Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References However, patients with hypertrophic obstructive cardiomyopathy and idiopathic hypertrophic subaortic stenosis are at increased risk of syncope and sudden death after exercise.51x51DeBusk, R, Drory, Y, Goldstein, I et al. Management of sexual dysfunction in patients with cardiovascular disease: recommendations of the Princeton Consensus Panel. Am J Cardiol. 2000; 86: 62F–68F
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 links between hypertension and ED are increasingly recognized and the 2009 re-appraisal of European guidelines includes relevant statements.35,47 Erectile dysfunction is almost twice as frequent in hypertensive as in normotensive individuals and appears to be of higher severity. The relative risk of developing ED in hypertensive patients compared with normotensive individuals ranges from 1.3 to 6.9. Regarding pathophysiology, hypertension appears to cause ED per se, through a multitude of mechanisms that include prolonged exposure to elevated levels of systemic blood pressure, endothelial dysfunction, and circulation of vasoactive substance (with a pivotal role of angiotensin II) that lead to structural and functional alterations in the penile arteries. The largely unfounded (see earlier paragraph) notoriety of antihypertensive treatment for causing ED is one of the most predominant causes for non-adherence and discontinuation of antihypertensive therapy, and therefore, patients should be properly informed by physicians. Phosphodiesterase type 5 inhibitors are effective in hypertensive patients with ED and they can safely be co-administered with antihypertensive medication.39 Specifically for alpha-blockers, low starting doses of PDE5 inhibitors are preferred in patients already on alpha-blocker treatment, and likewise, low starting doses of alpha-blockers are encouraged in patients taking PDE5 inhibitors. Of clinical significance is that hypertensive men with ED are more likely to comply with their antihypertensive medication when under PDE5 inhibitors.
A limitation of the study is that the researchers did not assess the effects of untreated erectile dysfunction, or conversely, the effect of having an active sex life without taking erectile dysfunction drugs. The researchers also were unable to account for socioeconomic status; as a next step, they are planning a larger study that will include more health records and complete information on marital status, educational level and disposable income. They are also pursuing a separate analysis of outcomes from erectile dysfunction drugs in men with Type 1 and Type 2 diabetes.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Theoretically, the risk of a cardiac event during sexual activity should be increased. Sexual activity is associated with an elevated heart rate, blood pressure level, and myocardial oxygen demand, and this increase in hemodynamic stress may result in myocardial ischemia.79x79Kimmel, SE. Sex and myocardial infarction: an epidemiologic perspective. Am J Cardiol. 2000; 86: 10F–13F
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
ED is easily and successfully treated! If your sex drive is unaffected, but you experience problems achieving or sustaining erection for a period of four to five weeks, you may have ED. Talk to your doctor immediately. Don’t delay—erectile dysfunction doesn’t “just go away!” Additionally, ED could be a sign of a serious, even life-threatening complication, such as congestive heart failure or kidney disease. Ignoring your ED because it’s embarrassing could jeopardize your health.
Gutiérrez-González, Enrique; Castelló, Adela; Fernández-Navarro, Pablo; Castaño-Vinyals, Gemma; Llorca, Javier; Salas-Trejo, Dolores; Salcedo-Bellido, Inmaculada; Aragonés, Nuria; Fernández-Tardón, Guillermo; Alguacil, Juan; Gracia-Lavedan, Esther; García-Esquinas, Esther; Gómez-Acebo, Inés; Amiano, Pilar; Romaguera, Dora; Kogevinas, Manolis; Pollán, Marina; Pérez-Gómez, Beatriz. “Dietary Zinc and Risk of Prostate Cancer in Spain: MCC-Spain Study.” Nutrients. Jan 2019, 11(1).
Crucial to the understanding of the relationship between ED and CVD and the management of ED patients within the context of the (potential) CVD were the consecutive Princeton Consensus Recommendations (I: 2000, II: 2005, and III: 2012). The reader is strongly encouraged to refer to the most recent, third (2012) Princeton Consensus.30 Key notions in the assessment and management of the patient with organic ED are that (i) he should be considered at increased CVD risk until recommended checks suggest otherwise, and (ii) ED identifies increased CVD risk in the presence or absence of CVD symptoms or history.
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Penile vibratory stimulator is a battery operated device with oscillating discs that can provide excitation of afferent penile nerves at various regulated frequency and amplitudes. PVS has been utilised to activate the ejaculatory reflex for patients with spinal cord injury above T10 seeking to collect retrogradely ejaculated semen in fertility treatment (10). The Viberect is a vibratory stimulation handheld device approved by FDA for treatment of ED. It is clamp-shaped with two oscillating discs facing each other near the tips, and the glans penis is placed between the two oscillating discs to receive concurrent dorsal and ventral stimulation at adjustable frequencies and amplitudes.

“I’m hoping this study will drive that (tie) a little bit harder and faster so that physicians will routinely be including ED when they’re screening patients for cardiovascular disease,” he said. “Doctors should ask the question and consider whether hardening of the arteries is occurring, ask about family history and signs or symptoms like chest pain with exertion, and spend the requisite amount of time to find out what’s going on.”
Age is a critical risk factor for the development of ED and endothelial dysfunction.4,5 ED is the most common condition occurring in middle-aged and older men.5 Kinsey et al. reported that 25 % of 65-year-old men and 75 % of ≥80-year-old men have ED.39 Moreover, ageing also decreases endothelial function, which is responsible for IHD.5 The incidence and severity of ED increases with age (a man aged 70 years is three-times more likely to have ED than a man aged 40 years).40
Taking one of these tablets will not automatically produce an erection. Sexual stimulation is needed first to cause the release of nitric oxide from your penile nerves. These medications amplify that signal, allowing some men to function normally. Oral erectile dysfunction medications are not aphrodisiacs, will not cause excitement and are not needed in men who get normal erections.
The discovery in 1992 of the second messenger of cavernosal smooth muscle relaxation was the critical step that led to the era of nonhormonal oral drug therapy for ED. In 1998, the multicenter trial of sildenafil in the treatment of ED was published in the New England Journal of Medicine, and the era of the phosphodiesterase type 5 (PDE-5) inhibitor began.1 For 5 years, sildenafil was the primary therapy for men with EDDM. Recently, 2 new PDE-5 inhibitors, vardenafil and tadalafil, were introduced.
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
Diabetes is one of the most common causes of ED. Men who have Diabetes are three times more likely to have Erectile Dysfunction than men who do not have Diabetes. Among men with ED, those with Diabetes are likely to have experienced the problem as much as 10 to 15 years earlier than men without Diabetes. A recent study of a clinic population revealed that 5% of the men with ED also had undiagnosed Diabetes. The risk of ED increases with the number of years you have Diabetes and the severity of your Diabetes. Even though 20% to 75% of men with Diabetes have ED, it can be successfully managed in almost all men.
Although ED is a common complication of diabetes, its effect on quality of life is not well understood. Recent work for the Exploratory Comprehensive Evaluation of Erectile Dysfunction (ExCEED) database demonstrates that in the general population of patients presenting to their urologist, ED negatively affects both general and disease-specific health-related quality of life (HRQOL).35 While this study provides insight into the detrimental affect of ED on quality of life, the cohort is somewhat selected, in that all of the patients were seen in sexual dysfunction clinics and therefore may have been more likely to be bothered by their condition and to report worse quality of life.
• Medications: About 25 percent of ED cases are caused by drugs. Many medications, including common medicines prescribed for diabetes and its complications, can cause ED. The most common offenders are blood pressure drugs, antihistamines, antidepressants, tranquilizers, appetite suppressants, and cimetidine (an ulcer drug). In addition, over-the-counter medications, including certain eye drops and nose drops, have been associated with ED. That does not mean you should stop taking these medications! Rather, you should discuss them with your doctor to determine whether a different dosage, an alternate medicine, or additional treatments will resolve the ED.
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