Some commonly prescribed cardiovascular drugs (beta-blockers, diuretics, angiotensin-converting enzyme inhibitors, etc.) contribute to ED.18 Previous studies have shown a strong association between ED and diuretics in patients treated with hydrochlorothiazide or chlorthalidone.19,20 It has also been shown that patients treated with first-generation non-selective beta-blockers, such as propranolol, had more frequent ED than those treated with a placebo.21
Cardiovascular disease and erectile dysfunction (ED) are closely interrelated disease processes. Erectile dysfunction reportedly affects 10 million to 20 million men in the United States and more than 100 million men worldwide. Each year, about 500,000 persons in the United States survive a myocardial infarction, and an estimated 11 million have existing cardiovascular disease, making the issue of sexual function and cardiac disease relevant to many patients. We explore the relationship between ED and the presence of cardiovascular disease in the general population. We also review the prevalence and pathophysiological associations of ED and cardiovascular disease. The risks of sexual activity for patients with cardiovascular disease are discussed, as are prevention and treatment strategies for ED in this patient population.
The use of shock wave therapy has revolutionized the treatment of many aspects of medicine. High intensity extracorporeal shockwave therapy has been used for the treatment of nephro-urolithiasis while medium intensity shockwave therapy is used by orthopaedic surgeons to treat joint pain as well as tendinitis. Low intensity shockwaves therapy was first noted to improve ischaemia-induced myocardial dysfunction in animal studies when low intensity shockwaves were applied to porcine myocardium (13). Shockwaves induces a localized stress on cell membranes in the same way that shear stress affects endothelial cell membranes (14) and this triggers the release of angiogenic factors, such as increased NO production through increased activity of endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS), platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) (15). These shockwaves also cause membrane hyperpolarization (16), activation of the Ras signaling pathway, non-enzymatic synthesis of NO and induction of stress fibers and intercellular gaps (17).

*** 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.
When it comes to combating heart disease, most information sources promote drugs and surgery as the only viable options, with lip service to dietary advice that simply does not work. As a result, the demand for high-tech, expensive, but largely ineffective medical care is soaring, causing medical costs and insurance rates to skyrocket. This chase for "cures" is both financially devastating and futile. Morbidity and premature mortality from heart disease continue to rise, with no sign of abating.
When it comes to boosting sexual performance, many men will walk all over God’s green earth looking for ways to maintain a good sex life. Luckily men, all you have to do is walk — not run — 2 miles a day. This, along with other healthier lifestyle interventions can help obese men reduce their risk of ED, or even “reverse” current impotence, according to a 2005 study. This comes of importance, since maintaining a trim waistline is a good defense for ED, as men with a 42-inch waist are 50 percent more likely to have ED than those with a 32-inch waist. Getting to a healthy weight and maintaining it is a good strategy for preventing and treating ED.
Other effective Diabetic Erectile Dysfunction Treatment therapies available include (a) an intraurethral suppository of the vasodilator drug alprostadil (prostaglandin E1), (b) intracavernosal self injection (penile self injection) of the non-specific PDE drug papaverine, the non-selective alpha-adrenergic antagonist phentolamine, and the vasodilator prostaglandin E1, used alone or in combination, or (c) penile prostheses (penile implants).
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.

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].
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References However, patients with hypertrophic obstructive cardiomyopathy and idiopathic hypertrophic subaortic stenosis are at increased risk of syncope and sudden death after exercise.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
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).
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Nitrates have only modest antianginal effects and offer no prognostic benefit for mild recurrent angina or unstable angina. Therefore, such anginal symptoms occurring after sildenafil use should be treated with other nonnitrate antianginal agents such as β-blockers.15x15Taylor, HA Jr. Sexual activity and the cardiovascular patient: guidelines. Am J Cardiol. 1999; 84: 6N–10N

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.


Several other facts support the close relationship between sexual dysfunction and CV disease. Endothelial dysfunction mediated by decreased nitric-oxide bioavailability as well as atherosclerotic lesions constitute a common pathophysiologic substrate affecting both CV disease and erectile dysfunction, a disease considered to be primarily of vascular origin[76,80-82]. Several traditional CV risk factors (diabetes mellitus, hypertension, dyslipidemia, and smoking) are frequently found in individuals with erectile dysfunction, conferring a detrimental cardiovascular burden to them. More interestingly, the increased cardiovascular risk observed in those patients is independent of the aforementioned CV risk factors[81-88].


Third, men with Diabetes need to control their blood sugar levels. When your blood sugar is not under control, your body does not produce enough Nitric Oxide (NO) and vascular tissues don’t respond as effectively to NO. When enough blood flows into the penis, penile veins close off and block the blood from flowing out. This process results in an erection. If your body does not produce enough NO or if your penile tissues do not respond to NO, the pressure of the blood flowing into your penis is not sufficient to trap the blood, you penis will not get hard.


Some research even suggests the effect of blood pressure drugs may be more psychological than physical. When ED occurs after a man begins to take a new medication, it's possible that anxiety about his health, rather than the medication, may trigger the problem. And being aware of possible side effects may make a man more likely to recognize them as abnormal.

In DM patients with a documented androgen deficiency, testosterone replacement may correct or facilitate the treatment of ED.7 A transdermal testosterone gel or patch, or intramuscular testosterone cypionate are the alternatives. Oral testosterone is contraindicated in the United States due to hepatotoxicity, but a new product has been developed that allows for buccal absorption of testosterone. Thyroid supplements rarely alleviate EDDM.


At the same time, people with diabetes are susceptible to a type of blood vessel damage known as endothelial dysfunction. A recent study found that men with ED are at a greater risk of heart disease, which is also associated with endothelial dysfunction. If blood vessels aren't in good working order, the penis may not get enough blood for an erection.
Ginseng is the most common ingredient among top-selling supplements for men’s sexual health (36). The English word ginseng derives from the Chinese term renshen. Ren means “person” and shen means “plant root”. This plant has been named in this manner as its roots resemble the lower limbs of a human, Traditionally, ginseng has been used to restore and enhance the normal well-being of the body. The effects are due to ginseng’s reactions with the central nervous system, metabolism, immune function and cardiovascular system. The principal active compounds are triterpene saponins known as ginsenosides. Animal studies have suggested that specific ginsenosides may be responsible for ginseng-mediated effects on copulatory behavior (37). Ginsenoside induces smooth muscle relaxation by hyperpolarizing the smooth muscle membrane via activation of large-conductance KCa channels (38).
The common associations between cardiovascular disease and ED have led some researchers to explore whether onset of ED can be an effective predictor of the presence of cardiovascular disease. A study of 40 patients with cardiac disease found an association between sexual dysfunction and the presence of cardiovascular disease, as well as a correlation between the severity of ED and the number of coronary arteries with extensive atherosclerosis.16x16Greenstein, A, Chen, J, Miller, H, Matzkin, H, Villa, Y, and Braf, Z. Does severity of ischemic coronary disease correlate with erectile function?. Int J Impot Res. 1997; 9: 123–126

And diabetes affects more than the blood system. “Diabetes also results in nerve dysfunction and, in the penile shaft, [eventually] the muscle starts to atrophy and is replaced by scar tissue or collagen rather than smooth muscle. That’s the ultimate end result in men,” explains urologist Ajay Nehra, MD, professor of urology at the Mayo Clinic in Rochester, Minn. That scenario — damage to all the tissues that support your penis — is what could happen if you do not get and keep your diabetes under control.

Crossref | PubMed | Google ScholarSee all References Patients with vascular risk factors (diabetes mellitus, hypertension, heart disease, and hyperlipidemia) had significantly decreased peak systolic velocities and increased end-diastolic velocities. Patients with diabetes mellitus had increased end-diastolic velocities and decreased resistive indices, indicating a disorder of venous trapping during erections. Another study examined corpora cavernosal tissue removed at penile prosthesis placement in 21 diabetic men and 42 nondiabetic controls.23x23Saenz de Tejada, I, Goldstein, I, Azadzoi, K, Krane, RJ, and Cohen, RA. Impaired neurogenic and endothelium-mediated relaxation of penile smooth muscle from diabetic men with impotence. N Engl J Med. 1989; 320: 1025–1030
For patients who failed oral medical therapy or unable to tolerate the side effects, intracavernosal injection of vasoactive agents can often provide effective alternative. Various vasoactive agents such as alprostadil, papaverine or phentolamine have been used either as single agent or combination agents to potentiate the NO release and cavernosal smooth muscle vasodilation. However, intracavernosal injection therapy has high attrition rate and can be associated pain especially with alprostadil injection (2). The practice of isolating compounds and understanding its pharmacological attributes before using it as a drug therapy has been a strength of Western medicine.
Yes, and there’s the rub. High blood pressure, especially if untreated, can lead to erectile dysfunction (ED). So can medications your doctor prescribes to bring down your high blood pressure. Fortunately, not all meds cause ED. Thiazides, diuretics or “water pills,” are common ED culprits. So are beta blockers. These effective heart meds slow your system down, and also affect blood flow where you need it -- in your penis -- at the right time. Alpha blockers, another class of medications that lower high blood pressure, are less likely to cause ED. So talk with your good doc about medication choices and side effects, so you can choose the right med for you.
Abstract | Full Text PDF | PubMed | Scopus (1528) | Google ScholarSee all References After sexual intercourse, this risk increases approximately 2-fold, to 2 chances per million per hour, but only for the 2 hours after intercourse. For low-risk patients with no history of cardiovascular disease and an annual myocardial infarction risk of 1% per year, the risk increases to 1.01% with weekly sexual activity.8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409

Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References Risk of arrythmias after sexual intercourse was evaluated in 82 patients with stable coronary artery disease who were monitored with ambulatory ECG after sexual intercourse.81x81Drory, Y, Fisman, EZ, Shapira, Y, and Pines, A. Ventricular arrhythmias during sexual activity in patients with coronary artery disease. Chest. 1996; 109: 922–924


Penile erection is largely a vascular process, and the penile endothelium and smooth muscle tissue are very sensitive to functional and structural changes. Vasculogenic ED results from an impairment of endothelial dependent or independent smooth muscle relaxation (functional vascular ED, initial stages), occlusion of the cavernosal arteries by atherosclerosis (structural vascular ED, late stages), or a combination of these.3 Current data support a complex interplay between endothelial dysfunction, subclinical inflammation, and androgen deficiency (Figure 1). The relationship between ED and CAD at the clinical level is supported by this common pathophysiological basis. The ‘artery size’ hypothesis explains why patients with CAD frequently report ED before CAD detection.10 According to this hypothesis, for a given atherosclerotic burden, the smaller penile arteries suffer obstruction earlier than the larger coronary arteries (Figure 2). The same concept holds also true in the case of non-obstructing atherosclerosis: since the smaller penile artery have a greater endothelial surface and erection requires a large degree of vasodilation to occur when compared with arteries in other organs, the same degree of endothelial dysfunction will be symptomatic in these smaller vessels but subclinical in the larger ones (i.e. coronaries). In the same context, accelerated arterial ageing (as indicated by increased arterial stiffening that also affects large arteries of ED patients) may be a common background.11,12 Erectile dysfunction is associated with an incremental inflammatory and endothelial-pro-thrombotic activation.13 Interestingly, this activation is equal to that found in CAD patients with no ED, while when these two conditions are combined the burden is additive. Androgen deficiency may be also implicated in the common pathogenetic pathways of ED and CVD; however, this warrants further substantiation.2
With early detection, doctors can suggest preventive measures like statins, blood pressure meds, revamping eating habits and getting more exercise. Try these two exercises that can cut your risk of heart disease in half. The study researchers told Science Daily, “Our study supports a more aggressive CVD risk assessment and management for persons with erectile dysfunction, including young men who may otherwise be categorized as low-risk due to their young ages.” Check out the sexual health conditions affecting millennial men.
Quassinoids isolated from Tongkat Ali have been reputed to be anti-tumor, anti-malarial, anti-amoebic and anti-inflammatory. Its leaves are used for washing itches, its fruits for the treatment of dysentery, its bark used as a vermifuge, the taproots used for treatment of hypertension and the root bark for treatment of diarrhea and fever. The roots extracts are used for sexual dysfunction, aging, malaria, cancer, diabetes, anxiety, aches, constipation, exercise recovery, fever, increased energy, increased strength, leukemia, osteoporosis, stress and syphilis. Animal studies done on middle age sex rats showed enhancement of the sexual qualities in terms of hesitation time among middle aged rats (46).
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References During this period, 130 deaths were reported to the US FDA; 41 of these men died or had cardiac arrest within 4 to 5 hours after taking sildenafil, and 27 died or had cardiac arrest either during or immediately after sexual activity. The average age of these men was 64 years. Of the 77 men in this group who died of documented cardiovascular-related events, 41 died of definite or suspected myocardial infarction, 27 died after cardiac arrest, and 6 had symptoms of cardiac disease at the time of death. Sixteen of the men had taken nitroglycerin or organic nitrates in association with sildenafil; another 3 had nitroglycerin in their possession at the time of death. In 48 men, the cause of death was unknown, and another 3 died of cerebrovascular accidents. Overall, it was concluded that sildenafil was not associated with an excess of cardiovascular death.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (124) | Google ScholarSee all References This was a doubleblind, single-dose crossover study involving 41 men with stable coronary artery disease characterized by reproducible stable exertional angina. After taking either 10 mg of vardenafil or placebo, these men underwent treadmill exercise tolerance testing to 5 to 10 METs. Compared with placebo, vardenafil use did not result in a change in exercise treadmill time or time to first awareness of angina but significantly increased the time to ischemic threshold. At peak exercise levels, vardenafil did not cause a change in either heart rate or blood pressure level. This study concluded that 10 mg of vardenafil did not impair the ability of men with stable coronary artery disease to exercise at levels consistent with the exertion associated with sexual intercourse.
Due to their vasorelaxing effect, administration of PDE-5 inhibitors in hypertensive individuals was initially confronted with great suspicion. A wealth of clinical data however has proven that PDE-5 inhibitors are associated with few side effects and provoke a small and insignificant reduction in blood pressure with minimal heart rate alterations in both normotensive and hypertensive patients as well. As a matter of fact, they can be safely and effectively administered to hypertensive individuals even when they are already taking multiple antihypertensive agents[51-56]. The sole exception to the rule is co-administration with organic nitrates, which is an absolute contraindication due to profound and possibly hazardous hypotension effect[57,58]. Moreover, precaution should be taken when PDE-5 inhibitors are combined with a-blockers where, due to possible orthostatic hypotension effect, lower starting doses should be implemented in the therapeutic regime[59-62].
Dr. Eid also urges these patients to treat their diabetes in order to avoid developing ED for life. “They need to manage their diabetes and make sure they control it so the ED will not progress and will stabilize, as a result,” he said. “If the diabetes is controlled after the patient is first diagnosed, then the erections will come back. But if the patient has diabetes for many years, and suddenly decides it’s time to control it, they cannot prevent the damage that’s already been done.”
The 12-week study of 164 men, all with hypertension, was divided into 2 groups of 82, one group with sexual dysfunction, the other group reported normal sexual functioning. Both groups took losartan in dosages of 50 to 100 milligrams daily for the 12 weeks of the study. In the group of men with sexual dysfunction, 88 percent reported improvement in at least one area of sexual function and 73.7% reported an improved quality of life.

Relative risk and 95% confidence interval for erectile dysfunction and clinical events. Relative risk and 95% confidence interval for erectile dysfunction and total cardiovascular events (A), cardiovascular mortality (B), myocardial infarction (C), cerebrovascular events (D), and all-cause mortality (E). Studies are listed alphabetically. Boxes represent the relative risk and lines represent the 95% confidence interval for individual studies. The diamonds and their width represent the pooled relative risks and the 95% confidence interval, respectively. CVD, cardiovascular disease; DM, diabetes mellitus; HF, heart failure; GEN, general population. Numbers in brackets are the number of references in the text—and references with S are from Supplementary material online. With permission from Vlachopoulos et al.5


Due to their vasorelaxing effect, administration of PDE-5 inhibitors in hypertensive individuals was initially confronted with great suspicion. A wealth of clinical data however has proven that PDE-5 inhibitors are associated with few side effects and provoke a small and insignificant reduction in blood pressure with minimal heart rate alterations in both normotensive and hypertensive patients as well. As a matter of fact, they can be safely and effectively administered to hypertensive individuals even when they are already taking multiple antihypertensive agents[51-56]. The sole exception to the rule is co-administration with organic nitrates, which is an absolute contraindication due to profound and possibly hazardous hypotension effect[57,58]. Moreover, precaution should be taken when PDE-5 inhibitors are combined with a-blockers where, due to possible orthostatic hypotension effect, lower starting doses should be implemented in the therapeutic regime[59-62].
In men without cardiovascular disease, erectile dysfunction (ED) pills are very safe. The three rivals -- Viagra, Cialis, and Levitra -- have similar side effects, including headache, facial flushing, nasal congestion, diarrhea, backache, and, in a few Viagra or Levitra users, temporary impaired color vision (men with retinitis pigmentosa, a rare eye disease, should check with their ophthalmologists before using these medications).
Tribulus terrestris is a dicotyledonous herbal plant of the Zygophyllaceae family, used to increase serum testosterone levels, which has only been shown in animal studies (40). A prospective, randomized, double blind study of 30 men showed that Tribulus terrestris was not more effective than placebo on improving IIEF scores or serum total testosterone (41). Two accounts of hepato-nephrotoxicity have been reported in young men who ingested high doses of this herbal medication (42,43).
There are a number of reasons a man may not achieve the desired result from an oral erectile dysfunction drug. In some cases, a man may experience drug side effects severe enough to outweigh any potential benefit of taking the drug. Possible side effects of these drugs include headache, facial flushing, nasal congestion, and transient abnormal vision. (In October 2007, the FDA added a warning about sudden hearing loss to the package labels of oral erectile dysfunction drugs. While it’s not absolutely clear that the drugs can cause sudden hearing loss, a number of cases have been reported in men within hours or days of taking one of the drugs.)
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