Crossref | PubMed | Scopus (25) | Google ScholarSee all References In comparison, a randomized placebo-controlled trial of 65 patients given either placebo or 95 mg/d of sustained-release metoprolol for 4 months after percutaneous coronary angioplasty found no significant difference in sexual function between the 2 groups.44x44Franzen, D, Metha, A, Seifert, N, Braun, M, and Hopp, HW. Effects of beta-blockers on sexual performance in men with coronary heart disease: a prospective, randomized and double blinded study. Int J Impot Res. 2001; 13: 348–351
For over 25 years, Dr. Fuhrman has shown that it is possible to achieve sustainable weight loss and reverse heart disease, diabetes and many other illnesses using smart nutrition. In his medical practice, and through his books and PBS television specials, he continues to bring this life-saving message to hundreds of thousands of people around the world.
However, sildenafil should be used carefully with nitrates because their combination can result in severe hypotension and death.68 Both short- and long-acting nitrates are commonly prescribed to treat angina, but they have no prognostic benefit. In addition, there are numerous alternatives to treat angina, such as ranolazine and ivabradine, which do not interact with PDE5 inhibitors. As a result, patients with ED wishing to take PDE5 inhibitors can safely discontinue their nitrates and replace this treatment with the other anti-anginal agents.68
Erectile dysfunction is an accurate predictor of heart attacks and strokes in the future. Psychogenic components play a role in erectile dysfunction, but the most common and primary cause in most men is organic vascular insufficiency, meaning not enough blood gets to the penis. Erectile dysfunction usually occurs one to five years before a male manifests overt signs of cardiovascular disease. The first sign may be death.

ED is generally associated with significant changes in established cardiovascular risk factors. Atherosclerosis is the main cause of ED development in both the general population and patients with diabetes. However, the prevalence of ED is greater in patients with diabetes than in the general population.8 ED has been shown to occur at rates as high as 50 % in patients with CAD.9 A meta-analysis of 12 prospective cohort studies has provided evidence that ED is a predictor of IHD associated with an increased risk of CVD, stroke and all-cause mortality.10
Towards this direction, several sufficiently powered studies have demonstrated a higher incidence of erectile dysfunction in patients with coronary artery disease, either asymptomatic or overt. At the same time, patients with erectile dysfunction are more prone to have established coronary artery stenosis of more than 50% and consequently evident CV disease[75]. This is in conformity with the “artery size hypothesis” according to which smaller arteries (e.g., penile arteries) are the first to undergo a vascular lesion prior to the larger ones (e.g., coronary arteries). Moreover, in such patients erectile dysfunction is connected to the number of occluded vessels and more interestingly occurs over three years before coronary artery disease becomes apparent[76-80].
There’s some evidence that bark from the yohimbe tree can help with ED. The bark contains a substance called yohimbine. It’s been traditionally used in Africa as an aphrodisiac. Today, a pharmaceutical form of yohimbine (called yohimbine hydrochloride) is being studied to treat erectile dysfunction in men. However, it can cause severe side effects, including high blood pressure, tremors, and anxiety.

Feeling fatigued, very stressed, depressed or dealing with another mood-related issue that can lower libido. Sources of stress and diminished quality of life — such as “deteriorating economic position,” unhappiness with one’s job or other aspects that lower emotional health — are believed to be major causes for sexual dysfunction in both men and women
Crossref | PubMed | Scopus (171) | Google ScholarSee all References Incidence increased notably with age in this patient cohort: only 1.1% of diabetic men aged 21 to 30 years had ED compared with 47.1% of all diabetic patients older than 43 years. Diabetic patients often have other cardiovascular risk factors that may play a role in the development of ED. However, in an analysis of the PBI in 441 patients with ED and various cardiovascular risk factors (diabetes mellitus, hypertension, hyperlipidemia, tobacco use), diabetes was the only risk factor that was significantly and independently associated with a decrease in the PBI.7x7Virag, R, Bouilly, P, and Frydman, D. Is impotence an arterial disorder? a study of arterial risk factors in 440 impotent men. Lancet. 1985; 1: 181–184
Erectile dysfunction (ED) is generally defined as the persistent (at least 6 months) inability to achieve and maintain penile erection sufficient to allow satisfactory sexual performance.1 It is a common condition, and recent studies predict a higher prevalence of ED in the future.2 It is estimated that ED has affected more than 150 million men worldwide and this number will reach approximately 322 million by 2025.2,3 It has affected 30 million men in the US alone.4
First of all, libido (sexual desire) triggers a sympathetic (adrenaline-dependent) nervous system reaction mediated through the thoracic spinal cord. Also important is tactile stimulation, the pleasurable effect of touch, which is mediated through the acetylcholine-dependent parasympathetic nervous system. Both the sympathetic and parasympathetic forces regulate the release of nitric oxide—the universal artery-relaxing agent—from the cells lining the penile arteries and all its smaller branches. Nitric oxide causes the arteries to enlarge, increasing blood flow into the penile tissues. This is followed by compression of blood-draining penile veins, which causes blood to engorge the penis and create an erection.4
The incidence of ED is 42.0–57.0 % in men with CAD and 33.8 % in those who have diabetes with silent ischaemia, compared with 4.7 % in men without silent ischaemia.6 The prevalence of ED is likely to be higher than the reported figures, because men generally do not seek medical advice for ED.6 Erection is thought to be a process that is regulated by hormones and neurovascular mechanisms in cerebral and peripheral levels.7
Crucial to the understanding of the relationship between ED and CVD and the management of ED patients within the context of the (potential) CVD were the consecutive Princeton Consensus Recommendations (I: 2000, II: 2005, and III: 2012). The reader is strongly encouraged to refer to the most recent, third (2012) Princeton Consensus.30 Key notions in the assessment and management of the patient with organic ED are that (i) he should be considered at increased CVD risk until recommended checks suggest otherwise, and (ii) ED identifies increased CVD risk in the presence or absence of CVD symptoms or history.

Crossref | Google ScholarSee all References Other investigators have suggested these medications may exert a hormonal effect. β-Blockers have been associated with decreased free and total testosterone levels in placebo-controlled trials.39x39Rosen, RC and Weiner, DN. Cardiovascular disease and sleep-related erections. J Psychosom Res. 1997; 42: 517–530
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.
Diabetes, high blood pressure (hypertension), elevations in blood lipids or cholesterol are considered blood vessel problems and have all been associated with Erectile Dysfunction. The blood vessel abnormalities caused by these diseases affect vessels throughout the body and often produce other symptoms of vascular diseases. Diabetics and patients with hypertension frequently have heart disease. These conditions typically interfere with the ability of the penile vessels to work properly and ultimately cause ED.
Cardiovascular disease and erectile dysfunction (ED) are closely interrelated disease processes. Erectile dysfunction reportedly affects 10 million to 20 million men in the United States and more than 100 million men worldwide. Each year, about 500,000 persons in the United States survive a myocardial infarction, and an estimated 11 million have existing cardiovascular disease, making the issue of sexual function and cardiac disease relevant to many patients. We explore the relationship between ED and the presence of cardiovascular disease in the general population. We also review the prevalence and pathophysiological associations of ED and cardiovascular disease. The risks of sexual activity for patients with cardiovascular disease are discussed, as are prevention and treatment strategies for ED in this patient population.
Erection is a neurovascular event that involves spinal and supra spinal pathways. The final common pathway involves the release of nitric oxide (NO) from both endothelial cells and neurons, which acts as a vasodilator causing penile engorgement and erection. NO is degraded by the enzyme phosphodiesterase (PDE) type 5 in the penis. Erectile dysfunction (ED), defined as the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual performance, results when the neurovascular pathway is interrupted by medical conditions or drugs. A 15-item self-administered questionnaire, the International Index of Erectile Function (IIEF), is one of the most useful tools to evaluate erectile function (EF) in clinical trials, although of much less use in routine clinical practice. The MMAS (Massachusetts Male Aging Study) was the first major epidemiological investigation to study the prevalence of ED. The study found that ED was three times more common in patients with diabetes mellitus. The aetiopathogenesis of ED in diabetes is multifactorial, with vascular and neural factors being equally implicated. Hyperglycaemia is believed to give rise to biochemical perturbations that lead to these microvascular changes. In the MMAS, ED in diabetes was strongly correlated with glycaemic control, duration of disease and diabetic complications. The incidence increased with increasing age, duration of diabetes and deteriorating metabolic control, and was higher in individuals with type 2 diabetes than those with type 1.ED in men with diabetes often affects their quality of life and, as patients are often reluctant to come forward with their symptoms, a carefully taken history is one of the most useful approaches in identifying affected individuals. The PDE inhibitors have revolutionised the management of ED and oral drug therapy is currently first-line therapy for the condition. These agents act by potentiating the action of intracavernosal NO, thereby leading to a more sustained erection. Sildenafil was the first PDE5 inhibitor to undergo evaluation and has been studied extensively. More recently two other agents, vardenafil and tadalafil, have been introduced. All the drugs have been shown to be effective across a wide range of aetiologies of ED, including diabetes. The drugs have been shown to improve EF domain scores, penetration and maintenance of erection, resulting in more successful intercourse. Their effects are greater at higher doses. Sildenafil and vardenafil are shorter-acting agents, while tadalafil has a longer half-life allowing the user more flexibility in sexual activity. Common adverse effects include headache, nasal congestion and dyspepsia, all actions related to inhibition of PDE5. The drugs are generally well tolerated and withdrawal from the clinical studies as a result of drug-related adverse effects were rare. The use of PDE5 inhibitors in the presence of oral nitrates is absolutely contraindicated. The clinical studies to date have not evaluated the use of one drug in the case of treatment failure with another agent. Sublingual apomorphine, which stimulates central neurogenic pathways, is a new agent and may be a suitable alternative in those patients in whom PDE5 inhibitors are ineffective or contraindicated. In clinical trials, all IIEF domains except sexual desire were found to have improved after apomorphine. The median times to erection in these studies were 18.9 and 18.8 minutes for the 2 and 3mg doses, respectively. Intraurethral and intracavernosal alprostadil may be a useful alternative when oral drug therapy is ineffective or contraindicated. The management of ED in the diabetic patient may often involve a multidisciplinary approach where psychosexual counselling and specialist urologist advice is required in addition to the skills and expertise of the diabetologist. Finally, the introduction of the new oral agents have completely revolutionised the management of ED and allowed more individuals to come forward for treatment.
Admitting to your doctor that you are having trouble achieving an erection can be difficult, but take comfort in the fact that they are not judging you and are there to improve your health and well-being. If you are just beginning a blood pressure treatment regimen and are beginning to experience erectile dysfunction, tell your doctor as soon as you can—they can solve the problem by simply changing the prescription.
Erectile dysfunction usually precedes cardiovascular events by 3 to 5 years. Therefore, sexual function should be incorporated into cardiovascular disease risk assessment for all men. Recently, algorithms for the management of patients with erectile dysfunction according to the risk for sexual activity and future cardiovascular events were proposed[91]. A comprehensive approach to cardiovascular risk reduction (comprising of both lifestyle changes and pharmacological treatment) will result in significant benefits on overall vascular health, including sexual function. Proper sexual counselling will exert beneficial effects on the quality of life of hypertensive patients with erectile dysfunction and will improve adherence to antihypertensive drug therapy[91].

 Other treatment options such as penile self-injection therapy, external vacuum pumps and the medicated urethral system for erection are on rare occasions an effective long-term treatment. A very small percentage of men will continue with these treatments as evidenced by a very high drop out rate and a very low refill rate for these treatments. These procedures require extensive planning which interfere with sexual spontaneity and are really not a realistic long-term treatment for young patients with permanent ED. 
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Rates of severe cardiovascular adverse effects were also similar at 1.7 per 1000 person-years of treatment with sildenafil compared with 1.0 events per 1000 personyears with placebo treatment.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
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

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.

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.
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.
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."

The obvious risks are the same that accompany any surgery: infection, pain, bleeding, and scarring. If for some reason the prosthesis or parts become damaged or dislocated, surgical removal may be necessary. With a general success rate of about 90 percent, any of the devices will restore erections, but they will not affect sexual desire, ejaculation, or orgasm.
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