While a widely held perception is that CVD drugs cause ED, data attest towards the contrary and some agents may be even beneficial.41 Only thiazide diuretics lead clearly to ED, while some older beta-blockers also do so, but the side-effect of ED was very low (∼3%) when the patient was blinded for the drug administration.42 In fact, the vasodilating nebivolol may even improve erectile function.35,43 ACE-inhibitors, angiotensin-receptor blockers, and calcium-channel blockers are reported to have neutral or even a positive effect on erectile function35,41,43 but more evidence is needed. Regarding statins, the largest body of evidence point towards a beneficial effect.44 A negative effect has been reported in high statin doses, possibly related to a potential reduction in serum testosterone levels, but this dose dependency warrants further investigation. In terms of patient management, when ED onset and therapy initiation are linked and a cause-and-effect association is presumed, a short period of drug withdrawal with monitoring for ED resolution for verification may be an option. In patients who developed ED long after the initiation of CV drug treatment, sexual dysfunction is less likely to be drug associated and PDE5 inhibition therapy may be initiated.
Apart from their beneficial effect in erectile dysfunction and their safe profile in antihypertensive medication, PDE-5 inhibitors have even more advantages to demonstrate. Several lines of evidence has proven that patients receiving PDE-5 inhibitors are more likely to initiate an antihypertensive regime and more willing to add a new agent to their existing treatment, a fact that raises significantly patient’s adherence and as a matter of fact control of high blood pressure and quality of life[63,64]. Moreover, a handful of clinical data has demonstrated the considerable vasodilating and anti-proliferative properties of PDE-5 inhibitors in the pulmonary vasculature, establishing them as a first-line treatment in patients with pulmonary arterial hypertension[65,66]. The same properties have been considered as potentially responsible for improving microcirculation in patients with secondary Raynaud phenomenon and ameliorating cardiopulmonary exercise performance in patients with heart failure[67,68]. In addition, the therapeutic implementation of PDE-5 inhibitors has expanded in the field of benign prostate hyperplasia-lower urinary tract symptoms (BPH-LUTS). The common pathophysiologic substrate between erectile dysfunction and BPH-LUTS has rendered PDE-5 inhibitors an effective treatment which significantly improves measures of both conditions while at the same time exhibits high efficacy and safety. The beneficial effect is much more pronounced when taking into consideration the fact that a-blockers, the mainstay of therapy for benign prostate hyperplasia frequently provoke sexual side effects, erectile dysfunction included[69].
In subsequent clinical studies, a surprisingly high percentage of EDDM patients–10% to 20%–claimed that the placebo "improved my erections," thus indicating a psychological basis for their ED. In the latter half of the 1980s, objective means were developed that could help determine if a EDDM patient had organic or psychogenic ED. The absence of rigid sleep erections confirmed by penile monitors was one criterion for organic ED. The failure of vasoactive agents (papaverine, Trimix, or prostaglandin E-1 [PGE-1]) injected into the corpora cavernosa to induce penile rigidity was another criterion for organic disease. Intracavernosal maintenance flow rates during pharmacocavernosometry and maximum cavernosal arterial flow during penile Doppler ultrasonography were additional determinants.

Crossref | PubMed | Scopus (443) | Google ScholarSee all References Nitroglycerin and other NO donors work through the same NO-cGMP pathway that sildenafil affects, thereby decreasing vascular resistance and blood pressure level.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
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
Abstract | Full Text | Full Text PDF | PubMed | Scopus (30) | Google ScholarSee all References Penile sympathetic stimulation flows through several pathways, including the sympathetic chain ganglia, which also supply such structures as the heart and vascular system. Sympathetic tone precipitates release of norepinephrine from penile adrenergic nerves, resulting in tonic contraction of cavernosal smooth muscle and its vasculature, thereby keeping the penis flaccid.9x9Andersson, K and Stief, C. Penile erection and cardiac risk: pathophysiologic and pharmacologic mechanisms. Am J Cardiol. 2000; 86: 23F–26F

For many men, stopping smoking is an erectile dysfunction remedy, particularly when ED is the result of vascular disease, which occurs when blood supply to the penis becomes restricted because of blockage or narrowing of the arteries. Smoking and even smokeless tobacco can also cause the narrowing of important blood vessels and have the same negative impact. 

In particular, patients are classified into three categories (low, intermediate, high) depending on their CV risk profile. Individuals with controlled hypertension belong to the low-risk group where sexual dysfunction can be safely managed with the approved medical therapies regardless of the number or class (with the exception of b-blockers and diuretics) of agents of the patient’s antihypertensive regime. Moreover, patients of this group can safely initiate or reinstitute sexual activity without any need for additional cardiovascular evaluation.
Abstract | Full Text PDF | PubMed | Scopus (105) | Google ScholarSee all References Aspirin and β-blocker use have been suggested to decrease the risk of cardiovascular events with sexual activity, although their benefit has not been proved definitively.79x79Kimmel, SE. Sex and myocardial infarction: an epidemiologic perspective. Am J Cardiol. 2000; 86: 10F–13F
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?
While additional investigation is usually necessary, the medical and sexual history is essential and frequently the most revealing aspect of the ED assessment process. Questionnaires are an integral part of the history. The International Index of Erectile Function (IIEF), a 15-item, self-evaluation questionnaire is a validated instrument for assessing erectile function, orgasmic function, desire and satisfaction after sexual relations.8 An abridged version of the IIEF is a 5-item questionnaire the Sexual Health Inventory for Men (SHIM) or IIEF-5 (Table 2). Responses to the five questions range from 1 (worst) to 5 (best). Questions 2 to 4 may be graded 0 (if there is no sexual activity, or no sexual intercourse attempt) and the final score ranges from 1 to 25 points; a descending score indicates worsening of erectile function, with values ≤21 being diagnostic of ED.8 Importantly, validated questionnaires correlate with the extend of CAD9 and improve the predictive value of ED for total cardiovascular events compared with a single-question ED diagnosis.5 It cannot be overemphasized that the SHIM can be effectively used not only by andrologists and urologists but by a wide array of medical specialists, such as cardiologists, diabetologists, primary care physicians, etc.
Obesity is a strong predictor of ED as it is associated with other risk factors, such as diabetes, hyperlipidaemia and hypertension.4 Obesity increases the risk of ED by 30–90 % and acts as an independent risk factor for CVD. Obese men with ED have greater impairment in endothelial function than non-obese men with ED.5 Moreover, high BMI causes low testosterone levels, which in turn leads to ED, as observed in a prospective trial involving 7,446 participants.50
In Eastern medicine, animal products are commonly used for their perceived health benefits. The philosophy “like nourishes like”, suggests that consuming the organ of an animal will bring benefits to the corresponding organ in one’s body is a common belief. Men seeking greater potency have turned to eating penises from goats, bull, deer, horses, seals and other mammals in the form of cooked dishes or herbal preparations. While there is no scientific evidence supporting this practice, the cultural beliefs remain strong and supplements containing extracts from animal penises are readily available in the form of capsules, often mixed with herbal compounds pitching similar erectogenic properties. A significant proportion of these potency-inducing supplements in Asia have been found to contain PDE5-inhibitors substrates such as tadalafil and sildenafil (30). However uncontrolled use of illicit PDE5-inhibitors under the guise of natural supplements remains a health threat to the general public.
Obesity is a strong predictor of ED as it is associated with other risk factors, such as diabetes, hyperlipidaemia and hypertension.4 Obesity increases the risk of ED by 30–90 % and acts as an independent risk factor for CVD. Obese men with ED have greater impairment in endothelial function than non-obese men with ED.5 Moreover, high BMI causes low testosterone levels, which in turn leads to ED, as observed in a prospective trial involving 7,446 participants.50
This form of therapy has a response rate of well over 70%. The sympathetic nervous system normally maintains the penis in a flaccid or non-erect state. All of the vasoactive drugs, when injected into the corpora cavernosae, inhibit or override sympathetic inhibition to encourage relaxation of the smooth muscle trabeculae. The rush of blood engorges the penile corpora cavernosae sinusoidal spaces and creates an erection.
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.
Erectile dysfunction is defined as the inability to attain or maintain a penile erection sufficient for satisfactory sexual performance. Cases of ED may be classified as predominantly organic in nature, predominantly psychogenic, or mixed. Usual organic aetiologies are vasculogenic, hormonal, and neurogenic. Owing to the relationship of vasculogenic ED with CVD, it is important to distinguish men with predominantly vasculogenic ED from those with predominantly psychogenic ED or non-vasculogenic organic ED.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (37) | Google ScholarSee all References Other studies have proposed that the strain involved with intercourse in older patients is less associated with physical exertion and more closely related to sexual arousal.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
Penile implants - are generally used if physical damage (like an accident) makes the anatomical parts needed for an erection not work. These are inserted by surgery and can provide a permanent treatment choice if others fail to work. The implants can be semi-rigid or inflatable. They can be pretty expensive and are not usually available on the NHS.
A study published in May 2014 in The Journal of Sexual Medicine found that some men can reverse erectile dysfunction with healthy lifestyle changes, such as exercise, weight loss, a varied diet, and good sleep. The Australian researchers also showed that even if erectile dysfunction medication is required, it's likely to be more effective if you implement these healthy lifestyle changes.
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.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (272) | Google ScholarSee all References Most adverse effects are mild and are related primarily to vasodilation (headache, flushing, nasal congestion), gastrointestinal disturbances (dyspepsia), or retinal effects such as vision changes.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Not enough info for you? No problem. Nerd out on erectile dysfunction with these studies and research from the most trusted sources on the interwebs. If you have any questions or you think we missed something important, leave a comment or book a consultation with me or one of these trained professionals and we’ll get you on the way to a healthier manhood.
Abstract | Full Text PDF | PubMed | Scopus (3562) | Google ScholarSee all References During a 9-year follow-up study of 513 of these men who had no ED at the first study, the risk of new-onset ED was analyzed.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
Phosphodiesterase Inhibitors. The cornerstone of first-line therapy is the PDE-5 inhibitor. No other class of oral agents approaches the efficacy of PDE-5 inhibitors. Yohimbine, trazodone, phentolamine, L-arginine, and OTC herbal remedies have been used with very limited success. The superiority of yohimbine over placebo in the treatment of organic ED is a matter of dispute.9 A recent trazodone study failed to detect any difference between trazodone and placebo on sexual function.10 Oral phentolamine, although available in Mexico, has not been approved by the US FDA for the treatment of ED. Apomorphine, a central dopaminergic receptor drug, has recently been voluntarily withdrawn from FDA consideration for the treatment of ED. The efficacy of ginkgo biloba and Korean red ginseng has yet to be demonstrated by randomized, placebo-controlled trials.
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.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (124) | Google ScholarSee all References This was a doubleblind, single-dose crossover study involving 41 men with stable coronary artery disease characterized by reproducible stable exertional angina. After taking either 10 mg of vardenafil or placebo, these men underwent treadmill exercise tolerance testing to 5 to 10 METs. Compared with placebo, vardenafil use did not result in a change in exercise treadmill time or time to first awareness of angina but significantly increased the time to ischemic threshold. At peak exercise levels, vardenafil did not cause a change in either heart rate or blood pressure level. This study concluded that 10 mg of vardenafil did not impair the ability of men with stable coronary artery disease to exercise at levels consistent with the exertion associated with sexual intercourse.

Crossref | PubMed | Scopus (53) | Google ScholarSee all References This study found that, although hypertensive patients had more coronary artery disease, no direct evidence supported an association between hypertension and arteriogenic impotence, as measured by the PBI, peak systolic velocity, and resistive index, in patients with mild to moderate hypertension.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (25) | Google ScholarSee all References Hemodynamic stress also may cause rupture of a vulnerable atherosclerotic plaque resulting in angina, myocardial infarction, or sudden cardiac death.80x80Muller, JE. Triggering of cardiac events by sexual activity: findings from a case-crossover analysis. Am J Cardiol. 2000; 86: 14F–18F

27. Haahr MK, Jensen CH, Toyserkani NM, et al. Safety and Potential Effect of a Single Intracavernous Injection of Autologous Adipose-Derived Regenerative Cells in Patients with Erectile Dysfunction Following Radical Prostatectomy: An Open-Label Phase I Clinical Trial. EBioMedicine 2016;5:204-10. 10.1016/j.ebiom.2016.01.024 [PMC free article] [PubMed] [CrossRef]
Abstract | Full Text | Full Text PDF | PubMed | Scopus (207) | Google ScholarSee all References Adverse-effect profiles of headaches, flushing, rhinitis, and dyspepsia, without visual changes, mimic those of vardenafil.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
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.
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
A nutrient-dense, plant-rich (Nutritarian) diet is a huge defense. When men eat for optimal health, they protect their heart, prostate, brain, and, in effect, the entire body. A nutrient-dense, plant-rich (Nutritarian) diet floods the body with protective nutrients, and supports a healthy weight. It not only normalizes risk factors for heart disease and diabetes, but also offers a substantial level of protection against common cancers.
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.

The links between hypertension and ED are increasingly recognized and the 2009 re-appraisal of European guidelines includes relevant statements.35,47 Erectile dysfunction is almost twice as frequent in hypertensive as in normotensive individuals and appears to be of higher severity. The relative risk of developing ED in hypertensive patients compared with normotensive individuals ranges from 1.3 to 6.9. Regarding pathophysiology, hypertension appears to cause ED per se, through a multitude of mechanisms that include prolonged exposure to elevated levels of systemic blood pressure, endothelial dysfunction, and circulation of vasoactive substance (with a pivotal role of angiotensin II) that lead to structural and functional alterations in the penile arteries. The largely unfounded (see earlier paragraph) notoriety of antihypertensive treatment for causing ED is one of the most predominant causes for non-adherence and discontinuation of antihypertensive therapy, and therefore, patients should be properly informed by physicians. Phosphodiesterase type 5 inhibitors are effective in hypertensive patients with ED and they can safely be co-administered with antihypertensive medication.39 Specifically for alpha-blockers, low starting doses of PDE5 inhibitors are preferred in patients already on alpha-blocker treatment, and likewise, low starting doses of alpha-blockers are encouraged in patients taking PDE5 inhibitors. Of clinical significance is that hypertensive men with ED are more likely to comply with their antihypertensive medication when under PDE5 inhibitors.
Now that we better appreciate the complex sequence of events necessary for erections to occur, it’s no surprise that testosterone alone yields less than perfect results. Erectile dysfunction represents more than just low testosterone, which is just one facet of the spectrum of dysfunctional phenomena that cause sexual dysfunction. Nonetheless, when testosterone is combined with popular drugs like Viagra®, success is enhanced to an even greater degree—orgasmic function improves, along with erectile capacity and libido.20 Testosterone also activates penile nitric oxide; ultrasound studies have demonstrated a 27% increase in arterial blood flow into the penis with testosterone supplementation.23
Does drinking water improve erectile dysfunction? Erectile dysfunction or ED is a common concern for men. Everyday factors, such as hydration levels, may affect a person's ability to get or maintain an erection. Drinking water may, therefore, help some men with ED. In this article, learn about the link between hydration and ED, and other factors that can cause ED. Read now
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