The choice is yours. You do not have to die of a heart attack, and you do not have to have erectile dysfunction. Both are the result of dietary choices, and you can make a choice right now to protect your life. Do you want to die of a heart attack or don’t you? If you don’t, then are you willing to do what it takes to reduce your risk almost 100 percent? I don’t know about you, but for me, just dropping my risk 20 to 40 percent with medical care is not enough. I want maximum protection.
Abstract | Full Text PDF | PubMed | Scopus (105) | Google ScholarSee all References Aspirin and β-blocker use have been suggested to decrease the risk of cardiovascular events with sexual activity, although their benefit has not been proved definitively.79x79Kimmel, SE. Sex and myocardial infarction: an epidemiologic perspective. Am J Cardiol. 2000; 86: 10F–13F
Despite physician’s inexperience and patient’s reluctance to disclose sexual dysfunction problems, attempts to estimate the magnitude of this clinical condition have predicted that over 150 million men worldwide experience some degree of erectile dysfunction. Several studies have demonstrated a wide range regarding the prevalence of erectile dysfunction, which is even higher in patients with essential hypertension where the relative risk is approximately two times higher than in normotensive individuals[6-11]. The etiology can be found in the structural and functional abnormalities of the penile arteries induced by high blood pressure. Smooth muscle hypertrophy, stenotic lesions due to atherosclerosis and impaired blood flow are among the prominent structural alterations whereas endothelial dysfunction and the defective nitric oxide-induced vasodilatory mechanism belong to the main functional abnormalities induced by increased blood pressure[12,13]. As a matter of fact, sexual dysfunction is encountered more frequently that it is indeed believed underlining the need for a more proper and concrete assessment.
Erectile dysfunction (ED) is highly prevalent affecting at least 50 % of men with diabetes mellitus (DM). DM may cause ED through a number of pathophysiological pathways. These include neuropathy, endothelial dysfunction, cavernosal smooth muscle structural/functional changes, and hormonal changes. Lifestyle changes, diabetes control, and treatment of hypogonadism are important as the first step in ED management since there is no curative treatment for ED. Phosphodiesterase type 5 inhibitors (PDE5i) are the first-line treatment option. Intracavernous administration of vasoactive drugs is commonly used as a second-line medical treatment when PDE5i have failed. Alprostadil is the most widely used drug in this second-line setting. The combination of papaverine, phentolamine, and alprostadil represents the most efficacious intracavernous pharmacologic treatment option that may save non-responders to alprostadil. Penile prosthesis implantation can be considered in treatment refractory cases, with excellent functional and safety results in the properly informed patients.
Erectile dysfunction (ED) is defined as the persistent inability to attain and maintain an erection that is sufficient to permit satisfactory sexual performance (1). The current pharmaco-therapeutic research in ED focuses on underlying endothelial dysfunction as the root cause for ED and introduction of phosphodiesterase type 5 inhibitors to potentiate nitric oxide (NO) action and cavernosal smooth muscle vasodilation, has revolutionized modern ED treatment over the past two decades (2). In contrast to Western Medicine, the traditional and complementary medicine (TCM) aims at restoration and better overall bodily regulation with medicine to invigorate qi (energy) in vital organs such as kidney, spleen and liver; to enhance physical fitness, increase sexual drive, stabilize the mind and improve the overall situation resulting in natural and harmonious sexual life (3).
Diabetic damage doesn’t stop with these small vessels, he said. “You really have two parallel situations: You need blood flow that feeds the muscle of the penis, and you need an artery dedicated to bringing blood rapidly when a man becomes aroused and wants to be sexually active,” he said. “That artery is also affected by diabetes. They’ll say ‘I can get a partial erection, but I can’t maintain it.’ ”
Nebivolol seems to have an advantage over other beta-blockers when used to treat men with hypertension and ED. It has additional vasodilating effects because it stimulates endothelial release of nitric oxide (NO), resulting in relaxation of smooth muscle in the corpus cavernosum, allowing penile erection.25 Despite limited studies, nebivolol does not seem to worsen erectile function and some studies have demonstrated significant improvement in erectile function with nebivolol compared with second-generation cardioselective beta-blockers.23,26–28
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.
Erectile dysfunction is common in the patient with cardiovascular disease. It is an important component of the quality of life and it also confers an independent risk for future cardiovascular events. The usual 3-year time period between the onset of erectile dysfunction symptoms and a cardiovascular event offers an opportunity for risk mitigation. Thus, sexual function should be incorporated into cardiovascular disease risk assessment for all men. A comprehensive approach to cardiovascular risk reduction (comprising of both lifestyle changes and pharmacological treatment) improves overall vascular health, including sexual function. Proper sexual counselling improves the quality of life and increases adherence to medication. This review explores the critical connection between erectile dysfunction and cardiovascular disease and evaluates how this relationship may influence clinical practice. Algorithms for the management of patient with erectile dysfunction according to the risk for sexual activity and future cardiovascular events are proposed.
The cardiovascular adverse effects of sildenafil use have been studied extensively. Phosphodiesterase type 5, although located primarily in the genitalia, also can be found throughout the systemic vasculature, although other PDEs predominate there10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
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

Ginseng, specifically “red ginseng,” is known as the “herbal Viagra” that helps puts to rest men’s bedroom woes. Red ginseng is when the root has been steamed and then dried. The ginseng root is the part of the plant that is mostly used as a natural remedy when in its supplement form. However, the plant must be grown for a minimum of five years before it can be used. In a 2008 review, seven studies on red ginseng and ED, ranging in dosages from 600 to 1,000 milligrams three times a day, were found to provide evidence for the effectiveness of the herb in ED treatment.


Abstract | Full Text PDF | PubMed | Scopus (19) | Google ScholarSee all References However, there has been disagreement regarding the effects of diuretics on erectile function; many studies found that only rarely have these medications been implicated convincingly as the cause of a patient's ED.36x36Wein, AJ and Van Arsdalen, KN. Drug-induced male sexual dysfunction. Urol Clin North Am. 1988; 15: 23–31
Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Avoiding sexual activity between 6 AM and noon may be recommended to higher-risk patients because this is the time of peak incidence of most arrhythmias, myocardial ischemia, sudden cardiac death, and cerebrovascular accidents.1x1Muller, JE. Sexual activity as a trigger for cardiovascular events: what is the risk?. Am J Cardiol. 1999; 84: 2N–5N
This form of therapy has a response rate of well over 70%. The sympathetic nervous system normally maintains the penis in a flaccid or non-erect state. All of the vasoactive drugs, when injected into the corpora cavernosae, inhibit or override sympathetic inhibition to encourage relaxation of the smooth muscle trabeculae. The rush of blood engorges the penile corpora cavernosae sinusoidal spaces and creates an erection.
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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