Table 1 offers elements for distinction between organic and psychogenic disease.7 Of note is that in cases of organic origin, a psychogenic component may co-exist. The most common organic aetiology of ED is vasculogenic (see below ‘ED and CAD: common pathophysiology’).2,3 Co-existence of vascular disease, advancing age, and the presence of CVD risk factors and metabolic disorders increase the likelihood that ED is of vasculogenic aetiology.
A recent systematic review and meta-analysis of relevant studies in this field confirmed that erectile dysfunction is associated with increased risk of CV events and all-cause mortality[89]. The pooled relative risks were 1.44 (95%CI: 1.27-1.63) for total CV events, 1.19 (95%CI: 0.97-1.46) for CV mortality, 1.62 (95%CI: 1.34-1.96) for myocardial infarction, 1.39 (95%CI: 1.23-1.57) for cerebrovascular events, and 1.25 (95%CI: 1.12-1.39) for all-cause mortality, for men with vs without erectile dysfunction. Of note, the relative risk was higher in intermediate-compared with high- or low-CV-risk populations and with younger age, with obvious clinical implications. Interestingly, the relative risks were higher when erectile dysfunction was diagnosed with the use of a questionnaire compared with a single question (RR = 1.61; 95%CI: 1.38-1.86 vs RR = 1.27; 95%CI: 1.18-1.37, respectively; P = 0.006).
De Berardis et al.6 assessed general HRQOL in 1,460 men with type 2 diabetes in Italy. Within the cohort, 615 men reported that they never experienced ED, 346 stated that they occasionally had ED, and 449 stated that they frequently had ED. They then compared general HRQOL among these three groups. In the univariate analysis, they found that degree of ED negatively correlated with general HRQOL scores in all eight domains of the Short Form 36 (SF-36) health survey questionnaire. In the multivariate analysis, ED was not independently associated with physical function, bodily pain, or role limitations due to physical problem scores but was independently associated with general HRQOL outcomes in the domains of general health (P = 0.004), role limitations due to emotional problems (P = 0.001), vitality (P = 0.001), social functioning (P = 0.01), and overall mental health (P = 0.002). Another study examining the effect of ED on quality of life in hemodialysis patients, more than half of whom had diabetes, also noted an independent, negative effect of ED on the emotional domains of general HRQOL.39
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.
Heart disease and erectile dysfunction can be related. In fact, ED and heart disease are considered two signs of the same disease process. The smaller arteries in the penis are affected by atherosclerosis sooner, perhaps three or more years before they cause heart disease symptoms.11 A large international study found that men with ED were more likely to die from heart causes; have a heart attack, stroke or be admitted to the hospital with heart failure than men with no or mild ED.12
Crossref | Google ScholarSee all References A 1985 study found that ED accounted for 400,000 outpatient visits and 30,000 hospital admissions per year in the United States, with a direct total cost of $146 million.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

The study, which retrospectively tracked more than 43,000 men for an average of 3.3 years, found that men prescribed phosphodiesterase-5 (PDE5) inhibitors—the type of erectile dysfunction drug sold under the names Viagra, Levitra, Cialis and others—after their first heart attack were 38 percent less likely to die from any cause. No survival benefit was seen among men taking alprostadil, another type of erectile dysfunction drug that works through a different mechanism.


Crossref | PubMed | Scopus (174) | Google ScholarSee all References All these men had ED and twice underwent symptom-limited supine bicycle exercise echocardiography 1 hour after taking either sildenafil (50 mg or 100 mg) or placebo. This study found no significant changes in resting heart rate, diastolic blood pressure level, or wall motion score index, and the exercise capacity of the 2 groups was similar. Both groups had similar numbers of patients who experienced dyspnea and/or chest pain, had a positive exercise echocardiographic test, and had exercise-induced wall motion abnormalities. Sildenafil caused a mean decrease of 7 mm Hg in the resting systolic blood pressure level compared with the placebo group. In conclusion, this study showed that in patients with stable coronary artery disease, sildenafil caused no change in symptoms, exercise endurance, or presence/extent of exercise-induced ischemia as measured by exercise echocardiography.

Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References The use of any NO-donor medications should be avoided for 24 hours after the last dose of sildenafil and even longer if there is a suspected prolonged half-life secondary to such conditions as renal insufficiency.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Causes of ED may be of primary developmental origin or secondary. Lack of sex hormone in the early developmental stage of male children is the major cause of primary ED. The secondary cause of ED involves arteriosclerosis, diabetes or psychogenic disturbances. Other secondary factors may include hypertension, hyperlipidaemia, obesity and tobacco use. The primary causes of ED are beyond the scope of this review; we will not be discussing the neurovascular mechanisms pertaining to ED and will focus on the relationship between IHD and ED.

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.
Most studies into the effect of beta-blockers on ED point to negative effects of first- and second-generation beta-blockers, while beta-blockers with vasodilating effects can improve erectile function. Alpha-blockers, calcium channel blockers, and angiotensin-converting enzyme inhibitors seem to have a neutral effect on erectile function. Multiple previous studies have demonstrated a beneficial effect of angiotensin receptor blockers on erectile function and they should probably be the favoured antihypertensive agents in patients with ED.29

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.

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
Abstract | Full Text | Full Text PDF | PubMed | Scopus (53) | Google ScholarSee all References Erectile dysfunction is a common physiological disorder. According to estimates from the National Institutes of Health, ED affects 10 million to 20 million men in the United States; another 10 million men are affected by partial ED, defined as present but diminished erectile function.2x2NIH Consensus Development Panel on Impotence. NIH Consensus Conference: impotence. JAMA. 1993; 270: 83–90

Phosphodiesterase Inhibitors. The cornerstone of first-line therapy is the PDE-5 inhibitor. No other class of oral agents approaches the efficacy of PDE-5 inhibitors. Yohimbine, trazodone, phentolamine, L-arginine, and OTC herbal remedies have been used with very limited success. The superiority of yohimbine over placebo in the treatment of organic ED is a matter of dispute.9 A recent trazodone study failed to detect any difference between trazodone and placebo on sexual function.10 Oral phentolamine, although available in Mexico, has not been approved by the US FDA for the treatment of ED. Apomorphine, a central dopaminergic receptor drug, has recently been voluntarily withdrawn from FDA consideration for the treatment of ED. The efficacy of ginkgo biloba and Korean red ginseng has yet to be demonstrated by randomized, placebo-controlled trials.
Furthermore, if feelings of sadness, bloating, or weight gain are prominent, it may be beneficial to measure a form of estrogen called estradiol. This form of estrogen can be elevated in men, particularly in those who are overweight, and may trigger these abnormal responses, increasing the risk of heart disease. Estradiol levels above 30 pg/mL are generally considered abnormal. Weight loss can help correct elevated estradiol, as can prescription “aromatase inhibitors,” such as Arimidex®. In addition, a nutritional supplement called chrysin has been shown in the laboratory to inhibit the aromatase enzyme that is responsible for converting testosterone to estradiol.24 You should consult your doctor to determine if this supplement may be helpful for you.
Arginine. The amino acid L-arginine, which occurs naturally in food, boosts the body's production of nitric oxide, a compound that facilitates erections by dilating blood vessels in the penis. Studies examining L-arginine's effectiveness against impotence have yielded mixed results. A 1999 trial published in the online journal BJU International found that high doses of L-arginine can help improve sexual function, but only in men with abnormal nitric oxide metabolism, such as that associated with cardiovascular disease. In another study, published in 2003 in the Journal of Sex & Marital Therapy, Bulgarian scientists reported that ED sufferers who took L-arginine along with the pine extract pycnogenol saw major improvements in sexual function with no side effects. Arginine can be helpful, says Geo Espinosa, ND, director of the Integrative Urological Center at NYU Langone Medical Center. Espinosa says that men with known cardiovascular problems should take it only with a doctor's supervision; L-arginine can interact with some medications.
Cardiovascular tolerance for sex is based on “functional reserve,” which corresponds to how closely the cardiovascular response to sex (in terms of heart rate, blood pressure level, and oxygen consumption) approaches the patient's peak response to exercise.85x85DeBusk, RF. Evaluating the cardiovascular tolerance for sex. Am J Cardiol. 2000; 86: 51F–56F
Causes of ED may be of primary developmental origin or secondary. Lack of sex hormone in the early developmental stage of male children is the major cause of primary ED. The secondary cause of ED involves arteriosclerosis, diabetes or psychogenic disturbances. Other secondary factors may include hypertension, hyperlipidaemia, obesity and tobacco use. The primary causes of ED are beyond the scope of this review; we will not be discussing the neurovascular mechanisms pertaining to ED and will focus on the relationship between IHD and ED.
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
Erectile dysfunction is very common as men age. Erectile dysfunction is frequently a sign of atherosclerosis, a clogging or narrowing of the blood vessels that causes heart attacks. Erectile dysfunction usually comes 3 to 5 years before a heart attack, so after ED is diagnosed, there is time to treat atherosclerosis and prevent a heart attack. Treating atherosclerosis involves diet, exercise, and medications, if necessary. Talk with your doctor about a broken sex life, and you might be able to prevent a broken heart.
Despite its limitations in detecting CVD without significant stenosis, EST (with or without imaging) can further define the cardiovascular risk in patients with ED and no overt CAD and may be particularly helpful for identifying silent CAD in patients with diabetes. Chemical stress tests are appropriate for patients who cannot complete an EST or in whom ECG is non-interpretable. In patients with established CVD, an interpretable EST is mandatory in the indeterminate risk category and is at the discretion of the cardiologist in the low risk category (Table 3B), since it determines exercise ability and estimates cardiovascular risk associated with sexual activity.
Crossref | PubMed | Scopus (53) | Google ScholarSee all References This study found that, although hypertensive patients had more coronary artery disease, no direct evidence supported an association between hypertension and arteriogenic impotence, as measured by the PBI, peak systolic velocity, and resistive index, in patients with mild to moderate hypertension.
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
In Western medicine approach, health and disease are clearly divided entities. The emphasis is on protection of the individual body from disease or how to replace the body’s lost functions. Antibiotic therapy is used to combat harmful bacteria during infections, exogenous synthetic hormones are used to replace hormone-deficient individuals and artificial prostheses are applied when an organ loses its functions. This is very different from the holistic Eastern approach where the treatment entity is taken as a whole, and the objective is to seek harmony between different bodily systems.
Like the case of untreated hypertensive patients, evaluation of sexual dysfunction in hypertensive patients under antihypertensive regime, should primarily exclude other concomitant diseases and pharmaceutical agents. Consecutively, a competent physician with advanced communicational skills should try to “discover” medically induced erectile dysfunction since a vast majority of patients being under complex antihypertensive regimes usually attribute the undesirable effect to normal aging thus not relating it to their current medication. Moreover, even physicians seldom report the cases of sexual dysfunction associated with certain medications. When medically induced sexual dysfunction is finally disclosed and a shift in medication is deemed necessary, b-blockers along with diuretics should generally be the first categories to be changed, unless they are deemed absolutely indicated for the individual patient. Ideally, an ARB could constitute the mainstay of therapy in these cases. If sexual dysfunction still persists, then more effective remedies should be elected paving the way for the introduction of phosphodiesterase-5 inhibitors (PDE-5).
In particular, patients are classified into three categories (low, intermediate, high) depending on their CV risk profile. Individuals with controlled hypertension belong to the low-risk group where sexual dysfunction can be safely managed with the approved medical therapies regardless of the number or class (with the exception of b-blockers and diuretics) of agents of the patient’s antihypertensive regime. Moreover, patients of this group can safely initiate or reinstitute sexual activity without any need for additional cardiovascular evaluation.
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

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.
Diabetes is known to sabotage two body parts that provide essential components of an erection: nerves and blood vessels. Studies suggest that diabetic nerve damage (neuropathy) is the most important risk factor for ED in people with diabetes. If pelvic nerves that trigger penis muscles to relax are impaired, there may be a break in the chain between brain and penis, disrupting erection. Some researchers suspect that an inadequate supply of oxygen to the nerves causes this damage.
Before taking any medication for erectile dysfunction, including over-the-counter supplements and herbal remedies, get your doctor's OK. Medications for erectile dysfunction do not work in all men and might be less effective in certain conditions, such as after prostate surgery or if you have diabetes. Some medications might also be dangerous if you:
Severe testosterone deficiency, known as “hypogonadism,” is present in approximately 2–35% of men with erectile dysfunction.19 However, lesser degrees of deficiency are common, perhaps present in the majority, depending on the definition of “low” applied, the method of measurement, and the parameter being used to define testosterone (total, free, or bioavailable) deficiency.19,20 Most authorities agree that a total testosterone level below 300 ng/dL is clearly low, and that 300–400 ng/dL is low to low-to-normal. Most studies using testosterone replacement for erectile dysfunction have attempted to achieve blood levels of 450–850 ng/dL.
Crossref | PubMed | Scopus (23) | Google ScholarSee all References, 73x73Rajagopalan, P, Mazzu, A, Xia, C, Dawkins, R, and Sundaresan, P. Effect of high-fat breakfast and moderate-fat evening meal on the pharmacokinetics of vardenafil, an oral phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction. J Clin Pharmacol. 2003; 43: 260–267
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.
Causes of ED may be of primary developmental origin or secondary. Lack of sex hormone in the early developmental stage of male children is the major cause of primary ED. The secondary cause of ED involves arteriosclerosis, diabetes or psychogenic disturbances. Other secondary factors may include hypertension, hyperlipidaemia, obesity and tobacco use. The primary causes of ED are beyond the scope of this review; we will not be discussing the neurovascular mechanisms pertaining to ED and will focus on the relationship between IHD and ED.
Some commonly prescribed cardiovascular drugs (beta-blockers, diuretics, angiotensin-converting enzyme inhibitors, etc.) contribute to ED.18 Previous studies have shown a strong association between ED and diuretics in patients treated with hydrochlorothiazide or chlorthalidone.19,20 It has also been shown that patients treated with first-generation non-selective beta-blockers, such as propranolol, had more frequent ED than those treated with a placebo.21
airdone/ShutterstockErectile dysfunction (ED) is a serious issue for men, which helps explain all the prescription drugs, over-the-counter treatments, and herbal concoctions that claim to cure ED. (In fact, it’s one of the top nine health risks men need to watch out for.) But before any guy decides to take matters into his own hands, he should talk to his doctor about a heart checkup: A new study published in the journal Vascular Medicine suggests ED can signal cardiovascular concerns.
Chlamydia and erectile dysfunction: What's the link? Some people who have chlamydia also experience erectile dysfunction (ED), which involves problems getting or maintaining an erection. Chlamydia can infect the prostate gland, leading to prostatitis, pain, and ED. In this article, learn more about the link between this common infection and ED, and treatments for both. Read now
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