Sexual dysfunction is a common problem of increasing incidence that is associated with multiple co-morbid conditions and chronic diseases. In heart failure, however, exact numbers are unknown, in part secondary to under-reporting and under-interrogating by health care providers. A genderspecific questionnaire was modified from established sexual dysfunction questionnaires to correspond to a non-randomized outpatient heart failure population, to assess the prevalence and demographic distribution of sexual dysfunction and potential treatments expectations. Onehundred patients in a stable hemodynamic condition in New York Heart Association classes I-III participated. Eighty-seven percent of women were diagnosed with female sexual dysfunction compared to 84% of men with erectile dysfunction. Eighty percent of women reported reduced lubrication, which resulted in frequent unsuccessful intercourse in 76%. Thirty-six percent of patients thought that sexual activity could harm their current cardiac condition; 75% of females and 60% of men stated that no physicians ever asked about potential sexual problems. Fifty-two percent of men considered sexual activity in their current condition as an essential aspect of quality of life and 61% were interested in treatment to improve sexual function. Sexual dysfunction appears to be high in prevalence in both men and women with chronic compensated heart failure and represents a reduction in quality of life for most. Despite the fact that most patients are interested in receiving therapy to improve sexual dysfunction, treatment options are rarely discussed or initiated.

Chronic heart failure (HF) and erectile dysfunction (ED) are 2 highly prevalent disorders that frequently occur concomitantly. Coronary artery disease, HF, and ED share several common risk factors, including diabetes mellitus, hypertension, smoking, and dyslipidemia. Additionally, the distinct physiologic sequelae of HF create unique organic and psychologic factors contributing to ED in this patient population. Standard HF therapy with beta-receptor blockers, digoxin and thiazide diuretics may worsen sexual dysfunction owing to medication side effects. This may, in turn, lead to noncompliance in misguided efforts to retain satisfactory sexual activity, with secondary worsening of cardiac capacity. This review describes the unique aspects of ED in the HF population.

Chronic heart failure (HF) is an increasingly common cardiovascular disorder. The goal of healthcare 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.

Phosphodiesterase-5 (PDE-5) inhibitors selectively inhibit PDE-5 enzymes that are present in various tissues like penile tissue, platelets, vascular, and smooth muscle tissue. The drug's actions on these tissues have lead to the successful therapeutic use in patients suffering from conditions such as erectile dysfunction (ED) and pulmonary hypertension. PDE-5 inhibitors (PDE-5i) act on the erectile tissue causing penile smooth muscle relaxation and vasodilatation leading to penile erection. In addition, in particular when used in conjunction with prostaglandin inhibitors, PDE-5i cause vasodilatation in pulmonary vasculature hence decreasing both the pulmonary arterial pressure and resistance. PDE-5i have also shown to mildly decrease blood pressure, increase cardiac index, and increase coronary blood flow in experimental animals as well as in human studies. The Food and Drug Administration (FDA) has approved three PDE-5i for the treatment of ED: sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis) and one for pulmonary hypertension: sildenafil (Revatio). These agents are highly selective for PDE-5 enzymes as compared to other subclasses of PDE enzymes and have the almost identical pharmacological action but slightly different pharmacokinetics. Only little data exist about long-term use of PDE-5i and their effects on different organ system. This paper reviews the current information available on chronic PDE-5 inhibitor use.

IntroductionThe present study determined whether late-ischemia/early reperfusion therapy with the β1-adrenergic receptor (AR) blocker esmolol and phosphodiesterase III inhibitor milrinone reduced left ventricular (LV) myocardial infarct size (IS).Methods and ResultsIn an ischemia/reperfusion rat model (30-min ischemia/4-hr reperfusion), esmolol, milrinone or esmolol + milrinone were intravenous (IV) infused over 10 min (from the last 5min of ischemia to the first 5min of reperfusion). LV-IS were 48.9 ± 8.9%, 41.5 ± 5.4%, 25.8 ± 7.7% and 16.8 ± 7.3% for saline, esmolol, milrinone, and esmolol + milrinone, respectively (n = 12/group). Esmolol + milrinone further reduced LV-IS compared with esmolol or milrinone alone (p < 0.05). LV-IS-reduction induced by esmolol + milrinone was eliminated in the presence of protein kinase A-(PKA)-inhibitor (Rp-cAMPS) or Akt-inhibitor (AKT 1/2 kinase inhibitor). In mixed rat ventricular cardiomyocyte cultures, intra-ischemic application of esmolol, milrinone or esmolol + milrinone reduced myocyte death rates by 5.5%, 13.3%, and 16.8%, respectively, compared with saline (p < 0.01). This cell protective effect by esmolol + milrinone was abrogated in the presence of PKA-inhibitor or Akt-inhibitor. Esmolol, milrinone or esmolol + milrinone increased myocardial PKA activity by 22%, 28% and 59%, respectively, compared with saline (n = 6, p < 0.01). No non-specific adverse effect of Rp-cAMPS on myocytes was identified in a purified myocyte preparation during hypoxia/re-oxygenation. Antiapoptotic pathways were assessed by measuring myocardial phosphorylated Akt (pAkt) levels combined with terminal dUTP nick-end labelling staining analysis. Ten minutes following infusion of esmolol, milrinone or esmolol + milrinone, there were 1.7-, 2.7-, and 6-fold increase in tissue pAkt levels, respectively. This esmolol + milrinone induced pAkt activation was abolished in the presence of PKA inhibitor. Esmolol, milrinone and esmolol + milrinone reduced myocyte apoptosis rates by 22%, 37% and 60%, respectively, compared with saline (p < 0.01).ConclusionsLate-ischemia/early reperfusion therapy with esmolol + milrinone additively reduces LV-IS associated with robust activation of myocardial PKA and subsequent Akt-antiapoptotic pathway.

Erectile dysfunction (ED) is increasingly considered as one manifestation of systemic vascular disease. Accordingly, ED and coronary artery disease share mutual risk factors and frequently coexist. Sexual health is an important aspect of our patients' lives, and ED is a common concern of the cardiovascular patient. Despite this, sexual function is under-addressed in the cardiac patient. Even when this topic is broached by the primary care physician or urologist, ED frequently remains untreated due to safety concerns involving cardiac disease and other comorbidities. This article describes our experience with this unique patient population, as well as our approach to building a multidisciplinary clinic designed to specifically address the important issue of ED in the cardiac patient.

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