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.

“The presence of erectile dysfunction portends a higher risk of future cardiovascular events, particularly in intermediate-risk men, and may serve as an opportunity for intensification of cardiovascular risk prevention strategies,” wrote Boston University heart specialists Naomi Hamburg, MD and Matt Kluge, MD, in an accompanying editorial. “The findings add to the growing evidence supporting additional trials to determine the clinical impact of erectile dysfunction screening and the appropriate cardiovascular directed evaluation and treatment of men with erectile dysfunction.”
Finding a potential early sign of heart disease is vital: Every minute in the United States someone dies from a heart disease-related event. Doctors know to watch for risks like obesity and high blood pressure; however, Men’s Health reports 50 percent of men who die from heart disease have never had one of these symptoms. For younger men, treating ED as an indicator of heart health could be a lifesaver.

In men without cardiovascular disease, erectile dysfunction (ED) pills are very safe. The three rivals -- Viagra, Cialis, and Levitra -- have similar side effects, including headache, facial flushing, nasal congestion, diarrhea, backache, and, in a few Viagra or Levitra users, temporary impaired color vision (men with retinitis pigmentosa, a rare eye disease, should check with their ophthalmologists before using these medications).
Abstract | Full Text PDF | PubMed | Scopus (29) | Google ScholarSee all References After controlling for diabetes mellitus, tobacco use, and hyperlipidemia, hypertension was not found to be an independent predictor of vasculogenic ED in 440 impotent men as measured by the PBI.7x7Virag, R, Bouilly, P, and Frydman, D. Is impotence an arterial disorder? a study of arterial risk factors in 440 impotent men. Lancet. 1985; 1: 181–184
The first step in the process is always to reevaluate if the medication that’s causing the problem is even necessary in the first place. Do you still need the medication(s) that you’re taking? When you’re experiencing medically induced ED, this has to be your starting point. Obviously you shouldn’t make this decision on your own. However, reevaluating your need for medication can be a simple conversation with your doctor. Remind your healthcare provider of the medications you’re taking, and explain any symptoms or side effects—like ED. Going off of medication might sound like an extreme step, but I’ve seen many examples of this in practice.
The third Princeton Consensus (Expert Panel) Conference recommends assessing cardiovascular risk in all patients with ED and CVD. This refers to estimating the risk of mortality and morbidity associated with sexual activity. The current recommendations classify patients into low-, intermediate- and high-risk, based on their New York Heart Association class.57 The consensus also recommended that all patients with ED and CVD should undergo lifestyle changes, such as exercise, smoking cessation, healthy diet and weight reduction. These measures are likely to reduce cardiovascular risk and improve erectile function.58
Experimental in vivo studies have implicated central and peripheral neuropathy, impaired neurotransmission, and endothelial dysfunction in the pathogenesis of diabetic ED.26,27 Copulatory behavior and penile reflexes are uniformly impaired 4–12 months after the onset of diabetes in the BB rat.26,27 McVary et al.26 found that peripheral neuropathy accounts for only part of the dysfunctional findings, and that spinal sexual reflexes were also severely impaired.
Testosterone therapy in hypogonadism modulates metabolic components associated with CV risk. The majority of prospective clinical studies indicates that treatment achieving testosterone levels within physiological limits has beneficial or neutral effects on a lipid profile other than HDL-C, beneficial or neutral effects on inflammatory mediators, and generally beneficial effects on glycaemic state.25 The lean body mass is typically increased in hypogonadal subjects, and visceral adiposity is decreased in several studies and unchanged in the remainder. Such metabolic effects have raised interest on the potential impact on cardiovascular health. Regarding symptoms in patients with pre-existing cardiovascular conditions (angina or heart failure) TTh has been either neutral or beneficial.25 Regarding CVD risk, available clinical trial data indicate that the use of testosterone in middle-aged to elderly men does not increase cardiovascular risk25 with the exception of one study in very frail (substantial limitation of mobility and a high rate of comorbidities) elderly subjects that used an off-label high, and rapid escalation, dosing regimen.46 Prospective data from large, well-designed, long-term trials of TTh are warranted.
Heart disease and erectile dysfunction can be related. In fact, ED and heart disease are considered two signs of the same disease process. The smaller arteries in the penis are affected by atherosclerosis sooner, perhaps three or more years before they cause heart disease symptoms.11 A large international study found that men with ED were more likely to die from heart causes; have a heart attack, stroke or be admitted to the hospital with heart failure than men with no or mild ED.12
I have cared for hundreds of men with erectile dysfunction that have reversed their condition with a Nutritarian diet and the judicious use of dietary supplements. I have cared for hundreds of heart patients with angina and advanced heart disease, who have turned their backs on invasive cardiac procedures, recovered from angina and opened up the closed blood vessels in their diseased hearts. Out of thousands of men with advanced heart and erectile problems who have followed my nutritional advice, I have never had a patient suffer a heart attack or cardiac related death.
Core tip: The prevalence of erectile dysfunction is approximately 2-fold higher in hypertensive patients compared to normotensive individuals. However, erectile dysfunction remains under-reported, under-recognized, and under-treated in hypertensive patients. Lifestyle modification should be the mainstay of treating erectile dysfunction in patients with untreated hypertension. Switching antihypertensive therapy should be considered in treated hypertensive patients, unless administered drugs are absolutely indicated for the individual patient. Otherwise, phosphodiesterase-5 inhibitors should be used, since they are both effective and safe in hypertensive patients. Finally, erectile dysfunction offers the opportunity to recognize asymptomatic cardiovascular disease with obvious benefits for cardiovascular event prevention.
PubMed | Google ScholarSee all References They evaluated 40 patients with coronary artery disease who underwent coronary artery catheterization and whose penile brachial index (PBI) was measured by Doppler ultrasonography. Although a positive correlation was noted between the PBI and the severity of coronary artery obstruction, the relationship was not strong. Also, the degree of PBI abnormality did not effectively stratify the patients according to the severity of their coronary artery blockage. This study concluded that the PBI used alone would not be an effective predictor of ischemic heart disease.
Some research even suggests the effect of blood pressure drugs may be more psychological than physical. When ED occurs after a man begins to take a new medication, it's possible that anxiety about his health, rather than the medication, may trigger the problem. And being aware of possible side effects may make a man more likely to recognize them as abnormal.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (46) | Google ScholarSee all References The significant sympathetic discharge associated with sexual intercourse may contribute to the development of arrythmias in susceptible patients.81x81Drory, Y, Fisman, EZ, Shapira, Y, and Pines, A. Ventricular arrhythmias during sexual activity in patients with coronary artery disease. Chest. 1996; 109: 922–924
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.
Men with diabetes are at a higher risk of erectile dysfunction or impotence, especially if their diabetes is not well controlled. Erectile dysfunction means you cannot have an erection that is sufficient to perform sexual intercourse. Many men experience short-term episodes of erectile dysfunction but, for about one in 10 men, the problem may continue.
In the past 6 years, the FDA has approved three oral agents for the treatment of ED: sildenafil, vardenafil, and tadalafil. All three are phosphodiesterase type 5 (PDE-5) inhibitors and work by potentiating the effect of nitric oxide in the penis. In particular, they block the hydrolysis of cyclic guanosine monophosphate to guanosine 5'-monophosphate, thus enhancing nitric oxide–mediated smooth muscle relaxation, increasing blood flow to the penis and facilitating erection.
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
Normal penile erection is controlled by two mechanisms: reflex erection and psychogenic erection. Reflex erection occurs by directly touching the shaft of the penis, while psychogenic erection occurs by erotic or emotional stimuli. ED is a condition where erection does not take place by either mechanism. ED can occur because of hormonal imbalance, neural disorders or lack of adequate blood supply to the penis.54 Lack of blood supply can be a result of impaired endothelial function associated with CAD.54

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.


Apart from their beneficial effect in erectile dysfunction and their safe profile in antihypertensive medication, PDE-5 inhibitors have even more advantages to demonstrate. Several lines of evidence has proven that patients receiving PDE-5 inhibitors are more likely to initiate an antihypertensive regime and more willing to add a new agent to their existing treatment, a fact that raises significantly patient’s adherence and as a matter of fact control of high blood pressure and quality of life[63,64]. Moreover, a handful of clinical data has demonstrated the considerable vasodilating and anti-proliferative properties of PDE-5 inhibitors in the pulmonary vasculature, establishing them as a first-line treatment in patients with pulmonary arterial hypertension[65,66]. The same properties have been considered as potentially responsible for improving microcirculation in patients with secondary Raynaud phenomenon and ameliorating cardiopulmonary exercise performance in patients with heart failure[67,68]. In addition, the therapeutic implementation of PDE-5 inhibitors has expanded in the field of benign prostate hyperplasia-lower urinary tract symptoms (BPH-LUTS). The common pathophysiologic substrate between erectile dysfunction and BPH-LUTS has rendered PDE-5 inhibitors an effective treatment which significantly improves measures of both conditions while at the same time exhibits high efficacy and safety. The beneficial effect is much more pronounced when taking into consideration the fact that a-blockers, the mainstay of therapy for benign prostate hyperplasia frequently provoke sexual side effects, erectile dysfunction included[69].
Before a man concludes that oral drugs don’t work for him, he should have his testosterone levels checked to rule out hormone deficiency as the cause of (or as a contributor to) his sexual dysfunction. Other symptoms of low testosterone include a low sex drive and infertility. Checking testosterone levels requires a blood test. If a man’s levels of testosterone are decreased or at the lower end of normal, his doctor may prescribe supplemental testosterone therapy, either as testosterone injections or testosterone gel, which is applied daily to the skin. In some cases, testosterone therapy alone can resolve sexual dysfunction, or it can be combined with the use of oral erectile dysfunction drugs.
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