Erection is a neurovascular event that involves spinal and supra spinal pathways. The final common pathway involves the release of nitric oxide (NO) from both endothelial cells and neurons, which acts as a vasodilator causing penile engorgement and erection. NO is degraded by the enzyme phosphodiesterase (PDE) type 5 in the penis. Erectile dysfunction (ED), defined as the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual performance, results when the neurovascular pathway is interrupted by medical conditions or drugs. A 15-item self-administered questionnaire, the International Index of Erectile Function (IIEF), is one of the most useful tools to evaluate erectile function (EF) in clinical trials, although of much less use in routine clinical practice. The MMAS (Massachusetts Male Aging Study) was the first major epidemiological investigation to study the prevalence of ED. The study found that ED was three times more common in patients with diabetes mellitus. The aetiopathogenesis of ED in diabetes is multifactorial, with vascular and neural factors being equally implicated. Hyperglycaemia is believed to give rise to biochemical perturbations that lead to these microvascular changes. In the MMAS, ED in diabetes was strongly correlated with glycaemic control, duration of disease and diabetic complications. The incidence increased with increasing age, duration of diabetes and deteriorating metabolic control, and was higher in individuals with type 2 diabetes than those with type 1.ED in men with diabetes often affects their quality of life and, as patients are often reluctant to come forward with their symptoms, a carefully taken history is one of the most useful approaches in identifying affected individuals. The PDE inhibitors have revolutionised the management of ED and oral drug therapy is currently first-line therapy for the condition. These agents act by potentiating the action of intracavernosal NO, thereby leading to a more sustained erection. Sildenafil was the first PDE5 inhibitor to undergo evaluation and has been studied extensively. More recently two other agents, vardenafil and tadalafil, have been introduced. All the drugs have been shown to be effective across a wide range of aetiologies of ED, including diabetes. The drugs have been shown to improve EF domain scores, penetration and maintenance of erection, resulting in more successful intercourse. Their effects are greater at higher doses. Sildenafil and vardenafil are shorter-acting agents, while tadalafil has a longer half-life allowing the user more flexibility in sexual activity. Common adverse effects include headache, nasal congestion and dyspepsia, all actions related to inhibition of PDE5. The drugs are generally well tolerated and withdrawal from the clinical studies as a result of drug-related adverse effects were rare. The use of PDE5 inhibitors in the presence of oral nitrates is absolutely contraindicated. The clinical studies to date have not evaluated the use of one drug in the case of treatment failure with another agent. Sublingual apomorphine, which stimulates central neurogenic pathways, is a new agent and may be a suitable alternative in those patients in whom PDE5 inhibitors are ineffective or contraindicated. In clinical trials, all IIEF domains except sexual desire were found to have improved after apomorphine. The median times to erection in these studies were 18.9 and 18.8 minutes for the 2 and 3mg doses, respectively. Intraurethral and intracavernosal alprostadil may be a useful alternative when oral drug therapy is ineffective or contraindicated. The management of ED in the diabetic patient may often involve a multidisciplinary approach where psychosexual counselling and specialist urologist advice is required in addition to the skills and expertise of the diabetologist. Finally, the introduction of the new oral agents have completely revolutionised the management of ED and allowed more individuals to come forward for treatment.
Diuretics: Diuretics are also referred to as water pills. They can make the flow of blood to your penis less intense. This makes getting an erection difficult. Diuretics are also known to lower zinc levels, which can decrease the amount of testosterone your body makes. In turn, this can decrease your sex drive. It may also affect your muscle contraction.

ED is easily and successfully treated! If your sex drive is unaffected, but you experience problems achieving or sustaining erection for a period of four to five weeks, you may have ED. Talk to your doctor immediately. Don’t delay—erectile dysfunction doesn’t “just go away!” Additionally, ED could be a sign of a serious, even life-threatening complication, such as congestive heart failure or kidney disease. Ignoring your ED because it’s embarrassing could jeopardize your health.


The safety of PDE5 inhibitors in patients with IHD has been shown in multiple trials. Arruda-Olson et al. investigated the safety of sildenafil during exercise stress tests in patients with IHD to ascertain whether the drug induces or exacerbates myocardial ischaemia. This was a prospective, randomised crossover study that demonstrated safety of sildenafil when given 1 hour before an exercise stress test.69 Another study that investigated 120 trials of sildenafil revealed that the rates of MI and cardiovascular death with sildenafil are as low as with placebo.70
If you have been diagnosed with heart disease or have already had a heart attack and are experiencing erectile dysfunction, it is critical that you discuss erectile dysfunction medication with your physician before considering taking it. Popular erectile dysfunction medications such as Viagra (sildenafil), Cialis (tadalafil) and Levitra (vardenafil) can interact with a range of cardiovascular disease medications. Interactions are possible with blood pressure medications; blood thinners such as Coumadin (warfarin), nitrates for the treatment of chest pain, and antiarrhythmia medication for the treatment of irregular heart rhythms.
Dey J. “Evaluation and treatment of erectile dysfunction in men with diabetes mellitus.” Mayo Clinic Proceedings 77. 2002. 276-282. Shabsigh R. “Erectile Dysfunction in Men with Diabetes Mellitus.” Men’s Sexual Health Consult Collection. 2006 Nov. Moore C, Wang R. “Pathophysiology and treatment of diabetic erectile dysfunction.” Asian J Andrology. 2006 Nov. 8: 67-684. Penson D, Latini D, Lubeck D, Wallace K, Henning J, Lue T. “Do impotent men with diabetes have more severe erectile dysfunction and worse quality of life than general population of impotent patients?” Diabetes Care 26. 2003. 1093-1099. Sun P, Cameron A, Seftel A, Shabsigh R, Niederberger C, Guay A. “Erectile dysfunction – an observable marker of diabetes mellitus? A large national epidemiological study.” Journal of Urology 176. 2006. 1081-1085.
To date, there are no studies directly comparing the effectiveness of these three agents among diabetic men with ED, so it is impossible to state that one agent is superior to another in terms of effectiveness in diabetic patients. However, there are an number of studies that compare the individual agents to placebo in diabetic men with ED. For example, Boulton et al.41 completed a 12-week double-blind, placebo-controlled randomized clinical trial of the effectiveness of sildenafil in 219 men with ED and type 2 diabetes. They found that sildenafil resulted in a significant improvement in the ability to both achieve and maintain an erection adequate for sexual intercourse in men with type 2 diabetes. In a similar study, Rendell et al.42 randomized 268 diabetic men with ED to receive either sildenafil in a dose-escalation manner or placebo. At the conclusion of the 12-week study, 56% of the patients in the sildenafil arm reported improved erections, compared to 10% in the placebo arm (P < 0.001). Additionally, 61% of patients in the diabetic arm reported at least one successful attempt at sexual intercourse in the final month of the study, compared to 22% in the control arm (P < 0.001). Similar randomized studies have documented the effectiveness of both tadalafil43 and vardenafil44 in the treatment of diabetes-related ED.
If you have several atherosclerotic risk factors or symptoms of heart disease, your doctor might do additional tests to look for atherosclerosis in the coronary arteries. A stress test involves monitoring the heart with an electrocardiogram or images before and after exercise. An angiogram, or cardiac catheterization, involves entering a blood vessel in the leg or wrist to pass instruments into the heart to directly visualize the coronary arteries. During this procedure, atherosclerosis can be treated by inflating a balloon or placing a metal stent in the coronary blood vessel to keep it open. If you and your doctor begin a treatment plan to prevent atherosclerosis at the first sign of ED, then you may significantly delay or prevent the need for these more invasive procedures.

Physical and emotional stress — whether over-exercising, under-sleeping or just dealing with everyday stressors like work and a busy schedule — causes an increase in “stress hormones,” including cortisol and adrenaline. Stress can lower desire for sex. This is because stress can contribute to fatigue or preoccupation with other tasks. It can also significantly affect blood flow by increasing inflammation.
Gazzaruso C,  Solerte SB,  Pujia A,  Coppola A,  Vezzoli M,  Salvucci F,  Valenti C,  Giustina A,  Garzaniti A. Erectile dysfunction as a predictor of cardiovascular events and death in diabetic patients with angiographically proven asymptomatic coronary artery disease: a potential protective role for statins and 5-phosphodiesterase inhibitors, J Am Coll Cardiol , 2008, vol. 51 (pg. 2040-2044)https://doi.org/10.1016/j.jacc.2007.10.069
Getting blood glucose under control is a good anti-ED tactic. Men with diabetes and poor blood glucose control are two to five times as likely to have ED as those with good control. One study in a group of men who had had type 1 diabetes for up to 15 years with minor complications found that intensive blood glucose control lowered the risk of ED compared with conventional treatment. A study in men with type 2 diabetes found that lowering A1C (average blood glucose in the past two to three months) below 7 percent and reducing blood pressure through a combination of medication, diet, and exercise improved sexual functioning.
To reduce the risk of side effects from these medications, including sexual problems, take medications exactly as prescribed. If you still have side effects, talk to your doctor about other possible medications that may have fewer side effects. On the other hand, you should not take any medication that promotes and erection while on medication to lower blood pressure.
Basaria S,  Coviello AD,  Travison TG,  Storer TW,  Farwell WR,  Jette AM,  Eder R,  Tennstedt S,  Ulloor J,  Zhang A,  Choong K,  Lakshman KM,  Mazer NA,  Miciek R,  Krasnoff J,  Elmi A,  Knapp PE,  Brooks B,  Appleman E,  Aggarwal S,  Bhasin G,  Hede-Brierley L,  Bhatia A,  Collins L,  LeBrasseur N,  Fiore LD,  Bhasin S. Adverse events associated with testosterone administration, N Engl J Med , 2010, vol. 36 (pg. 109-122)https://doi.org/10.1056/NEJMoa1000485

Apart from their beneficial effect in erectile dysfunction and their safe profile in antihypertensive medication, PDE-5 inhibitors have even more advantages to demonstrate. Several lines of evidence has proven that patients receiving PDE-5 inhibitors are more likely to initiate an antihypertensive regime and more willing to add a new agent to their existing treatment, a fact that raises significantly patient’s adherence and as a matter of fact control of high blood pressure and quality of life[63,64]. Moreover, a handful of clinical data has demonstrated the considerable vasodilating and anti-proliferative properties of PDE-5 inhibitors in the pulmonary vasculature, establishing them as a first-line treatment in patients with pulmonary arterial hypertension[65,66]. The same properties have been considered as potentially responsible for improving microcirculation in patients with secondary Raynaud phenomenon and ameliorating cardiopulmonary exercise performance in patients with heart failure[67,68]. In addition, the therapeutic implementation of PDE-5 inhibitors has expanded in the field of benign prostate hyperplasia-lower urinary tract symptoms (BPH-LUTS). The common pathophysiologic substrate between erectile dysfunction and BPH-LUTS has rendered PDE-5 inhibitors an effective treatment which significantly improves measures of both conditions while at the same time exhibits high efficacy and safety. The beneficial effect is much more pronounced when taking into consideration the fact that a-blockers, the mainstay of therapy for benign prostate hyperplasia frequently provoke sexual side effects, erectile dysfunction included[69].
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.

Crossref | PubMed | Scopus (539) | Google ScholarSee all References Possible etiologies for ED secondary to hypertension include vascular damage due to hypertensive changes as well as hormonal abnormalities such as elevated prolactin levels.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


Men can judge themselves pretty harshly when it comes to their performance in between the sheets. The unsettling fear of not being able to rise to the occasion becomes a reccurring nightmare for men that is often equated with failure, loss of dignity, and masculinity. If you suffer from erectile dysfunction (ED), don’t be so hard on yourself, since impotence can almost always be improved with treatment, without having to rely on Viagra or other medications. Whether you suffer from ED, or hope to prevent the condition, here are six tips to overcome impotence without the side effects of the little blue pill.
Figure. Progression of atherosclerosis. Endothelial dysfunction occurs early in atherosclerosis and prevents blood vessels from dilating properly. When the blood vessels that supply the penis are not able to dilate during sexual stimulation because of endothelial dysfunction, the penis cannot fill with blood, and the man develops erectile dysfunction. As atherosclerosis progresses, plaques build up in blood vessels and blood flow is slowed, further worsening erectile function. A heart attack occurs when an atherosclerotic plaque in a coronary artery ruptures, a blood clot forms over the plaque, and blood flow to the heart muscle is completely blocked. Atherosclerotic risk factors (black arrows) worsen cardiovascular health; modification of these risk factors (red arrows) improves cardiovascular health.
Dey J. “Evaluation and treatment of erectile dysfunction in men with diabetes mellitus.” Mayo Clinic Proceedings 77. 2002. 276-282. Shabsigh R. “Erectile Dysfunction in Men with Diabetes Mellitus.” Men’s Sexual Health Consult Collection. 2006 Nov. Moore C, Wang R. “Pathophysiology and treatment of diabetic erectile dysfunction.” Asian J Andrology. 2006 Nov. 8: 67-684. Penson D, Latini D, Lubeck D, Wallace K, Henning J, Lue T. “Do impotent men with diabetes have more severe erectile dysfunction and worse quality of life than general population of impotent patients?” Diabetes Care 26. 2003. 1093-1099. Sun P, Cameron A, Seftel A, Shabsigh R, Niederberger C, Guay A. “Erectile dysfunction – an observable marker of diabetes mellitus? A large national epidemiological study.” Journal of Urology 176. 2006. 1081-1085.

Second-generation cardioselective beta-blockers (atenolol, metoprolol, bisoprolol, etc.) can also lead to ED. Atenolol was shown to cause significant reduction of sexual activity compared with placebo in a double-blind, parallel-arm study.22 The same study also showed a significant reduction in testosterone levels with atenolol versus valsartan. An open, prospective study of hypertensive men treated with atenolol, metoprolol and bisoprolol for at least 6 months showed high prevalence of ED – approaching 66 % – in these patients.23
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.
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.

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.
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 (335) | Google ScholarSee all References Glycemia, as measured by glycosylated hemoglobin, also has been associated with the risk of developing ED in diabetic patients.21x21Klein, R, Klein, BE, Lee, KE, Moss, SE, and Cruickshanks, KJ. Prevalence of self-reported erectile dysfunction in people with long-term IDDM. Diabetes Care. 1996; 19: 135–141
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.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (272) | Google ScholarSee all References Between 1987 and 1989, the Massachusetts Male Aging Study (MMAS), a community-based random sample observational study of 1709 men, used self-administered sexual activity questionnaires to gather information about noninstitutionalized men aged 40 to 70 years in cities near Boston.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
Although the results provide evidence that PDE5 inhibitors may benefit heart health, the retrospective study design makes it impossible to ascertain direct cause and effect, Andersson noted. It is possible that using erectile dysfunction drugs simply indicates a more active sex life, which could itself contribute to, or be a marker of, a heart-healthy lifestyle overall.
Older age. A man’s risk increases past the age of 40, as age is the variable most strongly associated with impotence. This is due to changing hormones, higher risk for heart problems and those affecting circulation, and decreased sexual desire that often occurs with increasing age. For example, based on findings from the National Health and Social Life Survey, it’s been found that “men between 50–60 years old are more than 3 times as likely to experience erection problems and to report low sexual desire compared to men aged 18 to 29 years.” (3)
A number of over-the-counter herbal supplements claim to treat ED. However, according to the Mayo Clinic, you should avoid products labeled as “herbal Viagra.” These supplements can increase blood flow and cause dangerous drops in blood pressure. Risk may be particularly high for men who are using nitrates. Herbal Viagra can also interact with other prescription drugs. Herbal Viagra products may contain potentially toxic compounds that aren’t listed on the label.

Yohimbe A number of clinical trials have shown that the primary component of this bark from an African tree can improve sexual dysfunction associated with selective-serotonin reuptake inhibitors (SSRIs) used to treat depression. This herb has been linked to a number of side effects, including increased blood pressure, fast or irregular heartbeat, and anxiety. Yohimbe shouldn't be used without a doctor's supervision.
If you can't take one of these oral medications, your physician may have you try Caverject (alprostadil for injection), a hormone that you inject into your penis using a fine needle, or Muse (alprostadil urogenital), a tiny suppository that you insert into the tip of the penis. Both of these will bring on an erection within five to 15 minutes without sexual stimulation.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References The risk after sexual activity in these patients is unknown, although vasodilators should be avoided because they may increase the intraventricular gradient.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
Levine GN,  Steinke EE,  Bakaeen FG,  Bozkurt B,  Cheitlin MD,  Conti JB,  Foster E,  Jaarsma T,  Kloner RA,  Lange RA,  Lindau ST,  Maron BJ,  Moser DK,  Ohman EM,  Seftel AD,  Stewart WJ. Sexual activity and cardiovascular disease: a scientific statement from the American Heart Association, Circulation , 2012, vol. 125 (pg. 1058-1072)https://doi.org/10.1161/CIR.0b013e3182447787
Abstract | Full Text | Full Text PDF | PubMed | Scopus (207) | Google ScholarSee all References Adverse-effect profiles of headaches, flushing, rhinitis, and dyspepsia, without visual changes, mimic those of vardenafil.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446

Abstract | Full Text | Full Text PDF | PubMed | Scopus (56) | Google ScholarSee all References However, subsequent studies of older patients who had sexual intercourse in their home and were monitored with ambulatory ECG reported significantly lower heart rates and blood pressure levels.84x84Stein, RA. Cardiovascular response to sexual activity. Am J Cardiol. 2000; 86: 27F–29F


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
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.
Crossref | PubMed | Scopus (53) | Google ScholarSee all References A study of 24 patients with ED and untreated essential hypertension showed decreased levels of free and total serum testosterone compared with normal controls.31x31Hughes, GS, Mathur, RS, and Margolius, HS. Sex steroid hormones are altered in essential hypertension. J Hypertens. 1989; 7: 181–187
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

The prevalence of erectile dysfunction is approximately 2-fold higher in hypertensive patients compared to normotensive individuals. However, erectile dysfunction remains under-reported, under-recognized, and under-treated in hypertensive patients. Hypertension per se and antihypertensive drug therapy may contribute to the development of erectile dysfunction in patients with arterial hypertension. The management of erectile dysfunction in hypertensive patients is tricky and should take into account the different effects of antihypertensive drug categories on erectile function. Lifestyle modification should be the mainstay of treating erectile dysfunction in patients with untreated hypertension. Switching antihypertensive therapy should be considered in treated hypertensive patients, unless administered drugs are absolutely indicated for the individual patient. Otherwise, PDE-5 inhibitors should be used, since they are both effective and safe in hypertensive patients. Finally, erectile dysfunction offers the opportunity to recognize asymptomatic cardiovascular disease and better characterize the relevant risk with obvious benefits for cardiovascular disease prevention.


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.

Your choice of blood pressure medications could make a difference in the bedroom (or wherever you like to have sex). Thiazides (diuretics or “water pills”) and beta blockers are the most likely to cause erectile dysfunction (ED), while alpha blockers the least likely. Alpha blockers work by reducing nerve impulses to blood vessels, allowing blood to pass more easily. Ask your doctor whether these or other blood pressure medications are best for you.
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.
The mechanisms of action by which antihypertensive medications cause ED are currently unknown. Some investigators have theorized that antihypertensive medications affect erectile function by decreasing blood pressure, which reduces the perfusion pressure needed to maintain sufficient blood flow for erections through atherosclerotic penile arteries.37x37Benet, AE and Melman, A. The epidemiology of erectile dysfunction. Urol Clin North Am. 1995; 22: 699–709

Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References However, if optimally treated with β-blockers, lipid-lowering agents, and aspirin, these patients have no significantly increased cardiovascular risk associated with sexual activity, although they should receive appropriate risk information.88x88Jackson, G. The use of sildenafil in heart disease [editorial]. Hosp Med. 2000; 61: 526–527
Stem cell therapy is an attractive treatment modality and an appealing option for tissue regenerative therapy for ED. Stem cells are pluripotent cells that can be produced from multiple regions within the body. They have the potential to divide and differentiate into numerous kinds of human cells, such as endothelial cells and smooth muscle.79 The efficacy and safety of gene and stem cell therapy in patients with ED and IHD need to be extensively investigated because both seem to have the potential to correct underlying abnormalities in ED. This would be a huge development in terms of management options for patients with ED and IHD.
Many products contain undocumented “fillers” that can cause allergic reactions.  In recent years, the FDA has found over 300 herbal products that contain hidden, deceptively labeled, or dangerous ingredients4. And since 2015, the FDA has released public warnings on more than 160 ED supplements and “male enhancement” products found to contain dangerous ingredients and contaminants5 .   An independent study of FDA data, conducted in 2018, found almost 800 herbal supplements that contained unlisted ingredients6.
A variety of personal habits and lifestyle choices have been linked to ED. In some ways, this is a good thing, since habits can be broken and choices reconsidered. What's more, many of the lifestyle factors that contribute to sexual problems are ones that affect overall health and well-being, both physical and mental. Addressing these factors, therefore, can have benefits beyond improving erectile dysfunction.

Crossref | PubMed | Scopus (174) | Google ScholarSee all References This study concluded that patients who have stable coronary artery disease who can exercise to 4.5 metabolic equivalents (METs) with a negative or mildly positive stress test and without angina or hypotension can safely take sildenafil. Physicians who prescribe sildenafil should counsel their patients that, if they have chest pain or other cardiac symptoms with sexual intercourse, they should not take nitrates and should immediately call their physician.66x66Jackson, G. Sexual intercourse and stable angina pectoris. Am J Cardiol. 2000; 86: 35F–37F
Crossref | PubMed | Scopus (335) | Google ScholarSee all References Glycemia, as measured by glycosylated hemoglobin, also has been associated with the risk of developing ED in diabetic patients.21x21Klein, R, Klein, BE, Lee, KE, Moss, SE, and Cruickshanks, KJ. Prevalence of self-reported erectile dysfunction in people with long-term IDDM. Diabetes Care. 1996; 19: 135–141
Testosterone cypionate and testosterone enanthate injections are used for replacement therapy in patients with low testosterone. Other formulations, such as gels and patches, are recommended in older patients with chronic conditions.57 Serum prostate specific antigen should be measured before starting testosterone replacement, then 3–6 months after starting the treatment, followed by annual measurement.74
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
Cavallini, G., Modenini, F., Vitali, G., & Koverech, A. (2005, November). Acetyl-L-carnitine plus propionyl-L-carnitine improve efficacy of sildenafil in treatment of erectile dysfunction after bilateral nerve-sparing radical retropubic prostatectomy. Urology, 66(5), 1080-5. Retrieved from http://www.sciencedirect.com/science/article/pii/S0090429505006515
Yohimbe A number of clinical trials have shown that the primary component of this bark from an African tree can improve sexual dysfunction associated with selective-serotonin reuptake inhibitors (SSRIs) used to treat depression. This herb has been linked to a number of side effects, including increased blood pressure, fast or irregular heartbeat, and anxiety. Yohimbe shouldn't be used without a doctor's supervision.
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.
According to the Cleveland Clinic, “because erectile dysfunction is caused by a complex set of psychosocial, neurologic, and vascular factors, a specific cause in a patient may remain ambiguous.” The root causes are often related to a blockage or dysfunction of blood vessels. For example, ED can be due to conditions like atherosclerosis or diabetes, hormonal imbalances or problems related to mental health. It’s been found that common causes typically include one or more of the following factors: (2)
When it comes to combating heart disease, most information sources promote drugs and surgery as the only viable options, with lip service to dietary advice that simply does not work. As a result, the demand for high-tech, expensive, but largely ineffective medical care is soaring, causing medical costs and insurance rates to skyrocket. This chase for "cures" is both financially devastating and futile. Morbidity and premature mortality from heart disease continue to rise, with no sign of abating.
Relaxation of erectile tissue requires nitric oxide from nonadrenergic-noncholinergic neurons and the endothelium.21 Penile tissue from diabetic men with ED demonstrates impaired neurogenic and endothelium-mediated relaxation of smooth muscle,22 increased accumulation of advanced glycation end products (AGEs),23 and upregulation arginase, a competitor with nitric oxide synthase for its substrate L-arginine.24 Normal responses to direct smooth muscle relaxants in most of these studies implies that the impairments are due to decreased synthesis, release, or activity of nitric oxide. The fundamental mechanisms mediating these changes are thought to be the same as for other diabetic complications: increased polyol pathway flux, intracellular accumulation of AGEs, activation of protein kinase C, and increased flux through the hexosamine pathway.25
×