Table 3 is a suggested algorithm for the assessment of patients and their further categorization and handling. There are parts of investigation that are common for patients both with and without CVD, while additional elements of investigation are helpful in categorizing the patient without CVD to the appropriate risk category. Determination of exercise ability and stress testing is crucial to the assessment (see also below ‘Exercise ability: the risk of sexual activity’). Patients without established CVD or diabetes should be evaluated for their risk of future events according to risk scores (SCORE or Framingham). Patients with established CVD or diabetes are by default considered at increased risk. Patients with adequate exercise ability or a negative stress test can initiate or resume sexual activity and begin treatment for ED. In patients with a positive stress test or in high-risk patients, sexual activity should be deferred until the cardiac condition has been treated and stabilized. In all cases, patient follow-up and reassessment is recommended.
In another scientific article published in 2015 in the American Journal of Lifestyle Medicine, respondents who were not taking cholesterol-lowering medication experienced an average 42 mg/dl decrease in LDL cholesterol and an average decrease in triglycerides of 79.5 mg/dl about one year after switching to a Nutritarian diet. Furthermore, case histories presented in that publication documented atherosclerosis reversal.7
ED is a common disease affecting men with IHD. Endothelial dysfunction is the link between ED and IHD and both diseases share the same aetiology, risk factors and pathogenesis. Aggressive control of these risk factors – along with lifestyle modification – is recommended to improve symptoms of ED and reduce cardiovascular risk. PDE5 inhibitors remain the first-choice treatment for ED in IHD patients and they have been shown to be safe and effective. However, PDE5 inhibitors can potentiate the hypotensive effect of nitrates so concomitant administration of sildenafil and nitrates is contraindicated. Gene and stem cell therapy are being investigated as a future therapies for ED.
Patients who use this therapy should be trained under the guidance of a urologist, and sterile technique must be used. The drugs must be injected into the shaft of the penis and into one of the penile erectile bodies (corpus cavernosum) 10–15 min before intercourse. Most patients do not complain of pain upon injection. Sexual stimulation is not required, and resulting erections may last for hours. Side effects include penile pain and priapism. The cost is about $12–20 per injection.
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
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
Abstract | Full Text | Full Text PDF | PubMed | Scopus (30) | Google ScholarSee all References Penile sympathetic stimulation flows through several pathways, including the sympathetic chain ganglia, which also supply such structures as the heart and vascular system. Sympathetic tone precipitates release of norepinephrine from penile adrenergic nerves, resulting in tonic contraction of cavernosal smooth muscle and its vasculature, thereby keeping the penis flaccid.9x9Andersson, K and Stief, C. Penile erection and cardiac risk: pathophysiologic and pharmacologic mechanisms. Am J Cardiol. 2000; 86: 23F–26F
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
PubMed | Google ScholarSee all References As with sildenafil, use of nitrate or NO-donor medications is contraindicated while taking tadalafil because of the potential for marked hypotensive interactions.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
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
For patients who failed oral medical therapy or unable to tolerate the side effects, intracavernosal injection of vasoactive agents can often provide effective alternative. Various vasoactive agents such as alprostadil, papaverine or phentolamine have been used either as single agent or combination agents to potentiate the NO release and cavernosal smooth muscle vasodilation. However, intracavernosal injection therapy has high attrition rate and can be associated pain especially with alprostadil injection (2). The practice of isolating compounds and understanding its pharmacological attributes before using it as a drug therapy has been a strength of Western medicine.
Myocardial ischaemia is caused by the reduction of coronary blood flow as a result of fixed or dynamic epicardial coronary artery stenosis, abnormal constriction or deficient relaxation of coronary microcirculation, or because of reduced oxygen-carrying capacity of the blood.56 Atherosclerosis is the major cause of myocardial ischaemia. Plaque that develops in atherosclerosis can rupture causing platelet aggregation and subsequent thrombus formation, which leads to MI. The other mechanisms of myocardial ischaemia are encountered far less than atherosclerosis. Endothelial dysfunction has an important role in the progression of atherosclerosis. Endothelial dysfunction enhances the intimal proliferation and malregulation that results in plaque destabilisation in the arteries.6 This process, coupled with paradoxical vasoconstriction, can result in major cardiovascular events such as MI.32
A number of over-the-counter herbal supplements claim to treat ED. However, according to the Mayo Clinic, you should avoid products labeled as “herbal Viagra.” These supplements can increase blood flow and cause dangerous drops in blood pressure. Risk may be particularly high for men who are using nitrates. Herbal Viagra can also interact with other prescription drugs. Herbal Viagra products may contain potentially toxic compounds that aren’t listed on the label.
In another study from ExCEED, Penson et al.38 compared erectile function and disease-specific quality of life of men with ED and diabetes to those of men with ED without diabetes. They found that those with diabetes reported significantly worse erectile function (P = 0.004) and intercourse satisfaction (P = 0.04) than those without diabetes. Importantly, the diabetic patients also reported that ED had a significantly worse psychological impact on their overall emotional life than did their nondiabetic counterparts (P = 0.01). Interestingly, no differences were noted between the two groups in the psychological impact of ED on the sexual experience.
Three FDA-approved oral medications, sildenafil, tadalafil, and vardenafil are available. These drugs are phosphodiesterase type 5 (PDE-5) inhibitors that can prolong levels of cGMP in tissue allowing improved smooth muscle relaxation, thus facilitating an erection. PDE-5 inhibitor drugs are effective in 56-63% of diabetic men with ED. More stringent glycemic control can improve these results. Men with testosterone deficiency may benefit from a combination of oral ED medication and testosterone supplementation.
The obvious risks are the same that accompany any surgery: infection, pain, bleeding, and scarring. If for some reason the prosthesis or parts become damaged or dislocated, surgical removal may be necessary. With a general success rate of about 90 percent, any of the devices will restore erections, but they will not affect sexual desire, ejaculation, or orgasm.
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].
This category of treatments includes external vacuum therapies: devices that go around the penis and produce erections by increasing the flow of blood in, while constricting the flow out. Such devices imitate a natural erection, and do not interfere with orgasm. External vacuum therapy mechanisms are approximately 95 percent successful in causing and sustaining an erection. All are portable, and costs range between $200-$500, covered under most insurance plans and Medicare Part B.
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
Having ED means that all, most, or some of the time, the penis fails to become or stay hard enough for sexual intercourse. If, on rare occasions, you cannot get an erection, you do not have ED. You also do not have ED if you have a decrease in sexual desire, have premature ejaculation, or if you fail to ejaculate or reach orgasm. ED means that you can’t get or keep an erection.
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