Erectile dysfunction as a marker for vascular disease

A body of evidence from basic science and clinical research is emerging to provide a compelling argument for endothelial dysfunction as a central etiologic factor in the development of atherosclerosis and systemic vascular diseases (hypertension, dyslipidemia, diabetes, ischemic heart disease, stroke, or claudication). Erectile dysfunction (ED) is another prevalent vascular disorder that, like cardiovascular disease, is now thought to be caused by endothelial dysfunction. In fact, a burgeoning literature is now available that suggests that ED may be an early marker for atherosclerosis, cardiovascular risk, and subclinical systemic vascular disease. The emerging awareness of ED as a barometer for vascular health and occult cardiovascular disease represents a unique opportunity for primary prevention of vascular disease in all men. Although the implications of this relationship for primary and secondary prevention of cardiovascular disease are not fully appreciated, the available literature makes a strong argument for the role of ED as an early marker for the development of significant cardiovascular risk factors and cardiovascular disease.     

Erectile dysfunction and HTLV-I infection: a silent problem

The human T-lymphotropic virus type I (HTLV-I) is a retrovirus associated with a chronic myelopathy known as HTLV-I-Associated Myelopathy or Tropical Spastic Paraparesis (HAM/TSP). The main objective was to assess the frequency of erectile dysfunction (ED) in HTLV-I-infected individuals from Salvador and other cities from Bahia, Brazil, as well as to verify if sexual dysfunction correlates with urinary symptoms and overall neurological impairment. From January 2001 to April 2004, 218 HTLV-I carriers (111 male and 107 female subjects) had complete clinical, neurological, and urological evaluation. They were assessed using standardized questionnaires to determine urinary complaints (Urinary Distress Inventory) and ED (Brief Male Sexual Function Inventory). Neurological impairment was established by Expanded Disability Status Scale (EDSS) from 0 to 10. HAM/TSP was considered as EDSS> or =2. A total of 17 males had clinically defined HAM/TSP (group 1). From the 94 HTLV-I-infected males, 62 were selected (group 2) and paired by age with patients in group 1. A total of 79 individuals were selected for this study. The age ranged from 35 to 81 y (mean=47.9+/-9.65). The percentage of ED in the studied population was 40.5%. In the HAM/TSP group, ED frequency was 88.2%. The associations among sexual dissatisfaction, erectile dysfunction, urinary symptoms (frequency, nocturia, and urgency) and EDSS> or =2 were statistically significant. In HAM/TSP, there is a slow and progressive degeneration of the lateral funiculus of the spinal cord. HTLV-I-infected individuals present a high frequency of ED and it is closely associated to urinary symptoms and the overall neurological picture. The HTLV-I carriers already had prominent compromise of the sexual activity.     

Erectile dysfunction as an early sign of cardiovascular disease

A body of evidence from basic science and clinical research is emerging to provide a compelling argument for endothelial dysfunction as a central etiologic factor in the development of atherosclerosis and vascular disease (ischemic heart disease, stroke, and claudication). Erectile dysfunction (ED) is another prevalent vascular disorder that is now thought to be caused by endothelial dysfunction. In fact, a burgeoning literature is now available that suggests that ED may be an early marker for atherosclerosis and cardiovascular disease (CVD). The emerging awareness of ED as a barometer for CVD represents a unique opportunity to enhance preventive vascular health in men. The diagnosis of ED could become a powerful clinical tool to improve early detection of atherosclerosis and initiate prompt aggressive medical management of associated cardiovascular risk factors.     

Erectile dysfunction in smokers: a penile dynamic and vascular study

In this study, we aimed to determine the hemodynamic mechanisms through which cigarette smoking, as an independent risk factor, induces erectile dysfunction (ED). We performed a standard ED evaluation that included history; a physical exam; and serum glucose, testosterone, and prolactin levels. We then excluded ED patients with abnormal androgen profiles and patients with ED risk factors other than smoking. A total of 109 ED patients entered the study, including 71 current smokers and 38 nonsmokers. All patients then underwent extensive evaluation, including nocturnal penile tumescence and rigidity (NPTR) monitoring with Rigiscan, followed by pharmacopenile duplex ultrasonography (PPDU) and redosing pharmacocavernosometry (RPC). Results of the above tests were compared in the smoker and nonsmoker groups. We also performed receiver operating characteristic (ROC) curve analysis to determine which diagnostic parameter is most affected by cigarette smoking. The 4 most significant variates served as input features for a logistic regression model, designed to predict smoking. The average age for smokers and nonsmokers was 44.3 and 51.2 years, respectively (P = .02). Eighty-six percent of smokers had abnormal NPTR testing compared with 55% of nonsmokers (P = .02). The average peak systolic velocity (PSV) was 26.8 and 31.2 cm/s for smokers and nonsmokers, respectively, and this difference was not found to be statistically significant (P = .19) in this study. On performing RPC, an abnormal maintenance flow (MF) of >5 mL/min was detected in 89% of smokers and in 47% of nonsmokers, and the difference was significant (P < .01). With the use of smoking as the outcome, the ROC area of different diagnostic parameters was as follows: 0.79 for penile base rigidity, 0.58 for PSV, and 0.77 for MF. A logistic regression model that used the 4 most significant variates as input features yielded a ROC of 0.857. The results of NPTR testing in our smoker and nonsmoker groups indicated that ED in smokers is mainly of organic etiology. On the basis of the PPDU findings and the higher incidence of abnormal MF in the smoker group and its relatively high ROC value, we concluded that dysfunction of penile veno-occlusive mechanisms plays a substantial role in the development of ED in smokers.     

Erectile dysfunction as a predictor of cardiovascular disease

Although it has been recognized that erectile dysfunction (ED) and coronary artery disease share many of the same risk factors--smoking, dyslipidemia, diabetes and hypertension--just in the past few years several new studies now suggest that ED is an important early marker of the presence of coronary artery disease. Recent analyses suggest that ED symptoms occur prior to coronary artery disease symptoms and may be a predictor of future major cardiovascular events. Some of these new studies also suggest that ED is an independent risk factor for predicting cardiovascular events--that is independent of other well-established risk factors. Taken together, these new studies suggest that when a patient presents with ED, the patient should be questioned about cardiac health and cardiovascular risk factors. If cardiovascular risk factors are identified, they should be worked up and aggressively treated--as treatment of these risk factors may be life-saving.     

Erectile dysfunction due to atherosclerotic vascular disease: the development of an animal model.

An animal model was developed to study the pathophysiology of erectile dysfunction due to atherosclerotic vascular disease. Thirty one New Zealand white male rabbits were divided into control (n = 5) and treatment groups (n = 26). The control group was placed on a regular diet while the treatment group underwent balloon de-endothelialization of the aorto-iliac arteries and received 1.6% cholesterol and 4% triglyceride diet for eight weeks. After eight weeks in the control animals (n = 5), blood levels of cholesterol, triglycerides and low density lipoproteins, radiologic studies as well as hemodynamic parameters of erectile function were all normal. In the surviving treatment animals (n = 21) after the same time period, a significant increase in blood levels of cholesterol, triglyceride and low density lipoprotein were observed. In addition, 62% of these animals developed hypertension which was not observed in the control group. Angiographically, 10 animals (48%) demonstrated severe atherosclerotic lesions (75% to 100% occlusion of common or internal iliac arteries on one side and over 50% occlusion of the opposite side), five (24%) had moderate lesions (50 to 75% luminal occlusion of right and left common iliac or internal iliac arteries) and 6 revealed minimal lesions (less than 50% occlusion of the right and left common iliac or internal iliac arteries). Of the 15 animals with 50% or greater luminal occlusion of the iliohypogastric arteries, erectile dysfunction was found in 93% of cases. Due to the development of erectile dysfunction in 33% of animals with minimal occlusive lesions, it appears that factors, other than large vessel luminal occlusion, may exist in this animal model which adversely influence erectile function. This model may therefore be of further benefit in the study of other factors associated with atherosclerosis and impotence, such as the possible concomitant hypercholesterolemic and atherosclerotic-induced alterations in the local reactivity of corpus cavernosum smooth muscle and lacunar space endothelial cells.     

Blue toe syndrome--a warning sign of unsuspected vascular injury

A case report is presented of a young patient involved in a motor vehicle accident, who initially demonstrated no physical or radiologic evidence of thoracic injury. Six weeks later the patient was noted to have two blue toes. Arteriography done at that time demonstrated a previously unsuspected false aneurysm of the descending thoracic aorta. An embolic event in a patient with a history of major trauma should be considered a strong indication for arteriographic evaluation of the proximal arterial system.     

Erectile dysfunction in heart disease patients

Atherosclerosis is a general health problem that not only affects the coronary arteries but also (in men) the penile arteries, thus contributing to organic causes of erectile dysfunction (ED) in heart disease patients. These organic causes are intertwined with psychological and pharmacological causes because medication prescribed for heart disease patients may also cause ED. The incidence of ED after myocardial infarction ranges from 38 to 78%. As sexual intercourse involves physical exertion, the medical history, ventricular function determined through echocardiography, and stress testing are used to classify patients into various groups where coital activity represents a greater or lesser cardiovascular risk. The energy requirements for intercourse are not high, ranging from 3.7 metabolic equivalents (METs) of energy expenditure at resting state during the preorgasmic phase to 5 METs during orgasm. The Bruce protocol for exercise stress testing is a six-stage protocol with changes in the slope and speed of the treadmill. As a general rule, a patient who completes the first two stages of the Bruce protocol has a functional capacity greater than 7 METs, which is considered sufficient for sexual intercourse. The physician or cardiologist concerned should institute first-line treatment with oral drugs according to the indications listed below. If sexual activity is not contraindicated, the treatment of choice for ED in heart disease patients is oral therapy with sildenafil, except in those cases in which its use is contraindicated. Specific recommendations are discussed.     

Erectile dysfunction in patients with coronary artery disease

Recent studies suggest that erectile dysfunction (ED) may be an early marker of endothelial dysfunction and coronary artery disease (CAD). Conversely, patients with CAD commonly have ED. The phosphodiesterase 5 (PDE5) inhibitors are very effective for the treatment of ED in patients with CAD. Numerous studies show that this class of drugs is in general safe in patients with stable CAD and these agents do not exacerbate ischemia in men with CAD undergoing exercise stress testing. Analysis of placebo-controlled trials did not show an increase in cardiovascular events among men receiving PDE5 inhibitors, and post-marketing surveillance studies with sildenafil did not observe an increase in cardiovascular events compared to expected age-matched rates. Organic nitrates remain a contraindication for PDE5 inhibitors and alpha blockers have precautions/contraindications depending upon specific drugs. The Princeton Consensus Guidelines (soon to be updated) suggest a logical approach to the patient with CAD seeking therapy for sexual dysfunction.     

The drop sign, a radiographic warning sign of elbow instability

Persistent instability or redislocation is uncommon but of significant concern in treating elbow dislocations. Finding an objective, static radiographic sign that might correlate with the presence of instability was the purpose of this study. Pre- and post-reduction radiographs of 10 consecutive simple and complete adult elbow dislocations were reviewed and compared with radiographs of 20 consecutive adult elbows without any trauma history. A statistically significant measured increase in static ulnohumeral distance was noted on the routine unstressed post-reduction lateral radiographs of patients sustaining dislocation. We have termed this increased distance the drop sign. It differs from the radiographic ulnohumeral separation noted during O'Driscoll's test for posterolateral rotary instability, which is present only with axial compression. The drop sign becomes concerning only if persistent after the first reduction radiograph and may be a warning sign of the presence of instability.     

Erectile dysfunction and cardiac disease: Recommendations of the second princeton conference

Erectile dysfunction (ED) has been linked increasingly to cardiovascular risk factors and comorbidities. Considering the potential risk associated with sexual activity, guidelines were developed (Princeton I) for assessment and management of patients with varying degrees of cardiac risk. These guidelines were recently updated (Princeton II) based on new data concerning the link between ED and cardiovascular disease and the availability of additional phosphodiesterase type 5 inhibitors (vardenafil, tadalafil). Despite the need for careful risk assessment in all cases, sexual activity remains safe for the large majority of patients. However, all patients presenting with complaints of ED should be carefully assessed for the presence of cardiovascular risk factors (eg, obesity, hypertension, hyperlipidemia). Risk-factor modification, including lifestyle interventions (eg, exercise, weight loss) is strongly encouraged. Guidelines are presented for the management of acute coronary syndromes in patients taking phosphodiesterase type 5 inhibitors, including alternatives to the use of nitrates for these patients. Other drug interactions and the cardiovascular safety of testosterone replacement therapy are considered.     

Erectile dysfunction and coronary slow flow: distinct presentations of endothelial disease

The aim of the present study was to investigate degree of erectile dysfunction (ED) in males with slow coronary flow (SCF). Endothelial dysfunction was proposed to be the underlying mechanism in both diseases. A total of 29 male patients with slow coronary flow (mean age 45+/-7 years) and 23 male patients with normal coronary arteries (mean age 48+/-12 years) were included in the study. The severity of ED was determined according to the International Index of Erectile Function (IIEF) questionnaire. Mean IIEF scores in patients with SCF and control group were determined as 20.97+/-7.26 and 25.26+/-5.17, P=0.016. ED was detected in 45% (n=13) of SCF patients and 35% (n=8) of the control group (P=0.035). There was a negative correlation between the mean TIMI frame count and IIEF score between patients with SCF and controls (r=-0.31, P=0.029). These data suggest that ED is observed more frequently in patients with SCF phenomenon compared to patients with otherwise normal coronary angiograms.