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
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.
*** High-risk patients include those with unstable or refractory angina pectoris, uncontrolled hypertension, congestive heart failure (NYHA class IV), recent myocardial infarction without intervention (<2 weeks), high-risk arrhythmia (exercise-induced ventricular tachycardia, implanted internal cardioverter defibrillator with frequent shocks, and poorly controlled atrial fibrillation), obstructive hypertrophic cardiomyopathy with severe symptoms, and moderate to severe valve disease, particularly aortic stenosis.
Third, men with Diabetes need to control their blood sugar levels. When your blood sugar is not under control, your body does not produce enough Nitric Oxide (NO) and vascular tissues don’t respond as effectively to NO. When enough blood flows into the penis, penile veins close off and block the blood from flowing out. This process results in an erection. If your body does not produce enough NO or if your penile tissues do not respond to NO, the pressure of the blood flowing into your penis is not sufficient to trap the blood, you penis will not get hard.
Crossref | PubMed | Scopus (24) | Google ScholarSee all References Almost every class of antihyper-tensive medication has been implicated in causing ED; however, most of these studies, published as case reports or patient surveys, have been relatively subjective and uncontrolled.4x4Feldman, HA, Goldstein, I, Hatzichristou, DG, Krane, RJ, and McKinlay, JB. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol. 1994; 151: 54–61
Older age. A man’s risk increases past the age of 40, as age is the variable most strongly associated with impotence. This is due to changing hormones, higher risk for heart problems and those affecting circulation, and decreased sexual desire that often occurs with increasing age. For example, based on findings from the National Health and Social Life Survey, it’s been found that “men between 50–60 years old are more than 3 times as likely to experience erection problems and to report low sexual desire compared to men aged 18 to 29 years.” (3)
The use of shock wave therapy has revolutionized the treatment of many aspects of medicine. High intensity extracorporeal shockwave therapy has been used for the treatment of nephro-urolithiasis while medium intensity shockwave therapy is used by orthopaedic surgeons to treat joint pain as well as tendinitis. Low intensity shockwaves therapy was first noted to improve ischaemia-induced myocardial dysfunction in animal studies when low intensity shockwaves were applied to porcine myocardium (13). Shockwaves induces a localized stress on cell membranes in the same way that shear stress affects endothelial cell membranes (14) and this triggers the release of angiogenic factors, such as increased NO production through increased activity of endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS), platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) (15). These shockwaves also cause membrane hyperpolarization (16), activation of the Ras signaling pathway, non-enzymatic synthesis of NO and induction of stress fibers and intercellular gaps (17).
Most cases of sexual dysfunction are related to a physical cause. The most common causes are diabetes, heart disease, neurological trauma or disease, and side effects of medications. Stress and anxiety can also contribute to impotence. While most of the focus has been on men with erectile dysfunction, a number of women also suffer from this disorder.
A disruption anywhere along the complex chain of events will impair the capacity to have an erection. Any man who has experienced the frustration of male impotence knows that the consequences extend beyond physical dissatisfaction to anxiety, tension, and embarrassment. A common reason for failure of the erectile apparatus is disruption of the path leading to nitric oxide production and blood flow control.
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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.