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.

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.
Testosterone therapy in hypogonadism modulates metabolic components associated with CV risk. The majority of prospective clinical studies indicates that treatment achieving testosterone levels within physiological limits has beneficial or neutral effects on a lipid profile other than HDL-C, beneficial or neutral effects on inflammatory mediators, and generally beneficial effects on glycaemic state.25 The lean body mass is typically increased in hypogonadal subjects, and visceral adiposity is decreased in several studies and unchanged in the remainder. Such metabolic effects have raised interest on the potential impact on cardiovascular health. Regarding symptoms in patients with pre-existing cardiovascular conditions (angina or heart failure) TTh has been either neutral or beneficial.25 Regarding CVD risk, available clinical trial data indicate that the use of testosterone in middle-aged to elderly men does not increase cardiovascular risk25 with the exception of one study in very frail (substantial limitation of mobility and a high rate of comorbidities) elderly subjects that used an off-label high, and rapid escalation, dosing regimen.46 Prospective data from large, well-designed, long-term trials of TTh are warranted.
Crossref | PubMed | Scopus (174) | Google ScholarSee all References All these men had ED and twice underwent symptom-limited supine bicycle exercise echocardiography 1 hour after taking either sildenafil (50 mg or 100 mg) or placebo. This study found no significant changes in resting heart rate, diastolic blood pressure level, or wall motion score index, and the exercise capacity of the 2 groups was similar. Both groups had similar numbers of patients who experienced dyspnea and/or chest pain, had a positive exercise echocardiographic test, and had exercise-induced wall motion abnormalities. Sildenafil caused a mean decrease of 7 mm Hg in the resting systolic blood pressure level compared with the placebo group. In conclusion, this study showed that in patients with stable coronary artery disease, sildenafil caused no change in symptoms, exercise endurance, or presence/extent of exercise-induced ischemia as measured by exercise echocardiography.
Impotence, or erectile dysfunction (ED), is the inability for a man to sustain an erection long enough for normal, satisfying sexual intercourse.  To understand the underlying causes of impotence, it helps to know the basics about how an erection develops, along with potential problems that get in the way. Erections begin in the brain with a thought related to sexual desire. Then a chemical message travels from the brain to the penis. Blood flow to the penis increases as blood vessels leading to the reproductive system relax and allow for increased circulation.
In particular, patients are classified into three categories (low, intermediate, high) depending on their CV risk profile. Individuals with controlled hypertension belong to the low-risk group where sexual dysfunction can be safely managed with the approved medical therapies regardless of the number or class (with the exception of b-blockers and diuretics) of agents of the patient’s antihypertensive regime. Moreover, patients of this group can safely initiate or reinstitute sexual activity without any need for additional cardiovascular evaluation.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Phase 2 and 3 trials reported minimal associated cardiac adverse effects, which occurred in 3% of patients taking sildenafil and in 3.5% of patients receiving placebos.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Having your current medication checked – if you are taking medication already, it could be that your erection problems are a side effect. Have a doctor check whether this is the cause of your problems and if it is, you might be able to switch medications and then find that your erectile dysfunction goes away completely – or at least improves. Medications that can cause erection problems include:
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Crossref | PubMed | Scopus (165) | Google ScholarSee all References Typically, the response to sexual activity is no more than an increase in heart rate to 130 beats/min and an increase in systolic blood pressure level to 170 mm Hg.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
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.

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

Co-authors Stacy Mandras, M.D., Patricia Uber, Pharm. D., and Mandeep Mehra, M.D., conducted systematic independent literature searches using the MEDLINE database and examined a broad range of medical research that focused on chronic heart failure, sexual activity and sexual dysfunction. This literature included data from patient surveys and clinical trials.


The initial step in evaluating ED is a thorough sexual history and physical exam. The history can help in distinguishing between the primary and psychogenic causes. It is important to explore the onset, progression, and duration of the problem. If a man gives a history of “no sexual problems until one night,” the problem is most likely related to performance anxiety, disaffection, or an emotional problem. Aside from these causes, only radical prostatectomy or other overt genital tract trauma causes a sudden loss of male sexual function.
Crossref | Google ScholarSee all References Other investigators have suggested these medications may exert a hormonal effect. β-Blockers have been associated with decreased free and total testosterone levels in placebo-controlled trials.39x39Rosen, RC and Weiner, DN. Cardiovascular disease and sleep-related erections. J Psychosom Res. 1997; 42: 517–530

In the past 6 years, the FDA has approved three oral agents for the treatment of ED: sildenafil, vardenafil, and tadalafil. All three are phosphodiesterase type 5 (PDE-5) inhibitors and work by potentiating the effect of nitric oxide in the penis. In particular, they block the hydrolysis of cyclic guanosine monophosphate to guanosine 5'-monophosphate, thus enhancing nitric oxide–mediated smooth muscle relaxation, increasing blood flow to the penis and facilitating erection.

Ginkgo Biloba is promoted to treat conditions ranging from hypertension to Alzheimer’s dementia. There is evidence that shows improvement of memory enhancements in the geriatric population (47), improvement in terms of cognitive function via effect on cerebral vasculature (48), improvement of claudication distance and cutaneous ulcers in patients with peripheral vascular disease (49). Ginkgo Biloba extract is proposed to induce NO in endothelial cells and thus causing relaxation of vascular smooth muscles. Animal studies have reported relaxation of rabbit corpus cavernosal smooth muscle cells with the use of Ginkgo Biloba (50). Adverse effects include headaches, major bleeding (in patient who are taking warfarin concurrently) and seizures with reported fatality (36).
There have been some studies to suggest that a placebo effect that improves ED may work for some men. One study found that men taking an oral placebo pill showed as much improvement in ED symptoms as men who took actual medication to improve ED. Conversely, men who were given therapeutic suggestions to improve ED did not see signs of symptom improvement.
For oral erectile dysfunction medicines to work as desired, they must be used properly in the first place. This means taking the medicine 30–45 minutes before engaging in sexual intimacy; taking the drug on an empty stomach or at least avoiding a heavy or high-fat meal before taking the drug (this is especially important when using sildenafil); and engaging in adequate genital stimulation before attempting intercourse. Drinking small amounts of alcohol (one to two drinks) should not compromise the effectiveness of erectile dysfunction medicines, but larger amounts of alcohol can diminish a man’s ability to have an erection.
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