The drugs you take to lower your blood pressure may earn you lower marks in the bedroom, by leading to a bout of erectile dysfunction (ED), or the inability to get or maintain an erection during sex. High blood pressure medications such as beta blockers and diuretics do their life-saving job by lessening blood flow to your vital organs—and that includes down under. Less blood flow means no erection. The good news for guys is that not all high blood pressure medication cause ED. Talk with your doctor about switching to the ones that don't.
Get your diabetes under control. According to Dr. Nehra, the most important number you need to stay on top of is your A1C, which is a blood test that lets you know how well your blood sugar has been controlled for the past few months. Lifestyle changes can help and so can medications. Diabetes medications do not add to your risk for erectile dysfunction, says Nehra.
Crossref | PubMed | Scopus (53) | Google ScholarSee all References A study of 24 patients with ED and untreated essential hypertension showed decreased levels of free and total serum testosterone compared with normal controls.31x31Hughes, GS, Mathur, RS, and Margolius, HS. Sex steroid hormones are altered in essential hypertension. J Hypertens. 1989; 7: 181–187
Yohimbe. Before Viagra and the other prescription erectile dysfunction drugs became available, doctors sometimes prescribed a derivative of the herb yohimbe (yohimbine hydrochloride) to their patients suffering from ED. But experts say the medication is not particularly effective, and it can cause jitteriness and other problems. "It's not a great drug," says McCullough. "And I suspect the herb is not as potent as the pharmaceutical version." What's more, evidence shows that yohimbe is associated with high blood pressure, anxiety, headache, and other health problems. Experts discourage its use.
Characteristics that imply a higher risk is severe ED (SHIM 1–7) and ED duration >3 years.15,30 Vascular and circulating biomarkers may help to characterize further the patient with ED.23 Of the wide array of biomarkers that have been proposed for the assessment of cardiovascular risk in asymptomatic adults,34,35 some have been studied specifically in the context of ED.23Table 4 offers a critical evaluation of these biomarkers. Such tests should be considered as potentially helpful and thus recommended where available, but not mandatory.30 Despite its potent predictive ability recently shown,36 exposure to radiation with coronary artery calcium scoring should be carefully weighed. Although not specific for ED, it might be reasonable to evaluate biomarkers that have been proposed for the intermediate-risk patient such as uric acid, glycated haemoglobin, microalbuminuria, and lipoprotein-associated phospholipase A2.30
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.
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
Crossref | PubMed | Scopus (77) | Google ScholarSee all References Nitroglycerin is a vasodilator that is commonly used as an antianginal agent because of its ability to improve the imbalance between myocardial oxygen supply and demand.65x65Stamler, JS, Loh, E, Roddy, MA, Currie, KE, and Creager, MA. Nitric oxide regulates basal systemic and pulmonary vascular resistance in healthy humans. Circulation. 1994; 89: 2035–2040
Nehra A, Jackson G, Miner M, Billups KL, Burnett AL, Buvat J, Carson CC, Cunningham GR, Ganz P, Goldstein I, Guay AT, Hackett G, Kloner RA, Kostis J, Montorsi P, Ramsey M, Rosen R, Sadovsky R, Seftel AD, Shabsigh R, Vlachopoulos C, Wu FC. The Princeton III Consensus recommendations for the management of erectile dysfunction and cardiovascular disease, Mayo Clin Proc , 2012, vol. 87 (pg. 766-778)https://doi.org/10.1016/j.mayocp.2012.06.015
Conversely, and of significant clinical importance, is how often patients with ED as their first and sole clinical manifestation suffer from subclinical CAD.17 Previous studies reported a rate of inducible ischaemia by exercise stress testing (EST) in 22% (with a wide range of 5–56%) of ED patients reflecting differences in patient population, risk factors and criteria used for ED and CAD diagnosis. Interestingly, those patients further assessed with coronary angiography had obstructive atherosclerosis in >90% of cases.4,18 In a prospective angiographic study, we documented that 19% of ED patients suffer from clinically silent obstructive CAD.18
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.
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.
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.
If you’re taking medication to treat blood pressure, depression, pain, allergies, inflammation, seizures, or heart conditions, you’re one of the tens of millions of people at risk for medically induced erectile dysfunction. It’s just the nature of drug side effects. Yet erectile dysfunction is one of the least talked about side effects of prescription medication.
Figure. Progression of atherosclerosis. Endothelial dysfunction occurs early in atherosclerosis and prevents blood vessels from dilating properly. When the blood vessels that supply the penis are not able to dilate during sexual stimulation because of endothelial dysfunction, the penis cannot fill with blood, and the man develops erectile dysfunction. As atherosclerosis progresses, plaques build up in blood vessels and blood flow is slowed, further worsening erectile function. A heart attack occurs when an atherosclerotic plaque in a coronary artery ruptures, a blood clot forms over the plaque, and blood flow to the heart muscle is completely blocked. Atherosclerotic risk factors (black arrows) worsen cardiovascular health; modification of these risk factors (red arrows) improves cardiovascular health.
“I’m hoping this study will drive that (tie) a little bit harder and faster so that physicians will routinely be including ED when they’re screening patients for cardiovascular disease,” he said. “Doctors should ask the question and consider whether hardening of the arteries is occurring, ask about family history and signs or symptoms like chest pain with exertion, and spend the requisite amount of time to find out what’s going on.”
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.
Chronic heart failure often develops after other cardiac problems have damaged or weakened the heart, leaving it too weak or too stiff to fill and pump efficiently. Many underlying heart conditions can lead to heart failure. It can develop quickly after damage caused by a heart attack, or it can develop gradually after years of high blood pressure or coronary artery disease.
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.
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.
Erectile dysfunction (ED), or impotence, is when a man has difficulty getting or maintaining a strong enough erection for sexual intercourse or other sexual activity. It can be caused by stress, anxiety or excessive alcohol consumption. But it can also be a symptom of an underlying condition such as atherosclerosis (narrowing of the arteries), diabetes or high blood pressure. Some medications can cause erectile dysfunction, for example beta-blockers and diuretics (commonly used to treat a variety of heart-related conditions such as high blood pressure and heart failure).
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?
Alcohol consumption, bad nutrition, a sedentary lifestyle, excessive stress, psychological issues, relationship issues, use of illegal drugs and overuse of prescribed drugs, poor sleep habits and excessive physical activity are all contributing factors to ED. Ailments like diabetes, as well as low and high blood pressure, in addition to prostate cancer, may also result in ED.
Crossref | PubMed | Scopus (23) | Google ScholarSee all References, 73x73Rajagopalan, P, Mazzu, A, Xia, C, Dawkins, R, and Sundaresan, P. Effect of high-fat breakfast and moderate-fat evening meal on the pharmacokinetics of vardenafil, an oral phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction. J Clin Pharmacol. 2003; 43: 260–267
Crossref | PubMed | Scopus (528) | Google ScholarSee all References Sildenafil also has good efficacy in patients with ischemic heart disease, as shown by a retrospective subanalysis of data from 11 double-blind, placebo-controlled studies involving 3672 patients with ED and ischemic heart disease who were not taking nitrates.59x59Kloner, RA. Cardiovascular risk and sildenafil. Am J Cardiol. 2000; 86: 57F–61F
Abstract | PubMed | Scopus (136) | Google ScholarSee all References Other candidate mechanisms linking ED and cigarette smoking include hypercoagulability and increased platelet aggregation, increased release of free fatty acids and catecholamines, changes in NO synthetic pathways, and a possible direct toxic effect on vascular endothelium.13x13Chung, WS, Shim, BS, and Park, YY. Hemodynamic insult by vascular risk factors and pharmacologic erection in men with erectile dysfunction: Doppler sonography study. World J Urol. 2000; 18: 427–430
Although ED is a common complication of diabetes, its effect on quality of life is not well understood. Recent work for the Exploratory Comprehensive Evaluation of Erectile Dysfunction (ExCEED) database demonstrates that in the general population of patients presenting to their urologist, ED negatively affects both general and disease-specific health-related quality of life (HRQOL).35 While this study provides insight into the detrimental affect of ED on quality of life, the cohort is somewhat selected, in that all of the patients were seen in sexual dysfunction clinics and therefore may have been more likely to be bothered by their condition and to report worse quality of life.
Penile prosthesis implant remains the most effective and permanent treatment for ED. Penile prosthesis implants can be broadly divided into malleable and inflatable prostheses (20). Malleable penile prosthesis, also known as semi-rigid prosthesis, does not allow for (physiological) flaccid state of the penis. The patient can bend the prosthesis upwards for sexual intercourse and downwards for concealment. Although the angle of prosthesis concealment has improved with recent devices, however due to the constant rigid state of the penis, they are still less comfortable compared to their inflatable counterparts, are more likely to cause social embarrassment and associated with higher risk of implant erosions (21). However, malleable prosthesis still has its place for the treatment of ED as these implants are easier to handle, easier to place and would benefit patients with impaired manual dexterity.
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
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.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Another contraindication is the use of recreational drugs (“poppers”) that contain amyl nitrate. The guidelines also caution use in patients who have a high risk of cardiovascular effects, including patients with active coronary artery disease who are not taking nitrates, patients with congestive heart failure with a borderline low blood pressure level and low blood volume, or those with complicated multidrug antihypertensive regimens.
A man needs to try the medicine at least four times before he concludes that it doesn’t work for him. It is unlikely that a man with diabetes who has other medical problems such as high blood pressure, is taking multiple medicines, and has not had sexual intercourse for several years will be able to have an erection adequate for intercourse the first time he takes a pill. Most men need to try the medicine several times before they have the desired results.