“The presence of erectile dysfunction portends a higher risk of future cardiovascular events, particularly in intermediate-risk men, and may serve as an opportunity for intensification of cardiovascular risk prevention strategies,” wrote Boston University heart specialists Naomi Hamburg, MD and Matt Kluge, MD, in an accompanying editorial. “The findings add to the growing evidence supporting additional trials to determine the clinical impact of erectile dysfunction screening and the appropriate cardiovascular directed evaluation and treatment of men with erectile dysfunction.”
Arterial hypertension is a major risk factor for cardiovascular disease and affects approximately one third of the adult population worldwide. The vascular origin of erectile dysfunction is now widely accepted in the vast majority of cases. Erectile dysfunction is frequently encountered in patients with arterial hypertension and greatly affects their quality of life of hypertensive patients and their sexual partners. Therefore, the management of erectile dysfunction in hypertensive patients is of paramount importance. Unfortunately, erectile dysfunction remains under-reported, under-recognized, and under-treated in hypertensive patients, mainly due to the lack of familiarity with this clinical entity by treating physicians. This review aims to discuss the more frequent problems in the management of hypertensive patients with erectile dysfunction and propose ways to overcome these problems in everyday clinical practice.

Crossref | PubMed | Google ScholarSee all References Regular exercise can significantly decrease the patient's risk of having a myocardial infarction during sexual intercourse by increasing the patient's functional reserve, decreasing the heart rate, and increasing the stroke volume.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

The Massachusetts Male Aging Study of 1,290 men, aged 40–70 years, has documented the extraordinarily high prevalence of erectile dysfunction among aging men: 50% of men at 50 years of age, and 70% by age 70 have erectile dysfunction.2 Furthermore, a recent Italian study of men with severe heart disease has uncovered an astounding 93% with erectile dysfunction 24 months before their heart attack or onset of heart disease symptoms.3
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.
High blood pressure, otherwise known as hypertension, can contribute to erectile dysfunction (ED). Some of the medications used to treat high blood pressure can cause ED as well. According to the authors of one study, about 30 percent of men with high blood pressure also have had ED. Finding a medication that treats high blood pressure without causing ED is a goal of many men.

Abstract | Full Text | Full Text PDF | PubMed | Scopus (46) | Google ScholarSee all References The Princeton Consensus Panel provided guidelines (Table 4) for physicians regarding patients who are being evaluated for their level of risk in resuming sexual activity.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
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
Table 1 offers elements for distinction between organic and psychogenic disease.7 Of note is that in cases of organic origin, a psychogenic component may co-exist. The most common organic aetiology of ED is vasculogenic (see below ‘ED and CAD: common pathophysiology’).2,3 Co-existence of vascular disease, advancing age, and the presence of CVD risk factors and metabolic disorders increase the likelihood that ED is of vasculogenic aetiology.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (53) | Google ScholarSee all References Early work in this field, performed by Masters and Johnson in 1966, involved evaluation of young patients in a laboratory setting and found that heart rates and systolic blood pressure levels during sexual activity approached levels seen during maximal exercise.84x84Stein, RA. Cardiovascular response to sexual activity. Am J Cardiol. 2000; 86: 27F–29F
SOURCES: American Urological Association, "AUA Guideline on the Management of Erectile Dysfunction: Diagnosis and Treatment Recommendations." Barksdale, J. Pharmacotherapy, May 1999; vol 19: pp 573-581. Ferrario, C. Journal of Clinical Hypertension, November/December 2002; vol 4: pp 424-432. Fogari, R. American Journal of Hypertension, January 2001; vol. 14: pp 27-31. Grimm, R. Hypertension, January 1997; vol 29: pp 8-14. Llisteri, J. American Journal of the Medical Sciences, May 2001; vol. 321: pp 336-341. WebMD Medical Reference provided in collaboration with The Cleveland Clinic: "Hypertension: Treatment With ACE Inhibitors."

Few simple laboratory tests can help identify obvious causes of organic ED. Initial labs should include HbA1c, free testosterone, thyroid function tests, and prolactin levels. However, patients who do not respond to pharmacological therapy or who may be candidates for surgical treatment may require more in-depth testing, including nocturnal penile tumescence testing, duplex Doppler imaging, somatosensory evoked potentials, or pudendal artery angiography.


Evaluation of functional capacity is the mainstay for the management of patients with ED.30 However, it should be kept in mind that in men with heart failure sexual activity may affect the heart differently from physical activity of similar METS due to differences in psychological anticipation and sympathetic activation.30,49 Cardiac echocardiography may offer valuable information for left ventricular performance and valvular function. For risk categories of heart failure patients and their management, please refer to Table 3 and Figure 5.
L-arginine, an amino acid that is naturally present in the body and helps make nitric oxide, supports a successful erection. Nitric oxide is responsible for making the blood vessels relax, which helps sustain an erection for men. A 1999 study, observed the effects of six weeks of high-dose (5 grams/day) orally administered nitric oxide (NO) donor L-arginine on men with organic ED. Thirty-one percent of those who took 5 grams/day of L-arginine experienced significant improvements in sexual function. Burns told Medical Daily, “l-arginine and deer antler velvet” have been the most popular go-to natural treatments for men.
When antihypertensive medication comes to the fore, certain issues need to be carefully addressed. This is due to the fact that medically induced erectile dysfunction is one of the major reasons for non-adherence and treatment discontinuation, a reality that could have deleterious consequences on patient’s cardiovascular profile and health quality in the long term[38,39].
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
Although DM patients often correctly assume that their ED is of organic origin, a psychogenic component should be considered, especially in the younger patient. If this is the case, the patient may benefit from psychosocial therapy that includes anxiety reduction and desensitization, cognitivebehavioral intervention, sexual stimulation techniques, and interpersonal assertiveness with couples communication training.6 Not all healthcare providers offer these options. Freudian-based psychotherapy for EDDM has not been proved to be efficacious.
Crossref | PubMed | Google ScholarSee all References Risk factors for cardiovascular disease include diabetes mellitus, obesity, physical inactivity, hyperlipidemia, tobacco use, and hypertension. Often, the relative risk of each of these factors in the development of ED is difficult to assess because many patients with ED and cardiovascular disease have more than 1 risk factor. Another important consideration is the effect of cardiac disease itself on erectile function. A history of a prior myocardial infarction was not found to be a significant independent risk factor for ED in a study comparing sexual function in 50 patients who had a prior myocardial infarction with a control group of 50 patients.14x14Dhabuwala, CB, Kumar, A, and Pierce, JM. Myocardial infarction and its influence on male sexual function. Arch Sex Behav. 1986; 15: 499–504
The development of PDE5-inhibitors is a clear example of how Western medicine approached the problem of ED differently from Eastern medicine. The erectogenic effect of sildenafil (Viagra®) was discovered by accident when patients undergoing heart clinical trials reported better erections as a side effect after taking sildenafil. This observation led to further elucidation of the NO/cGMP signalling pathway and development of PDE5-inhibitors as a first-line therapy in ED (5).
Branded Viagra can now be bought over the counter in pharmacies, but please check with your GP first if you have a medical condition. It's important to use a reputable pharmacy, as there is a large market in counterfeit drugs for erectile dysfunction, especially over the internet. These contain varying amounts of the active ingredient and sometimes completely different drugs.
For those patients who cannot take erectile dysfunction medications, the authors counsel that an exercise training regimen may be an appropriate substitute therapy to enhance sexual function and quality of life. The authors stress that clinicians should focus on the sexual activity history of chronic heart failure patients and not ignore it, since addressing this element can substantially improve their quality of life.
It’s crucial that any underlying medical condition, such as angina or diabetes, is detected. So if you’re experiencing problems with ED, book an appointment with your doctor. He or she will assess and examine you to try to establish the cause of the problem, and may refer you for tests. Don’t take any medicine for ED without first discussing it with your doctor.
Phosphodiesterase Inhibitors. The cornerstone of first-line therapy is the PDE-5 inhibitor. No other class of oral agents approaches the efficacy of PDE-5 inhibitors. Yohimbine, trazodone, phentolamine, L-arginine, and OTC herbal remedies have been used with very limited success. The superiority of yohimbine over placebo in the treatment of organic ED is a matter of dispute.9 A recent trazodone study failed to detect any difference between trazodone and placebo on sexual function.10 Oral phentolamine, although available in Mexico, has not been approved by the US FDA for the treatment of ED. Apomorphine, a central dopaminergic receptor drug, has recently been voluntarily withdrawn from FDA consideration for the treatment of ED. The efficacy of ginkgo biloba and Korean red ginseng has yet to be demonstrated by randomized, placebo-controlled trials.
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
Three FDA-approved oral medications, sildenafil, tadalafil, and vardenafil are available. These drugs are phosphodiesterase type 5 (PDE-5) inhibitors that can prolong levels of cGMP in tissue allowing improved smooth muscle relaxation, thus facilitating an erection. PDE-5 inhibitor drugs are effective in 56-63% of diabetic men with ED. More stringent glycemic control can improve these results. Men with testosterone deficiency may benefit from a combination of oral ED medication and testosterone supplementation.
Nebivolol seems to have an advantage over other beta-blockers when used to treat men with hypertension and ED. It has additional vasodilating effects because it stimulates endothelial release of nitric oxide (NO), resulting in relaxation of smooth muscle in the corpus cavernosum, allowing penile erection.25 Despite limited studies, nebivolol does not seem to worsen erectile function and some studies have demonstrated significant improvement in erectile function with nebivolol compared with second-generation cardioselective beta-blockers.23,26–28
The American College of Cardiology is a 52,000-member medical society that is the professional home for the entire cardiovascular care team. The mission of the College is to transform cardiovascular care and to improve heart health. The ACC leads in the formation of health policy, standards and guidelines. The College operates national registries to measure and improve care, offers cardiovascular accreditation to hospitals and institutions, provides professional medical education, disseminates cardiovascular research and bestows credentials upon cardiovascular specialists who meet stringent qualifications.
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.
But closer questioning often revealed a very different story—men would admit that struggles to achieve an erection usually preceded a heart attack or other cardiac event by one, two, or three years. Back then, the pattern of erectile dysfunction and cardiac disease was so widespread, that most in the medical profession attributed it to simple “aging,” as common as wrinkles and constipation.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References Overall, sexual intercourse does not lead to an extremely exaggerated heart rate or blood pressure level when performed in a familiar setting with one's usual partner.82x82Hellerstein, HK and Friedman, EH. Sexual activity and the postcoronary patient. Arch Intern Med. 1970; 125: 987–999

In another study, 60 patients underwent stress exercise cardiovascular testing and Doppler ultrasonography for measurement of their cavernosal artery peak systolic velocity (PSV).17x17Kawanishi, Y, Lee, KS, Kimura, K et al. Screening of ischemic heart disease with cavernous artery blood flow in erectile dysfunctional patients. Int J Impot Res. 2001; 13: 100–103
Abstract | Full Text | Full Text PDF | PubMed | Scopus (37) | Google ScholarSee all References Other studies have proposed that the strain involved with intercourse in older patients is less associated with physical exertion and more closely related to sexual arousal.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

Like the case of untreated hypertensive patients, evaluation of sexual dysfunction in hypertensive patients under antihypertensive regime, should primarily exclude other concomitant diseases and pharmaceutical agents. Consecutively, a competent physician with advanced communicational skills should try to “discover” medically induced erectile dysfunction since a vast majority of patients being under complex antihypertensive regimes usually attribute the undesirable effect to normal aging thus not relating it to their current medication. Moreover, even physicians seldom report the cases of sexual dysfunction associated with certain medications. When medically induced sexual dysfunction is finally disclosed and a shift in medication is deemed necessary, b-blockers along with diuretics should generally be the first categories to be changed, unless they are deemed absolutely indicated for the individual patient. Ideally, an ARB could constitute the mainstay of therapy in these cases. If sexual dysfunction still persists, then more effective remedies should be elected paving the way for the introduction of phosphodiesterase-5 inhibitors (PDE-5).

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.’ ”
Some research even suggests the effect of blood pressure drugs may be more psychological than physical. When ED occurs after a man begins to take a new medication, it's possible that anxiety about his health, rather than the medication, may trigger the problem. And being aware of possible side effects may make a man more likely to recognize them as abnormal.
Based on this testing, EDDM patients were treated with behavioral therapy, intracavernosal (papaverine, PGE-1, or Trimix) or intraurethral PGE-1, a vacuum constriction device (VCD), or implantation of a penile prosthesis. Novel surgical procedures, ligation of incompetent cavernosal veins or penile revascularization, were seldom efficacious with EDDM and were soon abandoned. Although these nonsurgical therapies were efficacious, they were not widely requested because of their invasive or mechanical nature.
Diaclina (also known as Panzer’s Darkling Beetle), Korean bug are used as aphrodisiacs in China, Korea and Southeast Asia. These are consumed either whole or as compounds within capsules. It is felt that the aphrodisiac properties come by stimulating the urogenital structures. Flies have been studied for their aphrodisiac effects, including Spanish fly, Chinese cantharide, and Eastern-Indian cantharide (32). The active compound found in the dried and mashed up bodies of these flies is cantharidin, which is a pheromone produced in the accessory glands of the male flies’ genitals. Cantharidin, stimulates the urogenital tract, causing pelvic hyperemia and possibly erections. As cantharidin is toxic and its safety dose not well determined, its use cannot be recommended. Cantharidin is lethal at high doses and exposure can lead to gastrointestinal and urogenital hemorrhage as well as acute renal failure.
Cardiovascular tolerance for sex is based on “functional reserve,” which corresponds to how closely the cardiovascular response to sex (in terms of heart rate, blood pressure level, and oxygen consumption) approaches the patient's peak response to exercise.85x85DeBusk, RF. Evaluating the cardiovascular tolerance for sex. Am J Cardiol. 2000; 86: 51F–56F
Although a considerable number of patients report penile pain with IC injection therapy, it appears that diabetic men still have high compliance rates with therapy. In one study, 16 of 18 diabetic men continued IC injection therapy for 7 years, compared to 7 of 22 nondiabetic control subjects with ED.57 One possible explanation for this is that diabetic patients with ED have fewer options than do nondiabetic men with ED, who are more likely to have a successful response to oral PDE-5 agents, as documented in one study.58 Another explanation is the greater familiarity with needles and injections among men with diabetes than among their nondiabetic counterparts.

Viagra, Cialis, Levita, and Staxyn all work in a similar fashion and make it physically possible to get an erection when aroused. However, men whose blood pressure is poorly controlled and who take alpha-blockers for high blood pressure treatment should not take any of these treatments for erectile dysfunction as it may reduce blood pressure to critically low levels, causing fainting or sudden death. Also, you may be prohibited to use these drugs if you demonstrate any of the following:
There are other treatment options for erectile dysfunction (ED). Alprostadil is a medication that improves blood flow to the penis and improves erections. It can be given either by injection (Caverject and other brands) at the base of the penis or by putting an alprostadil gel (brand name MUSE) directly into the urethra, using a thin tube and a little lubricant so it slides in easily. The medicine is absorbed from the lining of the urethra into the surrounding tissues. The shot is less appealing to most people, of course, but more effective.
“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.”

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


The use of shock wave therapy has revolutionized the treatment of many aspects of medicine. High intensity extracorporeal shockwave therapy has been used for the treatment of nephro-urolithiasis while medium intensity shockwave therapy is used by orthopaedic surgeons to treat joint pain as well as tendinitis. Low intensity shockwaves therapy was first noted to improve ischaemia-induced myocardial dysfunction in animal studies when low intensity shockwaves were applied to porcine myocardium (13). Shockwaves induces a localized stress on cell membranes in the same way that shear stress affects endothelial cell membranes (14) and this triggers the release of angiogenic factors, such as increased NO production through increased activity of endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS), platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) (15). These shockwaves also cause membrane hyperpolarization (16), activation of the Ras signaling pathway, non-enzymatic synthesis of NO and induction of stress fibers and intercellular gaps (17).
Hey folks, It's great to have met you, I really do hope that you enjoyed this article and found it helpful and informative. I Suffered from ED for a few years before taking a short while to reverse it after going down the usual route of those little blue (and expensive) pills, (not an actual cure but a treatment to temporarily relieve the symptoms).Be sure to check out My Highly Recommended products and start taking positive steps in the right direction to cure your erectile dysfunction. And don't forget to grab your free copy of The Testosterone Report and The Morning Wood Report
PubMed | Google ScholarSee all References More recently, researchers have recognized that climbing stairs does not correlate closely with sexual activity in terms of autonomic, psychological, and emotional patterns of stress on the body.1x1Muller, JE. Sexual activity as a trigger for cardiovascular events: what is the risk?. Am J Cardiol. 1999; 84: 2N–5N
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.

“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.”
Due to their vasorelaxing effect, administration of PDE-5 inhibitors in hypertensive individuals was initially confronted with great suspicion. A wealth of clinical data however has proven that PDE-5 inhibitors are associated with few side effects and provoke a small and insignificant reduction in blood pressure with minimal heart rate alterations in both normotensive and hypertensive patients as well. As a matter of fact, they can be safely and effectively administered to hypertensive individuals even when they are already taking multiple antihypertensive agents[51-56]. The sole exception to the rule is co-administration with organic nitrates, which is an absolute contraindication due to profound and possibly hazardous hypotension effect[57,58]. Moreover, precaution should be taken when PDE-5 inhibitors are combined with a-blockers where, due to possible orthostatic hypotension effect, lower starting doses should be implemented in the therapeutic regime[59-62].
The Massachusetts Male Aging Study of 1,290 men, aged 40–70 years, has documented the extraordinarily high prevalence of erectile dysfunction among aging men: 50% of men at 50 years of age, and 70% by age 70 have erectile dysfunction.2 Furthermore, a recent Italian study of men with severe heart disease has uncovered an astounding 93% with erectile dysfunction 24 months before their heart attack or onset of heart disease symptoms.3
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
Diuretics: Also called water pills, this medication is a common treatment for reducing blood pressure. They work by getting rid of unnecessary water and salt in the urine. This essentially helps lower blood pressure and can make it easier for the heart to pump blood. Unfortunately, diuretics can reduce the blood flow to the penis, making erections difficult to achieve. Zinc levels have been known to diminish due to diuretic use, which may lead to a decreased production of overall testosterone.
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 (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
ED is a common complication of diabetes and people with diabetes are also prone to developing cardiovascular complications.48 The risk of ED is relatively high in patients with known CVD. This was supported by a study of men with known CVD, in which ED was substantially predictive of all-cause mortality and the composite of CVD death, admission for heart failure, MI and stroke.17 Macroangiopathy, microangiopathy and endothelial dysfunction are among the mechanisms by which diabetes causes ED.
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Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References However, α-blockers are a well-known cause of retrograde ejaculation secondary to a reversible relaxation of bladder neck smooth muscle.50x50Meinhardt, W, Kropman, RF, Vermeij, P, Nijeholt, AA, and Zwartendijk, J. The influence of medication on erectile function. Int J Impot Res. 1997; 9: 17–26
Abstract | Full Text PDF | PubMed | Scopus (3562) | Google ScholarSee all References During a 9-year follow-up study of 513 of these men who had no ED at the first study, the risk of new-onset ED was analyzed.5x5Feldman, HA, Johannes, CB, Derby, CA et al. Erectile dysfunction and coronary risk factors: prospective results from the Massachusetts Male Aging Study. Prev Med. 2000; 30: 328–338
In a study by Segal et al. (11), 4 out of 5 healthy individuals were able to achieve tumescence beyond 60% maximum rigidity when subjected to PVS using the Viberect® alone, with no other external visual sexual stimulation. In a randomized controlled study by Fode et al. (12) involving 68 men who underwent nerve-sparing radical prostatectomy, 30 men who received PVS to the frenulum daily for 6 weeks, using the Ferticare® vibrator, showed a trend towards better erections. After 1 year, 53% in the PVS group had an IIEF score ≥18 compared with 32% in the control group, although no statistical achievement was achieved. The role of PVS in penile rehabilitation is based on the postulation that PVS provides early activation of the parasympathetic erectile spinal centres at S2–S4 level, which result in early recovery of the neuropraxic cavernosal nerves.
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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