Abstract | Full Text | Full Text PDF | PubMed | Scopus (25) | Google ScholarSee all References Hemodynamic stress also may cause rupture of a vulnerable atherosclerotic plaque resulting in angina, myocardial infarction, or sudden cardiac death.80x80Muller, JE. Triggering of cardiac events by sexual activity: findings from a case-crossover analysis. Am J Cardiol. 2000; 86: 14F–18F
In contrast to Chinese ginseng, Korean ginseng is divided into three types, depending on how it is processed. Red Ginseng is harvested at the sixth year of cultivation and is steamed and dried. In addition to the effects mentioned regarding the effects of ginsenoside, red ginseng has been repoted to improve erectile function in a rat model of metabolic syndrome and it was also found to inhibit fibrosis of the corpus cavernosum of the penis (39). As with most herbal medicines, the concentration of ginsenoside are distributed unevenly throughout the ginseng plant and the concentrations in individual supplements can vary. Common side effects include headaches, insomnia, gastric upset, rash and constipation.
The great majority of ED cases in diabetic men have a physical cause, such as neuropathy or circulatory problems. In some cases, however, the cause of ED is psychological, including depression, guilt, or anxiety. With a thorough exam, the doctor should be able to determine whether the ED is psychological or physical in nature. If the cause is psychological, your doctor may refer you to a psychiatrist, psychologist, sex therapist, or marital counselor. Do not view such a diagnosis as an insult. Most psychologically-based ED is easily and successfully treated.
A thorough history (including cardiovascular symptoms, age, presence of risk factors and comorbid conditions such as obesity, hypertension, dyslipidaemia, pre-diabetes, CAD, peripheral artery disease, symptoms suggestive of sleep apnoea, family history of premature atherothrombotic CVD and lifestyle factors), assessment of ED severity (according to SHIM) and duration, and physical examination (for both heart and peripheral circulation pathology) are mandatory first-line elements of investigation. A resting electrocardiogram, measurement of fasting plasma glucose, and estimation of glomerular filtration rate are desirable tests that may be used to further characterize cardiovascular status and risk and to identify men who require additional cardiologic workup. Owing to the accumulating evidence supporting the link with CVD, the measurement of testosterone is recommended in all men with a diagnosis of organic ED, especially in those for whom phosphodiesterase type 5 (PDE5) inhibitor therapy failed.
Low testosterone levels have been observed inconsistently in STZ-induced diabetic and BB rats.18 Androgen deficiency in rats is associated with downregulation of the neuronal isoforms of nitric oxide synthase, suggesting a trophic effect of testosterone on peripheral erectile tissues. In humans, androgens play a larger role in sexual interest and motivation (libido) than in erectile capacity itself; penile erection is more resistant to androgen withdrawal than is sexual desire.19,20
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Since then, several other oral PDE-5 inhibitors have been developed, including vardenafil and tadalafil, which generated considerable interest in both the scientific and lay communities. There was also much concern about their safety, especially in men with cardiovascular disease. Compared with the 2 newer PDE-5 inhibitors vardenafil and tadalafil, sildenafil has been available for a much longer time; therefore, the vast majority of published cardiovascular safety studies have been performed on this medication. Recommended starting and maximum doses of oral PDE-5 inhibitors are shown in Table 1.

 Other treatment options such as penile self-injection therapy, external vacuum pumps and the medicated urethral system for erection are on rare occasions an effective long-term treatment. A very small percentage of men will continue with these treatments as evidenced by a very high drop out rate and a very low refill rate for these treatments. These procedures require extensive planning which interfere with sexual spontaneity and are really not a realistic long-term treatment for young patients with permanent ED. 


A significant proportion (ranging from ∼60 to 90%) of heart failure patients report ED and marked decrease in sexual interest, with ultimately one-quarter reporting cessation of sexual activity altogether.48 Erectile dysfunction contributes further to the poor quality of life and aggravates depression. Of interest, many heart failure patients place a greater importance on improving the quality of life (including sexual activity) than on improving survival. Sexual function correlates with the symptomatic status (i.e. NYHA functional class and 6-minute walk test).48 In the Evaluation of Role of Sexual Dysfunction in the Saarland (EROSS) Program, left ventricular dysfunction was a risk factor for ED independent of heart failure symptoms. While heart failure and ED share common pre-disposing risk factors, heart failure by itself can cause ED or affect engagement to sexual activity. Neurohumoral activation, medication (thiazides), limited exercise capacity, and depression are responsible.49
The most important way to protect your heart is to eat a Nutritarian diet and that means eating your G-BOMBS: greens, beans, onions, mushrooms, berries and seeds. Natural plant foods have numerous cardio-protective effects. For example, greens activate the Nrf2 system, which turns on natural detoxification mechanisms and protects blood vessels against inflammatory processes that lead to atherosclerotic plaque buildup.9
Erectile dysfunction is common in the CVD patient. It is an important component of the quality of life and it also confers an independent risk for future CV events. The usual 3-year time frame between the onset of ED symptoms and a CV event offers an opportunity for risk mitigation. Thus, sexual function should be incorporated into CVD risk assessment for all men. Algorithms for the management of patient with ED have been proposed according to the risk for sexual activity and future CV events. 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. Testosterone assessment may be useful for both diagnosis of ED, risk stratification and further management. There are issues to be addressed, such as whether PDE5 inhibition reduces CV risk. Management of ED requires a collaborative approach and the role of the cardiologist is pivotal.
To reduce the risk of side effects from these medications, including sexual problems, take medications exactly as prescribed. If you still have side effects, talk to your doctor about other possible medications that may have fewer side effects. On the other hand, you should not take any medication that promotes and erection while on medication to lower blood pressure.
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
On any matter relating to your health or well-being, please check with an appropriate health professional. No statement herein is to be construed as a diagnosis, treatment, preventative, or cure for any disease, disorder or abnormal physical state. The statements herein have not been evaluated by the Foods and Drugs Administration or Health Canada. Dr. Marchione and the doctors on the Bel Marra Health Editorial Team are compensated by Bel Marra Health for their work in creating content, consulting along with formulating and endorsing products.
 Other treatment options such as penile self-injection therapy, external vacuum pumps and the medicated urethral system for erection are on rare occasions an effective long-term treatment. A very small percentage of men will continue with these treatments as evidenced by a very high drop out rate and a very low refill rate for these treatments. These procedures require extensive planning which interfere with sexual spontaneity and are really not a realistic long-term treatment for young patients with permanent ED. 
Erections are extremely complicated and surprisingly fragile. Erections involve chemical signals, nerve impulses, complicated blood pressure changes, and overall fitness in systems ranging from your heart and hormones to your mood. When medication changes how one of these factors works—like blood pressure drops or depression medication—ED is a common side effect. The problem with these completely predictable medically induced side effects is how people react.

Artery size also explains the onset of ED before occurrence of CAD. Coronary arteries are 3–4 mm in diameter, while the penile artery is 1–2 mm in diameter.17 Endothelial dysfunction and plaque burden in the small arteries may cause symptoms of ED before they affect blood flow in large arteries. Also, an asymptomatic lipid-rich plaque in the coronary arteries carries the risk of rupture that leads to acute coronary syndrome or death, so ED may be predictive of these serious events without warning cardiac symptoms.17
Chlamydia and erectile dysfunction: What's the link? Some people who have chlamydia also experience erectile dysfunction (ED), which involves problems getting or maintaining an erection. Chlamydia can infect the prostate gland, leading to prostatitis, pain, and ED. In this article, learn more about the link between this common infection and ED, and treatments for both. Read now
*** 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.
Erectile dysfunction (ED) is commonly called impotence. It’s a condition in which a man can’t achieve or maintain an erection during sexual performance. Symptoms may also include reduced sexual desire or libido. Your doctor is likely to diagnose you with ED if the condition lasts for more than a few weeks or months. ED affects as many as 30 million men in the United States.
While a widely held perception is that CVD drugs cause ED, data attest towards the contrary and some agents may be even beneficial.41 Only thiazide diuretics lead clearly to ED, while some older beta-blockers also do so, but the side-effect of ED was very low (∼3%) when the patient was blinded for the drug administration.42 In fact, the vasodilating nebivolol may even improve erectile function.35,43 ACE-inhibitors, angiotensin-receptor blockers, and calcium-channel blockers are reported to have neutral or even a positive effect on erectile function35,41,43 but more evidence is needed. Regarding statins, the largest body of evidence point towards a beneficial effect.44 A negative effect has been reported in high statin doses, possibly related to a potential reduction in serum testosterone levels, but this dose dependency warrants further investigation. In terms of patient management, when ED onset and therapy initiation are linked and a cause-and-effect association is presumed, a short period of drug withdrawal with monitoring for ED resolution for verification may be an option. In patients who developed ED long after the initiation of CV drug treatment, sexual dysfunction is less likely to be drug associated and PDE5 inhibition therapy may be initiated.
The information provided on this site is for informational purposes only and is not intended as a substitute for advice from your physician or other health care professional or any information contained on or in any product label or packaging. You should not use the information on this site for diagnosis or treatment of any health problem or for prescription of any medication or other treatment. You should consult with a healthcare professional before starting any diet, exercise or supplementation program, before taking any medication, or if you have or suspect you might have a health problem. You should not stop taking any medication without first consulting your physician.

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.

Following the breakthrough in ED treatment using PDE5-inhibitors, Western medicine has now moved on to a new frontier of regenerative medicine, with stem cell and gene therapy leading the way (25). There is a practical need for novel therapy as a significant portion of diabetic or post-prostatectomy ED patients do not respond to oral pharmacotherapy. To date, stem cells derived from different sites including adipose tissue-derived stem cells, bone marrow mesenchymal stem cells and muscle-derived stem cells have been investigated using animal models for ED, to study their effects on neural, vascular, endothelial or smooth muscle regeneration (25,26).
Usually patients will try less invasive alternatives to treat impotence before opting for surgery. These alternatives may include supplements, herbs, lifestyle changes and even medications. In cases where other treatments do not work to resolve ED, surgery might be a last-resort option. Surgery involves implanting a penile prosthesis. This is a saline-filled silicone device or a malleable device. Although the likelihood of serious side effects is considered to be low, certain risks are associated with surgery to correct erectile dysfunction. These side effects may include: anesthetic risk, device infection, and device malfunction or mechanical failure. Some studies have found that five years following surgery around 10–20 percent of men experience device malfunction and failure. Infection rates are low. Around one percent of men who opt for this type of surgery get an infection.
High blood pressure and erectile dysfunction (ED) often go hand in hand. While having high blood pressure (hypertension) itself may not initially cause any symptoms, it will damage your arteries over time, leading them to become less flexible and progressively more narrow. This not only increases the risk of heart attacks and stroke, but has the potential to compromise blood flow to many organs in the body, including the penis, if left untreated.

Powerful clinical and scientific experience suggests a close link between erectile dysfunction and heart disease. Studies like the Health Professionals Follow-up Study have revealed the risk factors for erectile dysfunction to be very similar to those for heart disease. Hypertension, smoking, diabetes, high cholesterol, obesity, and physical inactivity all strongly predict sexual dysfunction in men, as they do heart disease.1
The vacuum constriction device consists of a vacuum cylinder, various sizes of tension rings, and a vacuum pump, either hand-operated or electric. The penis is placed in a cylinder to which a tension ring is attached. Air is evacuated from the cylinder by means of the pump, creating a vacuum, which produces the erection. The cylinder is removed, leaving the tension ring at the base of the penis to maintain the erection.
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