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.
Combination therapy has proven effective for some men who don’t respond adequately to oral medicines. The idea is to use two drugs with different mechanisms of action for better results. Commonly, sildenafil is used in combination with pellets of alprostadil (synthetic prostaglandin E1) that are inserted into the urethra (the tube in the penis that carries urine from the bladder to the outside of the body). Alprostadil also increases the blood supply to the penis, but by different means.
Erectile dysfunction (ED) is defined as the persistent inability to attain and maintain an erection that is sufficient to permit satisfactory sexual performance (1). The current pharmaco-therapeutic research in ED focuses on underlying endothelial dysfunction as the root cause for ED and introduction of phosphodiesterase type 5 inhibitors to potentiate nitric oxide (NO) action and cavernosal smooth muscle vasodilation, has revolutionized modern ED treatment over the past two decades (2). In contrast to Western Medicine, the traditional and complementary medicine (TCM) aims at restoration and better overall bodily regulation with medicine to invigorate qi (energy) in vital organs such as kidney, spleen and liver; to enhance physical fitness, increase sexual drive, stabilize the mind and improve the overall situation resulting in natural and harmonious sexual life (3).

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.
Although a considerable number of patients report penile pain with IC injection therapy, it appears that diabetic men still have high compliance rates with therapy. In one study, 16 of 18 diabetic men continued IC injection therapy for 7 years, compared to 7 of 22 nondiabetic control subjects with ED.57 One possible explanation for this is that diabetic patients with ED have fewer options than do nondiabetic men with ED, who are more likely to have a successful response to oral PDE-5 agents, as documented in one study.58 Another explanation is the greater familiarity with needles and injections among men with diabetes than among their nondiabetic counterparts.
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.
Clinical practice in TCM has been an exemplary case of customized treatment with holism epitomizes the essence of TCM. TCM encompasses these aspects, taking a holistic approach to patient’s problem and these methods combine body, mind and spirit, and healings are achieved via the concept of energy rather than matter, as in modern medicine. Compared to the complexity of modern science, which is the basis of Western medicine, this concept is easily understood and comprehended, and is readily accepted because of its holistic approach.
In a study by Segal et al. (11), 4 out of 5 healthy individuals were able to achieve tumescence beyond 60% maximum rigidity when subjected to PVS using the Viberect® alone, with no other external visual sexual stimulation. In a randomized controlled study by Fode et al. (12) involving 68 men who underwent nerve-sparing radical prostatectomy, 30 men who received PVS to the frenulum daily for 6 weeks, using the Ferticare® vibrator, showed a trend towards better erections. After 1 year, 53% in the PVS group had an IIEF score ≥18 compared with 32% in the control group, although no statistical achievement was achieved. The role of PVS in penile rehabilitation is based on the postulation that PVS provides early activation of the parasympathetic erectile spinal centres at S2–S4 level, which result in early recovery of the neuropraxic cavernosal nerves.
Montorsi P,  Ravagnani PM,  Galli S,  Rotatori F,  Veglia F,  Briganti A,  Salonia A,  Dehò F,  Rigatti P,  Montorsi F,  Fiorentini C. Association between erectile dysfunction and coronary artery disease. Role of coronary clinical presentation and extent of coronary vessels involvement: the COBRA trial, Eur Heart J , 2006, vol. 27 (pg. 2632-2639)https://doi.org/10.1093/eurheartj/ehl142

“The presence of erectile dysfunction portends a higher risk of future cardiovascular events, particularly in intermediate-risk men, and may serve as an opportunity for intensification of cardiovascular risk prevention strategies,” wrote Boston University heart specialists Naomi Hamburg, MD and Matt Kluge, MD, in an accompanying editorial. “The findings add to the growing evidence supporting additional trials to determine the clinical impact of erectile dysfunction screening and the appropriate cardiovascular directed evaluation and treatment of men with erectile dysfunction.”
Abstract | Full Text PDF | PubMed | Scopus (16) | Google ScholarSee all References These medications cause intracavernosal pressure changes in animal models, and human studies have noted deleterious effects on erectile function, decreased libido, and ejaculatory problems.42x42Weiss, RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician. 1991; 44: 2075–2082
The discovery in 1992 of the second messenger of cavernosal smooth muscle relaxation was the critical step that led to the era of nonhormonal oral drug therapy for ED. In 1998, the multicenter trial of sildenafil in the treatment of ED was published in the New England Journal of Medicine, and the era of the phosphodiesterase type 5 (PDE-5) inhibitor began.1 For 5 years, sildenafil was the primary therapy for men with EDDM. Recently, 2 new PDE-5 inhibitors, vardenafil and tadalafil, were introduced.
Keep your stress level down. Stress can interfere with sexual arousal and your ability to get an erection. Exercise, meditation, and setting aside time to do the things that you enjoy can help to keep your stress levels down and lessen your risk of ED. If you’re developing symptoms of anxiety or depression, consult your doctor. They may be able to refer you to a therapist who can help you work through anything that is causing you stress.
Like all diabetic complications, ED can occur even when you have followed your doctor’s advice and carefully managed your diabetes. Also like all diabetes complications, ED is less likely to occur with good blood sugar control. Poorly controlled diabetes and high cholesterol increase the chances of vascular complications, which may lead to ED or other circulatory problems. In addition, regular smoking and alcohol use can contribute to ED.
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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).

Oral medicines: The best known ED medications are the Big Three: Viagra (sildenafil citrate, made by Pfizer, Inc.), Levitra (vardenafil HCl, made by Bayer and GlaxoSmithKline), and Cialis (tadalafil, made by Eli Lilly). The three are chemically very similar, and all have proven very effective. Because they are effective, convenient, and relatively inexpensive (about nine dollars per pill), these medicines have become the treatment of choice for most men experiencing ED.

Low testosterone represents another link between erectile dysfunction and heart disease. A man’s testosterone levels gradually diminish beginning at age 30. By the time he reaches his 70s, testosterone levels may have dropped to a tenth of youthful levels. Diminishing testosterone levels contribute to loss of muscle, increased body fat, and reduced libido. Fatigue is common, as is depression. Low testosterone levels can also result in reduced concentration, irritability, passivity, loss of interest in activities, and even hypochondria.

A collection of risk factors that strongly predict heart disease—termed the metabolic syndrome—is also associated with erectile dysfunction. An increasingly prevalent condition, this syndrome includes low HDL, increased triglycerides, high blood sugar, and heightened inflammation and causes a three-fold or greater risk of heart attack, stroke, and diabetes. It is largely attributable to excess weight, poor diet, and inactivity and afflicts at least 47 million Americans, signaling that an epidemic of erectile dysfunction is sure to follow. Indeed, a survey of 2,400 men participating in a health screening revealed that metabolic syndrome increases the likelihood of erectile dysfunction by 48%.10

Contraindications for TTh include (for detailed listing, please refer to Buvat et al.45) patients with breast or prostate cancer, while patients with a palpable prostate nodule or induration, or prostate-specific antigen >4 ng/mL (or >3 ng/mL in men at high risk for prostate cancer, such as African-Americans or men with first-degree relatives with prostate cancer), should first undergo urological evaluation. Testosterone therapy is contraindicated also in patients with haematocrit >50% (TTh increases haematocrit) and uncontrolled congestive heart failure (risk of fluid retention). Risk for adverse CVD events may be increased in patients and with the mode of treatment epitomized in the study of Basaria et al.46 (see earlier).
Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References However, if optimally treated with β-blockers, lipid-lowering agents, and aspirin, these patients have no significantly increased cardiovascular risk associated with sexual activity, although they should receive appropriate risk information.88x88Jackson, G. The use of sildenafil in heart disease [editorial]. Hosp Med. 2000; 61: 526–527
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

If impotence affects you or someone you love, don’t lose hope. You may be suffering from a medical or emotional issue that is causing low libido or impotence — possibly interfering with both your confidence and relationship — but the good news is there are effective natural remedies for impotence that can help reverse this problem in most men. Around 70 percent of ED cases are resolved with natural impotence remedies that can help restore your sexual health.
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

With great interest we have read the recently published review by Vlachopoulos et al, a very detailed and extensive overview of erectile dysfunction in the cardiovascular patients. Guidelines for the management of erectile dysfunction with heart failure were noted, as well as advice about dealing with erectile dysfunction (ED) in patients with cardiovascular disease (CVD). However, many others have written similar reviews and guideline concerning the care for ED as well as (female) sexual dysfunction in CAD in the past years (1-4), cardiologists should be familiar with this matter by now. The problem is the actual translation of this knowledge into actions in cardiologists' daily clinical practice. Our research group performed a survey among Dutch cardiologists, aiming to evaluate their inquiry about erectile function in day-to-day practice, to detect their attitude towards this discussion and their perceived barriers for addressing sexual activity. Results from this survey indicated that cardiologists (n=414) did not routinely discuss erectile dysfunction: 48.7% indicated to discuss sexual function 'sometimes' and only 16.9% said to discuss the subject regularly. Of respondents, 41.5% marked that care for patients' sexual quality of life is not their responsibility. Nevertheless, 42% indicated that they would benefit from training to obtain knowledge about treatment of erectile and sexual dysfunction in cardiologic patients. Barriers not to inquire about sexual activity included 'the patient does not ask about it' (53.7%), 'I do not have an angle or motive to start about it'(45.9%), as well as time constraints (42.9%) and lack of training in dealing with sexual dysfunction (35.2%). The more experienced the cardiologist was the less he/she stated the need for training or for a referral directory(5). Since all cardiologists should, meanwhile, know that ED is part of their responsibility, as it is a sentinel marker of CVD(6). It is now case to pay attention to the implementation of the care for erectile and other sexual dysfunction in the cardiology practice. Our study suggests that physicians' experience in the field plays an important role in discussing sexual activity and that sexual healthcare can be improved with more education about the subject. Furthermore a directory of the available healthcare professionals for the referral of patients with sexual dysfunction was indicated as mandatory. We suggest that attention of cardiologists should not only be focused on writing about ED and CVD, attention should be diverted to the actual implementation of care for patients with ED as well, in order to improve patient-centered healthcare in cardiology.

Whereas management of sexual dysfunction in previously untreated hypertensive patients can be a challenging procedure, confronting the same clinical condition in individuals under antihypertensive regime can be even more demanding. In such cases there will always be a question hovering over physicians head. Is hypertension per se, antihypertensive medication or both, the causative factors provoking sexual dysfunction[15]?
Despite all the options and alternatives, sometimes there’s no suitable alternative to a prescription that contributes to ED. You might have an adverse reaction to an particular medication or an alternative is unavailable in your state, health insurance plan, or your budget. There are good reasons you were prescribed your original medication in the first place.
If your doctor says it's OK, you may be able to stop taking blood pressure medications temporarily to see if your sex life improves. To make sure your blood pressure remains within a safe range, you may need frequent blood pressure readings while you're not taking the blood pressure lowering medication that may be causing your sexual difficulties. This can be done with a home blood pressure monitoring device for convenience.
Second-generation cardioselective beta-blockers (atenolol, metoprolol, bisoprolol, etc.) can also lead to ED. Atenolol was shown to cause significant reduction of sexual activity compared with placebo in a double-blind, parallel-arm study.22 The same study also showed a significant reduction in testosterone levels with atenolol versus valsartan. An open, prospective study of hypertensive men treated with atenolol, metoprolol and bisoprolol for at least 6 months showed high prevalence of ED – approaching 66 % – in these patients.23
Vacuum therapy devices have a few disadvantages. One must interrupt foreplay to use them. You must use the correct-size tension ring and remove it, to prevent penile bruising, after sustaining the erection for 30 minutes. Initial use may produce some soreness. Such devices may be unsuitable for men with certain bleeding disorders. In general, vacuum constriction devices are successful in management of long-term ED.
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