Erectile dysfunction in the cardiology practice-a patients' perspective.

BACKGROUND: Erectile dysfunction (ED) is an independent risk factor for cardiovascular events sharing mutual risk factors with coronary artery disease. Several guidelines for the management of ED in cardiovascular disease have been proposed, recommending cardiologists to routinely inquire about erectile function. However, males' specific needs and wishes regarding sexual health care in cardiology are unknown. We sought to identify male patients' view concerning possible improvements in sexual health care and preferred forms of sexual counseling in the cardiology practice. METHODS: This is a cross-sectional multicentered survey study among randomly selected males visiting a cardiologist. RESULTS: Of 388 respondents, 296 questionnaires were eligible for analysis. Mean age of respondents was 62.9 years. Overall, 56% (n = 165) had ED, with up to 86% in patients with heart failure. Mean bother experienced due to ED was 5.93 (±2.57) on a 0 to 10 scale. Most respondents indicated to feel comfortable discussing sexual health with the cardiologists (88%). Of men with ED (n = 165), 46% would like to have a conversation with the cardiologist about possibilities to improve sexual function, 55% would be helped if questions could be asked during consultation with a specialized nurse, and 58% would appreciate written information. Of all respondents (n = 296), 28% ever tried a phosphodiesterase inhibitor; 4% received the prescription of the cardiologists. CONCLUSIONS: Erectile dysfunction is highly prevalent in patients with a variety of cardiovascular diagnosis and care for sexual function is mandatory. Patients indicated that above consultation with the cardiologist, both consultation with a specialized nurse and written information would be helpful.

A wandering defibrillator lead.

A 53-year-old woman was admitted because of sudden onset of severe chest pain and palpitations. Her medical history revealed an out-of-hospital cardiac arrest due to ventricular tachycardia caused by arrhythmogenic right ventricular cardiomyopathy for which an implantable cardioverter-defibrillator was implanted with epicardial patches. On 2D echocardiography, a mobile piece of lead was seen in the right atrium and right ventricle, loosely attached to the free wall of the right ventricule; 3D reconstruction confirmed this suggestion. Remarkably, the lead disappeared while performing the echocardiogram. A pulmonary artery fluoroscopy was performed. It had positioned itself in the right pulmonary artery. The lead could be extracted from the right pulmonary artery using an extraction device. We suggest that during a period of frequent bending physical activity, the lead must have started its journey by perforating through the free wall of the right ventricle and had then been carried away by the blood flow towards the right pulmonary artery. The lead must be a residue of an epicardial defibrillation lead, which has not been removed completely after the heart transplantation performed 10 years earlier. Perforations of pacemaker leads are not uncommon but as far as we know, such a witnessed dislocation and migration of an epicardial defibrillator lead has not been described before.

Familial occurrence of isolated non-compaction cardiomyopathy.

BACKGROUND AND AIMS: Isolated left ventricular non-compaction cardiomyopathy (LVNC) may have an autosomal dominant or X-linked recessive inheritance. We focus on the familial occurrence of LVNC after misdiagnosing this disorder in symptomatic patients in two families. After identification of the index patient we studied the families more intensively in order to unmask affected family members. METHODS AND RESULTS: LVNC was defined as an end-systolic non-compacted subendocardial layer of the left ventricular wall of at least twice the thickness of the subepicardial compacted layer (2D echocardiogram and MRI). This was studied in 13 patients in 2 families (A and B). LVNC was found in 3 out of 11 patients in family A. The grandmother was asymptomatic. Her daughter suffered from recurrent syncope and heart failure. Her daughter received a cardiac transplant because of progressive heart failure at the age of 14years. In family B, LVNC was found in 2 patients, a father and his son and presumed in a brother and a sister of the father who died suddenly at the age of 17 and 21years, respectively. CONCLUSIONS: In all symptomatic patients, proven LVNC was previously misdiagnosed as hypertrophic or dilated cardiomyopathy. Misdiagnosis may lead to insufficient treatment and will misdirect targeted molecular genetic analysis. LVNC was identified in seven patients in two families. Family screening may unmask affected family members for primary prevention including anti-coagulation and ICD-therapy.

Rapid intake of alcohol (binge drinking) inhibits platelet adhesion to fibrinogen under flow.

BACKGROUND: Moderate alcohol consumption is associated with decreased mortality from cardiovascular disease. Drinking large amounts in a short period (binge drinking) is associated with increased cardiovascular morbidity. We tested whether rapid consumption of a large dose of alcohol affects platelet aggregation and adhesion. METHODS: Healthy volunteers (n = 20) were asked to drink three glasses of alcohol or red wine in a 45-min period. Thereafter, another 45 min was allowed for absorption of alcohol. Ninety minutes after the start of the experiment, blood was collected. This entire cycle was repeated once, resulting in consumption of six alcohol-containing drinks in 3 hr. Adenosine-diphosphate (ADP)-induced aggregation was measured and platelet adhesion to fibrinogen and collagen was measured in a perfusion chamber at shear rates of 300/sec and 1600/sec. Platelet coverage and aggregate size were measured. RESULTS: Acute alcohol intake significantly increased platelet aggregation in suspension when stimulated with low concentrations of ADP (0.1 and 0.5 microg/ml). This effect was not observed when consuming red wine. In contrast, adhesion to fibrinogen was significantly inhibited by alcohol but not red wine at high shear rate after six drinks (p = 0.025). The inhibition was accompanied by a reduction in aggregate size at 90 and 180 min after the start of the experiment. Adhesion to collagen was not altered by either alcohol or red wine. CONCLUSIONS: Rapid intake of alcohol increases platelet aggregation, which might contribute to the increased mortality associated with binge drinking. Red wine does not show increased platelet aggregation, which might support the reduction of cardiovascular disease in red wine consumers. However, alcohol inhibits platelet adhesion to fibrinogen-coated surface under flow. The diminished adhesion might contribute to the cardioprotective effects of alcohol.