A similar situation develops in the fragile penile circulation. Any disturbance in nitric oxide production lowers the capacity to dilate penile arteries, impairing penile engorgement for erection. Release of nitric oxide is readily sabotaged by many conditions, including elevated levels of cholesterol, high blood pressure, increased triglycerides, smoking, metabolic syndrome and diabetes, and excessive consumption of dietary saturated fat.9 If an artery’s inner wall can’t produce nitric oxide, an abnormal constriction of the arteries to the penis follows, effectively choking off blood flow.
Relation between erectile dysfunction prevalence and type of coronary syndrome (A). Time interval (months) between erectile dysfunction and coronary artery disease symptom onset in chronic coronary syndrome according to the number of vessels involved (B). ACS, acute coronary syndrome; CCS, chronic coronary syndrome, G1: ACS and 1-VD; G2: ACS and 2-,3-VD; G3: CCS. VD, vessel disease; C: the control group with normal coronary angiography. With permission from Montorsi et al.15
Other effective Diabetic Erectile Dysfunction Treatment therapies available include (a) an intraurethral suppository of the vasodilator drug alprostadil (prostaglandin E1), (b) intracavernosal self injection (penile self injection) of the non-specific PDE drug papaverine, the non-selective alpha-adrenergic antagonist phentolamine, and the vasodilator prostaglandin E1, used alone or in combination, or (c) penile prostheses (penile implants).
Co-authors Stacy Mandras, M.D., Patricia Uber, Pharm. D., and Mandeep Mehra, M.D., conducted systematic independent literature searches using the MEDLINE database and examined a broad range of medical research that focused on chronic heart failure, sexual activity and sexual dysfunction. This literature included data from patient surveys and clinical trials.
Men can judge themselves pretty harshly when it comes to their performance in between the sheets. The unsettling fear of not being able to rise to the occasion becomes a reccurring nightmare for men that is often equated with failure, loss of dignity, and masculinity. If you suffer from erectile dysfunction (ED), don’t be so hard on yourself, since impotence can almost always be improved with treatment, without having to rely on Viagra or other medications. Whether you suffer from ED, or hope to prevent the condition, here are six tips to overcome impotence without the side effects of the little blue pill.
Preclinical and clinical trials of these oral agents have clearly demonstrated that they are well tolerated by most DM patients and have an efficacy rate superior to other oral agents. The ultimate result is an improved quality of life (QOL) in EDDM patients. With a greater willingness of DM patients to discuss and seek treatment for ED, it is highly probable that the use of these oral agents will continue to increase. The goal of this article is to provide the physician and pharmacist with a background and working knowledge of these oral agents and their present-day alternatives.
Erectile dysfunction is common in the patient with cardiovascular disease. It is an important component of the quality of life and it also confers an independent risk for future cardiovascular events. The usual 3-year time period between the onset of erectile dysfunction symptoms and a cardiovascular event offers an opportunity for risk mitigation. Thus, sexual function should be incorporated into cardiovascular disease risk assessment for all men. A comprehensive approach to cardiovascular risk reduction (comprising of both lifestyle changes and pharmacological treatment) improves overall vascular health, including sexual function. Proper sexual counselling improves the quality of life and increases adherence to medication. This review explores the critical connection between erectile dysfunction and cardiovascular disease and evaluates how this relationship may influence clinical practice. Algorithms for the management of patient with erectile dysfunction according to the risk for sexual activity and future cardiovascular events are proposed.

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.


Another common reason for failures of oral therapy is the absence of sexual or genital stimulation prior to attempting sexual intercourse. These medicines facilitate an erection by increasing blood flow to the penis, but they do not act as an aphrodisiac or as an initiator of the erection. A man who is not “in the mood” or does not have adequate physical stimulation will not respond with an erection.
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