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.
DHEA is a hormone made by the human body. It’s a building block for testosterone. According to a study published in Urology, this supplement may be able to help men whose ED is related to having low testosterone. However, there’s no definitive evidence of this benefit. It’s clear that DHEA can cause various side effects, including liver damage and acne. Long-term use of DHEA can also cause hormonal imbalances.
No matter what erectile dysfunction treatment or treatments (whether herbal remedies or not) a man ultimately decides upon, experts say it's important to eat healthily and to avoid smoking and heavy drinking. Moreover, adequate exercise, stress reduction, and sleep can improve erectile dysfunction in many. In addition, says Lamm, "A loving, receptive, and responsive partner is a home run. After all, this is still a couple's issue."
The EDDM patient has a variety of firstline options. The risk factors for vascular disease are the risk factors for ED. First-line therapy begins with attempts to minimize or eliminate these factors. These include smoking cessation, regular exercise, tighter glycemic control by attention to dietary restrictions, addition of statin drugs to correct dyslipidemia, and moderation of alcohol ingestion. Although there is very limited evidence that these modifications will dramatically reverse ED, they certainly will sponsor improved general health.4
While a widely held perception is that CVD drugs cause ED, data attest towards the contrary and some agents may be even beneficial.41 Only thiazide diuretics lead clearly to ED, while some older beta-blockers also do so, but the side-effect of ED was very low (∼3%) when the patient was blinded for the drug administration.42 In fact, the vasodilating nebivolol may even improve erectile function.35,43 ACE-inhibitors, angiotensin-receptor blockers, and calcium-channel blockers are reported to have neutral or even a positive effect on erectile function35,41,43 but more evidence is needed. Regarding statins, the largest body of evidence point towards a beneficial effect.44 A negative effect has been reported in high statin doses, possibly related to a potential reduction in serum testosterone levels, but this dose dependency warrants further investigation. In terms of patient management, when ED onset and therapy initiation are linked and a cause-and-effect association is presumed, a short period of drug withdrawal with monitoring for ED resolution for verification may be an option. In patients who developed ED long after the initiation of CV drug treatment, sexual dysfunction is less likely to be drug associated and PDE5 inhibition therapy may be initiated.
Diaclina (also known as Panzer’s Darkling Beetle), Korean bug are used as aphrodisiacs in China, Korea and Southeast Asia. These are consumed either whole or as compounds within capsules. It is felt that the aphrodisiac properties come by stimulating the urogenital structures. Flies have been studied for their aphrodisiac effects, including Spanish fly, Chinese cantharide, and Eastern-Indian cantharide (32). The active compound found in the dried and mashed up bodies of these flies is cantharidin, which is a pheromone produced in the accessory glands of the male flies’ genitals. Cantharidin, stimulates the urogenital tract, causing pelvic hyperemia and possibly erections. As cantharidin is toxic and its safety dose not well determined, its use cannot be recommended. Cantharidin is lethal at high doses and exposure can lead to gastrointestinal and urogenital hemorrhage as well as acute renal failure.
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).
Testosterone therapy (TTh) should be reserved for patients who (i) are symptomatic (ED or reduced libido) of testosterone deficiency45 and (ii) they have biochemical evidence of low testosterone (TT <8 nmol/L or 2.3 ng/mL). In men with borderline TT (8–12 nmol/L or 2.3–3.5 ng/mL), a TTh trial (for 3–6 months and continuation if effective) may be envisaged. While adding a PDE5 inhibitor can be considered in men who have not improved with TTh, the usual clinical scenario is to add TTh in patients who have not responded to PDE5 inhibitors. Improvement is dependent on the testosterone levels with better results being obtained at lower levels of TT.45 Despite evidence of benefit in patients with pre-existing cardiovascular conditions (angina or heart failure), it should be emphasized that TTh is not a medication with cardiovascular indications.
Some doctors prefer to start a man on the lowest dose of an oral medicine and increase the dose until an effective one is found. Others prefer to start with the highest dose and go to a lower dose only if a man complains of side effects. In either case, it’s important for a man to communicate with his doctor to let him know how the dose he’s using is working.