Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References Although some case studies have reported a relationship between calcium channel blockers and ED, most studies suggest that this effect is minimal and that any relationship is likely secondary to a decrease in blood pressure with consequent reflex sympathetic activation.42x42Weiss, RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician. 1991; 44: 2075–2082

A component of the increased risk conferred by ED could be testosterone deficiency.24 Low testosterone leads to increased levels of total and LDL cholesterol, as well as to increased production of pro-inflammatory markers and mediators.25 Endothelial dysfunction and increased arterial wall thickness, stiffening, and calcification also ensue. On this basis it has been hypothesized that chronically lowered testosterone may increase CVD risk. Indeed, androgen deficiency has emerged as a predictor of CV events, as well as of all-cause and CV mortality, both in the general population and in patients with CV risk factors, with hypertension, with established CVD, and with ED.26 Viewed from the opposite angle, higher serum testosterone showed a protective role for CV events in elderly men.27 A 2010 meta-analysis limited to studies in middle-aged men found no association between total testosterone (TT) levels and CVD risk.28 However, a more recent meta-analysis involving a larger number of studies identified significant associations between androgen deficiency and increased risk of CVD and CVD mortality.29 It should be stressed, however, that the nature of these studies cannot prove causality. The possibility that low testosterone may be an epiphenomenon, marking poor general health rather than modulating CVD risk per se has to be explored.


Crossref | PubMed | Scopus (23) | Google ScholarSee all References In some elderly men, tadalafil could be detected in the bloodstream 6 days after oral ingestion.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446
In the early years of my cardiology practice, I was surprised by the number of men with heart disease who also suffered from impotence. In fact, being incapable of having an erection was the norm rather than the exception after heart attack. In those days, impotence was widely attributed to the psychological depression that often followed heart attack.

According to the Cleveland Clinic, “because erectile dysfunction is caused by a complex set of psychosocial, neurologic, and vascular factors, a specific cause in a patient may remain ambiguous.” The root causes are often related to a blockage or dysfunction of blood vessels. For example, ED can be due to conditions like atherosclerosis or diabetes, hormonal imbalances or problems related to mental health. It’s been found that common causes typically include one or more of the following factors: (2)

Another common reason for failures of oral therapy is the absence of sexual or genital stimulation prior to attempting sexual intercourse. These medicines facilitate an erection by increasing blood flow to the penis, but they do not act as an aphrodisiac or as an initiator of the erection. A man who is not “in the mood” or does not have adequate physical stimulation will not respond with an erection.
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