Abstract | Full Text | Full Text PDF | PubMed | Scopus (56) | Google ScholarSee all References Cardiologists use METs of oxygen consumption to compare the energy expenditure of different forms of 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
Low testosterone represents another link between erectile dysfunction and heart disease. A man’s testosterone levels gradually diminish beginning at age 30. By the time he reaches his 70s, testosterone levels may have dropped to a tenth of youthful levels. Diminishing testosterone levels contribute to loss of muscle, increased body fat, and reduced libido. Fatigue is common, as is depression. Low testosterone levels can also result in reduced concentration, irritability, passivity, loss of interest in activities, and even hypochondria.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (164) | Google ScholarSee all References Several double-blind, placebo-controlled studies have shown vardenafil to be more effective than placebo in the treatment of ED secondary to a wide range of other etiologies as well.71x71Hellstrom, WJ, Gittelman, M, Karlin, G..., and Vardenafil Study Group. Sustained efficacy and tolerability of vardenafil, a highly potent selective phosphodiesterase type 5 inhibitor, in men with erectile dysfunction: results of a randomized, double-blind, 26-week placebo-controlled pivotal trial. Urology. 2003; 61: 8–14
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
Alcohol consumption, bad nutrition, a sedentary lifestyle, excessive stress, psychological issues, relationship issues, use of illegal drugs and overuse of prescribed drugs, poor sleep habits and excessive physical activity are all contributing factors to ED. Ailments like diabetes, as well as low and high blood pressure, in addition to prostate cancer, may also result in ED.
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
However, sildenafil should be used carefully with nitrates because their combination can result in severe hypotension and death.68 Both short- and long-acting nitrates are commonly prescribed to treat angina, but they have no prognostic benefit. In addition, there are numerous alternatives to treat angina, such as ranolazine and ivabradine, which do not interact with PDE5 inhibitors. As a result, patients with ED wishing to take PDE5 inhibitors can safely discontinue their nitrates and replace this treatment with the other anti-anginal agents.68
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].
Yohimbine: The main component of an African tree bark, yohimbine is probably one of the most problematic of all natural remedies for ED. Some research suggests that yohimbine can improve a type of sexual dysfunction that is linked with a drug used to treat depression. However, studies have linked yohimbine to a number of side effects, which can include anxiety, increased blood pressure, and a fast, irregular heartbeat. Like all natural remedies, yohimbine should only be used after advice and under supervision from a doctor.
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
Perk J,  De Backer G,  Gohlke H,  Graham I,  Reiner Z,  Verschuren WM,  Albus C,  Benlian P,  Boysen G,  Cifkova R,  Deaton C,  Ebrahim S,  Fisher M,  Germano G,  Hobbs R,  Hoes A,  Karadeniz S,  Mezzani A,  Prescott E,  Ryden L,  Scherer M,  Syvänne M,  Scholte Op Reimer WJ,  Vrints C,  Wood D,  Zamorano JL,  Zannad F. European Guidelines on cardiovascular disease prevention in clinical practice (version 2012). The Fifth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of nine societies and by invited experts). Developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR), Eur Heart J , 2012, vol. 33 (pg. 1635-1701)https://doi.org/10.1093/eurheartj/ehs092
Uses and risks of viagra Viagra treats erectile dysfunction and pulmonary arterial hypertension. For sexual purposes, it helps someone with erectile dysfunction achieve and maintain an erection. However, Viagra can have unpleasant side effects, and an overdose can be serious. We cover everything you need to know about Viagra in this article. Read now
Erne P,  Schoenenberger AW,  Zuber M,  Burckhardt D,  Kiowski W,  Dubach P,  Resink T,  Pfisterer M. Effects of anti-ischaemic drug therapy in silent myocardial ischaemia type I: the Swiss Interventional Study on Silent Ischaemia type I (SWISSI I): a randomized, controlled pilot study, Eur Heart J , 2007, vol. 28 (pg. 2110-2117)https://doi.org/10.1093/eurheartj/ehm273
80. Montorsi F, Briganti A, Salonia A, Rigatti P, Margonato A, Macchi A, Galli S, Ravagnani PM, Montorsi P. Erectile dysfunction prevalence, time of onset and association with risk factors in 300 consecutive patients with acute chest pain and angiographically documented coronary artery disease. Eur Urol. 2003;44:360–364; discussion 364-365. [PubMed]
PubMed | Google ScholarSee all References However, other studies have noted that, when blood pressure levels are monitored after initiation of antihypertensive therapy, changes in blood pressure level are not correlated with sexual function.38x38Rosen, RC, Kostis, JB, Jekelis, A, and Taska, LS. Sexual sequelae of antihypertensive drugs: treatment effects on self-report and physiological measures in middle-aged male hypertensives. Arch Sex Behav. 1994; 23: 135–152
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.
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].
Faced with concern about ED pills and the heart, the FDA has urged caution in patients who have suffered heart attacks, strokes, or serious disturbances of the heart's pumping rhythm in the previous six months, in men with a history of congestive heart failure or unstable angina, and in men with low blood pressure or uncontrolled high blood pressure (above 170/110 mm Hg). Because certain medications can boost the blood levels of these drugs, men taking erythromycin or certain antifungal or anti-HIV medications should use only low-dose PDE-5 inhibitors. Reduced dosage is also important for men with advanced age and for those with significant kidney or liver disease.
Neurological (nerve and brain) diseases: The nervous system plays a vital part in achieving and maintaining an erection. It is common for men with conditions such as stroke, multiple sclerosis (MS), Alzheimer’s disease, Parkinson’s disease, and spinal cord injuries to experience ED. This is due to an interruption in the transmission of nerve impulses between the brain and the penis.
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.
Abnormalities in the vascular, neural, endocrine, muscular, or psychiatric systems can result in ED.2,3 EDDM is due to multisystemic disease. Atrophy or apoptosis of cavernosal smooth muscle can occur due to loss of Bcl-2 expression in cavernosal smooth muscle and lead to ED. Abnormal amounts of advanced glycation end products is a common occurrence. These chemicals may have an effect on potassium channels that facilitate intracellular calcium release and subsequent cavernosal smooth muscle relaxation. Connective tissue synthesis is increased due to transforming growth factor-beta. The decrease in smooth muscle and the increase in collagen decreases the compliance of the erectile tissue. Neuropathic damage to both the somatic and autonomic nerves has been clearly defined in DM. Partial occlusion of the pelvic or intracavernosal arteries, hypogonadotropic hypogonadism, and depression associated with a chronic illness (DM) can all play a primary or secondary role in the development of EDDM. On a molecular level, studies have demonstrated decreased levels of endothelial and neuronal nitric acid synthase (NS) and decreased cavernosal artery and sinusoidal response to nitric oxide. Abnormalities in nitric oxide rapidly render the functional syncytium of the corpora cavernosa unable to synchronously relax. As the patient with diabetes ages, the concentration of constrictors, including endothelin, prostanoids, and possibly angiotensin, increases as the production of the relaxants, including nitric oxide, vasointestinal peptide, and prostacyclin, decreases.
Crossref | PubMed | Scopus (35) | Google ScholarSee all References Also, if lower blood pressure level was the primary etiology of ED, all classes of antihypertensive agents should be expected to have relatively similar effects on erectile function because of their efficacy in lowering pressure, which has not been seen.6x6Kloner, RA. Erectile dysfunction and cardiovascular risk factors. Hosp Pract (Off Ed). 2001; 36: 41–44 (49-51.)
Crossref | PubMed | Scopus (23) | Google ScholarSee all References Vardenafil has been shown to be significantly more effective than placebo in the treatment of ED secondary to diabetes mellitus and after radical retropubic prostatectomy.69x69Goldstein, I, Young, JM, Fischer, J, Bangerter, K, Segerson, T, Taylor, T, and Vardenafil Diabetes Study Group. Vardenafil, a new phosphodiesterase type 5 inhibitor, in the treatment of erectile dysfunction in men with diabetes: a multicenter double-blind placebo-controlled fixed-dose study. Diabetes Care. 2003; 26: 777–783
Treatment of ED which was previously confined to invasive procedures, cavernosal injections or to rather ineffective oral medications was revolutionized in 1999 with the introduction of the orally administered PDE5 inhibitor sildenafil. Phosphodiesterase type 5 inhibitors are the first-line therapy for ED of organic aetiology unless there is a specific contraindication to their use. This class of agents is widely used because of its effectiveness and safety.38 Interactions with cardiovascular drugs have been minimal with the exception of nitrates and other nitric oxide (NO) donors (such as nicorandil), where co-administration may result in severe vasodilation and hypotension. However, nitrates are often overused in clinical practice; therefore, the option of their discontinuation should be considered. A strong body of clinical data shows that all three agents (sildenafil, tadalafil, and vardenafil) do not increase the risk of non-fatal myocardial infarction, stroke, or cardiovascular deaths. These drugs do not exacerbate ischaemia or worsen exercise tolerance in patients with known CAD who achieve levels of exercise comparable or greater than that achieved during sexual intercourse.38,39 Phosphodiesterase type 5 is expressed throughout the human body, including the pulmonary and systemic vasculature and hypertrophied myocardium. While currently their only additional indication, beyond ED, is idiopathic pulmonary hypertension (for sildenafil and tadalafil), they show potential to be of benefit in several other conditions, such as CAD and systolic heart failure.39 Mechanisms of benefit of PDE5 inhibitors include pulmonary and systemic vasodilation, increased myocardial contractility, reduced large artery stiffness and wave reflections, improved endothelial function, and reduced apoptosis, fibrosis and hypertrophy through mechanisms involving NO, cyclic guanosine monophosphate, protein kinase G and Rho kinase.39 A very important issue is whether treatment of ED per se (and not of its risk factors and comorbidities) will have an impact on cardiovascular risk. While this applies to all therapeutic modalities of ED, it is particularly pertinent for PDE5 inhibitors, since they represent the mainstay of ED therapy. Data are limited to date. Gazzaruso et al.21 showed a trend of PDE5 inhibitors to reduce cardiovascular morbidity and mortality in diabetic patients with silent CAD and ED, while Frantzen et al.40 showed that 2 years after the introduction of sildenafil, the relative risk of the incidence of CVD among men with ED compared with healthy men significantly decreased from 1.7 to 1.1.
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
Three longitudinal studies have estimated incidence rates of ED in men with diabetes. Unfortunately, none of these studies specifically examined men with type 2 disease. In a cohort of 278 diabetic men with type 1 or type 2 diabetes potent at study entry, the proportion of patients reporting ED at 5-year follow-up was 28%.7 A follow-up analysis of the Massachusetts Male Aging Study, a community-based cohort of men between 40 and 70 years of age, found that the incidence of ED in the diabetic men was 51/1,000 population-years.8 This figure was similar to the 68/1,000 person-years crude incidence rate of ED reported in a study of 1,010 men with diabetes.5 However, new studies need to be carried out in well-characterized populations of men with diabetes in order to better determine the incidence of ED and potential effects of interventions to reduce complications.
Alprostadil is an ED drug that comes in two forms. One form (Caverject, Caverject Impulse, or Edex) is injected into the side of the penis to increase blood flow and cause an erection within 5 to 20 minutes. Its effects last 1 hour or less. The most common side effect is pain. Other side effects include bruising, redness, numbness, bleeding, and irritation.
Abnormalities in the vascular, neural, endocrine, muscular, or psychiatric systems can result in ED.2,3 EDDM is due to multisystemic disease. Atrophy or apoptosis of cavernosal smooth muscle can occur due to loss of Bcl-2 expression in cavernosal smooth muscle and lead to ED. Abnormal amounts of advanced glycation end products is a common occurrence. These chemicals may have an effect on potassium channels that facilitate intracellular calcium release and subsequent cavernosal smooth muscle relaxation. Connective tissue synthesis is increased due to transforming growth factor-beta. The decrease in smooth muscle and the increase in collagen decreases the compliance of the erectile tissue. Neuropathic damage to both the somatic and autonomic nerves has been clearly defined in DM. Partial occlusion of the pelvic or intracavernosal arteries, hypogonadotropic hypogonadism, and depression associated with a chronic illness (DM) can all play a primary or secondary role in the development of EDDM. On a molecular level, studies have demonstrated decreased levels of endothelial and neuronal nitric acid synthase (NS) and decreased cavernosal artery and sinusoidal response to nitric oxide. Abnormalities in nitric oxide rapidly render the functional syncytium of the corpora cavernosa unable to synchronously relax. As the patient with diabetes ages, the concentration of constrictors, including endothelin, prostanoids, and possibly angiotensin, increases as the production of the relaxants, including nitric oxide, vasointestinal peptide, and prostacyclin, decreases.
Crossref | PubMed | Scopus (539) | Google ScholarSee all References After adjusting for age, vascular disease, psychiatric disease, hormonal factors, and marital status, a study of 4462 US Army veterans aged 31 to 49 years found an odds ratio of 1.8 for the risk of developing ED in men who smoked.26x26Mannino, DM, Klevens, RM, and Flanders, WD. Cigarette smoking: an independent risk factor for impotence?. Am J Epidemiol. 1994; 140: 1003–1008
Montorsi P,  Ravagnani PM,  Galli S,  Rotatori F,  Veglia F,  Briganti A,  Salonia A,  Dehò F,  Rigatti P,  Montorsi F,  Fiorentini C. Association between erectile dysfunction and coronary artery disease. Role of coronary clinical presentation and extent of coronary vessels involvement: the COBRA trial, Eur Heart J , 2006, vol. 27 (pg. 2632-2639)https://doi.org/10.1093/eurheartj/ehl142
Abnormalities in the vascular, neural, endocrine, muscular, or psychiatric systems can result in ED.2,3 EDDM is due to multisystemic disease. Atrophy or apoptosis of cavernosal smooth muscle can occur due to loss of Bcl-2 expression in cavernosal smooth muscle and lead to ED. Abnormal amounts of advanced glycation end products is a common occurrence. These chemicals may have an effect on potassium channels that facilitate intracellular calcium release and subsequent cavernosal smooth muscle relaxation. Connective tissue synthesis is increased due to transforming growth factor-beta. The decrease in smooth muscle and the increase in collagen decreases the compliance of the erectile tissue. Neuropathic damage to both the somatic and autonomic nerves has been clearly defined in DM. Partial occlusion of the pelvic or intracavernosal arteries, hypogonadotropic hypogonadism, and depression associated with a chronic illness (DM) can all play a primary or secondary role in the development of EDDM. On a molecular level, studies have demonstrated decreased levels of endothelial and neuronal nitric acid synthase (NS) and decreased cavernosal artery and sinusoidal response to nitric oxide. Abnormalities in nitric oxide rapidly render the functional syncytium of the corpora cavernosa unable to synchronously relax. As the patient with diabetes ages, the concentration of constrictors, including endothelin, prostanoids, and possibly angiotensin, increases as the production of the relaxants, including nitric oxide, vasointestinal peptide, and prostacyclin, decreases.

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.
If your physician advises you that the risks of taking an erectile dysfunction medication are too high, he or she can advise you of other treatment options that can enable you to resume sexual activity without risks of complications. These might also include screening to try to determine if your erectile dysfunction has a physiological basis in need of medical intervention, can be corrected through lifestyle changes or if it may have psychological roots. After all, a heart attack or diagnosis of heart disease can lead to depression, which can also affect libido. Talk with your doctor to establish a safe, effective plan for resuming intimacy after your heart disease diagnosis.

When counseling diabetic men who are considering a PDE-5 inhibitor for ED, it is important to set realistic expectations and explain that studies document that all three agents are less effective in diabetic patients than in the general population of men with ED.45–49 For additional information, readers are referred to the excellent review of the use of PDE-5 inhibitors in diabetic men by Vickers and Satyanarayana.50
The aetiology of predominantly psychogenic ED is multifactorial, and components may include psychiatric disorders (especially depression), interpersonal problems with the sexual partner or misconceptions about normal sexual activity. Identifying and getting treatment for those patients with psychogenic causes of ED such as depression that may also increase CVD risk is also important.
Erectile dysfunction (ED) is defined as the persistent inability to attain and maintain an erection that is sufficient to permit satisfactory sexual performance (1). The current pharmaco-therapeutic research in ED focuses on underlying endothelial dysfunction as the root cause for ED and introduction of phosphodiesterase type 5 inhibitors to potentiate nitric oxide (NO) action and cavernosal smooth muscle vasodilation, has revolutionized modern ED treatment over the past two decades (2). In contrast to Western Medicine, the traditional and complementary medicine (TCM) aims at restoration and better overall bodily regulation with medicine to invigorate qi (energy) in vital organs such as kidney, spleen and liver; to enhance physical fitness, increase sexual drive, stabilize the mind and improve the overall situation resulting in natural and harmonious sexual life (3).
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).
Erectile dysfunction (ED) is highly prevalent affecting at least 50 % of men with diabetes mellitus (DM). DM may cause ED through a number of pathophysiological pathways. These include neuropathy, endothelial dysfunction, cavernosal smooth muscle structural/functional changes, and hormonal changes. Lifestyle changes, diabetes control, and treatment of hypogonadism are important as the first step in ED management since there is no curative treatment for ED. Phosphodiesterase type 5 inhibitors (PDE5i) are the first-line treatment option. Intracavernous administration of vasoactive drugs is commonly used as a second-line medical treatment when PDE5i have failed. Alprostadil is the most widely used drug in this second-line setting. The combination of papaverine, phentolamine, and alprostadil represents the most efficacious intracavernous pharmacologic treatment option that may save non-responders to alprostadil. Penile prosthesis implantation can be considered in treatment refractory cases, with excellent functional and safety results in the properly informed patients.
In an open-label study, 8 patients monitored with a Swan-Ganz catheter were given a total of 40 mg of sildenafil in 4 intravenous transfusions (the equivalent of 1 to 3 times the plasma concentration after an oral dose of 100 mg).62x62Jackson, G, Benjamin, N, Jackson, N, and Allen, MJ. Effects of sildenafil citrate on human hemodynamics. Am J Cardiol. 1999; 83: 13C–20C
The art of acupuncture has become the new treatment for everything from back pain, depression, and even ED. Impotence could be more of a state of mind, and acupuncture may help. Through this alternative therapy, fine needles are placed in various parts of the body to relieve pain or stress. Although there are many mixed studies for acupuncture and ED, many tend to confirm positive results. A 1999 study found acupuncture improved the quality of erection and even restored sexual activity in 39 percent of participants.
Crossref | PubMed | Scopus (165) | Google ScholarSee all References Typically, the response to sexual activity is no more than an increase in heart rate to 130 beats/min and an increase in systolic blood pressure level to 170 mm Hg.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
Eastern medicine should be fully exploited, and integrated with modern medicine to combine the advantages of both TCM and Western medicine. More research should be conducted into the efficacy and safety of TCM, and integration of TCM and Western medicine may provide promising breakthroughs in future clinical treatment. This strategy may allow for the development of new therapeutic strategies based on concepts of TCM and integrated medicine. There is a need for multimodal therapy and holistic approach to treat men (and their partners) with ED through complementary use of herbal supplements and modern drug to optimize underlying medical comorbidities; acupuncture, exercise or massage to reduce stress and strengthen the body; introduction and escalation of various medical therapy with use of mechanical therapy to further enhance penile erection; and lastly surgical intervention in suboptimal or refractory ED cases.
High blood pressure and erectile dysfunction (ED) often go hand in hand. While having high blood pressure (hypertension) itself may not initially cause any symptoms, it will damage your arteries over time, leading them to become less flexible and progressively more narrow. This not only increases the risk of heart attacks and stroke, but has the potential to compromise blood flow to many organs in the body, including the penis, if left untreated.
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
The connection between diabetes and ED is related to your circulation and nervous system. Poorly controlled blood sugar levels can damage small blood vessels and nerves. Damage to the nerves that control sexual stimulation and response can impede a man’s ability to achieve an erection firm enough to have sexual intercourse. Reduced blood flow from damaged blood vessels can also contribute to ED.
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