Showing papers by "London Bridge Hospital published in 2010"

Erectile dysfunction and coronary artery disease prediction: Evidence-based guidance and consensus

Abstract: * A significant proportion of men with erectile dysfunction (ED) exhibit early signs of coronary artery disease (CAD), and this group may develop more severe CAD than men without ED (Level 1, Grade A). * The time interval among the onset of ED symptoms and the occurrence of CAD symptoms and cardiovascular events is estimated at 2-3 years and 3-5 years respectively; this interval allows for risk factor reduction (Level 2, Grade B). * ED is associated with increased all-cause mortality primarily due to increased cardiovascular mortality (Level 1, Grade A). * All men with ED should undergo a thorough medical assessment, including testosterone, fasting lipids, fasting glucose and blood pressure measurement. Following assessment, patients should be stratified according to the risk of future cardiovascular events. Those at high risk of cardiovascular disease should be evaluated by stress testing with selective use of computed tomography (CT) or coronary angiography (Level 1, Grade A). * Improvement in cardiovascular risk factors such as weight loss and increased physical activity has been reported to improve erectile function (Level 1, Grade A). * In men with ED, hypertension, diabetes and hyperlipidaemia should be treated aggressively, bearing in mind the potential side effects (Level 1, Grade A). * Management of ED is secondary to stabilising cardiovascular function, and controlling cardiovascular symptoms and exercise tolerance should be established prior to initiation of ED therapy (Level 1, Grade A). * Clinical evidence supports the use of phosphodiesterase 5 (PDE5) inhibitors as first-line therapy in men with CAD and comorbid ED and those with diabetes and ED (Level 1, Grade A). * Total testosterone and selectively free testosterone levels should be measured in all men with ED in accordance with contemporary guidelines and particularly in those who fail to respond to PDE5 inhibitors or have a chronic illness associated with low testosterone (Level 1, Grade A). * Testosterone replacement therapy may lead to symptomatic improvement (improved wellbeing) and enhance the effectiveness of PDE5 inhibitors (Level 1, Grade A). * Review of cardiovascular status and response to ED therapy should be performed at regular intervals (Level 1, Grade A).

Antiphospholipid syndrome (Hughes syndrome): 10 clinical topics.

Abstract: This year in Galveston, Texas, Silvia Pierangeli hosts the 13th International Congress on Antiphospholipid Antibodies. Twenty-six years after the first antiphospholipid syndrome meeting, the number of interested colleagues has multiplied, and the subject has become more scientifically understood. So also has the clinical picture. In this short contribution, I will highlight a number of clinical observations which may, or may not, contribute to our understanding of antiphospholipid syndrome.

Antiphospholipid syndrome, migraine and stroke

Abstract: It is over a quarter of a century since the description of the antiphospholipid (Hughes) syndrome (APS). This pro-thrombotic condition, characterized by the presence of antiphospholipid antibodies (aPL), results in an increased tendency to thrombosis and, in pregnancy, to recurrent miscarriage and other obstetric complications. Strikingly, APS can affect both veins and arteries, the latter leading, for example, to myocardial infarction and stroke. The brain appears to be particularly susceptible to the syndrome, with its attendant thrombosis and ischaemia, the neurological presentations ranging frommemory loss to movement disorders, from atypical multiple sclerosis to epilepsy. Additionally, some of these clinical associates of aPL may well have been under-recognizeduntil recently.Forexample, theassociationwith seizures (including temporal lobe epilepsy) first recognized in 1985, may well be substantial – a recent report suggesting that20%ofcasesof idiopathic teenage epilepsy were linked to aPL, for example. However, the two most important clinical neurological manifestations of Hughes syndrome are migraine and stroke. Migraine, in all its forms, is arguably the commonest clinical manifestation of the syndrome. Many Hughes syndrome patients presenting with thrombosis, transient ischaemic attacks (TIAs) or stroke at, say, the age of 40, give a history of severe headaches, often migrainous, dating back to childhood. Interestingly, there is often a family history of migraine, and a number of large family cohorts embracing migraine, APS and stroke are now being reported. Attempts at quantifying the prevalence of headache and migraine in Hughes syndrome (and in lupus) are limited by the well known difficulties in classification. This is doubly important as the links with cognitive impairment, in both lupus and in patients with antiphospholipid antibodies need clarification. For example, in a recent study of cognitive impairment in lupus, and its relationship to headache, Whitelaw and Spangenberg concluded that . . . ‘it is only APS (Hughes) syndrome which has been documented to produce impaired cognitive function in lupus’. The cause of the headache is uncertain. However, one of the most striking clinical observations is the often complete disappearance of the headaches when anticoagulation with heparin or warfarin is started, say, for a peripheral thrombosis, or with heparin prophylaxis in pregnancy. This observation has led to the use of a 2–3-week therapeutic trial of low-molecular-weight heparin in some cases of APS in which increasingly severe headaches are a feature. Stroke is now internationally recognized as an important manifestation of Hughes syndrome – the severity ranging from small TIAs to catastrophic fatal cerebral infarction. What is the relative contribution of Hughes syndrome to the huge medical social and economic problem of stroke? Published figures vary, ranging from 7% of all strokes to 41% in a major collaborative American stroke study. The latter study has, however, been criticised for a number of shortcomings, including the reliance on single aPL assessments. An important study from Rome found that in a younger population (under 45) a striking one in five of all strokes were associated with aPL. If such estimates are correct (and despite flaws in the standardization of aPL testing, clinical experience suggests that they are), then here we have a large group of individuals who, with a simple blood test, could be identified as being at risk of stroke and in whom preventative anti-aggregant or anticoagulant treatment could be instituted. Furthermore, a greater awareness of the fact that even on warfarin anticoagulation, patients with APS are at greater risk of thrombosis than from bleeding, would lead to more appropriate treatment. The discovery of the antiphospholipid syndrome has opened up new avenues for research in medicine and in epidemiology. Correspondence to: Graham Hughes, Head, The London Lupus Centre, London Bridge Hospital, London SE1 2PR, UK. Email: graham.hughes@hcaconsultant.co.uk

Hughes syndrome (antiphospholipid syndrome) and myocardial infarction

Abstract: Hughes syndrome (the antiphospholipid syndrome, APS) first described in clinical detail in 1983, is characterised by thrombosis, migraine, recurrent miscarriage and the presence of circulating antiphospholipid antibodies (1,2).