Since erectile dysfunction presents such an intimate relationship with CV parameters, it is easily deducted that it could constitute a powerful tool for detecting asymptomatic CV disease. Consequently, recognition of sexual dysfunction in a hypertensive individual should prompt further diagnostic procedures and therapeutic interventions in order to disclose its silent cardiovascular risk and improve patient’s quality of life and life expectancy.

Cardiovascular disease and erectile dysfunction (ED) are closely interrelated disease processes. Erectile dysfunction reportedly affects 10 million to 20 million men in the United States and more than 100 million men worldwide. Each year, about 500,000 persons in the United States survive a myocardial infarction, and an estimated 11 million have existing cardiovascular disease, making the issue of sexual function and cardiac disease relevant to many patients. We explore the relationship between ED and the presence of cardiovascular disease in the general population. We also review the prevalence and pathophysiological associations of ED and cardiovascular disease. The risks of sexual activity for patients with cardiovascular disease are discussed, as are prevention and treatment strategies for ED in this patient population.
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The number of men reporting improvement was at 88% during the study. The number of men involved in the study who reported impotence dropped from 75.3 % to 11.8%. The results of this study raise hope for men who have quit taking other blood pressure medications because they interfered with sexual function. Sexual dysfunction was defined for the study as decreased libido, impotence and poor sexual satisfaction.

The drugs come in several strengths. Most men should start with a low to moderate dose. The dose can be adjusted depending on the results. Men with potential problems should always start with the lowest dose. Every man should avoid consuming alcohol before taking these drugs. Men who do not respond to a full dose on two or three different occasions should try other treatments.
Based on this testing, EDDM patients were treated with behavioral therapy, intracavernosal (papaverine, PGE-1, or Trimix) or intraurethral PGE-1, a vacuum constriction device (VCD), or implantation of a penile prosthesis. Novel surgical procedures, ligation of incompetent cavernosal veins or penile revascularization, were seldom efficacious with EDDM and were soon abandoned. Although these nonsurgical therapies were efficacious, they were not widely requested because of their invasive or mechanical nature.
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

Since erectile dysfunction presents such an intimate relationship with CV parameters, it is easily deducted that it could constitute a powerful tool for detecting asymptomatic CV disease. Consequently, recognition of sexual dysfunction in a hypertensive individual should prompt further diagnostic procedures and therapeutic interventions in order to disclose its silent cardiovascular risk and improve patient’s quality of life and life expectancy.

Logically, ED secondary to testosterone deficiency should be treated by testosterone replacement. Testosterone levels in men decrease with age.4 Both epidemiological and observational studies have demonstrated that reduced testosterone is associated with increased cardiovascular risk. One meta-analysis showed lower testosterone and higher 17β oestradiol as significant risk predictors despite adjustment for age and body mass index.4 Patients with coronary artery disease (CAD) have been found to have lower testosterone levels than controls, and there is inverse correlation between testosterone and the incidence of major cardiovascular disease (CVD).4 A significant negative correlation has been reported between total testosterone levels and Framingham risk score.4 However, it has been pointed out that ‘It is unclear if this is a causal association or due to low testosterone being a biomarker of poor health’.4 Testosterone replacement as a treatment for …

Crossref | PubMed | Google ScholarSee all References Regular exercise can significantly decrease the patient's risk of having a myocardial infarction during sexual intercourse by increasing the patient's functional reserve, decreasing the heart rate, and increasing the stroke volume.8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409
The vascular endothelium has an important role in angiogenesis and vascular repair by producing regulatory substances, including NO, prostaglandin, endothelins, prostacyclin and angiotensin II. These regulatory factors regulate the blood flow to the penis by controlling smooth muscle contractility and subsequent vasoconstriction and vasodilatation. Generally, in erectile tissue, increased blood flow through the cavernosal artery increases shear stress and produces NO, which further relaxes the vascular smooth muscles and increases blood flow in the corpora cavernosa.54 These events cause penile erection. However, in ED, endothelial NO synthesis is reduced and there is increased endothelial cell death (Figure 2).55
Erectile dysfunction is common in the CVD patient. It is an important component of the quality of life and it also confers an independent risk for future CV events. The usual 3-year time frame between the onset of ED symptoms and a CV event offers an opportunity for risk mitigation. Thus, sexual function should be incorporated into CVD risk assessment for all men. Algorithms for the management of patient with ED have been proposed according to the risk for sexual activity and future CV events. 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. Testosterone assessment may be useful for both diagnosis of ED, risk stratification and further management. There are issues to be addressed, such as whether PDE5 inhibition reduces CV risk. Management of ED requires a collaborative approach and the role of the cardiologist is pivotal.
Crossref | PubMed | Scopus (53) | Google ScholarSee all References This study found that, although hypertensive patients had more coronary artery disease, no direct evidence supported an association between hypertension and arteriogenic impotence, as measured by the PBI, peak systolic velocity, and resistive index, in patients with mild to moderate hypertension.
The use of penile support device such as penile cast worn externally during intercourse has been tried to provide length and rigidity to the penile shaft (24). Each device can be customised to the patient’s penile size and provided an option for patients who are seeking non-pharmaceutical/non-invasive treatment, or have end-organ failure who may not be candidates for, or unable to afford, penile prosthesis implant.
Gazzaruso C,  Solerte SB,  Pujia A,  Coppola A,  Vezzoli M,  Salvucci F,  Valenti C,  Giustina A,  Garzaniti A. Erectile dysfunction as a predictor of cardiovascular events and death in diabetic patients with angiographically proven asymptomatic coronary artery disease: a potential protective role for statins and 5-phosphodiesterase inhibitors, J Am Coll Cardiol , 2008, vol. 51 (pg. 2040-2044)https://doi.org/10.1016/j.jacc.2007.10.069
Relaxation of erectile tissue requires nitric oxide from nonadrenergic-noncholinergic neurons and the endothelium.21 Penile tissue from diabetic men with ED demonstrates impaired neurogenic and endothelium-mediated relaxation of smooth muscle,22 increased accumulation of advanced glycation end products (AGEs),23 and upregulation arginase, a competitor with nitric oxide synthase for its substrate L-arginine.24 Normal responses to direct smooth muscle relaxants in most of these studies implies that the impairments are due to decreased synthesis, release, or activity of nitric oxide. The fundamental mechanisms mediating these changes are thought to be the same as for other diabetic complications: increased polyol pathway flux, intracellular accumulation of AGEs, activation of protein kinase C, and increased flux through the hexosamine pathway.25
Not enough info for you? No problem. Nerd out on erectile dysfunction with these studies and research from the most trusted sources on the interwebs. If you have any questions or you think we missed something important, leave a comment or book a consultation with me or one of these trained professionals and we’ll get you on the way to a healthier manhood.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References However, α-blockers are a well-known cause of retrograde ejaculation secondary to a reversible relaxation of bladder neck smooth muscle.50x50Meinhardt, W, Kropman, RF, Vermeij, P, Nijeholt, AA, and Zwartendijk, J. The influence of medication on erectile function. Int J Impot Res. 1997; 9: 17–26
Diabetes occurs when you have too much sugar circulating in your bloodstream. There are two main types of diabetes: type 1 diabetes, which affects less than 10 percent of those who have diabetes, and type 2 diabetes, which accounts for over 90 percent of diabetes cases. Type 2 diabetes often develops as a result of being overweight or inactive. Approximately 30 million Americans have diabetes, and about half of them are men.
Hi there and welcome to my site where I talk about natural solutions to a not often talked about and often embarrassing taboo topic. I talk about the main causes of the sexual dysfunction known as ED and suggest potential solutions for the causes and some lifestyle changes that you may need to make and the herbs or supplements you may need to take!.
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

Dr. Eid also urges these patients to treat their diabetes in order to avoid developing ED for life. “They need to manage their diabetes and make sure they control it so the ED will not progress and will stabilize, as a result,” he said. “If the diabetes is controlled after the patient is first diagnosed, then the erections will come back. But if the patient has diabetes for many years, and suddenly decides it’s time to control it, they cannot prevent the damage that’s already been done.”
There are a number of reasons a man may not achieve the desired result from an oral erectile dysfunction drug. In some cases, a man may experience drug side effects severe enough to outweigh any potential benefit of taking the drug. Possible side effects of these drugs include headache, facial flushing, nasal congestion, and transient abnormal vision. (In October 2007, the FDA added a warning about sudden hearing loss to the package labels of oral erectile dysfunction drugs. While it’s not absolutely clear that the drugs can cause sudden hearing loss, a number of cases have been reported in men within hours or days of taking one of the drugs.)
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