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 (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
With atherosclerosis, the blood vessels are not able to dilate properly, which is called endothelial dysfunction (see the Figure). Cholesterol builds up in the blood vessel walls and forms plaques, which make the vessels narrow and slow down blood flow. When a plaque becomes very advanced, it can completely stop blood from passing through, which is what happens in a heart attack. Atherosclerosis affects not only the blood vessels supplying the heart (coronary arteries), but also blood vessels throughout the entire body. Atherosclerosis causes angina (chest pain that is often exertional), heart attacks, strokes, claudication (pain in the legs with walking), and ED. Atherosclerosis affects different people in different places, but it often affects the penis first, then the heart and brain, and the legs last. Because the first stage of atherosclerosis, endothelial dysfunction, usually affects the penis first, ED can be a warning sign that a heart attack or a stroke may follow, often in the next 3 to 5 years. This warning sign can be a good thing if it alerts you and your doctor that you have atherosclerosis, because then you can take steps to treat the atherosclerosis and prevent a heart attack or stroke.
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.
Erectile dysfunction can occur as a side effect of medication taken for another health condition. Common culprits are high blood pressure meds, antidepressants, some diuretics, beta-blockers, heart medication, cholesterol meds, antipsychotic drugs, hormone drugs, corticosteroids, chemotherapy, and medication for male pattern baldness, among others.

Treatment of ED which was previously confined to invasive procedures, cavernosal injections or to rather ineffective oral medications was revolutionized in 1999 with the introduction of the orally administered PDE5 inhibitor sildenafil. Phosphodiesterase type 5 inhibitors are the first-line therapy for ED of organic aetiology unless there is a specific contraindication to their use. This class of agents is widely used because of its effectiveness and safety.38 Interactions with cardiovascular drugs have been minimal with the exception of nitrates and other nitric oxide (NO) donors (such as nicorandil), where co-administration may result in severe vasodilation and hypotension. However, nitrates are often overused in clinical practice; therefore, the option of their discontinuation should be considered. A strong body of clinical data shows that all three agents (sildenafil, tadalafil, and vardenafil) do not increase the risk of non-fatal myocardial infarction, stroke, or cardiovascular deaths. These drugs do not exacerbate ischaemia or worsen exercise tolerance in patients with known CAD who achieve levels of exercise comparable or greater than that achieved during sexual intercourse.38,39 Phosphodiesterase type 5 is expressed throughout the human body, including the pulmonary and systemic vasculature and hypertrophied myocardium. While currently their only additional indication, beyond ED, is idiopathic pulmonary hypertension (for sildenafil and tadalafil), they show potential to be of benefit in several other conditions, such as CAD and systolic heart failure.39 Mechanisms of benefit of PDE5 inhibitors include pulmonary and systemic vasodilation, increased myocardial contractility, reduced large artery stiffness and wave reflections, improved endothelial function, and reduced apoptosis, fibrosis and hypertrophy through mechanisms involving NO, cyclic guanosine monophosphate, protein kinase G and Rho kinase.39 A very important issue is whether treatment of ED per se (and not of its risk factors and comorbidities) will have an impact on cardiovascular risk. While this applies to all therapeutic modalities of ED, it is particularly pertinent for PDE5 inhibitors, since they represent the mainstay of ED therapy. Data are limited to date. Gazzaruso et al.21 showed a trend of PDE5 inhibitors to reduce cardiovascular morbidity and mortality in diabetic patients with silent CAD and ED, while Frantzen et al.40 showed that 2 years after the introduction of sildenafil, the relative risk of the incidence of CVD among men with ED compared with healthy men significantly decreased from 1.7 to 1.1.


In subsequent clinical studies, a surprisingly high percentage of EDDM patients–10% to 20%–claimed that the placebo "improved my erections," thus indicating a psychological basis for their ED. In the latter half of the 1980s, objective means were developed that could help determine if a EDDM patient had organic or psychogenic ED. The absence of rigid sleep erections confirmed by penile monitors was one criterion for organic ED. The failure of vasoactive agents (papaverine, Trimix, or prostaglandin E-1 [PGE-1]) injected into the corpora cavernosa to induce penile rigidity was another criterion for organic disease. Intracavernosal maintenance flow rates during pharmacocavernosometry and maximum cavernosal arterial flow during penile Doppler ultrasonography were additional determinants.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References The risk after sexual activity in these patients is unknown, although vasodilators should be avoided because they may increase the intraventricular gradient.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
Guidelines recommend that phosphodiesterase type 5 (PDE5) inhibitors are the first-line drug for the treatment of ED (Table 1). Sildenafil citrate was the first oral drug approved for ED in the US.59 The newer PDE5 inhibitors include vardenafil, tadalafil and avanafil. The inhibition of PDE5 enhances cyclic guanosine monophosphate (cGMP)-NO-mediated vasodilatation by preventing PDE5 catabolism of cGMP and so delaying detumescence. PDE5 inhibitors increase the number and duration of erections, as well as the percentage of successful sexual intercourse.60
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.
Crossref | PubMed | Scopus (539) | Google ScholarSee all References Possible etiologies for ED secondary to hypertension include vascular damage due to hypertensive changes as well as hormonal abnormalities such as elevated prolactin levels.30x30Jaffe, A, Chen, Y, Kisch, ES, Fischel, B, Alon, M, and Stern, N. Erectile dysfunction in hypertensive subjects: assessment of potential determinants. Hypertension. 1996; 28: 859–862
Like the case of untreated hypertensive patients, evaluation of sexual dysfunction in hypertensive patients under antihypertensive regime, should primarily exclude other concomitant diseases and pharmaceutical agents. Consecutively, a competent physician with advanced communicational skills should try to “discover” medically induced erectile dysfunction since a vast majority of patients being under complex antihypertensive regimes usually attribute the undesirable effect to normal aging thus not relating it to their current medication. Moreover, even physicians seldom report the cases of sexual dysfunction associated with certain medications. When medically induced sexual dysfunction is finally disclosed and a shift in medication is deemed necessary, b-blockers along with diuretics should generally be the first categories to be changed, unless they are deemed absolutely indicated for the individual patient. Ideally, an ARB could constitute the mainstay of therapy in these cases. If sexual dysfunction still persists, then more effective remedies should be elected paving the way for the introduction of phosphodiesterase-5 inhibitors (PDE-5).

Normal male sexual function requires a complex interaction of vascular, neurological, hormonal, and psychological systems. The initial obligatory event is acquisition and maintenance of an erect penis, which is a vascular phenomenon. Normal erections require blood flow into the corpora cavernosae and corpus spongiosum. As the blood accelerates, the pressure within the intracavernosal space increases dramatically to choke off penile venous outflow. This combination of increased intracavernosal blood flow and reduced venous outflow allows a man to acquire and maintain a firm erection.


But closer questioning often revealed a very different story—men would admit that struggles to achieve an erection usually preceded a heart attack or other cardiac event by one, two, or three years. Back then, the pattern of erectile dysfunction and cardiac disease was so widespread, that most in the medical profession attributed it to simple “aging,” as common as wrinkles and constipation.
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).
Most studies into the effect of beta-blockers on ED point to negative effects of first- and second-generation beta-blockers, while beta-blockers with vasodilating effects can improve erectile function. Alpha-blockers, calcium channel blockers, and angiotensin-converting enzyme inhibitors seem to have a neutral effect on erectile function. Multiple previous studies have demonstrated a beneficial effect of angiotensin receptor blockers on erectile function and they should probably be the favoured antihypertensive agents in patients with ED.29
The number of men reporting improvement was at 88% during the study. The number of men involved in the study who reported impotence dropped from 75.3 % to 11.8%. The results of this study raise hope for men who have quit taking other blood pressure medications because they interfered with sexual function. Sexual dysfunction was defined for the study as decreased libido, impotence and poor sexual satisfaction.
Erectile dysfunction is very common as men age. Erectile dysfunction is frequently a sign of atherosclerosis, a clogging or narrowing of the blood vessels that causes heart attacks. Erectile dysfunction usually comes 3 to 5 years before a heart attack, so after ED is diagnosed, there is time to treat atherosclerosis and prevent a heart attack. Treating atherosclerosis involves diet, exercise, and medications, if necessary. Talk with your doctor about a broken sex life, and you might be able to prevent a broken heart.
Mancia G,  Laurent S,  Agabiti-Rosei E,  Ambrosioni E,  Burnier M,  Caulfield MJ,  Cifkova R,  Clément D,  Coca A,  Dominiczak A,  Erdine S,  Fagard R,  Farsang C,  Grassi G,  Haller H,  Heagerty A,  Kjeldsen SE,  Kiowski W,  Mallion JM,  Manolis A,  Narkiewicz K,  Nilsson P,  Olsen MH,  Rahn KH,  Redon J,  Rodicio J,  Ruilope L,  Schmieder RE,  Struijker-Boudier HA,  van Zwieten PA,  Viigimaa M,  Zanchetti A. European Society of HypertensionReappraisal of European guidelines on hypertension management: a European Society of Hypertension Task Force document, J Hypertens , 2009, vol. 27 (pg. 2121-2158)https://doi.org/10.1097/HJH.0b013e328333146d
PubMed | Google ScholarSee all References They evaluated 40 patients with coronary artery disease who underwent coronary artery catheterization and whose penile brachial index (PBI) was measured by Doppler ultrasonography. Although a positive correlation was noted between the PBI and the severity of coronary artery obstruction, the relationship was not strong. Also, the degree of PBI abnormality did not effectively stratify the patients according to the severity of their coronary artery blockage. This study concluded that the PBI used alone would not be an effective predictor of ischemic heart disease.
Perk J,  De Backer G,  Gohlke H,  Graham I,  Reiner Z,  Verschuren WM,  Albus C,  Benlian P,  Boysen G,  Cifkova R,  Deaton C,  Ebrahim S,  Fisher M,  Germano G,  Hobbs R,  Hoes A,  Karadeniz S,  Mezzani A,  Prescott E,  Ryden L,  Scherer M,  Syvänne M,  Scholte Op Reimer WJ,  Vrints C,  Wood D,  Zamorano JL,  Zannad F. European Guidelines on cardiovascular disease prevention in clinical practice (version 2012). The Fifth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of nine societies and by invited experts). Developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR), Eur Heart J , 2012, vol. 33 (pg. 1635-1701)https://doi.org/10.1093/eurheartj/ehs092
Recent revised labeling for sildenafil states that there is a lack of controlled data for its use in patients with resting hypotension (<90/50 mm Hg) or hypertension (>170/110 mm Hg); a history of myocardial infarction, cerebrovascular accident, or life-threatening arrhythmia within the past 6 months; coronary artery disease or cardiac failure causing unstable angina; or retinitis pigmentosa and possible genetic disorders of retinal PDEs.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 (697) | Google ScholarSee all References Subsequent in vitro electrical stimulation of these tissue samples showed decreased neurogenic and endothelium-dependent smooth muscle relaxation in the tissue from the patients with diabetes. These effects persisted even after controlling for smoking and hypertension. Other studies have shown a heightened smooth muscle tone in patients with diabetes mellitus.24x24Christ, GJ, Stone, B, and Melman, A. Age-dependent alterations in the efficacy of phenylephrine-induced contractions in vascular smooth muscle isolated from the corpus cavernosum of impotent men. Can J Physiol Pharmacol. 1991; 69: 909–913
PubMed | Google ScholarSee all References This prolonged excretion half-life produces enhanced erections up to 36 hours after oral dosing, thereby potentially allowing for more spontaneous engagement of intercourse. The efficacy of tadalafil in the treatment of ED has been proved in randomized double-blind, placebo-controlled trials.78x78Porst, H, Padma-Nathan, H, Giuliano, F, Anglin, G, Varanese, L, and Rosen, R. Efficacy of tadalafil for the treatment of erectile dysfunction at 24 and 36 hours after dosing: a randomized controlled trial. Urology. 2003; 62: 121–125
A variety of personal habits and lifestyle choices have been linked to ED. In some ways, this is a good thing, since habits can be broken and choices reconsidered. What's more, many of the lifestyle factors that contribute to sexual problems are ones that affect overall health and well-being, both physical and mental. Addressing these factors, therefore, can have benefits beyond improving erectile dysfunction.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (37) | Google ScholarSee all References One MET is equal to a resting state, or 3.5 mL/kg per minute. The relative MET values of sexual activity compared with other forms of activity are shown in Table 3. In general, sexual activity is similar to mild or moderate activity for most patients either with or without coronary artery disease.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

Crossref | PubMed | Scopus (47) | Google ScholarSee all References Because of this perceived increase in risk, many couples are concerned about resuming sexual activity in the setting of cardiac disease. A study that monitored male patients after coronary artery bypass grafting found that 17% of patients and 35% of their partners were afraid of resuming sexual activity.1x1Muller, JE. Sexual activity as a trigger for cardiovascular events: what is the risk?. Am J Cardiol. 1999; 84: 2N–5N
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

In most men, ED is recognised as sharing vascular aetiology with IHD.17 ED and IHD share common risk factors, such as hypertension, hyperlipidaemia, diabetes, obesity, lack of physical exercise, cigarette smoking, poor diet, excess alcohol consumption and psychological stress, including depression.30 Endothelial dysfunction has been implicated as a common mechanism between CAD and ED and it has an important role in the development of atherosclerosis.31
If your physician advises you that the risks of taking an erectile dysfunction medication are too high, he or she can advise you of other treatment options that can enable you to resume sexual activity without risks of complications. These might also include screening to try to determine if your erectile dysfunction has a physiological basis in need of medical intervention, can be corrected through lifestyle changes or if it may have psychological roots. After all, a heart attack or diagnosis of heart disease can lead to depression, which can also affect libido. Talk with your doctor to establish a safe, effective plan for resuming intimacy after your heart disease diagnosis.
Second-generation cardioselective beta-blockers (atenolol, metoprolol, bisoprolol, etc.) can also lead to ED. Atenolol was shown to cause significant reduction of sexual activity compared with placebo in a double-blind, parallel-arm study.22 The same study also showed a significant reduction in testosterone levels with atenolol versus valsartan. An open, prospective study of hypertensive men treated with atenolol, metoprolol and bisoprolol for at least 6 months showed high prevalence of ED – approaching 66 % – in these patients.23
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).
The information provided on this site is for informational purposes only and is not intended as a substitute for advice from your physician or other health care professional or any information contained on or in any product label or packaging. You should not use the information on this site for diagnosis or treatment of any health problem or for prescription of any medication or other treatment. You should consult with a healthcare professional before starting any diet, exercise or supplementation program, before taking any medication, or if you have or suspect you might have a health problem. You should not stop taking any medication without first consulting your physician.
Abstract | Full Text PDF | PubMed | Scopus (16) | Google ScholarSee all References These medications cause intracavernosal pressure changes in animal models, and human studies have noted deleterious effects on erectile function, decreased libido, and ejaculatory problems.42x42Weiss, RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician. 1991; 44: 2075–2082
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
Currently, the preferred treatment for erectile dysfunction includes sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis). However, numerous experts have raised concerns about the use of these drugs in patients with chronic heart failure who also take nitrates (or other medications that relax and widen blood vessels). This drug combination has been shown to be dangerous, because it can increase the risk for a life-threatening drop in blood pressure.
Basaria S,  Coviello AD,  Travison TG,  Storer TW,  Farwell WR,  Jette AM,  Eder R,  Tennstedt S,  Ulloor J,  Zhang A,  Choong K,  Lakshman KM,  Mazer NA,  Miciek R,  Krasnoff J,  Elmi A,  Knapp PE,  Brooks B,  Appleman E,  Aggarwal S,  Bhasin G,  Hede-Brierley L,  Bhatia A,  Collins L,  LeBrasseur N,  Fiore LD,  Bhasin S. Adverse events associated with testosterone administration, N Engl J Med , 2010, vol. 36 (pg. 109-122)https://doi.org/10.1056/NEJMoa1000485
Counselling or sex therapy (58% of people find this works for them) –mind-related causes of erectile dysfunction can affect anyone. They are more likely if you experience erectile dysfunction at a younger age. Talking to a counsellor or therapist can help some people overcome erectile dysfunction related to these problems, possibly for good. They can also help you if your erectile dysfunction is causing you stress, as this can make matters worse.
In many of these cases, a discussion between the physician, the man with erectile dysfunction, and possibly his partner can help to resolve the issues leading to treatment failure. For men who experience severe side effects, can’t take the drugs for other reasons (such as taking medicines such as nitroglycerin), or don’t respond in spite of further education on the correct use of the drugs, there are other treatment options that can help most men remain sexually active.
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