Erectile dysfunction is frequent in patients with established CAD with prevalence rates ranging between 47 and 75% in studies.2,4,14 The AssoCiatiOn Between eRectile dysfunction and coronary Artery disease (COBRA) trial tested the hypothesis that the ED rate differs in CAD patients according to the clinical presentation (acute vs. chronic coronary syndromes) and the extent of vessel involvement (one vs. two to three vessel disease)15 (Figure 3). The overall ED prevalence in CAD patients was 47%, whereas in the normal coronary angiography group the ED rate was 24%. When separately considered, the ED rate was 22% in patients with acute coronary syndromes (ACS) and one-vessel disease and 55 and 65% in patients with ACS and multi-vessel disease and with chronic coronary syndrome, respectively. The study also showed that both severity (IIEF <10) and duration (>24 months) of ED were predictive of severe coronary involvement at angiography. This study offers pathophysiological and mechanistic explanations related to the clinical setting. In patients with multi-vessel disease, regardless of the clinical presentation, the advanced coronary and systemic atherosclerosis is the reason for the high rate of ED. However, in the setting of acute myocardial infarction with one-vessel disease, ED is far less frequent because the atherosclerotic burden is modest (i.e. abrupt occlusion of a single non-obstructing plaque in the absence of extensive atherosclerosis) in both the coronary and penile circulations.15,16
The initial event for normal erectile function is sexual stimulation. Subsequent to processing in the central nervous system neural impulses are conveyed along the spinal cord, exiting through the pelvic parasympathetic preganglionic nerves. These pelvic nerves form the pelvic plexus and send their message through first messenger, acetyl choline, to the cavernosal nerves. The cavernosal nerves enter erectile bodies (corpora cavernosa) (Figure 1). Here, their nerve endings release a second messenger, nitric oxide. Nitric oxide activates the enzyme guanylyl cyclase, which lyses guanosine triphosphate (GTP) to produce a third messenger, the intracellular cyclic guanosine monophosphate (cGMP). Ultimately, the result is a decrease of intracellular calcium and an opening of potassium channels with the resultant relaxation of vascular smooth muscle in the arteries, aterioles, and sinusoids of the corpora cavernosa. The sinusoids open and rapidly fill with blood. Finally, the distended sinusoids compress their drainage pathways (venules) against the fibroelastic covering of the cavernosal bodies (tunica albuginea) and trap the blood in cavernosal bodies. The combination of an increased inflow of blood into the penis and coincident markedly diminished outflow results in rapidly increasing intracavernosal pressure that ultimately approximates systolic pressure. At this pressure the penis has sufficient axial rigidity to permit vaginal penetration.

Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Sildenafil is taken orally 1 hour before anticipated sexual intercourse and enhances the normal response to sexual stimulation; however, it has no effect on erections in the absence of stimulation.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N


Crossref | PubMed | Scopus (23) | Google ScholarSee all References, 73x73Rajagopalan, P, Mazzu, A, Xia, C, Dawkins, R, and Sundaresan, P. Effect of high-fat breakfast and moderate-fat evening meal on the pharmacokinetics of vardenafil, an oral phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction. J Clin Pharmacol. 2003; 43: 260–267
Conversely, and of significant clinical importance, is how often patients with ED as their first and sole clinical manifestation suffer from subclinical CAD.17 Previous studies reported a rate of inducible ischaemia by exercise stress testing (EST) in 22% (with a wide range of 5–56%) of ED patients reflecting differences in patient population, risk factors and criteria used for ED and CAD diagnosis. Interestingly, those patients further assessed with coronary angiography had obstructive atherosclerosis in >90% of cases.4,18 In a prospective angiographic study, we documented that 19% of ED patients suffer from clinically silent obstructive CAD.18

However, sildenafil should be used carefully with nitrates because their combination can result in severe hypotension and death.68 Both short- and long-acting nitrates are commonly prescribed to treat angina, but they have no prognostic benefit. In addition, there are numerous alternatives to treat angina, such as ranolazine and ivabradine, which do not interact with PDE5 inhibitors. As a result, patients with ED wishing to take PDE5 inhibitors can safely discontinue their nitrates and replace this treatment with the other anti-anginal agents.68

Even if you do not take blood pressure drugs, you should get your blood pressure checked as high BP also can be a sign of ED. In fact, men with ED are about 38% more likely to have high blood pressure than those without ED, according to a study that examined the medical records of more than 1.9 million men. That is not too surprising, since ED often occurs in men who smoke or are overweight—both of which are common risk factors for high blood pressure.

Many products contain undocumented “fillers” that can cause allergic reactions.  In recent years, the FDA has found over 300 herbal products that contain hidden, deceptively labeled, or dangerous ingredients4. And since 2015, the FDA has released public warnings on more than 160 ED supplements and “male enhancement” products found to contain dangerous ingredients and contaminants5 .   An independent study of FDA data, conducted in 2018, found almost 800 herbal supplements that contained unlisted ingredients6.
The views expressed in this article intend to highlight alternative studies and induce conversation. They are the views of the author and do not necessarily represent the views of hims, and are for informational purposes only, even if and to the extent that this article features the advice of physicians and medical practitioners. This article is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment, and should never be relied upon for specific medical advice.

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.
Low intracavernosal nitric oxide synthase levels are found in people with diabetes, smokers, and men with testosterone deficiency. Interference with oxygen delivery or nitric oxide synthesis can prevent intracavernosal blood pressure from rising to a level sufficient to impede emissary vein outflow, leading to an inability to acquire or sustain rigid erection. Examples include decreased blood flow and inadequate intracavernosal oxygen levels when atherosclerosis involves the hypogastric artery or other feeder vessels and conditions, such as diabetes, that are associated with suboptimal nitric oxide synthase activity.
A sexually competent male must have a series of events occur and multiple mechanisms intact for normal erectile function. He must 1) have desire for his sexual partner (libido), 2) be able to divert blood from the iliac artery into the corpora cavernosae to achieve penile tumescence and rigidity (erection) adequate for penetration, 3) discharge sperm and prostatic/seminal fluid through his urethra (ejaculation), and 4) experience a sense of pleasure (orgasm). A man is considered to have ED if he cannot achieve or sustain an erection of sufficient rigidity for sexual intercourse. Most men, at one time or another during their life, experience periodic or isolated sexual failures. However, the term “impotent” is reserved for those men who experience erectile failure during attempted intercourse more than 75% of the time.

Jelqing is penile massage technique of ancient Arabic origin (52). Men who practise jelqing will stretch their penises while in a semi-erected state and repeatedly milk their penises from base to glans, with their thumb and index finger touching to form an “OK” hand sign around their penile shaft. This massage can be done daily with the aim to achieve greater penile length and harder erections. Unwanted side effects of bruising, pain and fibrosis had been reported. No studies have been done to evaluate the efficacy of jelqing objectively.


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.
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

Eastern medicine should be fully exploited, and integrated with modern medicine to combine the advantages of both TCM and Western medicine. More research should be conducted into the efficacy and safety of TCM, and integration of TCM and Western medicine may provide promising breakthroughs in future clinical treatment. This strategy may allow for the development of new therapeutic strategies based on concepts of TCM and integrated medicine. There is a need for multimodal therapy and holistic approach to treat men (and their partners) with ED through complementary use of herbal supplements and modern drug to optimize underlying medical comorbidities; acupuncture, exercise or massage to reduce stress and strengthen the body; introduction and escalation of various medical therapy with use of mechanical therapy to further enhance penile erection; and lastly surgical intervention in suboptimal or refractory ED cases.

Another study showed a forty percent increase of blood flow to the heart within one year of starting a dietary program designed similar to the one described in my book, The End of Heart Disease. Of pertinent note is that, in the same study, the patients following a high-protein Atkins’ diet decreased blood flow to the heart by forty percent in one year.8 These dangerous high-protein diets are a certain path to erectile impotence and a premature cardiac death.
Like all diabetic complications, ED can occur even when you have followed your doctor’s advice and carefully managed your diabetes. Also like all diabetes complications, ED is less likely to occur with good blood sugar control. Poorly controlled diabetes and high cholesterol increase the chances of vascular complications, which may lead to ED or other circulatory problems. In addition, regular smoking and alcohol use can contribute to ED.

The EDDM patient has a variety of firstline options. The risk factors for vascular disease are the risk factors for ED. First-line therapy begins with attempts to minimize or eliminate these factors. These include smoking cessation, regular exercise, tighter glycemic control by attention to dietary restrictions, addition of statin drugs to correct dyslipidemia, and moderation of alcohol ingestion. Although there is very limited evidence that these modifications will dramatically reverse ED, they certainly will sponsor improved general health.4

Physical and emotional stress — whether over-exercising, under-sleeping or just dealing with everyday stressors like work and a busy schedule — causes an increase in “stress hormones,” including cortisol and adrenaline. Stress can lower desire for sex. This is because stress can contribute to fatigue or preoccupation with other tasks. It can also significantly affect blood flow by increasing inflammation.
Crossref | PubMed | Scopus (23) | Google ScholarSee all References Only 1 published study has investigated the effect of vardenafil on cardiac function.75x75Thadani, U, Smith, W, Nash, S et al. The effect of vardenafil, a potent and highly selective phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction, on the cardiovascular response to exercise in patients with coronary artery disease. J Am Coll Cardiol. 2002; 40: 2006–2012
One study the authors reviewed measured these changes in middle-aged men with and without coronary artery disease. This study found that the peak heart rate during intercourse was lower than heart rates measured during the patients' normal daily activities. The study participants' peak oxygen consumption levels during intercourse were moderate -- comparable to their oxygen consumption levels during moderate activities such as walking on level ground at 3 to 4 miles per hour, climbing stairs slowly or doing general housework such as vacuuming.

The EDDM patient has a variety of firstline options. The risk factors for vascular disease are the risk factors for ED. First-line therapy begins with attempts to minimize or eliminate these factors. These include smoking cessation, regular exercise, tighter glycemic control by attention to dietary restrictions, addition of statin drugs to correct dyslipidemia, and moderation of alcohol ingestion. Although there is very limited evidence that these modifications will dramatically reverse ED, they certainly will sponsor improved general health.4
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
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.
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