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).
A collection of risk factors that strongly predict heart disease—termed the metabolic syndrome—is also associated with erectile dysfunction. An increasingly prevalent condition, this syndrome includes low HDL, increased triglycerides, high blood sugar, and heightened inflammation and causes a three-fold or greater risk of heart attack, stroke, and diabetes. It is largely attributable to excess weight, poor diet, and inactivity and afflicts at least 47 million Americans, signaling that an epidemic of erectile dysfunction is sure to follow. Indeed, a survey of 2,400 men participating in a health screening revealed that metabolic syndrome increases the likelihood of erectile dysfunction by 48%.10
The obvious risks are the same that accompany any surgery: infection, pain, bleeding, and scarring. If for some reason the prosthesis or parts become damaged or dislocated, surgical removal may be necessary. With a general success rate of about 90 percent, any of the devices will restore erections, but they will not affect sexual desire, ejaculation, or orgasm.
Crossref | PubMed | Scopus (56) | Google ScholarSee all References When matched for age, hypertension, diabetes, and tobacco use, no significant difference was noted in the presence of ED (42% in the myocardial infarction group vs 48% in the control group). However, the presence of severe congestive heart failure has been associated with increased ED. A study of 80 patients with New York Heart Association class III/IV congestive heart failure found that 40% of these patients had complete ED, and another 40% had either mild or moderate ED.15x15Taylor, HA Jr. Sexual activity and the cardiovascular patient: guidelines. Am J Cardiol. 1999; 84: 6N–10N
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.
Sexual dysfunction is a common, underappreciated complication of diabetes. Male sexual dysfunction among diabetic patients can include disorders of libido, ejaculatory problems, and erectile dysfunction (ED). All three forms of male dysfunction can cause significant bother for diabetic patients and can affect their quality of life. Despite this, health care providers often do not specifically ask their male diabetic patients about sexual function. This results in considerable underdiagnosis because patients are often reluctant or embarrassed to initiate discussion of these issues themselves. By not recognizing sexual dysfunction as a common organic sequel-lae of diabetes that should be addressed and treated, providers are missing an important opportunity to improve their patients' daily existence and quality of life.
Erectile dysfunction (ED) is a common disorder that affects the quality of life of many patients. It is prevalent in more than half of males aged over 60 years. Increasing evidence suggests that ED is predominantly a vascular disorder. Endothelial dysfunction seems to be the common pathological process causing ED. Many common risk factors for atherosclerosis such as diabetes, hypertension, smoking, obesity and hyperlipidaemia are prevalent in patients with ED and so management of these common cardiovascular risk factors can potentially prevent ED. Phosphodiesterase type 5 inhibitors provide short-term change of haemodynamic factors to help initiate and maintain penile erection. They have been shown to be an effective and safe treatment strategy for ED in patients with heart disease, including those with ischaemic heart disease and hypertension.
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
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.)