There’s one more thing to remember: A visit to a physician can be helpful even if a man doesn’t want to go near Viagra or try one of the alternatives. In some cases, a treatable medical condition such as low testosterone or depression could explain a case of ED. “Sexual health should not be viewed as a luxury, but rather as an essential component to wellness,” said urologist Ryan P. Terlecki, MD, of Wake Forest Baptist Health in North Carolina.
The same device is considered a vacuum erectile device (VED), when it is used to increase inflow of the blood to the penis without a constriction band. Regular use of VED in post-prostatectomy patient increases penile oxygenation and is accepted as a valid option in penile rehabilitation. Recent study reported transient increase in oxygenation to the glans penis and corporal bodies were detected by oximetry after VED was applied, providing proof for possible role for VED to counter the early penile hypoxia, cavernosal fibrosis and long-term ED after radical prostatectomy (9).
Diabetic damage doesn’t stop with these small vessels, he said. “You really have two parallel situations: You need blood flow that feeds the muscle of the penis, and you need an artery dedicated to bringing blood rapidly when a man becomes aroused and wants to be sexually active,” he said. “That artery is also affected by diabetes. They’ll say ‘I can get a partial erection, but I can’t maintain it.’ ”
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
The physical exam should focus on femoral and peripheral pulses, femoral bruits (vascular abnormalities), visual field defects (prolactinoma or pituitary mass), breast exam (hyperprolactinemia), penile strictures (Peyronie’s disease), testicle atrophy (testosterone deficiency), and asymmetry or masses (hypogonadism). A rectal exam allows for assessment of both the prostate and sphincter tone, abnormalities that are associated with autonomic dysfunction. Sacral and perineal neurological exam will help in assessing autonomic function.
PubMed | Google ScholarSee all References Unlike sildenafil, vardenafil has been associated with a slight prolongation of the QT interval and thus should not be used by patients with a congenital QT prolongation or by any patient currently taking antiarrhythmic medications.67x67Vardenafil (levitra) for erectile dysfunction. Med Lett Drugs Ther. 2003; 45: 77–78

"If you have an active sex life after a heart attack, it is probably safe to use PDE5 inhibitors," said Daniel Peter Andersson, MD, PhD, a postdoctoral researcher at Karolinska Institutet in Stockholm and the study's lead author. "This type of erectile dysfunction treatment is beneficial in terms of prognosis, and having an active sex life seems to be a marker for a decreased risk of death."
Crossref | PubMed | Scopus (71) | Google ScholarSee all References However, a double-blind, placebo-controlled study of 22 middle-aged men with hypercholesterolemia treated for 6 weeks with pravastatin or lovastatin showed improved erectile function with both medications.54x54Kostis, JB, Rosen, RC, and Wilson, AC. Central nervous system effects of HMG CoA reductase inhibitors: lovastatin and pravastatin on sleep and cognitive performance in patients with hypercholesterolemia. J Clin Pharmacol. 1994; 34: 989–996
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References However, patients with hypertrophic obstructive cardiomyopathy and idiopathic hypertrophic subaortic stenosis are at increased risk of syncope and sudden death after exercise.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

A deficiency of L-arginine, however, does not generally disrupt nitric oxide synthesis because L-arginine availability is not the rate-limiting step in this process. In fact, research over the past five years has identified an endogenous (occurs in the body naturally) inhibitor called “asymmetric dimethylarginine” or ADMA, an amino acid which blocks the production of nitric oxide. By acting as an L-arginine mimic, this damaging look-alike effectively elbows out L-arginine and pushes it off to the side in the biochemical pathway leading to the synthesis of nitric oxide. ADMA is relatively elevated in patients with hypertension, high levels of cholesterol, triglycerides, homocysteine and low-density lipoprotein (LDL), and low levels of high-density lipoprotein (HDL), as well as with aging itself. This inhibitor of nitric oxide synthesis may very well be the common factor shared by all of these abnormal conditions. Increased levels of this detrimental inhibitor (ADMA) block nitric oxide production, leading to endothelial dysfunction.

Erectile dysfunction started to become a household term after scientists discovered a drug to treat it. Nowadays, as anyone who watches TV can attest, there are several different medications for ED. Fifty to 70 percent of men with type 1 or type 2 diabetes respond to a class of drugs—including sildenafil (Viagra), var­denafil hydrochloride (Levitra), and tadalafil (Cialis)—called phosphodiesterase-5 inhibitors.


Erectile dysfunction started to become a household term after scientists discovered a drug to treat it. Nowadays, as anyone who watches TV can attest, there are several different medications for ED. Fifty to 70 percent of men with type 1 or type 2 diabetes respond to a class of drugs—including sildenafil (Viagra), var­denafil hydrochloride (Levitra), and tadalafil (Cialis)—called phosphodiesterase-5 inhibitors.
Ginkgo Biloba is promoted to treat conditions ranging from hypertension to Alzheimer’s dementia. There is evidence that shows improvement of memory enhancements in the geriatric population (47), improvement in terms of cognitive function via effect on cerebral vasculature (48), improvement of claudication distance and cutaneous ulcers in patients with peripheral vascular disease (49). Ginkgo Biloba extract is proposed to induce NO in endothelial cells and thus causing relaxation of vascular smooth muscles. Animal studies have reported relaxation of rabbit corpus cavernosal smooth muscle cells with the use of Ginkgo Biloba (50). Adverse effects include headaches, major bleeding (in patient who are taking warfarin concurrently) and seizures with reported fatality (36).
Crossref | PubMed | Scopus (174) | Google ScholarSee all References All these men had ED and twice underwent symptom-limited supine bicycle exercise echocardiography 1 hour after taking either sildenafil (50 mg or 100 mg) or placebo. This study found no significant changes in resting heart rate, diastolic blood pressure level, or wall motion score index, and the exercise capacity of the 2 groups was similar. Both groups had similar numbers of patients who experienced dyspnea and/or chest pain, had a positive exercise echocardiographic test, and had exercise-induced wall motion abnormalities. Sildenafil caused a mean decrease of 7 mm Hg in the resting systolic blood pressure level compared with the placebo group. In conclusion, this study showed that in patients with stable coronary artery disease, sildenafil caused no change in symptoms, exercise endurance, or presence/extent of exercise-induced ischemia as measured by exercise echocardiography.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Erectile dysfunction secondary to cardiovascular disease often responds well to the standard ED treatments developed over the past few decades. Penile prosthesis implantation was developed in the 1970s, followed by intracavernosal injections of vasoactive agents, including papaverine, phentolamine, and prostaglandin E1, introduced in the 1980s.11x11Nehra, A. Intracavernosal therapy: when oral agents fail. Curr Urol Rep. 2001; 2: 468–472
"Just because there is evidence doesn't mean it's good evidence," says Andrew McCullough, MD, associate professor of clinical urology at New York University Langone Medical Center in New York City, and one of the original clinical investigators for the ED drug Viagra (sildenafil). "And before men with ED start down the naturopathic route, it's smart to make sure that there isn't some underlying medical condition that needs to be corrected." Moreover, it is estimated that 30 million American men have erectile dysfunction, and 70% of cases are a result of a potentially deadly condition like atherosclerosis, kidney disease, vascular disease, neurological disease, or diabetes. Additionally, ED can also be caused by certain medications, surgical injury, and psychological problems.
Crossref | PubMed | Scopus (35) | Google ScholarSee all References Also, if lower blood pressure level was the primary etiology of ED, all classes of antihypertensive agents should be expected to have relatively similar effects on erectile function because of their efficacy in lowering pressure, which has not been seen.6x6Kloner, RA. Erectile dysfunction and cardiovascular risk factors. Hosp Pract (Off Ed). 2001; 36: 41–44 (49-51.)
Most importantly, herbal supplements are not well regulated in the United States.  Studies have shown that 40-50% of herbal supplements do not even contain the supposed main ingredient, and many contain substances that are not listed which may have dangerous side effects2.  Another study found that over two thirds of the products tested had substituted other plant species for the plants listed on the label, and a third of products also contained other fillers or contaminants3.  A study by the New York State Attorney General of herbal products sold at GNC, Target, Walgreens, and Walmart found that four out of every five products didn’t contain the ingredient they claimed!  Fourteen US states and territories have petitioned Congress to regulate the herbal supplements industry.
Normal male sexual function requires a complex interaction of vascular, neurological, hormonal, and psychological systems. The initial obligatory event is acquisition and maintenance of an erect penis, which is a vascular phenomenon. Normal erections require blood flow into the corpora cavernosae and corpus spongiosum. As the blood accelerates, the pressure within the intracavernosal space increases dramatically to choke off penile venous outflow. This combination of increased intracavernosal blood flow and reduced venous outflow allows a man to acquire and maintain a firm erection.
High blood pressure and erectile dysfunction (ED) often go hand in hand. While having high blood pressure (hypertension) itself may not initially cause any symptoms, it will damage your arteries over time, leading them to become less flexible and progressively more narrow. This not only increases the risk of heart attacks and stroke, but has the potential to compromise blood flow to many organs in the body, including the penis, if left untreated.
Gene therapy has the potential to become a future management option for patients with CAD and ED. Animal studies have been conducted to evaluate the effects of gene therapy. A rat model was studied by Bivalacqua et al. to evaluate the effect of the combination of eNOS gene therapy and sildenafil. This research suggested that erectile response was greater in male rats with diabetes treated with combination eNOS gene therapy and sildenafil, compared with male rats with diabetes treated with eNOS gene therapy or sildenafil alone.76–78
Ginseng, specifically “red ginseng,” is known as the “herbal Viagra” that helps puts to rest men’s bedroom woes. Red ginseng is when the root has been steamed and then dried. The ginseng root is the part of the plant that is mostly used as a natural remedy when in its supplement form. However, the plant must be grown for a minimum of five years before it can be used. In a 2008 review, seven studies on red ginseng and ED, ranging in dosages from 600 to 1,000 milligrams three times a day, were found to provide evidence for the effectiveness of the herb in ED treatment.
Crossref | PubMed | Scopus (35) | Google ScholarSee all References Also, if lower blood pressure level was the primary etiology of ED, all classes of antihypertensive agents should be expected to have relatively similar effects on erectile function because of their efficacy in lowering pressure, which has not been seen.6x6Kloner, RA. Erectile dysfunction and cardiovascular risk factors. Hosp Pract (Off Ed). 2001; 36: 41–44 (49-51.)
Erectile dysfunction (ED) can be treated by urologists or other specialists or even by your general practitioner. Your doctor may recommend medication that works by relaxing penis muscles and increasing blood flow into the penis. Other treatments include therapy, implants, surgery and lifestyle changes, like exercising regularly, losing weight and eating right.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References The use of any NO-donor medications should be avoided for 24 hours after the last dose of sildenafil and even longer if there is a suspected prolonged half-life secondary to such conditions as renal insufficiency.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
The third Princeton Consensus (Expert Panel) Conference recommends assessing cardiovascular risk in all patients with ED and CVD. This refers to estimating the risk of mortality and morbidity associated with sexual activity. The current recommendations classify patients into low-, intermediate- and high-risk, based on their New York Heart Association class.57 The consensus also recommended that all patients with ED and CVD should undergo lifestyle changes, such as exercise, smoking cessation, healthy diet and weight reduction. These measures are likely to reduce cardiovascular risk and improve erectile function.58
Erectile dysfunction is common in the patient with cardiovascular disease. It is an important component of the quality of life and it also confers an independent risk for future cardiovascular events. The usual 3-year time period between the onset of erectile dysfunction symptoms and a cardiovascular event offers an opportunity for risk mitigation. Thus, sexual function should be incorporated into cardiovascular disease risk assessment for all men. A comprehensive approach to cardiovascular risk reduction (comprising of both lifestyle changes and pharmacological treatment) improves overall vascular health, including sexual function. Proper sexual counselling improves the quality of life and increases adherence to medication. This review explores the critical connection between erectile dysfunction and cardiovascular disease and evaluates how this relationship may influence clinical practice. Algorithms for the management of patient with erectile dysfunction according to the risk for sexual activity and future cardiovascular events are proposed.
Penile erection is largely a vascular process, and the penile endothelium and smooth muscle tissue are very sensitive to functional and structural changes. Vasculogenic ED results from an impairment of endothelial dependent or independent smooth muscle relaxation (functional vascular ED, initial stages), occlusion of the cavernosal arteries by atherosclerosis (structural vascular ED, late stages), or a combination of these.3 Current data support a complex interplay between endothelial dysfunction, subclinical inflammation, and androgen deficiency (Figure 1). The relationship between ED and CAD at the clinical level is supported by this common pathophysiological basis. The ‘artery size’ hypothesis explains why patients with CAD frequently report ED before CAD detection.10 According to this hypothesis, for a given atherosclerotic burden, the smaller penile arteries suffer obstruction earlier than the larger coronary arteries (Figure 2). The same concept holds also true in the case of non-obstructing atherosclerosis: since the smaller penile artery have a greater endothelial surface and erection requires a large degree of vasodilation to occur when compared with arteries in other organs, the same degree of endothelial dysfunction will be symptomatic in these smaller vessels but subclinical in the larger ones (i.e. coronaries). In the same context, accelerated arterial ageing (as indicated by increased arterial stiffening that also affects large arteries of ED patients) may be a common background.11,12 Erectile dysfunction is associated with an incremental inflammatory and endothelial-pro-thrombotic activation.13 Interestingly, this activation is equal to that found in CAD patients with no ED, while when these two conditions are combined the burden is additive. Androgen deficiency may be also implicated in the common pathogenetic pathways of ED and CVD; however, this warrants further substantiation.2

In a prospective human phase 1 open-label and single-arm study reported by Haahr et al. (27), 17 men with refractory post radical prostatectomy ED were given a single intracavernosal injection of autologous adipose-derived regenerative cells (ADRCs) freshly isolated after a liposuction. The procedures were well-tolerated and over a 6-month follow-up period, 8 of 17 men showed improvement of their erectile function.

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After adjusting for cardiovascular risk factors including diabetes, heart failure and stroke, those taking PDE5 inhibitors were found to be markedly less likely to die than those taking alprostadil or no erectile dysfunction drugs. Filling more prescriptions for PDE5 inhibitors appeared to be associated with a greater benefit, although Andersson said that trend should be interpreted with caution because the study was not large enough for a definitive dose-response analysis.
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.
Diabetes mellitus is associated with both decreased erectile function and increased cardiovascular risk. The MMAS found that the age-adjusted probability of complete impotence was 3 times higher in patients with diabetes mellitus than in those without the disease.6x6Kloner, RA. Erectile dysfunction and cardiovascular risk factors. Hosp Pract (Off Ed). 2001; 36: 41–44 (49-51.)
It's an all too common problem: Roughly half of men with diabetes—and up to 25 percent of men overall—experience erectile dysfunction (ED) at some point in their lives. And it's a complicated problem, too, with diverse physical origins and complex emotional ramifications. Yet diabetes-related ED needn't be a no-sex sentence for men. There are ways to avoid this disorder and to treat it at any age. While much of the research on ED is still in its infancy, here is what science has to say so far.
"If you have an active sex life after a heart attack, it is probably safe to use PDE5 inhibitors," said Daniel Peter Andersson, MD, PhD, a postdoctoral researcher at Karolinska Institutet in Stockholm and the study's lead author. "This type of erectile dysfunction treatment is beneficial in terms of prognosis, and having an active sex life seems to be a marker for a decreased risk of death."
"Just because there is evidence doesn't mean it's good evidence," says Andrew McCullough, MD, associate professor of clinical urology at New York University Langone Medical Center in New York City, and one of the original clinical investigators for the ED drug Viagra (sildenafil). "And before men with ED start down the naturopathic route, it's smart to make sure that there isn't some underlying medical condition that needs to be corrected." Moreover, it is estimated that 30 million American men have erectile dysfunction, and 70% of cases are a result of a potentially deadly condition like atherosclerosis, kidney disease, vascular disease, neurological disease, or diabetes. Additionally, ED can also be caused by certain medications, surgical injury, and psychological problems.
Erections also require neural input to redirect blood flow into the corpora cavernosae. Psychogenic erections secondary to sexual images or auditory stimuli relay sensual input to the spinal cord at T-11 to L-2. Neural impulses flow to the pelvic vascular bed, redirecting blood flow into the corpora cavernosae. Reflex erections secondary to tactile stimulus to the penis or genital area activate a reflex arc with sacral roots at S2 to S4. Nocturnal erections occur during rapid-eye-movement (REM) sleep and occur 3–4 times nightly. Depressed men rarely experience REM sleep and therefore do not have nocturnal or early-morning erections.
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