After getting a diagnosis of ED, most patients can begin treatment right away, but treatment may be delayed for some patients until the health of the heart is more fully assessed or improved. The most common treatment for ED is a pill (phosphodiesterase-5 inhibitor; PDE5-I): Viagra (sildenafil), Cialis (tadalafil), or Levitra (vardenafil). Each of these pills improves erections when taken before sexual activity; alternatively, a low dose of Cialis can be taken once a day. These medicines work by allowing the blood vessels that supply blood to the penis to dilate better during sexual stimulation. The PDE5-Is decrease blood pressure a little bit, but they are safe with most other medications and with other blood pressure pills. The PDE5-Is are not safe with nitrate medications like nitroglycerin, Nitrostat, Nitro Paste, Imdur, isosorbide mononitrate, and Isordil. Mixing a PDE5-I with a nitrate medication could result in severely low blood pressure and even death. Inform all medical professionals (including the ambulance or emergency department) about your most recent ED pill ingestion so that nitrates can be avoided. If you have high blood pressure or benign prostatic hypertrophy (enlarged prostate) and take medicines called α-blockers, your doctor may need to start you on the lowest dose of the PDE5-I.

Research is mixed on the effectiveness of acupuncture as an erectile dysfunction cure, but one study published in November 2013 in the Journal of Alternative and Complementary Medicine found that acupuncture can be beneficial for men experiencing erectile dysfunction as a side effect of antidepressants, including selective serotonin reuptake inhibitors (SSRIs) and serotonin noradrenaline reuptake inhibitors (SNRIs).
Crossref | PubMed | Google ScholarSee all References These hormonal findings were supported by a study of 1132 men aged 30 to 79 years that found an inverse relationship between blood pressure and serum testosterone levels.32x32Khaw, KT and Barrett-Connor, E. Blood pressure and endogenous testosterone in men: an inverse relationship. J Hypertens. 1988; 6: 329–332
Conversely, and of significant clinical importance, is how often patients with ED as their first and sole clinical manifestation suffer from subclinical CAD.17 Previous studies reported a rate of inducible ischaemia by exercise stress testing (EST) in 22% (with a wide range of 5–56%) of ED patients reflecting differences in patient population, risk factors and criteria used for ED and CAD diagnosis. Interestingly, those patients further assessed with coronary angiography had obstructive atherosclerosis in >90% of cases.4,18 In a prospective angiographic study, we documented that 19% of ED patients suffer from clinically silent obstructive CAD.18
Crossref | PubMed | Scopus (171) | Google ScholarSee all References Incidence increased notably with age in this patient cohort: only 1.1% of diabetic men aged 21 to 30 years had ED compared with 47.1% of all diabetic patients older than 43 years. Diabetic patients often have other cardiovascular risk factors that may play a role in the development of ED. However, in an analysis of the PBI in 441 patients with ED and various cardiovascular risk factors (diabetes mellitus, hypertension, hyperlipidemia, tobacco use), diabetes was the only risk factor that was significantly and independently associated with a decrease in the PBI.7x7Virag, R, Bouilly, P, and Frydman, D. Is impotence an arterial disorder? a study of arterial risk factors in 440 impotent men. Lancet. 1985; 1: 181–184
Logically, ED secondary to testosterone deficiency should be treated by testosterone replacement. Testosterone levels in men decrease with age.4 Both epidemiological and observational studies have demonstrated that reduced testosterone is associated with increased cardiovascular risk. One meta-analysis showed lower testosterone and higher 17β oestradiol as significant risk predictors despite adjustment for age and body mass index.4 Patients with coronary artery disease (CAD) have been found to have lower testosterone levels than controls, and there is inverse correlation between testosterone and the incidence of major cardiovascular disease (CVD).4 A significant negative correlation has been reported between total testosterone levels and Framingham risk score.4 However, it has been pointed out that ‘It is unclear if this is a causal association or due to low testosterone being a biomarker of poor health’.4 Testosterone replacement as a treatment for …
Abstract | Full Text | Full Text PDF | PubMed | Scopus (46) | Google ScholarSee all References The significant sympathetic discharge associated with sexual intercourse may contribute to the development of arrythmias in susceptible patients.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
Sexual problems might mean you have a broken heart, literally. The most common sexual problem in men is erectile dysfunction (ED). ED affects up to 30 million men in the United States. Surprisingly, ED might be a sign of heart problems. It is important to discuss sexual health with your doctor. Not only can your doctor prescribe medications to improve sexual function, but together you may be able to prevent a major heart problem like a heart attack. This article outlines the steps that you should take if you think you have ED.
Since erectile dysfunction presents such an intimate relationship with CV parameters, it is easily deducted that it could constitute a powerful tool for detecting asymptomatic CV disease. Consequently, recognition of sexual dysfunction in a hypertensive individual should prompt further diagnostic procedures and therapeutic interventions in order to disclose its silent cardiovascular risk and improve patient’s quality of life and life expectancy.
Relative risk and 95% confidence interval for erectile dysfunction and clinical events. Relative risk and 95% confidence interval for erectile dysfunction and total cardiovascular events (A), cardiovascular mortality (B), myocardial infarction (C), cerebrovascular events (D), and all-cause mortality (E). Studies are listed alphabetically. Boxes represent the relative risk and lines represent the 95% confidence interval for individual studies. The diamonds and their width represent the pooled relative risks and the 95% confidence interval, respectively. CVD, cardiovascular disease; DM, diabetes mellitus; HF, heart failure; GEN, general population. Numbers in brackets are the number of references in the text—and references with S are from Supplementary material online. With permission from Vlachopoulos et al.5
The third Princeton Consensus (Expert Panel) Conference recommends assessing cardiovascular risk in all patients with ED and CVD. This refers to estimating the risk of mortality and morbidity associated with sexual activity. The current recommendations classify patients into low-, intermediate- and high-risk, based on their New York Heart Association class.57 The consensus also recommended that all patients with ED and CVD should undergo lifestyle changes, such as exercise, smoking cessation, healthy diet and weight reduction. These measures are likely to reduce cardiovascular risk and improve erectile function.58
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
Yohimbine is an indole alkaloid derived from the bark of the African yohimbe tree (33). Yohimbine has been noted to treat fatigue, depression, diabetes, and sexual dysfunction. A meta-analysis of seven placebo-controlled trials (34) deemed yohimbine superior to placebo for the treatment of ED with rare adverse events. The proposed mechanism of action (35) is via the inhibition of central alpha-2-adrenergic receptors, decreasing central inhibition of arousal, and increasing penile nerve stimulation resulting in increased NO. Common side effects include headache, sweating, agitation, hypertension and insomnia. Contraindications include patients on tricyclic antidepressants, anti-hypertensives and central nervous system stimulants.
The use of penile support device such as penile cast worn externally during intercourse has been tried to provide length and rigidity to the penile shaft (24). Each device can be customised to the patient’s penile size and provided an option for patients who are seeking non-pharmaceutical/non-invasive treatment, or have end-organ failure who may not be candidates for, or unable to afford, penile prosthesis implant.
You put your penis in the cylinder and start pumping. The suction creates a vacuum, so blood rushes in to fill the spaces in the spongy tissue of the penis, creating an erection. The erection lasts only as long as the blood stays in, so you slide the band down around the base of your penis, trapping the blood. It's safe to keep the band on for up to 30 minutes.

Excess LDL cholesterol in your blood gets deposited in arteries, the blood vessels that feed the heart and brain. These deposits can join with other substances to form plaque, a thick, hard deposit in the blood vessel that leads to atherosclerosis. Plaque can narrow the passageway inside the artery and pinch off the flow of blood to the heart muscle, and to the penis.
There are so many potential reasons a man might develop erectile dysfunction (ED), it's nearly impossible to generalize the best ways to treat it. What works for one man may not work for another simply because they are having problems for different reasons. That said, it may encouraging to hear that there are a variety of options that may be considered, from psychological counseling to lifestyle changes, medications to treatments and devices.

The third Princeton Consensus (Expert Panel) Conference recommends assessing cardiovascular risk in all patients with ED and CVD. This refers to estimating the risk of mortality and morbidity associated with sexual activity. The current recommendations classify patients into low-, intermediate- and high-risk, based on their New York Heart Association class.57 The consensus also recommended that all patients with ED and CVD should undergo lifestyle changes, such as exercise, smoking cessation, healthy diet and weight reduction. These measures are likely to reduce cardiovascular risk and improve erectile function.58

PubMed | Google ScholarSee all References In comparison, a study of 132 patients evaluated by penile duplex ultrasonography after intracorporeal papaverine injection found that hypertension alone was not an independent risk factor for vasculogenic ED.34x34Shabsigh, R, Fishman, IJ, Schum, C, and Dunn, JK. Cigarette smoking and other vascular risk factors in vasculogenic impotence. Urology. 1991; 38: 227–231
In most men, ED is recognised as sharing vascular aetiology with IHD.17 ED and IHD share common risk factors, such as hypertension, hyperlipidaemia, diabetes, obesity, lack of physical exercise, cigarette smoking, poor diet, excess alcohol consumption and psychological stress, including depression.30 Endothelial dysfunction has been implicated as a common mechanism between CAD and ED and it has an important role in the development of atherosclerosis.31
Physical and sexual activity can trigger acute cardiac events. In a recent meta-analysis, a significant association between acute cardiac events and episodic physical (relative risk 3.45 for myocardial infarction and 4.98 for sudden cardiac death) and sexual activity (relative risk 2.7 for myocardial infarction) was demonstrated.32 This association was attenuated among individuals with high levels of habitual physical activity (for every additional time per week the relative risk for myocardial infarction decreased by ∼45%, and the relative risk for sudden cardiac death decreased by 30%). The physical demands of sexual activity have been identified as follows. Studies conducted primarily in young married men showed that sexual activity with a person's usual partner is comparable with mild-to-moderate physical activity in the range of 3–4 metabolic equivalents of the task (METS).30,33 The heart rate rarely exceeds 130 b.p.m. and systolic blood pressure rarely exceeds 170 mmHg in normotensive individuals. Accordingly, demands during sexual activity correspond to walking 1.5 km (or 1 mile) on the flat in 20 min or briskly climbing two flights of stairs in 10 s. Generalization, however, may not characterize all individuals (especially those who are older, are less physically fit, or have CVD) or sexual activity circumstances (e.g. extramarital, unfamiliar setting, excessive food and alcohol consumption). Therefore, completing 4 min of the standard Bruce treadmill protocol (5–6 METS) without symptoms, ST segment changes, arrhythmias, or a fall in systolic BP identifies the safety of sexual activity.30,33

Actually the first simple step to managing your blood pressure is to start tracking it! Get an inexpensive blood pressure cuff at CVS or on Amazon. Download the free Hello Heart app (iOS, Android) from the iTunes Store and Google Play.  Start recording your daily blood pressure. Just the simple act of daily recording can have a very beneficial effect.


Erectile dysfunction (ED) is a common sexual problem affecting many men irrespective of cultures, beliefs and nationalities. While medical therapy for ED has been revolutionized by the advent of oral phosphodiesterase type 5 inhibitors and intracavernosal injection of vasoactive agents, recent technological advances such stem cell therapy, low intensity shock wave and newer generation of penile prosthesis implant offer hope to men who do not respond to conventional medical therapy. In contrast, traditional and complementary medicine (TCM) focuses on the restoration and better overall bodily regulation with the use of various herbal and animal products as well as exercises to invigorate qi (energy) in vital organs. Western medicine involves an analysis of ED symptom and underlying causes that contribute to ED, while TCM emphases the concept of holism and harmonization of body organs to achieve natural sexual life. The following article reviews our current understanding regarding the philosophical approach, and evaluates the evidence surrounding various ED therapies between mainstream Western Medicine and TCM.
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.
In the vessels that supply the heart, healthy arteries enlarge in diameter up to 50% during exercise when sufficient nitric oxide is present. Because of its brief half-life, a continual supply of nitric oxide is required for optimal effect. If the supply of nitric oxide is inadequate, endothelial dysfunction—a core factor in heart disease—is made worse. Endothelial dysfunction can trigger the growth of coronary plaque.8
Abstract | Full Text | Full Text PDF | PubMed | Scopus (30) | Google ScholarSee all References Increased cGMP levels cause intracellular calcium levels to decrease, resulting in relaxation of the corporeal smooth muscle, active dilatation of the penile arteries, arterioles, and sinusoids, and finally, increased arterial inflow and passive compression of penile venous outflow.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Until recently, erectile dysfunction (ED) was one of the most neglected complications of diabetes. In the past, physicians and patients were led to believe that declining sexual function was an inevitable consequence of advancing age or was brought on by emotional problems. This misconception, combined with men’s natural reluctance to discuss their sexual problems and physicians’ inexperience and unease with sexual issues, resulted in failure to directly address this problem with the majority of patients experiencing it.
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.
Since erectile dysfunction presents such an intimate relationship with CV parameters, it is easily deducted that it could constitute a powerful tool for detecting asymptomatic CV disease. Consequently, recognition of sexual dysfunction in a hypertensive individual should prompt further diagnostic procedures and therapeutic interventions in order to disclose its silent cardiovascular risk and improve patient’s quality of life and life expectancy.
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.
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.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Phosphodiesterase type 5 is found predominantly in the smooth muscle of the corpora cavernosa but can be found in smaller quantities in platelets and other vascular smooth muscle.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
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.
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.
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

The Massachusetts Male Aging Study of 1,290 men, aged 40–70 years, has documented the extraordinarily high prevalence of erectile dysfunction among aging men: 50% of men at 50 years of age, and 70% by age 70 have erectile dysfunction.2 Furthermore, a recent Italian study of men with severe heart disease has uncovered an astounding 93% with erectile dysfunction 24 months before their heart attack or onset of heart disease symptoms.3


There are other treatment options for erectile dysfunction (ED). Alprostadil is a medication that improves blood flow to the penis and improves erections. It can be given either by injection (Caverject and other brands) at the base of the penis or by putting an alprostadil gel (brand name MUSE) directly into the urethra, using a thin tube and a little lubricant so it slides in easily. The medicine is absorbed from the lining of the urethra into the surrounding tissues. The shot is less appealing to most people, of course, but more effective.
Control your blood sugar through your diet. Eating a diabetes-friendly diet will help you better control your blood sugar levels and lessen the amount of damage to your blood vessels and nerves. A proper diet geared at keeping your blood sugar levels in check can also improve your energy levels and mood, both of which can help reduce the risk of erectile dysfunction. You may consider working with a dietitian who is also a certified diabetes educator to help adjust your eating style.
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