• Medications: About 25 percent of ED cases are caused by drugs. Many medications, including common medicines prescribed for diabetes and its complications, can cause ED. The most common offenders are blood pressure drugs, antihistamines, antidepressants, tranquilizers, appetite suppressants, and cimetidine (an ulcer drug). In addition, over-the-counter medications, including certain eye drops and nose drops, have been associated with ED. That does not mean you should stop taking these medications! Rather, you should discuss them with your doctor to determine whether a different dosage, an alternate medicine, or additional treatments will resolve the ED.
Abstract | PubMed | Scopus (136) | Google ScholarSee all References In a prospective review of 3250 men aged 26 to 83 years without ED at their first examination, total cholesterol and high-density lipoprotein (HDL) cholesterol levels were found to be strongly predictive of onset of ED after controlling for age, diabetes mellitus, stress level, cardiovascular disease, and prostate disease.25x25Wei, M, Macera, CA, Davis, DR, Hornung, CA, Nankin, HR, and Blair, SN. Total cholesterol and high density lipoprotein cholesterol as important predictors of erectile dysfunction. Am J Epidemiol. 1994; 140: 930–937
Erectile dysfunction is the persistent inability to maintain an erection that is not firm enough or lasts long enough to have sexual intercourse. This is a common problem and at least 40 % of men suffer from erectile dysfunction at least occasionally. Manipal Fertility has been instrumental in bringing Men’s Health as an independent area of focus not only for fertility but also erectile dysfunction. We are the pioneers in introducing Non Invasive Shockwave therapy for Erectile Dysfunction.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Erectile dysfunction secondary to cardiovascular disease often responds well to the standard ED treatments developed over the past few decades. Penile prosthesis implantation was developed in the 1970s, followed by intracavernosal injections of vasoactive agents, including papaverine, phentolamine, and prostaglandin E1, introduced in the 1980s.11x11Nehra, A. Intracavernosal therapy: when oral agents fail. Curr Urol Rep. 2001; 2: 468–472
Penile prosthesis implant remains the most effective and permanent treatment for ED. Penile prosthesis implants can be broadly divided into malleable and inflatable prostheses (20). Malleable penile prosthesis, also known as semi-rigid prosthesis, does not allow for (physiological) flaccid state of the penis. The patient can bend the prosthesis upwards for sexual intercourse and downwards for concealment. Although the angle of prosthesis concealment has improved with recent devices, however due to the constant rigid state of the penis, they are still less comfortable compared to their inflatable counterparts, are more likely to cause social embarrassment and associated with higher risk of implant erosions (21). However, malleable prosthesis still has its place for the treatment of ED as these implants are easier to handle, easier to place and would benefit patients with impaired manual dexterity.
Crossref | PubMed | Scopus (23) | Google ScholarSee all References Similar to sildenafil, vardenafil produces a slight hypotensive effect with an average maximal decrease in blood pressure level of 5 to 10 mm Hg.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446
Although the results provide evidence that PDE5 inhibitors may benefit heart health, the retrospective study design makes it impossible to ascertain direct cause and effect, Andersson noted. It is possible that using erectile dysfunction drugs simply indicates a more active sex life, which could itself contribute to, or be a marker of, a heart-healthy lifestyle overall.
In subsequent clinical studies, a surprisingly high percentage of EDDM patients–10% to 20%–claimed that the placebo "improved my erections," thus indicating a psychological basis for their ED. In the latter half of the 1980s, objective means were developed that could help determine if a EDDM patient had organic or psychogenic ED. The absence of rigid sleep erections confirmed by penile monitors was one criterion for organic ED. The failure of vasoactive agents (papaverine, Trimix, or prostaglandin E-1 [PGE-1]) injected into the corpora cavernosa to induce penile rigidity was another criterion for organic disease. Intracavernosal maintenance flow rates during pharmacocavernosometry and maximum cavernosal arterial flow during penile Doppler ultrasonography were additional determinants.
Several other facts support the close relationship between sexual dysfunction and CV disease. Endothelial dysfunction mediated by decreased nitric-oxide bioavailability as well as atherosclerotic lesions constitute a common pathophysiologic substrate affecting both CV disease and erectile dysfunction, a disease considered to be primarily of vascular origin[76,80-82]. Several traditional CV risk factors (diabetes mellitus, hypertension, dyslipidemia, and smoking) are frequently found in individuals with erectile dysfunction, conferring a detrimental cardiovascular burden to them. More interestingly, the increased cardiovascular risk observed in those patients is independent of the aforementioned CV risk factors[81-88].
Counselling or sex therapy (58% of people find this works for them) –mind-related causes of erectile dysfunction can affect anyone. They are more likely if you experience erectile dysfunction at a younger age. Talking to a counsellor or therapist can help some people overcome erectile dysfunction related to these problems, possibly for good. They can also help you if your erectile dysfunction is causing you stress, as this can make matters worse.
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. 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).
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.
Your choice of blood pressure medications could make a difference in the bedroom (or wherever you like to have sex). Thiazides (diuretics or “water pills”) and beta blockers are the most likely to cause erectile dysfunction (ED), while alpha blockers the least likely. Alpha blockers work by reducing nerve impulses to blood vessels, allowing blood to pass more easily. Ask your doctor whether these or other blood pressure medications are best for you.
Sildenafil should be taken 1–2 h before intercourse. It is important to tell patients that the drug’s effectiveness requires sexual stimulation. One patient in our clinic recently complained that he had no effect from taking sildenafil. It was later discovered that he took the pill and then sat on his couch and read a book about how to grow tomatoes!
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
Diuretics: Also called water pills, this medication is a common treatment for reducing blood pressure. They work by getting rid of unnecessary water and salt in the urine. This essentially helps lower blood pressure and can make it easier for the heart to pump blood. Unfortunately, diuretics can reduce the blood flow to the penis, making erections difficult to achieve. Zinc levels have been known to diminish due to diuretic use, which may lead to a decreased production of overall testosterone.
There are a number of herbs and supplements for use in men with ED. However, the overall quality of the studies evaluating these treatments has been low. Therefore, evidence for the effectiveness and safety of these therapies is limited. Many of these therapies have known risks, and there’s a possibility that other risks are yet to be discovered. Always use CAM therapies with caution.
The pathophysiological basis for the predictive ability of ED has been discussed above. It should be emphasized, however, that ED should not only be viewed as a manifestation of obstructive CAD that could be identified by ischaemia revealing tests. Owing to the inflammatory and pro-thrombotic activation of the disease,13 it should also be regarded as an early warning sign of an imminent acute event (mainly acute myocardial infarction)22 due to the rupture of a subclinical plaque, and thus identification of the risk should ideally include plaque vulnerability tests. Finally, an issue that has important clinical implications is by how long the clinical manifestation of ED precedes the clinical manifestation of CAD. According to studies, men with ED and no cardiac symptoms have an increased incidence of experiencing a cardiac event, both acute and chronic, in the ensuing 2–5 years, thus providing a ‘window of opportunity’ for risk reduction management in these patients.2
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 blood pressure medications that do not cause erectile dysfunction (ED). Some older blood pressure medications, especially beta blockers and thiazide diuretics, are the most likely to cause ED as a side effect. Better options include calcium channel blockers, which lower high blood pressure through a different mechanism. Don't just go off your medications, though; high blood pressure itself is a common cause of ED, so lowering your blood pressure is an important part of your ED treatment plan. And if you stop taking your blood pressure medications 'cold turkey', your blood pressure could actually sky rocket, putting you at risk for a heart attack or a stroke. Work with your doctor on ways to lower your blood pressure without lowering your sex drive.
A significant proportion (ranging from ∼60 to 90%) of heart failure patients report ED and marked decrease in sexual interest, with ultimately one-quarter reporting cessation of sexual activity altogether.48 Erectile dysfunction contributes further to the poor quality of life and aggravates depression. Of interest, many heart failure patients place a greater importance on improving the quality of life (including sexual activity) than on improving survival. Sexual function correlates with the symptomatic status (i.e. NYHA functional class and 6-minute walk test).48 In the Evaluation of Role of Sexual Dysfunction in the Saarland (EROSS) Program, left ventricular dysfunction was a risk factor for ED independent of heart failure symptoms. While heart failure and ED share common pre-disposing risk factors, heart failure by itself can cause ED or affect engagement to sexual activity. Neurohumoral activation, medication (thiazides), limited exercise capacity, and depression are responsible.49
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.
In fact, one common reason many younger men visit their doctor is to get erectile dysfunction medication. Often, men with erectile dysfunction suffer with diabetes or heart disease, or may be sedentary or obese, but they don’t realize the impact of these health conditions on sexual function. Along with erectile dysfunction treatment, the doctor may recommend managing the illness, being more physically active, or losing weight.
Penile implants - are generally used if physical damage (like an accident) makes the anatomical parts needed for an erection not work. These are inserted by surgery and can provide a permanent treatment choice if others fail to work. The implants can be semi-rigid or inflatable. They can be pretty expensive and are not usually available on the NHS.
First of all, libido (sexual desire) triggers a sympathetic (adrenaline-dependent) nervous system reaction mediated through the thoracic spinal cord. Also important is tactile stimulation, the pleasurable effect of touch, which is mediated through the acetylcholine-dependent parasympathetic nervous system. Both the sympathetic and parasympathetic forces regulate the release of nitric oxide—the universal artery-relaxing agent—from the cells lining the penile arteries and all its smaller branches. Nitric oxide causes the arteries to enlarge, increasing blood flow into the penile tissues. This is followed by compression of blood-draining penile veins, which causes blood to engorge the penis and create an erection.4
Crossref | PubMed | Scopus (72) | Google ScholarSee all References This study found that the mean PSV was a better predictor of the presence of cardiovascular disease than stratification by standard cardiac risk factors such as diabetes mellitus, hypertension, obesity, and smoking. The researchers recommended that persons with no history of prior perineal trauma and with a PSV lower than 35 mL/s should undergo exercise testing before receiving treatment of ED because these patients had a 42% risk of having ischemic heart disease. However, other investigators questioned the utility of using penile arterial flow to predict the presence of ischemic heart disease.18x18Chiu, AW, Chen, KK, Chen, MT, Chang, LS, and Chang, MS. Penile brachial index in impotent patients with coronary artery disease. Eur Urol. 1991; 19: 213–216
Crossref | PubMed | Scopus (71) | Google ScholarSee all References However, a double-blind, placebo-controlled study of 22 middle-aged men with hypercholesterolemia treated for 6 weeks with pravastatin or lovastatin showed improved erectile function with both medications.54x54Kostis, JB, Rosen, RC, and Wilson, AC. Central nervous system effects of HMG CoA reductase inhibitors: lovastatin and pravastatin on sleep and cognitive performance in patients with hypercholesterolemia. J Clin Pharmacol. 1994; 34: 989–996