Towards this direction, several sufficiently powered studies have demonstrated a higher incidence of erectile dysfunction in patients with coronary artery disease, either asymptomatic or overt. At the same time, patients with erectile dysfunction are more prone to have established coronary artery stenosis of more than 50% and consequently evident CV disease[75]. This is in conformity with the “artery size hypothesis” according to which smaller arteries (e.g., penile arteries) are the first to undergo a vascular lesion prior to the larger ones (e.g., coronary arteries). Moreover, in such patients erectile dysfunction is connected to the number of occluded vessels and more interestingly occurs over three years before coronary artery disease becomes apparent[76-80].

Crossref | PubMed | Google ScholarSee all References The risk of myocardial infarction with sexual activity has been estimated to be less than 3% in high-risk patients with prior cardiovascular disease if they can exercise to more than 7 METs without symptoms.89x89Moss, AJ and Benhorin, J. Prognosis and management after a first myocardial infarction. N Engl J Med. 1990; 322: 743–753
These medications don’t work for everyone but they are easy to use and work for around 60% of people who try them. They work by making it easier to get an erection by reducing the effect of (inhibiting) the chemical PDE-5. This chemical is used in the body to make sure there isn’t too much blood in the penis during an erection, but if you have erectile dysfunction then this chemical ends up over-compensating.
The research is based on a Swedish national database of health records that includes all hospitals in Sweden. Researchers analyzed the records of men age 80 years or younger who were hospitalized for a first heart attack between 2007 and 2013. Tracking the men for an average of 3.3 years following this first heart attack, they compared outcomes among those who subsequently filled a prescription for a PDE5 inhibitor or alprostadil to those who did not. Overall just over 7 percent of men were prescribed an erectile dysfunction drug, 92 percent of whom were prescribed a PDE5 inhibitor and 8 percent of whom were prescribed alprostadil.

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 …
Admitting to your doctor that you are having trouble achieving an erection can be difficult, but take comfort in the fact that they are not judging you and are there to improve your health and well-being. If you are just beginning a blood pressure treatment regimen and are beginning to experience erectile dysfunction, tell your doctor as soon as you can—they can solve the problem by simply changing the prescription.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Another contraindication is the use of recreational drugs (“poppers”) that contain amyl nitrate. The guidelines also caution use in patients who have a high risk of cardiovascular effects, including patients with active coronary artery disease who are not taking nitrates, patients with congestive heart failure with a borderline low blood pressure level and low blood volume, or those with complicated multidrug antihypertensive regimens.

This may seem like a lot to manage at a glance, however, just focus on one step at a time. If it is more exercise you want to start with, park your car further away from the front door at work so you have to walk a little more every day. Or go out on a walk to make your phone calls.  If you need to eat better,  try low-fat meat and chicken for lunch. Just keep it simple and don’t try to do it all at once.
While all three forms of male sexual dysfunction can be found among diabetic men, this review will focus on the most common form, ED, because the literature is most mature in this area. Defined as the inability to achieve or maintain an erection sufficient for satisfactory sexual performance, ED is highly prevalent in diabetic men1 and is almost always organic in its etiology. Given that many patients feel that their ED is “in their heads” and that “their provider will dismiss any sexual problems they might bring up,”2 it may be a relief for patients to learn that their ED is physical, related to their diabetes, and treatable. To this end, the goal of this article is to review the epidemiology, pathophysiology, quality of life effect, and treatment of ED in men with type 2 diabetes.
Crossref | PubMed | Scopus (174) | Google ScholarSee all References This study concluded that patients who have stable coronary artery disease who can exercise to 4.5 metabolic equivalents (METs) with a negative or mildly positive stress test and without angina or hypotension can safely take sildenafil. Physicians who prescribe sildenafil should counsel their patients that, if they have chest pain or other cardiac symptoms with sexual intercourse, they should not take nitrates and should immediately call their physician.66x66Jackson, G. Sexual intercourse and stable angina pectoris. Am J Cardiol. 2000; 86: 35F–37F
Treatment of ED which was previously confined to invasive procedures, cavernosal injections or to rather ineffective oral medications was revolutionized in 1999 with the introduction of the orally administered PDE5 inhibitor sildenafil. Phosphodiesterase type 5 inhibitors are the first-line therapy for ED of organic aetiology unless there is a specific contraindication to their use. This class of agents is widely used because of its effectiveness and safety.38 Interactions with cardiovascular drugs have been minimal with the exception of nitrates and other nitric oxide (NO) donors (such as nicorandil), where co-administration may result in severe vasodilation and hypotension. However, nitrates are often overused in clinical practice; therefore, the option of their discontinuation should be considered. A strong body of clinical data shows that all three agents (sildenafil, tadalafil, and vardenafil) do not increase the risk of non-fatal myocardial infarction, stroke, or cardiovascular deaths. These drugs do not exacerbate ischaemia or worsen exercise tolerance in patients with known CAD who achieve levels of exercise comparable or greater than that achieved during sexual intercourse.38,39 Phosphodiesterase type 5 is expressed throughout the human body, including the pulmonary and systemic vasculature and hypertrophied myocardium. While currently their only additional indication, beyond ED, is idiopathic pulmonary hypertension (for sildenafil and tadalafil), they show potential to be of benefit in several other conditions, such as CAD and systolic heart failure.39 Mechanisms of benefit of PDE5 inhibitors include pulmonary and systemic vasodilation, increased myocardial contractility, reduced large artery stiffness and wave reflections, improved endothelial function, and reduced apoptosis, fibrosis and hypertrophy through mechanisms involving NO, cyclic guanosine monophosphate, protein kinase G and Rho kinase.39 A very important issue is whether treatment of ED per se (and not of its risk factors and comorbidities) will have an impact on cardiovascular risk. While this applies to all therapeutic modalities of ED, it is particularly pertinent for PDE5 inhibitors, since they represent the mainstay of ED therapy. Data are limited to date. Gazzaruso et al.21 showed a trend of PDE5 inhibitors to reduce cardiovascular morbidity and mortality in diabetic patients with silent CAD and ED, while Frantzen et al.40 showed that 2 years after the introduction of sildenafil, the relative risk of the incidence of CVD among men with ED compared with healthy men significantly decreased from 1.7 to 1.1.
The causes of ED are numerous but generally fall into two categories: organic or psychogenic. The organic causes can be subdivied into five categories: vascular, traumatic/postsurgical, neurological, endocrine-induced, and drug-induced. Examples of the psychogenic causes are depression, performance anxiety, and relationship problems. In people with diabetes, the main risk factors are neuropathy, vascular insufficiency, poor glycemic control, hypertension, low testosterone levels, and possibly a history of smoking.
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
The development of PDE5-inhibitors is a clear example of how Western medicine approached the problem of ED differently from Eastern medicine. The erectogenic effect of sildenafil (Viagra®) was discovered by accident when patients undergoing heart clinical trials reported better erections as a side effect after taking sildenafil. This observation led to further elucidation of the NO/cGMP signalling pathway and development of PDE5-inhibitors as a first-line therapy in ED (5).
Physical and emotional stress — whether over-exercising, under-sleeping or just dealing with everyday stressors like work and a busy schedule — causes an increase in “stress hormones,” including cortisol and adrenaline. Stress can lower desire for sex. This is because stress can contribute to fatigue or preoccupation with other tasks. It can also significantly affect blood flow by increasing inflammation.
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
• Blood Vessels: Diabetes damages blood vessels, especially the smallest blood vessels such as those in the penis. Diabetes can also cause heart disease and other circulatory problems. Proper blood flow is absolutely crucial to achieving erection. “Erection is a hydraulic phenomenon that occurs involuntarily,” says Arturo Rolla, MD, of Harvard University School of Medicine. “Nobody can will an erection!” Anything that limits or impairs blood flow can interfere with the ability to achieve an erection, no matter how strong one’s sexual desire.
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