reduced libido) of testosterone deficiency45 and (ii) they have biochemical evidence of low testosterone (TT <8 nmol/L or 2.3 ng/mL). In men with borderline TT (8–12 nmol/L or 2.3–3.5 ng/mL), a TTh trial (for 3–6 months and continuation if effective) may be envisaged. While adding a PDE5 inhibitor can be considered in men who have not improved with TTh, the usual clinical scenario is to add TTh in patients who have not responded to PDE5 inhibitors. Improvement is dependent on the testosterone levels with better results being obtained at lower levels of TT.45 Despite evidence of benefit in patients with pre-existing cardiovascular conditions (angina or heart failure), it should be emphasized that TTh is not a medication with cardiovascular indications.
The connection between diabetes and ED is related to your circulation and nervous system. Poorly controlled blood sugar levels can damage small blood vessels and nerves. Damage to the nerves that control sexual stimulation and response can impede a man’s ability to achieve an erection firm enough to have sexual intercourse. Reduced blood flow from damaged blood vessels can also contribute to ED.
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