Low testosterone levels have been observed inconsistently in STZ-induced diabetic and BB rats.18 Androgen deficiency in rats is associated with downregulation of the neuronal isoforms of nitric oxide synthase, suggesting a trophic effect of testosterone on peripheral erectile tissues. In humans, androgens play a larger role in sexual interest and motivation (libido) than in erectile capacity itself; penile erection is more resistant to androgen withdrawal than is sexual desire.19,20
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 discovery in 1992 of the second messenger of cavernosal smooth muscle relaxation was the critical step that led to the era of nonhormonal oral drug therapy for ED. In 1998, the multicenter trial of sildenafil in the treatment of ED was published in the New England Journal of Medicine, and the era of the phosphodiesterase type 5 (PDE-5) inhibitor began.1 For 5 years, sildenafil was the primary therapy for men with EDDM. Recently, 2 new PDE-5 inhibitors, vardenafil and tadalafil, were introduced.

Table 3Metabolic Equivalent (MET) Values for Various Physical Activities56x56Wallis, 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


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
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.
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 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
Getting blood glucose under control is a good anti-ED tactic. Men with diabetes and poor blood glucose control are two to five times as likely to have ED as those with good control. One study in a group of men who had had type 1 diabetes for up to 15 years with minor complications found that intensive blood glucose control lowered the risk of ED compared with conventional treatment. A study in men with type 2 diabetes found that lowering A1C (average blood glucose in the past two to three months) below 7 percent and reducing blood pressure through a combination of medication, diet, and exercise improved sexual functioning.
In a prospective human phase 1 open-label and single-arm study reported by Haahr et al. (27), 17 men with refractory post radical prostatectomy ED were given a single intracavernosal injection of autologous adipose-derived regenerative cells (ADRCs) freshly isolated after a liposuction. The procedures were well-tolerated and over a 6-month follow-up period, 8 of 17 men showed improvement of their erectile function.
When counseling diabetic men who are considering a PDE-5 inhibitor for ED, it is important to set realistic expectations and explain that studies document that all three agents are less effective in diabetic patients than in the general population of men with ED.45–49 For additional information, readers are referred to the excellent review of the use of PDE-5 inhibitors in diabetic men by Vickers and Satyanarayana.50
Abstract | Full Text | Full Text PDF | PubMed | Scopus (25) | Google ScholarSee all References Hemodynamic stress also may cause rupture of a vulnerable atherosclerotic plaque resulting in angina, myocardial infarction, or sudden cardiac death.80x80Muller, JE. Triggering of cardiac events by sexual activity: findings from a case-crossover analysis. Am J Cardiol. 2000; 86: 14F–18F
This form of therapy has a response rate of well over 70%. The sympathetic nervous system normally maintains the penis in a flaccid or non-erect state. All of the vasoactive drugs, when injected into the corpora cavernosae, inhibit or override sympathetic inhibition to encourage relaxation of the smooth muscle trabeculae. The rush of blood engorges the penile corpora cavernosae sinusoidal spaces and creates an erection.
Crossref | PubMed | Scopus (42) | Google ScholarSee all References Apomorphine does not appear to have any notable cardiovascular adverse effects and has been used successfully in Europe. However, apomorphine use has been associated with other unpleasant adverse effects such as nausea and emesis, and the drug has not been approved by the US Food and Drug Administration (FDA) for use in the United States.
medicines called alpha-blockers such as Hytrin (terazosin
HCl), Flomax (tamsulosin HCl), Cardura (doxazosin
mesylate), Minipress (prazosin HCl), Uroxatral (alfuzosin HCl),
 Jalyn (dutasteride and tamsulosin HCl), or Rapaflo (silodosin).
Alpha-blockers are sometimes prescribed for prostate
problems or high blood pressure. In some patients, the use
of Sildenafil with alpha-blockers can lead to a drop in blood pressure or to fainting
27. Haahr MK, Jensen CH, Toyserkani NM, et al. Safety and Potential Effect of a Single Intracavernous Injection of Autologous Adipose-Derived Regenerative Cells in Patients with Erectile Dysfunction Following Radical Prostatectomy: An Open-Label Phase I Clinical Trial. EBioMedicine 2016;5:204-10. 10.1016/j.ebiom.2016.01.024 [PMC free article] [PubMed] [CrossRef]
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Talk with your doctor about your sexual health. Do not be shy or embarrassed. Your doctor has probably dealt with this issue before. If your doctor is an older man, he might even have ED. First, your doctor will figure out what is causing your ED, which can usually be done just by talking with you. Next, your doctor will look for risk factors for atherosclerosis (the Table) by asking you questions, checking your blood pressure, and performing a few blood tests. Identifying and successfully treating atherosclerotic risk factors can reduce the chance of developing major vascular events (heart attacks and strokes).
Abnormalities in the vascular, neural, endocrine, muscular, or psychiatric systems can result in ED.2,3 EDDM is due to multisystemic disease. Atrophy or apoptosis of cavernosal smooth muscle can occur due to loss of Bcl-2 expression in cavernosal smooth muscle and lead to ED. Abnormal amounts of advanced glycation end products is a common occurrence. These chemicals may have an effect on potassium channels that facilitate intracellular calcium release and subsequent cavernosal smooth muscle relaxation. Connective tissue synthesis is increased due to transforming growth factor-beta. The decrease in smooth muscle and the increase in collagen decreases the compliance of the erectile tissue. Neuropathic damage to both the somatic and autonomic nerves has been clearly defined in DM. Partial occlusion of the pelvic or intracavernosal arteries, hypogonadotropic hypogonadism, and depression associated with a chronic illness (DM) can all play a primary or secondary role in the development of EDDM. On a molecular level, studies have demonstrated decreased levels of endothelial and neuronal nitric acid synthase (NS) and decreased cavernosal artery and sinusoidal response to nitric oxide. Abnormalities in nitric oxide rapidly render the functional syncytium of the corpora cavernosa unable to synchronously relax. As the patient with diabetes ages, the concentration of constrictors, including endothelin, prostanoids, and possibly angiotensin, increases as the production of the relaxants, including nitric oxide, vasointestinal peptide, and prostacyclin, decreases.
It is recommended that testosterone be measured in patients with ED because low levels are a reliable measure of hypogonadism. Hypogonadism is not only a treatable cause of ED, but can also lead to reduced or lack of response to PDE5 inhibitors.73 Testosterone deficiency is also associated with increased cardiovascular and all-cause mortality.74 Levels >350 ng/dl do not usually require replacement, but in patients with testosterone <230 ng/dl, replacement can usually be beneficial.57 In patients with congestive heart failure, testosterone replacement can lead to fluid retention, so caution is advised. In these patients, the aim should be to keep testosterone levels in the middle range, i.e. 350–600 ng/dl.57
Abstract | Full Text | Full Text PDF | PubMed | Scopus (56) | Google ScholarSee all References However, subsequent studies of older patients who had sexual intercourse in their home and were monitored with ambulatory ECG reported significantly lower heart rates and blood pressure levels.84x84Stein, RA. Cardiovascular response to sexual activity. Am J Cardiol. 2000; 86: 27F–29F
The aetiology of predominantly psychogenic ED is multifactorial, and components may include psychiatric disorders (especially depression), interpersonal problems with the sexual partner or misconceptions about normal sexual activity. Identifying and getting treatment for those patients with psychogenic causes of ED such as depression that may also increase CVD risk is also important.
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.

Clinical practice in TCM has been an exemplary case of customized treatment with holism epitomizes the essence of TCM. TCM encompasses these aspects, taking a holistic approach to patient’s problem and these methods combine body, mind and spirit, and healings are achieved via the concept of energy rather than matter, as in modern medicine. Compared to the complexity of modern science, which is the basis of Western medicine, this concept is easily understood and comprehended, and is readily accepted because of its holistic approach.
Chronic heart failure often develops after other cardiac problems have damaged or weakened the heart, leaving it too weak or too stiff to fill and pump efficiently. Many underlying heart conditions can lead to heart failure. It can develop quickly after damage caused by a heart attack, or it can develop gradually after years of high blood pressure or coronary artery disease.

Since 1998, when sildenafil (brand name Viagra) first came on the market, oral therapy has been successfully used to treat erectile dysfunction in many men with diabetes. (Sildenafil was followed in 2003 by the drugs tadalafil [Cialis], vardenafil [Levitra] and avanafil [Stendra], which work in much the same way.) Some 50% of men with Type 1 diabetes who try the drugs report improved erections, and some 60% men with Type 2 diabetes do, too. However, that leaves a large percentage of men with diabetes and erectile dysfunction who do not respond to therapy with one of these pills. This article takes a look at what can be done to treat those men who do not respond to oral therapy.
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