Chronic heart failure (HF) is an increasingly common cardiovascular disorder. The goal of health-care providers is to optimize quality of life in this population, including sexual health. Up to 75% of patients with HF report erectile dysfunction (ED). As HF is a condition with distinct physiologic sequelae, some unique organic and psychological factors contributing to ED in this patient population have been identified, along with risk factors common to the development of coronary artery disease, HF and ED. This review describes contributing factors to ED in the setting of HF and highlights treatment considerations for this distinct patient population.
Erectile dysfunction (ED) is the persistent inability to achieve and/or maintain a penile erection sufficient for satisfactory sexual performance.1 Data from the Massachusetts Male Aging study showed that 52% of men aged 40–70 y reported some degree of ED.2 As heart failure is another highly prevalent condition that shares many risk factors with ED, it is not surprising that ED and HF frequently occur concomitantly. In a cohort of 62 male and female clinic outpatients with HF, approximately three-quarters reported compromised libido and ED.3 In our own patient population, at least 75% of patients with chronic HF reported ED (unpublished). Interestingly, HF patients place greater importance on symptomatic improvement and thereby quality of life, rather than longer survival.4 Sexuality and a satisfying sexually active life is an important component of quality of life.5, 6
ED and cardiac disease
Numerous studies have shown that ED shares several modifiable risk factors with cardiovascular disease including atherosclerosis,7 hypertension, hyperlipidemia, diabetes mellitus,8 smoking,9 obesity and sedentary lifestyle.10 Table 1 shows the estimated prevalence of ED in various conditions including coronary artery disease and in the presence of cardiovascular risk factors. More specific data are difficult to obtain due to concomitant presence of more than one risk factor in most of the patients diagnosed with ED. Data from several studies involving patients with cardiac disease have shown a high prevalence, 42–75%, of ED in this patient population.11, 12, 13, 14, 15, 16 Of interest are studies that have shown a significant correlation between the presence of vasculogenic ED and clinically evident or subclinical ischemic heart disease. Kaiser et al7 demonstrated that the presence of arteriogenic ED (using penile Doppler ultrasonography) was associated with a high prevalence of clinically apparent atherosclerosis, particularly in men aged >50 y. Greenstein et al17 also reported a significant correlation between ED and the number of occluded coronary arteries. Similar findings were recently reported by Solomon et al.11 Other investigators have found incidence rates of occult cardiovascular disease in men with ED as high as 15–30%.18, 19
Causes of ED in patients with heart failure
Patients with heart failure may experience ED for reasons similar to the general population, and the etiology may be polyfactoral. However, there are social, psychological, physiological and drug-related consequences specific to heart failure that may account for the high incidence of ED, and that warrant specialized consideration. Table 2 summarizes the various causes of ED and their possible mechanism in patients with HF (Table 3).
Cardiac capacity and exercise tolerance
Sexual activity is closely linked to a patient's exercise tolerance and conditioning. While it is difficult to standardize sexual exertion between patients and their partners, it is thought that the ‘average’ coitus requires the expenditure of approximately five metabolic equivalents, or roughly the same amount of oxygen consumption as a brisk walk up to two flights of stairs.20 Exercise capacity in chronic HF is determined by a patient's ability to increase heart rate and stroke volume beyond a submaximal stage of exercise.21 In HF, this ability is disturbed by a lack of preload response, autonomic dysregulation and excessive vascular resistance, secondary to neurohormonal activation. Jaarsma et al3 found a significant relationship between a patient's level of sexual function and results of the 6-min walk test. There is also a significant but weaker link between NYHA functional class and sexual performance. No significant correlation was found between sexual function and EF.3 However, in severely compromised left ventricular function, that is, patients in NYHA classes 3 and 4, reduced cardiac capacity might be causing the failure of hemodynamic physiology to adequately perform any physical exertion including satisfactory sexual intercourse.
Certainly psychogenic causes of ED such as depression and anxiety may be confounded in HF patients. This may be primarily due to the belief of a poor prognosis and the significant impact of cardiac symptoms in every-day life.22 Depression in this population is multifactoral,23, 24 and fluctuates with the natural evolution of heart failure symptoms. Therefore, cardiovascular disease, ED and depression have been proposed to form a mutually reinforcing triad.25 Performance anxiety and fear of death during sexual activity also contributes to ED.26 It is unknown, however, whether treatment of depression using selective serotonin-reuptake antagonists improves ED in heart failure patients, since in particular this class of drug is well known for its deleterious effects on erectile function and libido.
Vasculogenic causes of ED are common, and can be subdivided into (a) arterial insufficiency and (b) endothelial dysfunction. As ischemic cardiomyopathy is the most common cause of HF in the United States, many HF patients have underlying atherosclerosis. Atherosclerosis accounts for approximately 40% of ED in men greater than 50 y of age,7 and is at least in part due to reduced arterial inflow into the penile corpora cavernosa.27 This might be caused by intimal hyperplasia of the penile vessels, plaque deposition, focal stenosis or, more frequently, sclerosis, and thus reduced blood flow through the common iliac and the hypogastric as well as pudendal arteries.
Endothelial dysfunction appears to be a systemic phenomenon, affecting not only the coronary but also almost all peripheral circulation. Studies to establish whether basal nitric oxide (NO) production is altered in HF patients have yielded conflicting results.28, 29, 30, 31, 32 One study by Maguire et al33 supports previous observations that NO does not contribute to basal vascular tone in patients with HF. It has been suggested that endothelial damage could result in a reduction in the availability of endothelium-derived NO from either decreased production or increased breakdown. Decreased production may be due to mRNA downregulation of the endothelial enzymes NO synthase and cyclooxygenase, both of which are required for the production of endothelium-derived vasodilators. This deficiency appears to be specific to the physiologic state of heart failure.34 Another hypothesis is that underlying atherosclerosis alters the L-arginine–NO pathway, decreasing NO production.35, 36, 37, 38 Oxygen-derived free radicals have also been associated with inhibition of endothelium-dependent vasodilation, suggesting that rapid inactivation of NO may be caused by increased free radical production.39 Other possible mechanisms of endothelial dysfunction include cell surface receptor abnormalities or alterations at the G-protein level, which may account for decreased efficacy of free NO, as seen in atherosclerosis.40
Heart failure is associated with increased circulating vasoconstrictors such as endothelin (ET),41, 42 as well as a reduction in vasodilators such as prostacyclin.43 ET-1 potently induces slowly developing, long-lasting contractions in the CC and penile vessels, and has been suggested to contribute to the maintenance of corpus cavernosal smooth muscle tone.44, 45 ETs may have important effects on penile pathophysiology as modulators of other contractile agents (eg noradrenalin),46, 47, 48 cellular proliferation and/or phenotypic expression.49 This pathophysiologic state, with an abundance of potent vasoconstrictors in the setting of impaired vasodilatory mechanisms, prohibits the vascular events necessary to achieve and maintain an adequate erection.
Vascular smooth muscle abnormalities
In addition to impaired endothelium-dependent vasodilation, HF patients also appear to have dysfunctional endothelium-independent vasodilatation.33, 50 Some evidence suggests that over time arterial compliance decreases.51, 52 Abnormal smooth muscle function may result from altered responsiveness or impaired diffusion of NO through the arterial wall. Impaired smooth muscle responsiveness is thought to result, in part, from alterations in intracellular cGMP function.53 When combined with endothelium-dependent mechanisms, these pathophysiologic variations may further confound ED.
Drug therapy in heart failure and ED
While treating heart failure may attenuate some of these physiologic adaptations, several of commonly prescribed medications may actually cause or worsen ED. In general, published data on the prevalence of ED with the use of various medications is limited by the number or sample size of studies. Logistically, it can also be difficult to excise medication effects from the consequences of underlying diseases such as heart failure, hypertension and atherosclerosis. To date, there have been no studies establishing whether or not the collective medical treatment of heart failure has beneficial, deleterious or any net effect on sexual function.
In a community-based epidemiological study of 1709 men, analysis of data on multiple antihypertensive, vasodilator and cardiac medications revealed that digoxin use had the highest association with complete ED.54 The mechanism underlying digoxin-associated changes in sexual function remains poorly understood. Early studies by Stoffer et al55 and Neri et al56 attributed sexual dysfunction to hormonal alterations observed with digoxin use; these changes include higher serum estrogen coupled with lower testosterone and luteinizing hormone levels. More recent studies of healthy male volunteers and cardiac patients have failed to confirm a relationship between digoxin use and changes in serum hormone levels.57, 58, 59 Some studies on human corpus cavernosum tissue indicate that sodium-pump activity also has a role in the regulation of erectile function, with pump inhibition causing contraction and diminution of NO-induced relaxation.60 Gupta et al54 studied the effect of digoxin on sodium-pump activity in human corporeal smooth muscle strips in vitro. They concluded that digoxin-associated alteration of human sexual function may be due to corporeal smooth muscle pump inhibition, which promotes contraction and impedes NO-induced relaxation.
Beta-adrenergic receptor blockers
Beta-blockers are believed to have negative effects on erectile function.61 Some theories point to adverse effects of decreased perfusion pressure or a direct (but unknown) effect on smooth muscle. Support for the latter mechanism is derived from the observation that despite pressure-lowering effects, treatment with alpha-adrenergic receptor blockers is not associated with ED, and that this class of medications may actually improve pre-existing sexual dysfunction.62 Beta-adrenergic blocking agents may cause ED by potentiating alpha-1 adreno-receptor-mediated contraction of corporal smooth muscle in the penis.1 However, it is surprising and unclear why not all or even the majority of treated patients experience such (side) effects. A prospective, randomized, double-blind study showed that patients' sex lives were unaffected by metoprolol treatment.63 In another study, Wassertheil et al6 demonstrated that the beta-adrenergic blocker atenolol did not affect sexual function. In a study of 96 men with newly diagnosed cardiovascular disease and without ED, 31% reported ED after beginning treatment with atenolol and being informed of its possible adverse sexual side effects. In contrast, only 3% of men who were similarly treated reported ED when they were blinded to the study drug, suggesting that ED with beta-blockers is related to patient knowledge of these potential side effects.64 To the contrary, Croog et al found propranolol use to be associated with significant sexual dysfunction. More recently, carvedilol has become a preferred agent for beta-blocker therapy in HF patients. A recent study comparing carvedilol with the angiotensin-receptor blocker valsartan demonstrated a decline in sexual activity within the carvedilol-treated group. Notably, these patients were hypertensive treated with high doses of carvedilol, and patients with comorbidities such as diabetes mellitus and coronary atherosclerosis were excluded. Additionally, it is unknown if these data represent deleterious effects of carvedilol or beneficial effects of valsartan.65 The discrepancy of the effects of various beta-blockers and dosages may be related to a differential action on peripheral structures and or the central nervous system.66 In summary, the effects of beta-blockade on sexual function in the HF population have not been clearly defined. Overall most beta-blockers appear to be associated with worsening of ED. It is not quite clear whether beta-blockers do cause ED per se. Further investigation is needed to clarify the role of beta-blockers on erectile function in different and larger populations.
While sexual disorders caused by diuretics have been reported, the mechanism remains ill-defined.61 In all, 10–20% of patients taking thiazide diuretics may experience a decline in sexual function.67 Wassertheil et al6 demonstrated that the thiazide chlorthalidone causes sexual dysfunction. Similar findings were seen with the use of hydrochlorothiazide as monotherapy for hypertension in a small study of 12 patients.68 In another study among 177 patients treated with either methyldopa or propranolol for hypertension, total sexual symptom distress score worsened with the addition of hydrochlorothiazide, with significant worsening in the group taking propranolol. Among patients taking captopril, no change in baseline scores appeared for any sexual symptoms with the addition of hydrochlorothiazide.69 The aldosterone antagonist spironolactone is considered standard therapy for HF patients and can also cause erectile failure, gynecomastia and decreased libido secondary to its anti-androgen effects.1 These side effects have not been reported and yet not studied with the use of eplerenone, which is a newer, more selective mineralocorticoid receptor antagonist.70
ACE inhibitors and angiotensin receptor blockers
The impact of ACE inhibitors and ARBs on ED is unclear. Croog et al71 found that the ACE inhibitor captopril actually enhances sexual function. These findings are supported by DiBianco's72 reports that 40–80% of patients treated with ACE inhibitors experienced improved functional status and sexual function. It has been suggested that potential favorable sexual effects of captopril were secondary to improved cardiac function; however, sufficient data to support this hypothesis do not exist. There is even less information available regarding the effects of ARBs on sexual function. One Japanese study reported that in hypertensive patients switched from calcium channel blockers to candesartan, those patients less than 65 y of age experienced improved sexual function.73 Another study comparing the sexual side effects of the ARB valsartan with the beta-blocker carvedilol demonstrated that following an initial statistically insignificant decline in sexual frequency, continuous therapy with valsartan was associated with recovery or improvement of sexual activity.74 This favorable sexual profile of valsartan was confirmed by Dusing,75 who reported a reduction in ED with improved orgasmic function, intercourse and overall sexual satisfaction in hypertensive patients treated for 6 months. A more precise definition of the role these agents play in the sexual functioning in patient with chronic HF remains to be elucidated.
Electrical therapy/cardiac resynchronization for heart failure
The placement of a biventricular pacemaker for chronic resynchronization therapy has become increasingly common for HF treatment. In general, there is a paucity of data evaluating the effects of cardiac pacemakers on sexual or erectile function. One small study reported that while treating arrhythmias with pacemaker implantation improved quality of life in general, but it did not improve sexual function.76 Currently, there is no data evaluating the sexual effects of HF patients treated with resynchronization therapy.
Sexual function in cardiac patients
The effects of a significant cardiac condition on the vitality of a patient's sex life have not been elaborately explored. There are, however, some small studies demonstrating a general deterioration in this aspect of a patient's life after experiencing a cardiac event.
Sexual function in patients with heart failure
Jaarsma and colleagues studied 62 heart failure patients via questionnaire to determine alterations in a patient's emotional, social and sexual function. Most patients experienced a decreased libido, less frequency of coitus, negative changes in sexual performance and a general dissatisfaction related to their sexual function. In this report, however, these changes did not affect the relationship with the patient's spouses.3 In a cohort of >300 heart failure patients, >90% reported reduced libido and erectile problems, which was independent of the NYHA functional class (unpublished).
Sexual function post myocardial infarction
After myocardial infarction (MI), only two-thirds of male patients returned to satisfying sexual relations within 6 weeks, with 90% achieving at least pre-MI levels of sexual function by 1 y. Importantly, most patients also experience a decrease in frequency of sexual relations.77, 78, 79 Female patients at 18 months post-MI reported slightly lower rates of return to a ‘normal’ sexual function, with 73% having attempted to resume sexual relations with their husbands.80 Another comparison between men and women which was performed to determine whether there are gender differences in the quantity and quality of sexual activity showed that a first MI appears to reduce the frequency of and satisfaction with sexual activity of women and men equally.81
Sexual function postcoronary artery bypass surgery
In a prospective evaluation of patients postcoronary artery bypass surgery, Langeluddecke et al82 found a significant (though modest) improvement in patient's marital relationships, level of sexual interest and level of sexual activity compared with the presurgical status. These findings were consistent with previous studies.83 In another study by Papadopoulos et al,84 134 patients were interviewed about the impact of surgery on their sexuality; 39% of patients reported decreased frequency of sexual activity, with 17% of patients and 35% of their partners expressing fear of resuming sexual activity.
Sexual function postheart transplantation
Mulling et al85 conducted a survey in a cohort of 71 heart transplant recipient patients to assess the sexual interest, ability and activity before and after cardiac transplant. The authors found that libido remained unchanged before and after cardiac transplant. In contrast, erectile rigidity and orgasmic ability were impaired before and surprisingly declined further after transplantation. Intercourse frequency was relatively infrequent post-transplant and was related to problems with erectile rigidity. However, it needs to be emphasized that these data were published in 1991, that is, prior to modern heart failure therapy and prior to the development of PDE-5 inhibitors.
Treatment of ED in heart failure patients
Optimize heart failure therapy
First priority for patients with HF and ED should be to optimize heart failure management, according to the newly updated ACC/AHA guidelines.86 Even though there is no data published whether optimized heart failure therapy improves ED, it is assumed that reduced symptoms and improved exercise capacity contribute to improved sexual activity.
Secondly, drugs with potential side effects of sexual dysfunction should be avoided and—if possible—replaced. Prior to any use of PDE-5 inhibitors or other aphrodisiacs due to our experience, we try to (1) avoid digoxin, (2) avoid thiazide diuretics, (3) replace beta-blockers, for example, propranolol with either metoprolol or carvedilol (due to their alpha-blocking effects) and (4) replace spironolactone with eplerenone. The above approach should be considered only if clinically feasible without worsening function or symptoms, and if affordable by the patients.
Oral phosphodiesterase inhibitors
In March 1998, sildenafil citrate (Viagra®) became the first approved oral drug for ED in the United States. The role of sildenafil and other PDE-5 inhibitors is to enhance cGMP-NO-mediated vasodilatation with resulting improvement of erectile function.87, 88, 89
Vardenafil (Levitra®) and tadalafil (Cialis®) are newer PDE-5 inhibitors that appear to be as effective as sildenafil.90, 91, 92, 93, 94 All PDE-5 inhibitors are contraindicated with concomitant nitrate or any NO donator use (nitroprusside, molsidomine, etc).95 Although these newer agents may not have additional cardiac risks compared with sildenafil, there is less clinical information related to the safety of these drugs available in patients with heart disease.
The American College of Cardiology and the American Heart Association in their 1999 consensus document expressed concerns regarding the lack of cardiovascular safety data from controlled clinical trials of sildenafil in men who had ED and congestive HF. Caution was raised for the potential interaction of sildenafil with vasodilators commonly used in congestive HF treatment, potentially resulting in clinically significant hypotension. In this consensus statement, HF was listed as a relative contraindication for the use of sildenafil.96 Katz et al undertook a multicenter, prospective, randomized, double-blind, placebo-controlled, flexible-dose study, which addressed concerns raised by the consensus statement. The results demonstrated that flexible dosing of sildenafil from 25 to 100 mg was well tolerated, improved erectile function and increased satisfaction with sexual performance in ambulatory subjects who had mild to moderate congestive HF compared with subjects who received placebo.97 These findings were in accord with two previous small investigations of the effects of sildenafil in patients with HF.98, 99 No clinical safety data on the use of newer phosphodiesterase inhibitors, vardenafil and tadalfil, is available in the heart failure patient population.
Treatment options other than sildenafil can be pursued in patients with HF as they would be in the general population. As far as we know, there are no specific cardiovascular effects of androgen replacement therapy, intraurethral suppository, penile injection therapy, penile prosthesis or vacuum-assisted erection devices, as well as no long-term negative therapy effects have been reported in heart failure patients.
Men who are not candidates for or who fail treatment with an oral agent may select second-line therapies such as intraurethral prostaglandins, penile injection therapy, hormone therapy or a vacuum erection device. Since this might be unpleasant for some, these patients may be candidates for surgical intervention such as penile angioplasty, penile revascularization or implantation of a penile prosthesis.
Percutaneous angioplasty for ED
Percutaneous transluminal angioplasty (PTA) is common semi-invasive interventional method used for coronary arteries, peripheral arteries and, more recently, carotid arteries with a low complication rate. Little data exist, however, for the treatment of ED. High-quality diagnostic angiographic studies and their accurate interpretation are prime requirements for proper patient selection. Venogenic impotence must be excluded by cavernosometry and cavernosography.100 Only patients with focal atherosclerotic lesions in either the hypogastric (internal iliac), common iliac or even the pudendal arteries might be potential candidates for PTA. Only few small studies have reported success rates of 57–84% with resolution of ED after PTA of the common and external/internal iliac arteries and the internal pudendal arteries.101, 102, 103 Owing to our limited experience with individual successfully treated men, we believe that PTA represents a future potential treatment option for a selected group of patients; however, randomized controlled studies are required to establish its definitive role in the treatment of arteriogenic impotence.
Penile revascularization surgery is a rational and effective treatment for ED resulting from localized arterial lesions. Among vascular surgeons performing surgical revascularization, the accepted criteria for arteriogenic ED include: age<50 or 55 y, a negative response to intracavernosal injection tests, fewer than one or two cardiovascular risk factors, no history of diabetes mellitus and normal corporal veno-occlusive function,104, 105 which—unfortunately—represents the minority of affected patients. It is assumed that increased intracavernosal pressure is achieved by revascularization surgery, but studies to demonstrate this are lacking. Different approaches have been reported such as anastomizing the inferior epigastric artery to the corpus cavernosum (Michal et al106); to the dorsal penile artery (Michael 2107); to the deep dorsal vein (Virag et al108); and an anastamosis between the inferior epigastric artery and the deep dorsal vein and artery of the penis (Hauri109). A recent study by Kawanishi et al111 found penile revascularization surgery treatment suitable only for young men with no significant difference in the subjective outcome between the so-called Furlow–Fisher modification of the Virag V (FFV5; Furlow et al110) procedure and the Hauri procedure. Currently, revascularization surgery for ED represents a therapeutical alternative for a limited group of patients, with a vascular anatomy and morphology suitable for graft anastomoses, who failed all other noninvasive options as well as for a limited group of vascular surgeons.
Treatment of depression
Psychological counseling may help alleviate symptoms of depression and thereby help restore sexual function. While antidepressant drugs can be used, it should be noted that many of the newer and more effective antidepressants, in particular selective serotonin reuptake inhibitors (SSRI, such as fluoxetine, sertraline and paroxetine) can decrease libido and worsen erectile function.112 Trazodone, clomipramine and other tricyclic antidepressants, however, can cause delayed or retarded ejaculation (a side effect that actually may be beneficial for some men who are suffering from premature ejaculation).24, 113 It is unclear, however, whether well-controlled, treated depression does improve sexual function in patients with ED while the drug's side effects might worsen sexual function, resulting in a zero net balance. An ethically reasonable approach to this dilemma is to adequately treat depression and to counteract SSRIs side effects by use of PDE-5 inhibitors.
Hemodynamic stress reduction
It is possible to reduce physiologic demands of sexual activity, which is recommended in patients with heart failure. It has been assumed that man would perform less physical work during sexual intercourse in supine (as opposed to the man-on-top) position. However, there appears to be very little114 or no significant difference115 in hemodynamic parameters between the two positions, even though this may vary individually. It has also been suggested that patients should avoid eating large meals or alcohol use just before sexual intercourse and avoid extremes of temperature.116 Patients may be advised to engage in sexual activity when they feel well rested (in the morning rather than at the end of the day), and, interestingly, it has been proposed that the use of waterbeds may also reduce the number of metabolic equivalents required for sexual activity.3 However, most of these recommendations are intuitive and not based on controlled scientific data.
Investigators have documented that many cardiac patients are uncomfortable discussing issues concerning sexual activity or function.78 Many patients may become noncompliant with their heart failure medical regimen since they read the packet inserts’ side-effect profile on sexual function and strongly believe it causes or aggravates their sexual problems. Patients and spouses have informational needs about their sexual problems, specifically with regard to a change in frequency, interest and ability to have sex; most patients are also interested in having their concerns addressed.117 To dispel their fears and anxiety, couples need to receive information about the physiological requirements of sexual activity, the pathophysiology of heart failure (including its treatment) relative to sexual function and the psychological sequelae of heart failure. Westlake et al117 also found a disparity between the individuals' and their sexual partners' perception of the changes in their sexual relationship, reinforcing that instructions and counseling should be directed at both parties. This finding has been observed in previous studies as well.118, 119, 120, 121, 122 Advanced heart failure does not necessarily mean the end of satisfying sexual relations, but it is important that health-care professionals address the changes related to the disease, clarify misconceptions and provide appropriate counseling, in particular in patients with chronic heart failure.
Further clinical studies with selective antagonists of ET receptors might be considered given their established elevation in HF and causative role in ED. The Rho A/Rho kinase pathway is emerging as a novel player in the regulation of penile erection, and future investigations may further define its role in ED and HF.123 Neovascularization is an emerging approach to the reversal of impaired cavernosal artery flow. Intracavernosal injection of vascular growth factors has been demonstrated to be feasible in animal models.124 Also, gene therapy may be a treatment of the future. Studies are currently being conducted in animals with gene transfer of endothelial nitric oxide synthase to the penis of aged rats for the potential application of gene therapy for the treatment of ED.125
ED is highly prevalent among patients with HF, and can significantly and adversely affect quality of life. Causes of ED in HF patients are multifactorial, and may be due to direct vascular etiologies, reduced cardiac capacity, neurohormonal changes or treatment regimens specific to HF. Despite the unique issues of sexual dysfunction in the setting of HF, most patients are not receiving adequate counseling in this matter. Addressing the sexual concerns of these patients is important, as it may improve medical compliance as well as quality of life. Currently available effective oral medical treatment options are limited to the PDE-5 inhibitor sildenafil, which targets the NO/cGMP pathway. Sufficient safety data on the newer PDE-5 inhibitors in HF patients is lacking. Sexual function and potential dysfunction requires increased awareness among cardiologists, adequate assessment and appropriate counseling. Interestingly, in our experience, most patients with ED and chronic stable heart failure can be successfully treated for their erectile problems.
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Rastogi, S., Rodriguez, J., Kapur, V. et al. Why do patients with heart failure suffer from erectile dysfunction? A critical review and suggestions on how to approach this problem. Int J Impot Res 17, S25–S36 (2005). https://doi.org/10.1038/sj.ijir.3901426
- erectile dysfunction
- heart failure
- phosphodiesterase inhibitors
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