This may seem like a lot to manage at a glance, however, just focus on one step at a time. If it is more exercise you want to start with, park your car further away from the front door at work so you have to walk a little more every day. Or go out on a walk to make your phone calls.  If you need to eat better,  try low-fat meat and chicken for lunch. Just keep it simple and don’t try to do it all at once.
PubMed | Google ScholarSee all References Interestingly, this study found no association between erectile function and the number of years or packs per day of cigarette use. In contrast, a study of 314 current smokers with ED found that the number of cigarettes smoked inversely correlated with penile rigidity as measured by nocturnal penile tumescence.27x27Hirshkowitz, M, Karacan, I, Howell, JW, Arcasoy, MO, and Williams, RL. Nocturnal penile tumescence in cigarette smokers with erectile dysfunction. Urology. 1992; 39: 101–107
As ED has become more prevalent among the U.S. population, entrepreneurs have set out to serve this patient population by introducing a variety of non-invasive devices to help correct the condition. There’s the penis pump, which includes a plastic tube that fits over the penis and a hand or battery-powered pump attached to the tube, and a band that circles the base of the penis when it becomes erect.

Yet another common erectile dysfunction treatment that can be used in combination with oral drugs is a vacuum pump. This device consists of a plastic cylinder, a pump, a set of constriction bands, and a water-soluble lubricant. The lubricant is applied to the base of the penis to help form an airtight seal. The cylinder is placed over the flaccid penis and held tight against the pelvis. The pump is used to create a vacuum within the cylinder, drawing blood into the penis. Once the penis is engorged with blood, a constriction band is rolled off the cylinder to near the base of the penis. The constriction band is helpful for men with venous leakage, in which blood flows out of the penis as fast as it flows in. However, it should be left on for no more than 30 minutes at a time.
Impotence, or erectile dysfunction (ED), is the inability for a man to sustain an erection long enough for normal, satisfying sexual intercourse.  To understand the underlying causes of impotence, it helps to know the basics about how an erection develops, along with potential problems that get in the way. Erections begin in the brain with a thought related to sexual desire. Then a chemical message travels from the brain to the penis. Blood flow to the penis increases as blood vessels leading to the reproductive system relax and allow for increased circulation.
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.

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The second way relates to the risk associated with the sexual activity in a patient with either overt or occult CVD. In this case, the diagnosis of ED should prompt an initial cardiovascular assessment based on the history and clinical examination in order to define the baseline risk according to (i) the likelihood of silent CAD18,31 (especially since ED patients have a high probability to have silent CAD) or to the stage of clinically evident CAD, (ii) other cardiovascular conditions either unrelated, or related to ED (e.g. heart failure, peripheral arterial disease).
David F. Penson, MD, MPH, is an associate professor of urology and preventive medicine in the Keck School of Medicine at the University of Southern California, in Los Angeles. Hunter Wessells, MD, is an associate professor of urology at the University of Washington School of Medicine and chief of urology at Harborview Medical Center in Seattle, Wash.
The term “heart disease” is often used interchangeably with the term “cardiovascular disease.” Cardiovascular disease generally refers to conditions that involve narrowed or blocked blood vessels that can lead to a heart attack, chest pain (angina) or stroke. Other heart conditions, such as those that affect your heart’s muscle, valves or rhythm, also are considered forms of heart disease.
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
Hyperlipidemia has been implicated in the development of ED by several different mechanisms. Hyperlipidemia is associated with development of atherosclerotic blood vessel disease, thus contributing to vasculogenic impotence. Penile vascular changes have been noted in impotent patients with elevated serum lipids.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

Crossref | PubMed | Scopus (335) | Google ScholarSee all References Additionally, the presence of nephropathy has been correlated with onset of ED, as has the length of time the patient has had diabetes; most of these patients experience ED within 10 years of being diagnosed as having insulin-dependent or non–insulin-dependent diabetes mellitus.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
Based on this testing, EDDM patients were treated with behavioral therapy, intracavernosal (papaverine, PGE-1, or Trimix) or intraurethral PGE-1, a vacuum constriction device (VCD), or implantation of a penile prosthesis. Novel surgical procedures, ligation of incompetent cavernosal veins or penile revascularization, were seldom efficacious with EDDM and were soon abandoned. Although these nonsurgical therapies were efficacious, they were not widely requested because of their invasive or mechanical nature.
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.
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
Abstract | Full Text | Full Text PDF | PubMed | Scopus (37) | Google ScholarSee all References One MET is equal to a resting state, or 3.5 mL/kg per minute. The relative MET values of sexual activity compared with other forms of activity are shown in Table 3. In general, sexual activity is similar to mild or moderate activity for most patients either with or without coronary artery disease.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
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
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Even if you do not take blood pressure drugs, you should get your blood pressure checked as high BP also can be a sign of ED. In fact, men with ED are about 38% more likely to have high blood pressure than those without ED, according to a study that examined the medical records of more than 1.9 million men. That is not too surprising, since ED often occurs in men who smoke or are overweight—both of which are common risk factors for high blood pressure.
Recent revised labeling for sildenafil states that there is a lack of controlled data for its use in patients with resting hypotension (<90/50 mm Hg) or hypertension (>170/110 mm Hg); a history of myocardial infarction, cerebrovascular accident, or life-threatening arrhythmia within the past 6 months; coronary artery disease or cardiac failure causing unstable angina; or retinitis pigmentosa and possible genetic disorders of retinal PDEs.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
In men without cardiovascular disease, erectile dysfunction (ED) pills are very safe. The three rivals -- Viagra, Cialis, and Levitra -- have similar side effects, including headache, facial flushing, nasal congestion, diarrhea, backache, and, in a few Viagra or Levitra users, temporary impaired color vision (men with retinitis pigmentosa, a rare eye disease, should check with their ophthalmologists before using these medications).
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
Guidelines recommend that phosphodiesterase type 5 (PDE5) inhibitors are the first-line drug for the treatment of ED (Table 1). Sildenafil citrate was the first oral drug approved for ED in the US.59 The newer PDE5 inhibitors include vardenafil, tadalafil and avanafil. The inhibition of PDE5 enhances cyclic guanosine monophosphate (cGMP)-NO-mediated vasodilatation by preventing PDE5 catabolism of cGMP and so delaying detumescence. PDE5 inhibitors increase the number and duration of erections, as well as the percentage of successful sexual intercourse.60
To understand what happens in ED, it's helpful to know some anatomical basics. When aroused by either sensory or mental stimuli, the brain sends a signal through the nerves to the penis, causing the muscles there to relax. This opens up space for blood to flow in and engorge the penis. A membrane within the penis traps blood inside to help maintain the erection, which subsides when the penile muscles contract, forcing blood back into the rest of the body. Any number of things can go wrong in this process, leading to erectile dysfunction.
Medicines known as PDE5 inhibitors can help two-thirds of men with ED. These include Viagra (sildenafil), Cialis (tadalafil) and Levitra (vardenafil). You may need to take several doses over time before they work properly, and you may need to adjust the dose. National guidelines say you can be prescribed these drugs from six months after a heart attack, providing your condition is stable.
Crossref | PubMed | Google ScholarSee all References Patients with vascular risk factors (diabetes mellitus, hypertension, heart disease, and hyperlipidemia) had significantly decreased peak systolic velocities and increased end-diastolic velocities. Patients with diabetes mellitus had increased end-diastolic velocities and decreased resistive indices, indicating a disorder of venous trapping during erections. Another study examined corpora cavernosal tissue removed at penile prosthesis placement in 21 diabetic men and 42 nondiabetic controls.23x23Saenz de Tejada, I, Goldstein, I, Azadzoi, K, Krane, RJ, and Cohen, RA. Impaired neurogenic and endothelium-mediated relaxation of penile smooth muscle from diabetic men with impotence. N Engl J Med. 1989; 320: 1025–1030
Obesity is a strong predictor of ED as it is associated with other risk factors, such as diabetes, hyperlipidaemia and hypertension.4 Obesity increases the risk of ED by 30–90 % and acts as an independent risk factor for CVD. Obese men with ED have greater impairment in endothelial function than non-obese men with ED.5 Moreover, high BMI causes low testosterone levels, which in turn leads to ED, as observed in a prospective trial involving 7,446 participants.50
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.
Third, men with Diabetes need to control their blood sugar levels. When your blood sugar is not under control, your body does not produce enough Nitric Oxide (NO) and vascular tissues don’t respond as effectively to NO. When enough blood flows into the penis, penile veins close off and block the blood from flowing out. This process results in an erection. If your body does not produce enough NO or if your penile tissues do not respond to NO, the pressure of the blood flowing into your penis is not sufficient to trap the blood, you penis will not get hard.
Abstract | Full Text PDF | PubMed | Scopus (49) | Google ScholarSee all References Also, cigar smoking and passive exposure to cigarette smoke have been shown to significantly predict onset of ED.5x5Feldman, HA, Johannes, CB, Derby, CA et al. Erectile dysfunction and coronary risk factors: prospective results from the Massachusetts Male Aging Study. Prev Med. 2000; 30: 328–338

There are few data specifically relating to the effectiveness of vacuum erection devices (VEDs) in diabetic men with ED. In a single-center study of 44 men with diabetes who choose VED for the treatment of ED in the early 1990s, 75% reported that they were able to achieve erections satisfactory for intercourse with the use of the device.51 However, the manner in which patients were accrued to this study probably biased its findings, resulting in substantially higher effectiveness rates than are normally observed in clinical practice. A recent review of the use of VEDs in the general treatment of ED notes that satisfaction rates with this therapy are much lower, varying between 20 and 50%.52
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References Overall, sexual intercourse does not lead to an extremely exaggerated heart rate or blood pressure level when performed in a familiar setting with one's usual partner.82x82Hellerstein, HK and Friedman, EH. Sexual activity and the postcoronary patient. Arch Intern Med. 1970; 125: 987–999
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.
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.
The physical exam should focus on femoral and peripheral pulses, femoral bruits (vascular abnormalities), visual field defects (prolactinoma or pituitary mass), breast exam (hyperprolactinemia), penile strictures (Peyronie’s disease), testicle atrophy (testosterone deficiency), and asymmetry or masses (hypogonadism). A rectal exam allows for assessment of both the prostate and sphincter tone, abnormalities that are associated with autonomic dysfunction. Sacral and perineal neurological exam will help in assessing autonomic function.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References, 56x56Wallis, RM, Corbin, JD, Francis, SH, and Ellis, P. Tissue distribution of phosphodiesterase families and the effects of sildenafil on tissue cyclic nucleotides, platelet function, and the contractile responses of trabeculae carneae and aortic rings in vitro. Am J Cardiol. 1999; 83: 3C–12C
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.
Normal male sexual function requires a complex interaction of vascular, neurological, hormonal, and psychological systems. The initial obligatory event is acquisition and maintenance of an erect penis, which is a vascular phenomenon. Normal erections require blood flow into the corpora cavernosae and corpus spongiosum. As the blood accelerates, the pressure within the intracavernosal space increases dramatically to choke off penile venous outflow. This combination of increased intracavernosal blood flow and reduced venous outflow allows a man to acquire and maintain a firm erection.
The information provided on this site is for informational purposes only and is not intended as a substitute for advice from your physician or other health care professional or any information contained on or in any product label or packaging. You should not use the information on this site for diagnosis or treatment of any health problem or for prescription of any medication or other treatment. You should consult with a healthcare professional before starting any diet, exercise or supplementation program, before taking any medication, or if you have or suspect you might have a health problem. You should not stop taking any medication without first consulting your physician.
Crossref | Google ScholarSee all References Different classes of β-blockers have been postulated to have differential effects on erectile function, with the nonselective β-blockers (eg, propranolol) having more deleterious effects than the more cardioselective medications (eg, atenolol, metoprolol).42x42Weiss, RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician. 1991; 44: 2075–2082
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.

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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
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
In another study, 60 patients underwent stress exercise cardiovascular testing and Doppler ultrasonography for measurement of their cavernosal artery peak systolic velocity (PSV).17x17Kawanishi, Y, Lee, KS, Kimura, K et al. Screening of ischemic heart disease with cavernous artery blood flow in erectile dysfunctional patients. Int J Impot Res. 2001; 13: 100–103

Side effects of sildenafil are similar to those from taking niacin or any vasodilator, namely, headaches, lightheadedness, dizziness, and flushing. Some individuals experience a bluish tinge of their cornea, which makes them feel as if they are wearing light blue–tinted sunglasses. This effect can last for several hours. Syncope and myocardial infarction, the most serious side effects, are seen in men who are also taking nitrates for coronary heart disease. Sildenafil also has adverse effects in people with hypertrophic cardiomyopathy because a decrease in preload and after load in the cardiac output can increase the outflow obstruction, culminating in an unstable hemodynamic state.
In years past, before nitric oxide and its role in the erectile response was appreciated, testosterone was used to treat sexual dysfunction in men. It proved a partial success as a standalone therapy, resulting in improved erectile potency in 40–60% of men with low-to-normal testosterone levels. The likelihood of success increased, however, if starting testosterone levels were low (usually defined as below 300 ng/dL), in which case improved erections were experienced by as many as 65% of men, compared with 16.7% receiving placebo; topical testosterone preparations were also noted to be superior to oral replacement or injections.21 These findings were confirmed by another study that showed testosterone produced modest improvements in erectile function and libido in men with low-to-normal testosterone levels.22
Another common reason for failures of oral therapy is the absence of sexual or genital stimulation prior to attempting sexual intercourse. These medicines facilitate an erection by increasing blood flow to the penis, but they do not act as an aphrodisiac or as an initiator of the erection. A man who is not “in the mood” or does not have adequate physical stimulation will not respond with an erection.
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