Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References Risk of arrythmias after sexual intercourse was evaluated in 82 patients with stable coronary artery disease who were monitored with ambulatory ECG after sexual intercourse.81x81Drory, Y, Fisman, EZ, Shapira, Y, and Pines, A. Ventricular arrhythmias during sexual activity in patients with coronary artery disease. Chest. 1996; 109: 922–924
Other effective Diabetic Erectile Dysfunction Treatment therapies available include (a) an intraurethral suppository of the vasodilator drug alprostadil (prostaglandin E1), (b) intracavernosal self injection (penile self injection) of the non-specific PDE drug papaverine, the non-selective alpha-adrenergic antagonist phentolamine, and the vasodilator prostaglandin E1, used alone or in combination, or (c) penile prostheses (penile implants).
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.
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).
Despite all the options and alternatives, sometimes there’s no suitable alternative to a prescription that contributes to ED. You might have an adverse reaction to an particular medication or an alternative is unavailable in your state, health insurance plan, or your budget. There are good reasons you were prescribed your original medication in the first place.
Oral medications (Viagra™, Cialis™, Levitra™ and Stendra™) are a common first step to treat ED, but they don’t work for everyone – especially men with heart disease. Men taking nitrates for heart disease or those taking alpha blocking agents for blood pressure are generally not candidates for oral ED medication.13 In addition, some medications simply do not work for certain men. When ED medication is not the answer, there are other options.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (53) | Google ScholarSee all References Coital position has not been shown to play a role in increased cardiovascular risk; similar peak heart rates and blood pressure levels are evident with either the man or the woman in the superior position during intercourse.90x90Nemec, ED, Mansfield, L, and Kennedy, JW. Heart rate and blood pressure responses during sexual activity in normal males. Am Heart J. 1976; 92: 274–277
In contrast to Chinese ginseng, Korean ginseng is divided into three types, depending on how it is processed. Red Ginseng is harvested at the sixth year of cultivation and is steamed and dried. In addition to the effects mentioned regarding the effects of ginsenoside, red ginseng has been repoted to improve erectile function in a rat model of metabolic syndrome and it was also found to inhibit fibrosis of the corpus cavernosum of the penis (39). As with most herbal medicines, the concentration of ginsenoside are distributed unevenly throughout the ginseng plant and the concentrations in individual supplements can vary. Common side effects include headaches, insomnia, gastric upset, rash and constipation.
Testosterone therapy in hypogonadism modulates metabolic components associated with CV risk. The majority of prospective clinical studies indicates that treatment achieving testosterone levels within physiological limits has beneficial or neutral effects on a lipid profile other than HDL-C, beneficial or neutral effects on inflammatory mediators, and generally beneficial effects on glycaemic state.25 The lean body mass is typically increased in hypogonadal subjects, and visceral adiposity is decreased in several studies and unchanged in the remainder. Such metabolic effects have raised interest on the potential impact on cardiovascular health. Regarding symptoms in patients with pre-existing cardiovascular conditions (angina or heart failure) TTh has been either neutral or beneficial.25 Regarding CVD risk, available clinical trial data indicate that the use of testosterone in middle-aged to elderly men does not increase cardiovascular risk25 with the exception of one study in very frail (substantial limitation of mobility and a high rate of comorbidities) elderly subjects that used an off-label high, and rapid escalation, dosing regimen.46 Prospective data from large, well-designed, long-term trials of TTh are warranted.
Preclinical and clinical trials of these oral agents have clearly demonstrated that they are well tolerated by most DM patients and have an efficacy rate superior to other oral agents. The ultimate result is an improved quality of life (QOL) in EDDM patients. With a greater willingness of DM patients to discuss and seek treatment for ED, it is highly probable that the use of these oral agents will continue to increase. The goal of this article is to provide the physician and pharmacist with a background and working knowledge of these oral agents and their present-day alternatives.
Luckily, awareness of ED as a significant and common complication of diabetes has increased in recent years, mainly because of increasing knowledge of male sexual function and the rapidly expanding armamentarium of novel treatments being developed for impotence. Studies of ED suggest that its prevalence in men with diabetes ranges from 35–75% versus 26% in general population. The onset of ED also occurs 10–15 years earlier in men with diabetes than it does in sex-matched counterparts without diabetes.
The recommended dosage of sildenafil is 50 mg/day, usually taken 1 hour before sexual activity. This dose may be increased to 100 mg or decreased to 25 mg based on side effects.6 PDE5 inhibitors also have a beneficial effect in the treatment of heart failure with reduced ejection fraction as well as pre- and post-capillary pulmonary hypertension. The use of PDE5 inhibitors in the treatment of right heart failure and left ventricular failure associated with combined pre- and post-capillary pulmonary hypertension has been well studied.71,72
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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.
The pilot study by Vardi et al. (18) showed that LIESWT was effective in treating men with ED, suggesting a physiologic impact of LIESWT on cavernosal hemodynamics. The LIESWT is an effective penile rehabilitation tool that improves erectile function and potentially reverses underlying ED. Recent meta-analysis (19) of 14 studies showed that LiESWT could significantly improve the International Index of Erectile Function (IIEF) [mean difference: 2.00; 95% confidence interval (CI), 0.99–3.00; P<0.0001] and Erection Hardness Score (EHS) (risk difference: 0.16; 95% CI, 0.04–0.29; P=0.01). In addition, the therapeutic efficacy was noted to last for at least 3 months. LiESWT has been cited to a potential cure for ED, unlike other well established non-surgical methods of treatment (i.e., PDE5i, ICI and VED) being on demand treatments.
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.
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]
Crossref | PubMed | Scopus (25) | Google ScholarSee all References In comparison, a randomized placebo-controlled trial of 65 patients given either placebo or 95 mg/d of sustained-release metoprolol for 4 months after percutaneous coronary angioplasty found no significant difference in sexual function between the 2 groups.44x44Franzen, D, Metha, A, Seifert, N, Braun, M, and Hopp, HW. Effects of beta-blockers on sexual performance in men with coronary heart disease: a prospective, randomized and double blinded study. Int J Impot Res. 2001; 13: 348–351
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.
Admitting to your doctor that you are having trouble achieving an erection can be difficult, but take comfort in the fact that they are not judging you and are there to improve your health and well-being. If you are just beginning a blood pressure treatment regimen and are beginning to experience erectile dysfunction, tell your doctor as soon as you can—they can solve the problem by simply changing the prescription.
It is recommended that testosterone be measured in patients with ED because low levels are a reliable measure of hypogonadism. Hypogonadism is not only a treatable cause of ED, but can also lead to reduced or lack of response to PDE5 inhibitors.73 Testosterone deficiency is also associated with increased cardiovascular and all-cause mortality.74 Levels >350 ng/dl do not usually require replacement, but in patients with testosterone <230 ng/dl, replacement can usually be beneficial.57 In patients with congestive heart failure, testosterone replacement can lead to fluid retention, so caution is advised. In these patients, the aim should be to keep testosterone levels in the middle range, i.e. 350–600 ng/dl.57
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 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).
Abstract | PubMed | Scopus (136) | Google ScholarSee all References Another study evaluated 32 hypertensive men with ED and 78 normotensive men with ED with regard to age, body mass index, hormonal profile, penile arterial flow, risk factors for arterial disease, psychiatric disease, and neurologic disease measured by pudendal nerve conduction studies.30x30Jaffe, A, Chen, Y, Kisch, ES, Fischel, B, Alon, M, and Stern, N. Erectile dysfunction in hypertensive subjects: assessment of potential determinants. Hypertension. 1996; 28: 859–862
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 it comes to scientific development, in Western medicine, an analytic approach is often used to identify and resolve medical challenges. A hypothesis is first derived through general observations of a phenomenon. A research plan is then carefully designed and data collected. Once sufficient data is collected, critical statistical evaluations are done and conclusions are drawn (4). Every aspects of a disease entity are studied from macroscopic to microscopic views, down to the cellular and molecular levels. The deep understanding of the role of cGMP-specific phosphodiesterase type 5 enzymes in ED and the use of phosphodiesterase-5 inhibitors in treatment of ED exemplifies the success of this approach.
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).
ED is generally associated with significant changes in established cardiovascular risk factors. Atherosclerosis is the main cause of ED development in both the general population and patients with diabetes. However, the prevalence of ED is greater in patients with diabetes than in the general population.8 ED has been shown to occur at rates as high as 50 % in patients with CAD.9 A meta-analysis of 12 prospective cohort studies has provided evidence that ED is a predictor of IHD associated with an increased risk of CVD, stroke and all-cause mortality.10
Since 1998, when sildenafil (brand name Viagra) first came on the market, oral therapy has been successfully used to treat erectile dysfunction in many men with diabetes. (Sildenafil was followed in 2003 by the drugs tadalafil [Cialis], vardenafil [Levitra] and avanafil [Stendra], which work in much the same way.) Some 50% of men with Type 1 diabetes who try the drugs report improved erections, and some 60% men with Type 2 diabetes do, too. However, that leaves a large percentage of men with diabetes and erectile dysfunction who do not respond to therapy with one of these pills. This article takes a look at what can be done to treat those men who do not respond to oral therapy.