The drugs come in several strengths. Most men should start with a low to moderate dose. The dose can be adjusted depending on the results. Men with potential problems should always start with the lowest dose. Every man should avoid consuming alcohol before taking these drugs. Men who do not respond to a full dose on two or three different occasions should try other treatments.
A considerable number of patients with ED can have psychogenic factors as the only cause, or in combination with organic causes of ED. Depression, low self-esteem and social stresses are among the psychogenic factors that can lead to ED. Depression is an independent risk factor for both ED and IHD; these three disease conditions are interlinked.51 Psychogenic ED can be managed by multiple psychological interventions such as cognitive behavioural therapy, couples counselling and guided sexual stimulation techniques.52
Crossref | PubMed | Scopus (697) | Google ScholarSee all References Subsequent in vitro electrical stimulation of these tissue samples showed decreased neurogenic and endothelium-dependent smooth muscle relaxation in the tissue from the patients with diabetes. These effects persisted even after controlling for smoking and hypertension. Other studies have shown a heightened smooth muscle tone in patients with diabetes mellitus.24x24Christ, GJ, Stone, B, and Melman, A. Age-dependent alterations in the efficacy of phenylephrine-induced contractions in vascular smooth muscle isolated from the corpus cavernosum of impotent men. Can J Physiol Pharmacol. 1991; 69: 909–913
Vacuum therapy devices have a few disadvantages. One must interrupt foreplay to use them. You must use the correct-size tension ring and remove it, to prevent penile bruising, after sustaining the erection for 30 minutes. Initial use may produce some soreness. Such devices may be unsuitable for men with certain bleeding disorders. In general, vacuum constriction devices are successful in management of long-term ED.
Some blood pressure medicines can also cause erectile dysfunction. Thiazide diuretics and beta-blockers are most likely to cause problems, but this is not a common effect of these medicines and will not happen to everyone. If you are taking either of these medicines and are worried about erectile dysfunction, your GP may be able to change your medicines.
Ginseng. Korean red ginseng has long been used to stimulate male sexual function, but few studies have tried systematically to confirm its benefits. In one 2002 study involving 45 men with significant ED, the herb helped alleviate symptoms of erectile dysfunction and brought "enhanced penile tip rigidity." Experts aren't sure how ginseng might work, though it's thought to promote nitric oxide synthesis. "I would recommend ginseng [for men with ED]," says Espinosa. Discuss with your doctor before taking it since ginseng can interact with drugs you may already be taking and cause allergic reactions.
The EDDM patient has a variety of firstline options. The risk factors for vascular disease are the risk factors for ED. First-line therapy begins with attempts to minimize or eliminate these factors. These include smoking cessation, regular exercise, tighter glycemic control by attention to dietary restrictions, addition of statin drugs to correct dyslipidemia, and moderation of alcohol ingestion. Although there is very limited evidence that these modifications will dramatically reverse ED, they certainly will sponsor improved general health.4
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
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.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References, 56x56Wallis, RM, Corbin, JD, Francis, SH, and Ellis, P. Tissue distribution of phosphodiesterase families and the effects of sildenafil on tissue cyclic nucleotides, platelet function, and the contractile responses of trabeculae carneae and aortic rings in vitro. Am J Cardiol. 1999; 83: 3C–12C
Penile Injection Medication: This is just what it sounds like. Injected at home directly into the penis, the medication alprostadil produces erection by relaxing certain muscles, increasing blood flow into the penis and restricting outflow. Although some sources report an 80 percent success rate, the therapy has disadvantages, such as risks of infection, pain, and scarring—fibrosis—in the penis, and it may also cause priapism. A popular version of this medication is Upjohn Corporation’s Caverject. The MUSE System, by VIVUS, involves the same medicine (a pellet of alprostadil) applied with an eye-dropper-like applicator, directly into the urethra.
Penile implants - are generally used if physical damage (like an accident) makes the anatomical parts needed for an erection not work. These are inserted by surgery and can provide a permanent treatment choice if others fail to work. The implants can be semi-rigid or inflatable. They can be pretty expensive and are not usually available on the NHS.
Joel Fuhrman, M.D. is a board-certified family physician, six-time New York Times bestselling author and internationally recognized expert on nutrition and natural healing, who specializes in preventing and reversing disease through nutritional methods. Dr. Fuhrman coined the term “Nutritarian” to describe his longevity-promoting, nutrient dense, plant-rich eating style.
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
Abstract | Full Text PDF | PubMed | Scopus (49) | Google ScholarSee all References Also, cigar smoking and passive exposure to cigarette smoke have been shown to significantly predict onset of ED.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
"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."
Abstract | Full Text | Full Text PDF | PubMed | Scopus (328) | Google ScholarSee all References Their mean resting systolic and diastolic blood pressure levels decreased by 6% and 11%, respectively, compared with baseline. These patients also experienced a mild decrease in mean resting right atrial pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, and cardiac output. However, the hemodynamic response to exercise was preserved. Phase 2 and 3 trials showed no difference in the rate of adverse events between sildenafil and placebo in patients being treated with antihypertensive medications. The effects of sildenafil on blood pressure level were similar in patients who were taking antihypertensive medications compared with those who were not. In healthy volunteers, no consistent or significant doserelated electrocardiographic (ECG) changes were noted at 1 and 2 hours after doses of sildenafil ranging from 1.25 to 200 mg.3x3Zusman, RM, Morales, A, Glasser, DB, and Osterloh, IH. Overall cardiovascular profile of sildenafil citrate. Am J Cardiol. 1999; 83: 35C–44C
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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.
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. 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].
** Indeterminate risk patients include diabetics, those with mild or moderate stable angina pectoris, past myocardial infarction (2-8 wks) without intervention awaiting exercise electrocardiography, congestive heart failure (NYHA class III), and noncardiac sequelae of atherosclerotic disease (eg, peripheral artery disease and a history of stroke or transient ischemic attack); this patient with ED may require assessment for additional vascular disease using carotid intima-media thickness or ankle-brachial index and subsequent reclassification to low or high risk.
Erectile dysfunction (ED), or impotence, is when a man has difficulty getting or maintaining a strong enough erection for sexual intercourse or other sexual activity. It can be caused by stress, anxiety or excessive alcohol consumption. But it can also be a symptom of an underlying condition such as atherosclerosis (narrowing of the arteries), diabetes or high blood pressure. Some medications can cause erectile dysfunction, for example beta-blockers and diuretics (commonly used to treat a variety of heart-related conditions such as high blood pressure and heart failure).
For centuries, men have tried all sorts of natural remedies for erectile dysfunction (ED) -- the repeated inability to get or maintain an erection firm enough for sexual intercourse. But do they really work? It is simply not scientifically known at this point. Furthermore, you take these remedies at your own risk, because their safety profiles have not been established. What follows are commentaries by experts and reviews in the field of alternative treatments that are available over the counter for erectile dysfunction and impotence.
Crossref | PubMed | Scopus (53) | Google ScholarSee all References This study found that, although hypertensive patients had more coronary artery disease, no direct evidence supported an association between hypertension and arteriogenic impotence, as measured by the PBI, peak systolic velocity, and resistive index, in patients with mild to moderate hypertension.
Abstract | Full Text PDF | PubMed | Scopus (16) | Google ScholarSee all References These medications cause intracavernosal pressure changes in animal models, and human studies have noted deleterious effects on erectile function, decreased libido, and ejaculatory problems.42x42Weiss, RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician. 1991; 44: 2075–2082
Low testosterone levels have been observed inconsistently in STZ-induced diabetic and BB rats.18 Androgen deficiency in rats is associated with downregulation of the neuronal isoforms of nitric oxide synthase, suggesting a trophic effect of testosterone on peripheral erectile tissues. In humans, androgens play a larger role in sexual interest and motivation (libido) than in erectile capacity itself; penile erection is more resistant to androgen withdrawal than is sexual desire.19,20
With great interest we have read the recently published review by Vlachopoulos et al, a very detailed and extensive overview of erectile dysfunction in the cardiovascular patients. Guidelines for the management of erectile dysfunction with heart failure were noted, as well as advice about dealing with erectile dysfunction (ED) in patients with cardiovascular disease (CVD). However, many others have written similar reviews and guideline concerning the care for ED as well as (female) sexual dysfunction in CAD in the past years (1-4), cardiologists should be familiar with this matter by now. The problem is the actual translation of this knowledge into actions in cardiologists' daily clinical practice. Our research group performed a survey among Dutch cardiologists, aiming to evaluate their inquiry about erectile function in day-to-day practice, to detect their attitude towards this discussion and their perceived barriers for addressing sexual activity. Results from this survey indicated that cardiologists (n=414) did not routinely discuss erectile dysfunction: 48.7% indicated to discuss sexual function 'sometimes' and only 16.9% said to discuss the subject regularly. Of respondents, 41.5% marked that care for patients' sexual quality of life is not their responsibility. Nevertheless, 42% indicated that they would benefit from training to obtain knowledge about treatment of erectile and sexual dysfunction in cardiologic patients. Barriers not to inquire about sexual activity included 'the patient does not ask about it' (53.7%), 'I do not have an angle or motive to start about it'(45.9%), as well as time constraints (42.9%) and lack of training in dealing with sexual dysfunction (35.2%). The more experienced the cardiologist was the less he/she stated the need for training or for a referral directory(5). Since all cardiologists should, meanwhile, know that ED is part of their responsibility, as it is a sentinel marker of CVD(6). It is now case to pay attention to the implementation of the care for erectile and other sexual dysfunction in the cardiology practice. Our study suggests that physicians' experience in the field plays an important role in discussing sexual activity and that sexual healthcare can be improved with more education about the subject. Furthermore a directory of the available healthcare professionals for the referral of patients with sexual dysfunction was indicated as mandatory. We suggest that attention of cardiologists should not only be focused on writing about ED and CVD, attention should be diverted to the actual implementation of care for patients with ED as well, in order to improve patient-centered healthcare in cardiology.
Several other facts support the close relationship between sexual dysfunction and CV disease. Endothelial dysfunction mediated by decreased nitric-oxide bioavailability as well as atherosclerotic lesions constitute a common pathophysiologic substrate affecting both CV disease and erectile dysfunction, a disease considered to be primarily of vascular origin[76,80-82]. Several traditional CV risk factors (diabetes mellitus, hypertension, dyslipidemia, and smoking) are frequently found in individuals with erectile dysfunction, conferring a detrimental cardiovascular burden to them. More interestingly, the increased cardiovascular risk observed in those patients is independent of the aforementioned CV risk factors[81-88].
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.
Myocardial ischaemia is caused by the reduction of coronary blood flow as a result of fixed or dynamic epicardial coronary artery stenosis, abnormal constriction or deficient relaxation of coronary microcirculation, or because of reduced oxygen-carrying capacity of the blood.56 Atherosclerosis is the major cause of myocardial ischaemia. Plaque that develops in atherosclerosis can rupture causing platelet aggregation and subsequent thrombus formation, which leads to MI. The other mechanisms of myocardial ischaemia are encountered far less than atherosclerosis. Endothelial dysfunction has an important role in the progression of atherosclerosis. Endothelial dysfunction enhances the intimal proliferation and malregulation that results in plaque destabilisation in the arteries.6 This process, coupled with paradoxical vasoconstriction, can result in major cardiovascular events such as MI.32
Sexual intercourse is an infrequent cause of myocardial infarction. In a study of 1774 patients after myocardial infarction, only 1.5% of these events occurred within 2 hours of sexual intercourse, and sexual activity was considered a direct contributing factor in 0.9%.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
Diabetes is known to sabotage two body parts that provide essential components of an erection: nerves and blood vessels. Studies suggest that diabetic nerve damage (neuropathy) is the most important risk factor for ED in people with diabetes. If pelvic nerves that trigger penis muscles to relax are impaired, there may be a break in the chain between brain and penis, disrupting erection. Some researchers suspect that an inadequate supply of oxygen to the nerves causes this damage.
The links between hypertension and ED are increasingly recognized and the 2009 re-appraisal of European guidelines includes relevant statements.35,47 Erectile dysfunction is almost twice as frequent in hypertensive as in normotensive individuals and appears to be of higher severity. The relative risk of developing ED in hypertensive patients compared with normotensive individuals ranges from 1.3 to 6.9. Regarding pathophysiology, hypertension appears to cause ED per se, through a multitude of mechanisms that include prolonged exposure to elevated levels of systemic blood pressure, endothelial dysfunction, and circulation of vasoactive substance (with a pivotal role of angiotensin II) that lead to structural and functional alterations in the penile arteries. The largely unfounded (see earlier paragraph) notoriety of antihypertensive treatment for causing ED is one of the most predominant causes for non-adherence and discontinuation of antihypertensive therapy, and therefore, patients should be properly informed by physicians. Phosphodiesterase type 5 inhibitors are effective in hypertensive patients with ED and they can safely be co-administered with antihypertensive medication.39 Specifically for alpha-blockers, low starting doses of PDE5 inhibitors are preferred in patients already on alpha-blocker treatment, and likewise, low starting doses of alpha-blockers are encouraged in patients taking PDE5 inhibitors. Of clinical significance is that hypertensive men with ED are more likely to comply with their antihypertensive medication when under PDE5 inhibitors.
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.
The term “heart disease” is often used interchangeably with the term “cardiovascular disease.” Cardiovascular disease generally refers to conditions that involve narrowed or blocked blood vessels that can lead to a heart attack, chest pain (angina) or stroke. Other heart conditions, such as those that affect your heart’s muscle, valves or rhythm, also are considered forms of heart disease.
In men without cardiovascular disease, erectile dysfunction (ED) pills are very safe. The three rivals -- Viagra, Cialis, and Levitra -- have similar side effects, including headache, facial flushing, nasal congestion, diarrhea, backache, and, in a few Viagra or Levitra users, temporary impaired color vision (men with retinitis pigmentosa, a rare eye disease, should check with their ophthalmologists before using these medications).
A component of the increased risk conferred by ED could be testosterone deficiency.24 Low testosterone leads to increased levels of total and LDL cholesterol, as well as to increased production of pro-inflammatory markers and mediators.25 Endothelial dysfunction and increased arterial wall thickness, stiffening, and calcification also ensue. On this basis it has been hypothesized that chronically lowered testosterone may increase CVD risk. Indeed, androgen deficiency has emerged as a predictor of CV events, as well as of all-cause and CV mortality, both in the general population and in patients with CV risk factors, with hypertension, with established CVD, and with ED.26 Viewed from the opposite angle, higher serum testosterone showed a protective role for CV events in elderly men.27 A 2010 meta-analysis limited to studies in middle-aged men found no association between total testosterone (TT) levels and CVD risk.28 However, a more recent meta-analysis involving a larger number of studies identified significant associations between androgen deficiency and increased risk of CVD and CVD mortality.29 It should be stressed, however, that the nature of these studies cannot prove causality. The possibility that low testosterone may be an epiphenomenon, marking poor general health rather than modulating CVD risk per se has to be explored.
We need to keep in mind that angioplasty and bypass surgery have some significant adverse outcomes, including heart attacks, stroke and death. These invasive procedures only attempt to treat a small segment of the diseased heart, usually with only a temporary benefit. The patients treated with angioplasty and bypass will continue to experience progressive disability and most often die a premature death as a result of their heart disease.