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Showing papers by "London Bridge Hospital published in 2011"


Journal ArticleDOI
TL;DR: This review focuses on the multidirectional impact of low testosterone associated with obesity and the metabolic syndrome and its effects on erectile dysfunction and CVD risk in men with type 2 diabetes.
Abstract: Men with obesity, the metabolic syndrome, and type 2 diabetes have low total and free testosterone and low sex hormone–binding globulin (SHBG). Conversely, the presence of low testosterone and/or SHBG predicts the development of metabolic syndrome and type 2 diabetes. Visceral adiposity present in men with low testosterone, the metabolic syndrome, and/or type 2 diabetes acts through proinflammatory factors. These inflammatory markers contribute to vascular endothelial dysfunction with adverse sequelae such as increased cardiovascular disease (CVD) risk and erectile dysfunction. This review focuses on the multidirectional impact of low testosterone associated with obesity and the metabolic syndrome and its effects on erectile dysfunction and CVD risk in men with type 2 diabetes. Whenever possible in this review, we will cite recent reports (after 2005) and meta-analyses. ### Epidemiological studies of low testosterone, obesity, metabolic status, and erectile dysfunction Epidemiological studies support a bidirectional relationship between serum testosterone and obesity as well as between testosterone and the metabolic syndrome. Low serum total testosterone predicts the development of central obesity and accumulation of intra-abdominal fat (1–3). Also, low total and free testosterone and SHBG levels are associated with an increased risk of developing the metabolic syndrome, independent of age and obesity (1–3). Lowering serum T levels in older men with prostate cancer treated with androgen deprivation therapy increases body fat mass (4). Conversely, high BMI, central adiposity, and the metabolic syndrome are associated with and predict low serum total and to a lesser extent free testosterone and SHBG levels (1–3,5). Because obesity suppresses SHBG and as a result total testosterone concentrations, alterations in SHBG confound the relationship between testosterone and obesity. Low total testosterone or SHBG levels are associated with type 2 diabetes, independent of age, race, obesity, and criteria for diagnosis of diabetes (6,7). In longitudinal studies, low serum total and free testosterone …

309 citations


Journal ArticleDOI
TL;DR: Erectile dysfunction is a major problem with an increasing prevalence in cardiovascular high‐risk patients due to its association with cardiovascular risk factors and drugs used for evidence‐based treatment of cardiovascular diseases are reported to decrease erectile function.
Abstract: AIMS Erectile dysfunction is a major problem with an increasing prevalence in cardiovascular high-risk patients due to its association with cardiovascular risk factors. Drugs used for evidence-based treatment of cardiovascular diseases have been reported to decrease erectile function, but possible mechanisms are poorly characterised. METHODS MEDLINE, EMBASE and Cochrane Registry search were performed including manuscripts until January 2010. Searching terms are: 'erectile dysfunction or impotence' in combination with 'ACE-inhibitors', 'angiotensin', 'beta-blockers', 'calcium antagonist' and 'diuretics'. Animal studies, letters, reviews, case-reports and manuscripts other than English language and trials dealing with combination treatment are excluded. RESULTS Analysis of literature revealed five epidemiological trials evaluating the effect of different cardiovascular drugs on erectile function. There were eight trials evaluating the effect of beta-blockers, five trials evaluating the effect of ace-inhibitors or angiotensin-receptor-blockers and one trial evaluating the effect of diuretics on erectile function. Results of these trials demonstrate that only thiazide diuretics and beta-blockers except nebivolol may adversely influence erectile function. ACE-inhibitors, angiotensin-receptor-blockers and calcium-channel-blockers are reported to have no relevant or even a positive effect on erectile function. CONCLUSION Inappropriate patients' concerns about adverse effects of cardiovascular drugs on erectile function might limit the use of important medications in cardiovascular high-risk patients. Knowledge about the effects of drug-treatments on erectile function and about the major role of the endothelium in penile function might improve patients' adherence to evidence based treatment of cardiovascular diseases.

111 citations


Journal ArticleDOI
TL;DR: There are indications that the primary antiphospholipid syndrome will turn out to be more common than lupus, though this could still be a reflection of referral practice.
Abstract: A pro-thrombotic condition was described in 1983 which was characterised by the presence of circulating antiphospholipid antibodies, as well as peripheral thrombosis (e.g. DVT), a tendency to internal organ involvement, repeated miscarriage, and, occasionally, thrombocytopenia (aPL) (Hughes, Br Med J 287:1088–1089, 1983). Previously, there had been a number of observations, mainly in patients with lupus having “false positive” tests for syphilis, miscarriage and circulating lupus anticoagulants. The description in 1983 had three notable features (a) a detailed comprehensive clinical picture of the syndrome; (b) this description differed from other coagulopathies in showing a propensity for arterial thrombosis (e.g. stroke and heart attack); and (c) this was a syndrome quite independent from lupus. There are indications that the primary antiphospholipid syndrome will turn out to be more common than lupus, though this could still be a reflection of referral practice.

16 citations


Journal ArticleDOI
TL;DR: This review will elaborate the definition of cardiometabolic risk, apply the use of surrogate markers for cardiovascular risk stratification in men in addition to the traditional Framingham‐based markers, and examine minority men’s health and racial differences in these determinants of cardiovascular risk.
Abstract: Evaluation of cardiometabolic risk has become vital in primary prevention of adverse vascular events (coronary artery disease, heart attack, stroke or congestive heart failure), particularly in younger middle-aged men (40-60 years old). To discern the prevalence of events in these men, clinicians often stratify cardiovascular risk and treat according to traditional Framingham risk criteria. Yet it is evident that the traditional Framingham risk assigned to intermediate- and low-risk men will miss several of these individuals deemed at high 'cardiometabolic risk', also known as residual cardiovascular risk. This review will elaborate the definition of cardiometabolic risk and apply the use of surrogate markers for cardiovascular risk stratification in men in addition to the traditional Framingham-based markers. It will utilise both gender non-specific and gender-specific determinants of cardiometabolic risk. Lastly, it will examine minority men's health and racial differences in these determinants of cardiovascular risk. This analysis includes an electronic literature search utilising PubMed, EMBASE and MEDLINE databases to clarify the level of evidence for the stepwise utility of novel biomarkers for cardiometabolic risk in the male patient. This manuscript generates discussion of the utility of markers of cardiometabolic risk stratification. The following questions are summarised: (i) Are there non-traditional tests that might define this risk better than traditional markers? (ii) Will treatment based on this risk assessment augment present risk stratification and lower cardiovascular risk? (iii) What is known regarding racial differences surrounding cardiometabolic risk assessment? Traditional risk factors including Framingham Risk Score underestimate the overall 10 year and lifetime risk for the intermediate-risk younger middle-aged men<60 years of age. This fact is especially true in the minority population. We have graded the evidence of non-gender specific and gender-specific markers of cardiometabolic risk, thereby, allowing greater clarification of risk in this population. The pragmatic use of these novel markers of cardiometabolic risk may help stratify those individuals at greater lifetime risk than that noted by the Framingham Risk Score.

12 citations


Journal ArticleDOI
TL;DR: This yin–yang hypothesis is a general guide to how to interpret ADMA–NO interactions but can break down when viewed in detail, as both ADMA and SDMA can have other direct actions on the vasculature.

2 citations


Book ChapterDOI
01 Jan 2011
TL;DR: Though this chapter addresses an organic condition, it is important not to compartmentalize ED too rigidly – men with organic ED may, and often do, have psychological problems as well, and men with a predominantly psychological etiology may also have organic issues.
Abstract: The cardiovascular response to sexual activity worries a lot of men and women, particularly if a coronary or vascular event has already occurred. The fear of inducing another cardiac episode is fuelled by many myths including the assumption that sex is an extreme stress to the heart, driven to some extent by media/internet distortion. Adding the anxiety that treating ED may increase cardiac risk, and we have a recipe for relationship stress or breakdown and couple frustration. Many agree with the concept that ED is “a man’s problem but a couple’s concern” because it invariably is, though at times is not managed as such. Though this chapter addresses an organic condition, it is important not to compartmentalize ED too rigidly – men with organic ED may, and often do, have psychological problems as well, and men with a predominantly psychological etiology may also have organic issues.

1 citations


Journal ArticleDOI
01 Jan 2011-Lupus
TL;DR: As miscarriage is common, statistics and socio-economic constraints currently advocate the need for aPL testing only after 3 or more miscarriages – something that in the view of this author is debatable: a PL testing could protect against further miscarriages or even a tragic future late pregnancy loss.
Abstract: Once in a while, the stimulus for a research project comes not from a medical conference, or from a learned journal, but from an unlikely source – such as a newspaper. Even a throwaway newspaper. Thus, it was in my free daily London issue of the METRO, the headline appeared ‘‘Miscarriage link to risk of heart attack’’. The newspaper quoted a research paper from Heidelberg published online in the journal ‘‘Heart’’. A quarter of more than 11,500 women taking part in the study had suffered at least one miscarriage. Those who had more than three miscarriages were nine times more likely to have a subsequent heart attack, and a stillbirth increased the risk by 3.5 times. In response to the study, the British Heart Foundation said that in some cases of multiple miscarriages, women had previously undiagnosed heart and circulation disease which carried heart attack risks that may be unrelated to pregnancy. Do you believe that? Possibly in rare cases. For me, there is a far, far more likely link – antiphospholipid antibodies (aPL) and the antiphospholipid syndrome. Three decades of clinical experience since the description of the antiphospholipid syndrome have thrown up some clear clinical lessons in the world of obstetrics. The syndrome might be the commonest, treatable cause of recurrent miscarriage. Indeed, for late pregnancy loss the association with aPL is so strong that routine testing of all women with this tragic pregnancy outcome is considered mandatory – if only to alert obstetricians to the risks in any future pregnancy. Recognition of the syndrome has become an important component of obstetric care. But there is still a way to go. In particular, two weaknesses remain. Firstly, the decision as to whether to test after a single, or even two miscarriages. As miscarriage is common, statistics and socio-economic constraints currently advocate the need for aPL testing only after 3 or more miscarriages – something that in the view of this author is debatable: aPL testing could protect against further miscarriages or even a tragic future late pregnancy loss. This is an area which has been debated by APS experts and obstetricians for years, as clearly outlined in an excellent series of reviews at the 13 International Congress on Antiphospholipid Antibodies held in Galveston, April 2010, and elsewhere. The arguments are well rehearsed and based on selection and on the relatively small number of positive aPL/APS women seen in the ocean of miscarriage patients. However, one weakness of the ‘‘wait for 3 miscarriages’’ school is that studies are often limited to patients fulfilling the Sapporo criteria for APS. As with lupus, criteria are for classification rather than diagnosis and, as with lupus, clinical experience teaches us that there are many, many patients with less than classical APS, or in whom tests are borderline or even negative. The second weakness in obstetric care concerns the longer term follow-up. The aPL positive patient who, when treated, has a successful pregnancy, is congratulated, discharged and . . . . . .? The long (and sometimes short) term risks of aPL positivity are now well known and include DVT, pulmonary embolism, migraine and stroke. Another arterial thrombotic risk of APS is myocardial infarction. This complication, recognised early on in clinical descriptions of the syndrome has, if anything, been underreported. Recently, however, two major studies highlighted a strong link between the presence of aPL and heart attack. Greco and colleagues studied 344 acute coronary syndrome patients and found 40% aPL positive in one or more tests. Urbanus and colleagues looked at women under 50 with myocardial infarction or ischaemic stroke. The odds ratio for MI in aPL positive women and oral contraceptive was 22. Thus, it is possible that the excellent epidemiological study from Heidleberg linking miscarriage and later heart attack may have a clear – and measurable – link.

1 citations