Penile arterial supply (top) and venous drainage (middle), longitudinal views. Bottom, Transverse and longitudinal views of venous return. From Lue TF. Physiology of penile erection and pathophysiology of erectile dysfunction and priapism. In: Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ, eds. Campbell's Urology. Vol 2. 7th ed. Philadelphia, Pa: WB Saunders Co; 1998:1157-1179. With permission from Elsevier.
According to Harvard Special Health Report Erectile Dysfunction, one study in the European Heart Journal looked at men newly diagnosed with heart disease, but without ED, who started treatment with the beta-blocker atenolol (Tenormin). Some of the study participants were told about the sexual side effect of the blood pressure drug, and ED was reported by almost one-third of the participants. In contrast, among those who were not told the drug's name or its side effects, only 3% said they experienced ED.
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.
Until recently, erectile dysfunction (ED) was one of the most neglected complications of diabetes. In the past, physicians and patients were led to believe that declining sexual function was an inevitable consequence of advancing age or was brought on by emotional problems. This misconception, combined with men’s natural reluctance to discuss their sexual problems and physicians’ inexperience and unease with sexual issues, resulted in failure to directly address this problem with the majority of patients experiencing it.

But recently Brandon had some troubles keeping it up. At first, Kayla just thought it was her and that he needed some kind of a change to what they usually did, but later Brandon admitted that as of late, he just couldn’t seem to maintain an erection, and that it took way too much effort to go long. It wasn’t that he wasn’t aroused; his body just wasn’t keeping up.

airdone/ShutterstockErectile dysfunction (ED) is a serious issue for men, which helps explain all the prescription drugs, over-the-counter treatments, and herbal concoctions that claim to cure ED. (In fact, it’s one of the top nine health risks men need to watch out for.) But before any guy decides to take matters into his own hands, he should talk to his doctor about a heart checkup: A new study published in the journal Vascular Medicine suggests ED can signal cardiovascular concerns.

Some commonly prescribed cardiovascular drugs (beta-blockers, diuretics, angiotensin-converting enzyme inhibitors, etc.) contribute to ED.18 Previous studies have shown a strong association between ED and diuretics in patients treated with hydrochlorothiazide or chlorthalidone.19,20 It has also been shown that patients treated with first-generation non-selective beta-blockers, such as propranolol, had more frequent ED than those treated with a placebo.21
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.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Originally evaluated as a mild preload reducer and antianginal agent in its early phases of development, sildenafil's effect on male and female genitalia became quickly apparent.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 (95) | Google ScholarSee all References During this period, 130 deaths were reported to the US FDA; 41 of these men died or had cardiac arrest within 4 to 5 hours after taking sildenafil, and 27 died or had cardiac arrest either during or immediately after sexual activity. The average age of these men was 64 years. Of the 77 men in this group who died of documented cardiovascular-related events, 41 died of definite or suspected myocardial infarction, 27 died after cardiac arrest, and 6 had symptoms of cardiac disease at the time of death. Sixteen of the men had taken nitroglycerin or organic nitrates in association with sildenafil; another 3 had nitroglycerin in their possession at the time of death. In 48 men, the cause of death was unknown, and another 3 died of cerebrovascular accidents. Overall, it was concluded that sildenafil was not associated with an excess of cardiovascular death.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Sildenafil has a 4000-fold increased selectivity for PDE-5 over PDE-3, has negligible effects on heart rate, and has only a modest effect on blood pressure level in healthy persons, with an average systolic pressure decrease of 10 mm Hg with a single dose of 100 mg.3x3Zusman, RM, Morales, A, Glasser, DB, and Osterloh, IH. Overall cardiovascular profile of sildenafil citrate. Am J Cardiol. 1999; 83: 35C–44C
 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. 
27. Haahr MK, Jensen CH, Toyserkani NM, et al. Safety and Potential Effect of a Single Intracavernous Injection of Autologous Adipose-Derived Regenerative Cells in Patients with Erectile Dysfunction Following Radical Prostatectomy: An Open-Label Phase I Clinical Trial. EBioMedicine 2016;5:204-10. 10.1016/j.ebiom.2016.01.024 [PMC free article] [PubMed] [CrossRef]
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.
Crossref | PubMed | Google ScholarSee all References In study patients taking these medications compared with controls, significant decreases in total cholesterol and low-density lipoprotein cholesterol levels were found, as well as significant increases in length of maximal tumescence per nocturnal penile tumescence testing at 2 weeks. Hypoglycemia secondary to the use of insulin or hypoglycemic agents may result in ED or orgasmic dysfunction.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
The initial event for normal erectile function is sexual stimulation. Subsequent to processing in the central nervous system neural impulses are conveyed along the spinal cord, exiting through the pelvic parasympathetic preganglionic nerves. These pelvic nerves form the pelvic plexus and send their message through first messenger, acetyl choline, to the cavernosal nerves. The cavernosal nerves enter erectile bodies (corpora cavernosa) (Figure 1). Here, their nerve endings release a second messenger, nitric oxide. Nitric oxide activates the enzyme guanylyl cyclase, which lyses guanosine triphosphate (GTP) to produce a third messenger, the intracellular cyclic guanosine monophosphate (cGMP). Ultimately, the result is a decrease of intracellular calcium and an opening of potassium channels with the resultant relaxation of vascular smooth muscle in the arteries, aterioles, and sinusoids of the corpora cavernosa. The sinusoids open and rapidly fill with blood. Finally, the distended sinusoids compress their drainage pathways (venules) against the fibroelastic covering of the cavernosal bodies (tunica albuginea) and trap the blood in cavernosal bodies. The combination of an increased inflow of blood into the penis and coincident markedly diminished outflow results in rapidly increasing intracavernosal pressure that ultimately approximates systolic pressure. At this pressure the penis has sufficient axial rigidity to permit vaginal penetration.
This category of treatments includes external vacuum therapies: devices that go around the penis and produce erections by increasing the flow of blood in, while constricting the flow out. Such devices imitate a natural erection, and do not interfere with orgasm. External vacuum therapy mechanisms are approximately 95 percent successful in causing and sustaining an erection. All are portable, and costs range between $200-$500, covered under most insurance plans and Medicare Part B.
An equally valuable observation though, is the fact that sexual dysfunction could indeed indicate asymptomatic CV disease. A solid amount of evidence accumulated over the last years has pointed out towards that trend moving, hesitatingly though, sexual dysfunction in the surface of scientific interest. As such, commonly under-reported, under-recognized and under-treated, sexual dysfunction could indeed play its role in cardiovascular risk assessment and stratification.

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
PubMed | Google ScholarSee all References In comparison, a study of 132 patients evaluated by penile duplex ultrasonography after intracorporeal papaverine injection found that hypertension alone was not an independent risk factor for vasculogenic ED.34x34Shabsigh, R, Fishman, IJ, Schum, C, and Dunn, JK. Cigarette smoking and other vascular risk factors in vasculogenic impotence. Urology. 1991; 38: 227–231
The phrase “use it before you lose it” can be applied when it comes to helping men with ED regain normal erectile function. Pelvic exercises, more commonly known as kegel exercises, are used to promote urinary continence and sexual health. They help to strengthen the bulbocavernosus muscle, which does three things: allows the penis to engorge with blood during erection, it pumps during ejaculation, and it helps empty the urethra after urination, according to Healthline.

Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References During this period, 130 deaths were reported to the US FDA; 41 of these men died or had cardiac arrest within 4 to 5 hours after taking sildenafil, and 27 died or had cardiac arrest either during or immediately after sexual activity. The average age of these men was 64 years. Of the 77 men in this group who died of documented cardiovascular-related events, 41 died of definite or suspected myocardial infarction, 27 died after cardiac arrest, and 6 had symptoms of cardiac disease at the time of death. Sixteen of the men had taken nitroglycerin or organic nitrates in association with sildenafil; another 3 had nitroglycerin in their possession at the time of death. In 48 men, the cause of death was unknown, and another 3 died of cerebrovascular accidents. Overall, it was concluded that sildenafil was not associated with an excess of cardiovascular death.
Despite physician’s inexperience and patient’s reluctance to disclose sexual dysfunction problems, attempts to estimate the magnitude of this clinical condition have predicted that over 150 million men worldwide experience some degree of erectile dysfunction. Several studies have demonstrated a wide range regarding the prevalence of erectile dysfunction, which is even higher in patients with essential hypertension where the relative risk is approximately two times higher than in normotensive individuals[6-11]. The etiology can be found in the structural and functional abnormalities of the penile arteries induced by high blood pressure. Smooth muscle hypertrophy, stenotic lesions due to atherosclerosis and impaired blood flow are among the prominent structural alterations whereas endothelial dysfunction and the defective nitric oxide-induced vasodilatory mechanism belong to the main functional abnormalities induced by increased blood pressure[12,13]. As a matter of fact, sexual dysfunction is encountered more frequently that it is indeed believed underlining the need for a more proper and concrete assessment.

Since their introduction in the therapeutic field, more than a decade ago, PDE-5 inhibitors have revolutionized the treatment of sexual dysfunction. By blocking the activity of PDE-5 isoenzyme, localized throughout the smooth muscle cells of the vasculature (genital vessels included), PDE-5 inhibitors increase the levels of cyclic guanosine monophosphate thus exerting vasodilating properties and facilitating penile erection[40-42]. Due to these properties, sildenafil was the first drug of its class to receive wide acceptance. Its short half-life, food interactions and the associated visual disturbances however, paved the way for the development of newer PDE-5 inhibitors. As such vardenafil with its more rapid onset of action, and tadalafil with its longer half-life and the lack of food interactions or side effects, have offered significant alternatives to sildenafil[43-50].
Crossref | PubMed | Scopus (72) | Google ScholarSee all References This study found that the mean PSV was a better predictor of the presence of cardiovascular disease than stratification by standard cardiac risk factors such as diabetes mellitus, hypertension, obesity, and smoking. The researchers recommended that persons with no history of prior perineal trauma and with a PSV lower than 35 mL/s should undergo exercise testing before receiving treatment of ED because these patients had a 42% risk of having ischemic heart disease. However, other investigators questioned the utility of using penile arterial flow to predict the presence of ischemic heart disease.18x18Chiu, AW, Chen, KK, Chen, MT, Chang, LS, and Chang, MS. Penile brachial index in impotent patients with coronary artery disease. Eur Urol. 1991; 19: 213–216
Beta-blockers: A popular blood pressure medication that affects part of the nervous system in an attempt to slow and regulate heartbeats, helping reduce blood pressure. Unfortunately, this same part of the nervous system is also responsible for causing erections, and when beta blockers are used, it indirectly reduces the amount of blood flow to the penis.
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.
Smoking is an independent risk factor for ED. Tobacco smoking causes direct toxicity to endothelial cells, including decreased eNOS activity, increased adhesion expression and impaired regulation of thrombotic factors.6 A meta-analysis of 19 studies by Tengs and Osgood suggested that 40 % of the impotent men studied were current smokers compared with 28 % who had never smoked.49
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Tribulus terrestris is a dicotyledonous herbal plant of the Zygophyllaceae family, used to increase serum testosterone levels, which has only been shown in animal studies (40). A prospective, randomized, double blind study of 30 men showed that Tribulus terrestris was not more effective than placebo on improving IIEF scores or serum total testosterone (41). Two accounts of hepato-nephrotoxicity have been reported in young men who ingested high doses of this herbal medication (42,43).
The number of men reporting improvement was at 88% during the study. The number of men involved in the study who reported impotence dropped from 75.3 % to 11.8%. The results of this study raise hope for men who have quit taking other blood pressure medications because they interfered with sexual function. Sexual dysfunction was defined for the study as decreased libido, impotence and poor sexual satisfaction.
The second way relates to the risk associated with the sexual activity in a patient with either overt or occult CVD. In this case, the diagnosis of ED should prompt an initial cardiovascular assessment based on the history and clinical examination in order to define the baseline risk according to (i) the likelihood of silent CAD18,31 (especially since ED patients have a high probability to have silent CAD) or to the stage of clinically evident CAD, (ii) other cardiovascular conditions either unrelated, or related to ED (e.g. heart failure, peripheral arterial disease).
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.
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).
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.

Erectile dysfunction means that a man is not able to have sex because he cannot get or keep an erection. Erectile dysfunction affects >30% of men between 40 and 70 years of age. There are several different causes of ED, including depression, low testosterone, nerve problems, and some medications, but the most common cause is a problem with the blood vessels called atherosclerosis.


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
PDE-5 inhibitors amplify the intacavernosal production of cGMP in response to nitric oxide. This is achieved through the inhibition of cGMP's breakdown by the enzyme, PDE-5. If the predominant abnormality in the individual EDDM patient is molecular, the higher tissue levels of cGMP will overcome these inhibitory factors and the patient will regain erectile function. If the physical structure (eg, the compliance) of the cavernosal tissue has been significantly compromised by apoptosis of smooth muscle or increased collagen deposits, restoration of erectile function will not be achieved. These structural changes explain the lower efficacy rates of PDE-5 inhibitors in EDDM than in the general population.
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[14]. 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[15].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[16]. Interestingly, the beneficial effect of physical exercise on sexual dysfunction seems to be independent of its favorable impact on the general cardiovascular profile[17]. In terms of caloric reduction, Mediterranean diet exerts a positive effect on sexual function parameters of patients with metabolic syndrome[18]. 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[19].
Vascular disease: Vascular diseases are those that affect the blood vessels. These diseases include atherosclerosis (hardening of the arteries), hypertension (high blood pressure), and high cholesterol. These diseases, which account for 70% of physical-related causes of ED, restrict blood flow to the heart, the brain, and--in the case of ED--to the penis. Atherosclerosis alone accounts for 50%-60% of ED cases in men over age 60.

The connection between diabetes and ED is related to your circulation and nervous system. Poorly controlled blood sugar levels can damage small blood vessels and nerves. Damage to the nerves that control sexual stimulation and response can impede a man’s ability to achieve an erection firm enough to have sexual intercourse. Reduced blood flow from damaged blood vessels can also contribute to ED.

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