Crossref | PubMed | Google ScholarSee all References These hormonal findings were supported by a study of 1132 men aged 30 to 79 years that found an inverse relationship between blood pressure and serum testosterone levels.32x32Khaw, KT and Barrett-Connor, E. Blood pressure and endogenous testosterone in men: an inverse relationship. J Hypertens. 1988; 6: 329–332
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.
A significant proportion (ranging from ∼60 to 90%) of heart failure patients report ED and marked decrease in sexual interest, with ultimately one-quarter reporting cessation of sexual activity altogether.48 Erectile dysfunction contributes further to the poor quality of life and aggravates depression. Of interest, many heart failure patients place a greater importance on improving the quality of life (including sexual activity) than on improving survival. Sexual function correlates with the symptomatic status (i.e. NYHA functional class and 6-minute walk test).48 In the Evaluation of Role of Sexual Dysfunction in the Saarland (EROSS) Program, left ventricular dysfunction was a risk factor for ED independent of heart failure symptoms. While heart failure and ED share common pre-disposing risk factors, heart failure by itself can cause ED or affect engagement to sexual activity. Neurohumoral activation, medication (thiazides), limited exercise capacity, and depression are responsible.49
Erectile dysfunction (ED) is common in cardiac patients and shares the same risk factors--smoking, hypertension, hyperlipidaemia and diabetes mellitus. Sexual activity is not unduly stressful to the heart and, providing patients are properly assessed using established guidelines, sexual intercourse can be enjoyed without increased risk. The treatment of ED in patients with cardiovascular disease has been transformed by the introduction of the oral phosphodiesterase type 5 inhibitors, the first of which was sildenafil. Success in restoring erectile function is possible in up to 80% of patients (depending on the aetiology) with minimal adverse effects. A synergistic hypotensive effect with nitrates, and almost certainly nicorandil, is the only major contraindication. ED in asymptomatic patients may be a marker of silent vascular disease or increased vascular risk factors and should alert the physician to the need for cardiac risk screening. ED is common in patients with cardiovascular disease and should be routinely enquired about. ED is a distressing condition for the man and his partner, and severely impairs quality of life. Patients with cardiovascular disease and patients with diabetes represent the largest group of patients with ED, the majority of whom benefit from the drug therapies currently available. Addressing ED in patients with cardiovascular disease can lead to a substantial improvement in quality of life and success is not difficult to achieve.
Like the case of untreated hypertensive patients, evaluation of sexual dysfunction in hypertensive patients under antihypertensive regime, should primarily exclude other concomitant diseases and pharmaceutical agents. Consecutively, a competent physician with advanced communicational skills should try to “discover” medically induced erectile dysfunction since a vast majority of patients being under complex antihypertensive regimes usually attribute the undesirable effect to normal aging thus not relating it to their current medication. Moreover, even physicians seldom report the cases of sexual dysfunction associated with certain medications. When medically induced sexual dysfunction is finally disclosed and a shift in medication is deemed necessary, b-blockers along with diuretics should generally be the first categories to be changed, unless they are deemed absolutely indicated for the individual patient. Ideally, an ARB could constitute the mainstay of therapy in these cases. If sexual dysfunction still persists, then more effective remedies should be elected paving the way for the introduction of phosphodiesterase-5 inhibitors (PDE-5).
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
The Epimedium plant is a flowering perennial found throughout Asia and parts of the Mediterranean. Horny Goat Weed’s active ingredient is icariin, a falvonol glycoside and reputed to improve cardiovascular function, hormone regulation, modulation of immunological function and antitumor activity (44). Icariin has also been shown to have a PDE5i effect. Animal studies have been carried out showing improvements in penile hemodynamic parameters. There is one report of tachyarrhythmia and hypomania with the use of this herb (45).
In another scientific article published in 2015 in the American Journal of Lifestyle Medicine, respondents who were not taking cholesterol-lowering medication experienced an average 42 mg/dl decrease in LDL cholesterol and an average decrease in triglycerides of 79.5 mg/dl about one year after switching to a Nutritarian diet. Furthermore, case histories presented in that publication documented atherosclerosis reversal.7
Ginseng. Korean red ginseng has long been used to stimulate male sexual function, but few studies have tried systematically to confirm its benefits. In one 2002 study involving 45 men with significant ED, the herb helped alleviate symptoms of erectile dysfunction and brought "enhanced penile tip rigidity." Experts aren't sure how ginseng might work, though it's thought to promote nitric oxide synthesis. "I would recommend ginseng [for men with ED]," says Espinosa. Discuss with your doctor before taking it since ginseng can interact with drugs you may already be taking and cause allergic reactions.
When the diagnosis of vasculogenic sexual dysfunction has been carefully reached, physicians will have to come up with an effective treatment. Appropriate lifestyle measures and adoption of a healthier attitude could represent an initial, efficient and cost-effective treatment option. This is due to the fact that traditional CV risk factors such as hypertension, physical inactivity-obesity, smoking and dyslipidemia have been consistently linked with endothelial and consequently sexual dysfunction.In this context, it has been demonstrated that moderate physical activity can reduce up to 30% the risk of erectile dysfunction contrary to sedentary life, which exerts a deleterious effect. Interestingly, the beneficial effect of physical exercise on sexual dysfunction seems to be independent of its favorable impact on the general cardiovascular profile. In terms of caloric reduction, Mediterranean diet exerts a positive effect on sexual function parameters of patients with metabolic syndrome. Moreover, combined physical exercise and caloric restriction can result in weight reduction which in succession can reduce up to 30% the risk of obesity-associated erectile dysfunctio.
In many of these cases, a discussion between the physician, the man with erectile dysfunction, and possibly his partner can help to resolve the issues leading to treatment failure. For men who experience severe side effects, can’t take the drugs for other reasons (such as taking medicines such as nitroglycerin), or don’t respond in spite of further education on the correct use of the drugs, there are other treatment options that can help most men remain sexually active.