Normal penile erection is controlled by two mechanisms: reflex erection and psychogenic erection. Reflex erection occurs by directly touching the shaft of the penis, while psychogenic erection occurs by erotic or emotional stimuli. ED is a condition where erection does not take place by either mechanism. ED can occur because of hormonal imbalance, neural disorders or lack of adequate blood supply to the penis.54 Lack of blood supply can be a result of impaired endothelial function associated with CAD.54
A similar situation develops in the fragile penile circulation. Any disturbance in nitric oxide production lowers the capacity to dilate penile arteries, impairing penile engorgement for erection. Release of nitric oxide is readily sabotaged by many conditions, including elevated levels of cholesterol, high blood pressure, increased triglycerides, smoking, metabolic syndrome and diabetes, and excessive consumption of dietary saturated fat.9 If an artery’s inner wall can’t produce nitric oxide, an abnormal constriction of the arteries to the penis follows, effectively choking off blood flow.
Physical and sexual activity can trigger acute cardiac events. In a recent meta-analysis, a significant association between acute cardiac events and episodic physical (relative risk 3.45 for myocardial infarction and 4.98 for sudden cardiac death) and sexual activity (relative risk 2.7 for myocardial infarction) was demonstrated.32 This association was attenuated among individuals with high levels of habitual physical activity (for every additional time per week the relative risk for myocardial infarction decreased by ∼45%, and the relative risk for sudden cardiac death decreased by 30%). The physical demands of sexual activity have been identified as follows. Studies conducted primarily in young married men showed that sexual activity with a person's usual partner is comparable with mild-to-moderate physical activity in the range of 3–4 metabolic equivalents of the task (METS).30,33 The heart rate rarely exceeds 130 b.p.m. and systolic blood pressure rarely exceeds 170 mmHg in normotensive individuals. Accordingly, demands during sexual activity correspond to walking 1.5 km (or 1 mile) on the flat in 20 min or briskly climbing two flights of stairs in 10 s. Generalization, however, may not characterize all individuals (especially those who are older, are less physically fit, or have CVD) or sexual activity circumstances (e.g. extramarital, unfamiliar setting, excessive food and alcohol consumption). Therefore, completing 4 min of the standard Bruce treadmill protocol (5–6 METS) without symptoms, ST segment changes, arrhythmias, or a fall in systolic BP identifies the safety of sexual activity.30,33
Erectile dysfunction can be a symptom of heart disease. An erection is caused by engorgement of blood into the penile tissues which later becomes rigid for penetration. Men with heart problem suffer from an inadequate blood flow to the smooth tissues of the penis to achieve erection. A major cardiovascular disease known as Atherosclerosis is a result of fat accumulation in the arterial blood vessels. This build up of multiple plaques or fatty material causes the arteries to narrow and harden thus limiting blood flow. The arteries supplying your penis are smaller than those supplying your heart. In fact, ED can be an initial symptom of heart diseases like Atherosclerosis. Cardiovascular problems can also damage penile nerves and arteries, inhibiting erectile function. Experts found a consistent link between ED and heart disease. Other recent research conducted by health professionals has shown a direct connection between erection dysfunctions and heart problems.
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.
The incidence of ED is 42.0–57.0 % in men with CAD and 33.8 % in those who have diabetes with silent ischaemia, compared with 4.7 % in men without silent ischaemia.6 The prevalence of ED is likely to be higher than the reported figures, because men generally do not seek medical advice for ED.6 Erection is thought to be a process that is regulated by hormones and neurovascular mechanisms in cerebral and peripheral levels.7
Relaxation of erectile tissue requires nitric oxide from nonadrenergic-noncholinergic neurons and the endothelium.21 Penile tissue from diabetic men with ED demonstrates impaired neurogenic and endothelium-mediated relaxation of smooth muscle,22 increased accumulation of advanced glycation end products (AGEs),23 and upregulation arginase, a competitor with nitric oxide synthase for its substrate L-arginine.24 Normal responses to direct smooth muscle relaxants in most of these studies implies that the impairments are due to decreased synthesis, release, or activity of nitric oxide. The fundamental mechanisms mediating these changes are thought to be the same as for other diabetic complications: increased polyol pathway flux, intracellular accumulation of AGEs, activation of protein kinase C, and increased flux through the hexosamine pathway.25
An equally valuable observation though, is the fact that sexual dysfunction could indeed indicate asymptomatic CV disease. A solid amount of evidence accumulated over the last years has pointed out towards that trend moving, hesitatingly though, sexual dysfunction in the surface of scientific interest. As such, commonly under-reported, under-recognized and under-treated, sexual dysfunction could indeed play its role in cardiovascular risk assessment and stratification.
After analyzing 28 previous studies on the link between ED and heart disease, the researchers found a connection between erectile dysfunction and poor endothelial function. “Blood vessels are unable to fully dilate and allow blood to flow through,” explains Medicalnewstoday.com. “Endothelial dysfunction is an early sign of atherosclerosis, a condition in which plaque builds up in the arteries, raising the risk of heart attack and stroke.” The researchers also determined that there was a thickening of one of the inner two layers of the carotid artery—another heart-disease indicator.
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.
The safety of PDE5 inhibitors in patients with IHD has been shown in multiple trials. Arruda-Olson et al. investigated the safety of sildenafil during exercise stress tests in patients with IHD to ascertain whether the drug induces or exacerbates myocardial ischaemia. This was a prospective, randomised crossover study that demonstrated safety of sildenafil when given 1 hour before an exercise stress test.69 Another study that investigated 120 trials of sildenafil revealed that the rates of MI and cardiovascular death with sildenafil are as low as with placebo.70
The second way relates to the risk associated with the sexual activity in a patient with either overt or occult CVD. In this case, the diagnosis of ED should prompt an initial cardiovascular assessment based on the history and clinical examination in order to define the baseline risk according to (i) the likelihood of silent CAD18,31 (especially since ED patients have a high probability to have silent CAD) or to the stage of clinically evident CAD, (ii) other cardiovascular conditions either unrelated, or related to ED (e.g. heart failure, peripheral arterial disease).
Gutiérrez-González, Enrique; Castelló, Adela; Fernández-Navarro, Pablo; Castaño-Vinyals, Gemma; Llorca, Javier; Salas-Trejo, Dolores; Salcedo-Bellido, Inmaculada; Aragonés, Nuria; Fernández-Tardón, Guillermo; Alguacil, Juan; Gracia-Lavedan, Esther; García-Esquinas, Esther; Gómez-Acebo, Inés; Amiano, Pilar; Romaguera, Dora; Kogevinas, Manolis; Pollán, Marina; Pérez-Gómez, Beatriz. “Dietary Zinc and Risk of Prostate Cancer in Spain: MCC-Spain Study.” Nutrients. Jan 2019, 11(1).
A number of drugs are known to cause ED in patients with DM (Table 1). For example, many EDDM patients are on antihypertensive medications. Replacement of thiazides or beta-blockers with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may be sufficient to regain erectile ability.5 Furthermore, discontinuation of selective serotonin reuptake inhibitors, if these drugs are not essential for patient well-being, may be therapeutic. Careful monitoring following drug discontinuation will help to determine if ED is due to the medication or other underlying disorders. The benefits of continued drug therapy with these drugs should always be weighed against the likelihood of causing ED and impacting on the patient's QOL.
Since their introduction in the therapeutic field, more than a decade ago, PDE-5 inhibitors have revolutionized the treatment of sexual dysfunction. By blocking the activity of PDE-5 isoenzyme, localized throughout the smooth muscle cells of the vasculature (genital vessels included), PDE-5 inhibitors increase the levels of cyclic guanosine monophosphate thus exerting vasodilating properties and facilitating penile erection[40-42]. Due to these properties, sildenafil was the first drug of its class to receive wide acceptance. Its short half-life, food interactions and the associated visual disturbances however, paved the way for the development of newer PDE-5 inhibitors. As such vardenafil with its more rapid onset of action, and tadalafil with its longer half-life and the lack of food interactions or side effects, have offered significant alternatives to sildenafil[43-50].
The cardiovascular effects of sildenafil during exercise in patients with known or probable cardiovascular disease were studied in a randomized placebo-controlled trial of 105 men with a mean age of 66 years.63x63Arruda-Olson, AM, Mahoney, DW, Nehra, A, Leckel, M, and Pellikka, PA. Cardiovascular effects of sildenafil during exercise in men with known or probable coronary artery disease: a randomized crossover trial. JAMA. 2002; 287: 719–725
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
The connection between diabetes and ED is related to your circulation and nervous system. Poorly controlled blood sugar levels can damage small blood vessels and nerves. Damage to the nerves that control sexual stimulation and response can impede a man’s ability to achieve an erection firm enough to have sexual intercourse. Reduced blood flow from damaged blood vessels can also contribute to ED.
Crossref | PubMed | Scopus (72) | Google ScholarSee all References This study found that the mean PSV was a better predictor of the presence of cardiovascular disease than stratification by standard cardiac risk factors such as diabetes mellitus, hypertension, obesity, and smoking. The researchers recommended that persons with no history of prior perineal trauma and with a PSV lower than 35 mL/s should undergo exercise testing before receiving treatment of ED because these patients had a 42% risk of having ischemic heart disease. However, other investigators questioned the utility of using penile arterial flow to predict the presence of ischemic heart disease.18x18Chiu, AW, Chen, KK, Chen, MT, Chang, LS, and Chang, MS. Penile brachial index in impotent patients with coronary artery disease. Eur Urol. 1991; 19: 213–216
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.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (30) | Google ScholarSee all References Erections result from relaxation of the corpora cavernosa, which is mediated either by increasing intracellular cyclic guanosine monophosphate (cGMP) or cyclic adenosine monophosphate or by inhibition of their degradation. Increased parasympathetic tone results in a decrease in norepinephrine release and an increase in the release of acetylcholine; subsequently, NO synthase activity increases, which releases NO from both endothelial cells and nonadrenergic, noncholinergic neurons.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 (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.
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
Preclinical and clinical trials of these oral agents have clearly demonstrated that they are well tolerated by most DM patients and have an efficacy rate superior to other oral agents. The ultimate result is an improved quality of life (QOL) in EDDM patients. With a greater willingness of DM patients to discuss and seek treatment for ED, it is highly probable that the use of these oral agents will continue to increase. The goal of this article is to provide the physician and pharmacist with a background and working knowledge of these oral agents and their present-day alternatives.
These medications don’t work for everyone but they are easy to use and work for around 60% of people who try them. They work by making it easier to get an erection by reducing the effect of (inhibiting) the chemical PDE-5. This chemical is used in the body to make sure there isn’t too much blood in the penis during an erection, but if you have erectile dysfunction then this chemical ends up over-compensating.
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Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References The use of any NO-donor medications should be avoided for 24 hours after the last dose of sildenafil and even longer if there is a suspected prolonged half-life secondary to such conditions as renal insufficiency.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References When used in combination with NO-donor medications such as nitroglycerin, the modest blood pressure effects of sildenafil are potentiated, resulting in a significant decrease in systolic (21-55 mm Hg) and diastolic (up to 26 mm Hg) blood pressure levels, as well as vasodilatory symptoms such as headache, light-headedness, and nausea.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
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.
Just because a product claims to be natural doesn't mean it's safe. Many herbal remedies and dietary supplements can cause side effects and dangerous interactions when taken with certain medications. Talk to your doctor before you try an alternative treatment for erectile dysfunction — especially if you're taking medications or you have a chronic health problem such as heart disease or diabetes.
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
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.
When antihypertensive medication comes to the fore, certain issues need to be carefully addressed. This is due to the fact that medically induced erectile dysfunction is one of the major reasons for non-adherence and treatment discontinuation, a reality that could have deleterious consequences on patient’s cardiovascular profile and health quality in the long term[38,39].
Despite the existing controversies, available data so far imply the old generation b-blockers (e.g., propranolol) as the major culprits for sexual dysfunction with the newer ones (carvedilol, celiprolol) to exert a less pronounced negative effect[21-24]. A luminous exception to the rule, nebivolol, is a newer agent of its class which significantly ameliorates erectile dysfunction through increased nitric oxide generation, an effect consistently demonstrated in recent studies[25,26]. Diuretics, even on adjunct therapy, constitute another antihypertensive agent negatively associated with sexual function[27-29]. On the other hand, calcium antagonists and angiotensin converting enzyme inhibitors seem to demonstrate a neutral effect[30-32]. Interestingly, angiotensin receptor blockers (ARBs) by blocking the vasoconstrictive action of angiotensin II seem to positively affect erectile function and are thus regarded as a first-line treatment in hypertensive patients with erectile dysfunction[22,25,33-35].
Before Viagra hit the market in 1998, there was no proven treatment for erectile dysfunction that men could take in pill form. Doctors were interested in yohimbe, an herb that increases heart rate and blood pressure. Some doctors prescribed it to their patients in combination with other treatments for erectile dysfunction. Even then it was not a recommended treatment and is still not today. Studies have not proven that it works.
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.
To understand what happens in ED, it's helpful to know some anatomical basics. When aroused by either sensory or mental stimuli, the brain sends a signal through the nerves to the penis, causing the muscles there to relax. This opens up space for blood to flow in and engorge the penis. A membrane within the penis traps blood inside to help maintain the erection, which subsides when the penile muscles contract, forcing blood back into the rest of the body. Any number of things can go wrong in this process, leading to erectile dysfunction.
If you can't take one of these oral medications, your physician may have you try Caverject (alprostadil for injection), a hormone that you inject into your penis using a fine needle, or Muse (alprostadil urogenital), a tiny suppository that you insert into the tip of the penis. Both of these will bring on an erection within five to 15 minutes without sexual stimulation.
Diabetes mellitus is associated with both decreased erectile function and increased cardiovascular risk. The MMAS found that the age-adjusted probability of complete impotence was 3 times higher in patients with diabetes mellitus than in those without the disease.6x6Kloner, RA. Erectile dysfunction and cardiovascular risk factors. Hosp Pract (Off Ed). 2001; 36: 41–44 (49-51.)
According to Harvard Special Health Report Erectile Dysfunction, one study in the European Heart Journal looked at men newly diagnosed with heart disease, but without ED, who started treatment with the beta-blocker atenolol (Tenormin). Some of the study participants were told about the sexual side effect of the blood pressure drug, and ED was reported by almost one-third of the participants. In contrast, among those who were not told the drug's name or its side effects, only 3% said they experienced ED.
For many men, stopping smoking is an erectile dysfunction remedy, particularly when ED is the result of vascular disease, which occurs when blood supply to the penis becomes restricted because of blockage or narrowing of the arteries. Smoking and even smokeless tobacco can also cause the narrowing of important blood vessels and have the same negative impact.
Combination therapy has proven effective for some men who don’t respond adequately to oral medicines. The idea is to use two drugs with different mechanisms of action for better results. Commonly, sildenafil is used in combination with pellets of alprostadil (synthetic prostaglandin E1) that are inserted into the urethra (the tube in the penis that carries urine from the bladder to the outside of the body). Alprostadil also increases the blood supply to the penis, but by different means.