It is recommended that testosterone be measured in patients with ED because low levels are a reliable measure of hypogonadism. Hypogonadism is not only a treatable cause of ED, but can also lead to reduced or lack of response to PDE5 inhibitors.73 Testosterone deficiency is also associated with increased cardiovascular and all-cause mortality.74 Levels >350 ng/dl do not usually require replacement, but in patients with testosterone <230 ng/dl, replacement can usually be beneficial.57 In patients with congestive heart failure, testosterone replacement can lead to fluid retention, so caution is advised. In these patients, the aim should be to keep testosterone levels in the middle range, i.e. 350–600 ng/dl.57
Andersson said the results came as a surprise because erectile dysfunction is associated with an increased risk of heart disease in otherwise healthy men. However, previous studies have associated the use of PDE5 inhibitors with a decreased blood pressure in the left ventricle, which reduces the amount of work required to pump blood and therefore could help explain why the drugs might benefit people with heart failure. PDE5 inhibitors were initially developed to treat angina, a type of chest pain that results from constricted arteries.
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
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
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.

Crossref | PubMed | Scopus (539) | Google ScholarSee all References Aside from the economic costs, ED can have severe psychological effects, resulting in poor self-image, decreased self-esteem, depression, and mental stress, and negative effects on personal relationships.2x2NIH Consensus Development Panel on Impotence. NIH Consensus Conference: impotence. JAMA. 1993; 270: 83–90
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.

“If a diabetic patient has erectile dysfunction, it’s not enough to provide Viagra [sildenafil] or Cialis [tadalafil] and then send him on his merry way,” J. Francois Eid, MD, a New York City urologist, said at the annual meeting of the American Association of Diabetes Educators. “It’s important to let individuals know the drug has not cured the erectile dysfunction. If patients don’t take care of the diabetes, the erectile dysfunction progresses.”


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


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.
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Myocardial ischaemia is caused by the reduction of coronary blood flow as a result of fixed or dynamic epicardial coronary artery stenosis, abnormal constriction or deficient relaxation of coronary microcirculation, or because of reduced oxygen-carrying capacity of the blood.56 Atherosclerosis is the major cause of myocardial ischaemia. Plaque that develops in atherosclerosis can rupture causing platelet aggregation and subsequent thrombus formation, which leads to MI. The other mechanisms of myocardial ischaemia are encountered far less than atherosclerosis. Endothelial dysfunction has an important role in the progression of atherosclerosis. Endothelial dysfunction enhances the intimal proliferation and malregulation that results in plaque destabilisation in the arteries.6 This process, coupled with paradoxical vasoconstriction, can result in major cardiovascular events such as MI.32
The vacuum device is approved by USA Food and Drug Administration (FDA) for treatment of ED since 1982. Vacuum therapy (VT) works by creating a negative pressure environment around the penis through the use of a cylindrical housing attached to a pump mechanism, which can be manually-operated or battery-operated. Vacuum draws mixed arterial and venous blood into the corporal bodies and distends the corporal sinusoids to create an erected penis. If a pre-loaded constriction band is applied over the base of the penis to prevent outflow of blood and maintain tumescence for intercourse, it is considered a vacuum constriction device (VCD). It is recommended that the constriction band be removed within 30 mins to return the penis to its flaccid state, as prolonged application of the constriction band can compromise both arterial and venous blood flow (7). Some minor side effects associated with VCD are penile discomfort, coldness, numbness, bruising and pain on ejaculation. Major side effects such as penile skin necrosis, gangrene, urethral injury and Peyronie’s disease are very rare (8).
Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Theoretically, the risk of a cardiac event during sexual activity should be increased. Sexual activity is associated with an elevated heart rate, blood pressure level, and myocardial oxygen demand, and this increase in hemodynamic stress may result in myocardial ischemia.79x79Kimmel, SE. Sex and myocardial infarction: an epidemiologic perspective. Am J Cardiol. 2000; 86: 10F–13F

A penile prosthesis is another treatment option for men with erectile dysfunction. These devices are either malleable (bendable) or inflatable. The simplest type of prosthesis consists of a pair of malleable rods surgically implanted within the erection chambers of the penis. With this type of implant the penis is always semi-rigid and merely needs to be lifted or adjusted into the erect position to initiate sex. Today, many men choose a hydraulic, inflatable prosthesis, which allows a man to have an erection whenever he chooses and is much easier to conceal. It is also more natural.
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
Abstract | Full Text | Full Text PDF | PubMed | Scopus (164) | Google ScholarSee all References Several double-blind, placebo-controlled studies have shown vardenafil to be more effective than placebo in the treatment of ED secondary to a wide range of other etiologies as well.71x71Hellstrom, WJ, Gittelman, M, Karlin, G..., and Vardenafil Study Group. Sustained efficacy and tolerability of vardenafil, a highly potent selective phosphodiesterase type 5 inhibitor, in men with erectile dysfunction: results of a randomized, double-blind, 26-week placebo-controlled pivotal trial. Urology. 2003; 61: 8–14

Although the results provide evidence that PDE5 inhibitors may benefit heart health, the retrospective study design makes it impossible to ascertain direct cause and effect, Andersson noted. It is possible that using erectile dysfunction drugs simply indicates a more active sex life, which could itself contribute to, or be a marker of, a heart-healthy lifestyle overall.


One study the authors reviewed measured these changes in middle-aged men with and without coronary artery disease. This study found that the peak heart rate during intercourse was lower than heart rates measured during the patients' normal daily activities. The study participants' peak oxygen consumption levels during intercourse were moderate -- comparable to their oxygen consumption levels during moderate activities such as walking on level ground at 3 to 4 miles per hour, climbing stairs slowly or doing general housework such as vacuuming.
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]?

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


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.
Ginkgo biloba. Known primarily as a treatment for cognitive decline, ginkgo has also been used to treat erectile dysfunction -- especially cases caused by the use of certain antidepressant medications. But the evidence isn't very convincing. One 1998 study published in the Journal of Sex & Marital Therapy found that it did work. But a more rigorous study, published in Human Pharmacology in 2002, failed to replicate this finding. "Ginkgo has come out of fashion in the past few years," says Ronald Tamler, MD, assistant professor of medicine and codirector of the men's health program at Mount Sinai Medical Center in New York City. "That's because it doesn't do much. I can say that in my practice, I have not seen ginkgo work -- ever."
Sexual problems might mean you have a broken heart, literally. The most common sexual problem in men is erectile dysfunction (ED). ED affects up to 30 million men in the United States. Surprisingly, ED might be a sign of heart problems. It is important to discuss sexual health with your doctor. Not only can your doctor prescribe medications to improve sexual function, but together you may be able to prevent a major heart problem like a heart attack. This article outlines the steps that you should take if you think you have ED.
The first step in the process is always to reevaluate if the medication that’s causing the problem is even necessary in the first place. Do you still need the medication(s) that you’re taking? When you’re experiencing medically induced ED, this has to be your starting point. Obviously you shouldn’t make this decision on your own. However, reevaluating your need for medication can be a simple conversation with your doctor. Remind your healthcare provider of the medications you’re taking, and explain any symptoms or side effects—like ED. Going off of medication might sound like an extreme step, but I’ve seen many examples of this in practice.

Testosterone therapy in hypogonadism modulates metabolic components associated with CV risk. The majority of prospective clinical studies indicates that treatment achieving testosterone levels within physiological limits has beneficial or neutral effects on a lipid profile other than HDL-C, beneficial or neutral effects on inflammatory mediators, and generally beneficial effects on glycaemic state.25 The lean body mass is typically increased in hypogonadal subjects, and visceral adiposity is decreased in several studies and unchanged in the remainder. Such metabolic effects have raised interest on the potential impact on cardiovascular health. Regarding symptoms in patients with pre-existing cardiovascular conditions (angina or heart failure) TTh has been either neutral or beneficial.25 Regarding CVD risk, available clinical trial data indicate that the use of testosterone in middle-aged to elderly men does not increase cardiovascular risk25 with the exception of one study in very frail (substantial limitation of mobility and a high rate of comorbidities) elderly subjects that used an off-label high, and rapid escalation, dosing regimen.46 Prospective data from large, well-designed, long-term trials of TTh are warranted.
Finally, prevalence rates will be affected by whether the study population is accrued from a single hospital/clinic setting or from a more general population of men with diabetes. For example, Siu et al.4 studied 500 Chinese diabetic men (of which 97% had type 2 disease) seen at a single medical clinic in Hong Kong during 1999 and found the overall prevalence of ED to be 63.6%. Contrast this to Fedele et al.,5 who studied 9,756 diabetic men accrued from 178 diabetes centers in Italy. Among the 8,373 men with type 2 diabetes, only 37% reported ED, considerably less than in the Chinese study.

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


In contrast to Chinese ginseng, Korean ginseng is divided into three types, depending on how it is processed. Red Ginseng is harvested at the sixth year of cultivation and is steamed and dried. In addition to the effects mentioned regarding the effects of ginsenoside, red ginseng has been repoted to improve erectile function in a rat model of metabolic syndrome and it was also found to inhibit fibrosis of the corpus cavernosum of the penis (39). As with most herbal medicines, the concentration of ginsenoside are distributed unevenly throughout the ginseng plant and the concentrations in individual supplements can vary. Common side effects include headaches, insomnia, gastric upset, rash and constipation.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References The risk after sexual activity in these patients is unknown, although vasodilators should be avoided because they may increase the intraventricular gradient.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
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.

Crossref | Google ScholarSee all References A 1985 study found that ED accounted for 400,000 outpatient visits and 30,000 hospital admissions per year in the United States, with a direct total cost of $146 million.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


There are two kinds of penis implants. One kind is a rigid but flexible rod implanted in the penis. You bend it up for sex or down for daily living. The other kind is an inflatable implant. The device stores fluid in a reservoir under the skin of your abdomen or scrotum. You press on the reservoir to pump fluid into cylinders in the penis. That creates an erection. A valve drains the fluid out of the penis when you're done.
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.
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