Obesity and heart failure: when 'epidemics' collide

No abstract available

Socioeconomic deprivation and cardiovascular disease

Socioeconomic deprivation (SED) is inversely associated with mortality. The most deprived are at a higher risk of all cause mortality and cardiovascular mortality. However, only limited study of the relationship between SED and non-fatal cardiovascular disease has been previously undertaken. In those studies that have examined the relationship between SED and non-fatal cardiovascular disease, analyses have been limited to one form of cardiovascular disease (CVD), such as myocardial infarction or stroke and often prevalent disease. Furthermore, these studies have often failed to examine the association between SED and CVD whilst adjusting analyses for cardiovascular risk factors which are more prevalent in the most deprived. The aim of this work was to examine the association between SED and a number of cardiovascular outcomes after adjusting for the traditional cardiovascular risk factors of age, sex, smoking, blood pressure, diabetes mellitus and cholesterol. To determine is SED is in fact a risk factor for CVD after adjustment for these other risk factors, the relationship between SED and a number of fatal and non-fatal cardiovascular outcomes was examined. A number of forms of CVD were examined, including all coronary heart disease, myocardial infarction, stroke and heart failure A cohort of over 15,000 men and women who participated in the Renfrew Paisley cohort study was examined. These individuals were enrolled between 1974 and 1976 and underwent comprehensive screening for cardiorespiratory risk factors. They have since been followed for hospitalisations and deaths for 28 years. SED was measured using the Registrar General’s social class system and the Carstairs Morris index of deprivation. Rates of fatal and non-fatal outcomes were calculated, as were a number of composite outcomes. Adjusted analyses using multivariable regression were conducted to account for the risk factors of age, sex, smoking, blood pressure, diabetes and cholesterol. Further adjustment for the risk factors of lung function as measured by forced expiratory volume in 1 second, cardiomegaly on chest x-ray, body mass index, and a history of bronchitis was also made. The association between SED and the risk of recurrent cardiovascular hospitalisations, the burden of cardiovascular disease, as well as mortality and premature mortality was assessed for SED. I found that SED was associated with higher rates of hospitalisation for CVD disease in men and women irrespective of the measure of SED, either social class or the area based score of the Carstairs Morris index. This association persisted after adjustment for the traditional cardiovascular risk factors of age, sex, smoking, systolic blood pressure and diabetes and cholesterol. Further adjustment for lung function, the presence of bronchitis, body mass index and cardiomegaly on a chest x-ray did not explain the relationship between SED and each outcome. This risk was long lasting and persisted to the end of follow up. The strength of association of SED with coronary heart disease, myocardial infarction and stroke and all cause mortality was similar. The risk of a recurrent CVD hospitalisation was not higher in the most deprived after adjustment for CVD risk factors. However, I observed that SED was associated with higher mortality following an admission to hospital with CVD, before and after adjustment for cardiovascular risk factors of age, sex, smoking, systolic blood pressure, cholesterol and diabetes and after adjusting for the year of first developing cardiovascular disease. All cause mortality and cardiovascular mortality was highest in the most deprived. Again this association persisted after adjustment for cardiovascular risk factors. The most deprived also experienced longer hospital stays than the least deprived for a number of cardiovascular diseases including myocardial infarction and stroke. As a result the costs associated with cardiovascular disease admissions to hospital were highest in the most deprived despite their higher risk of dying during follow up. The cost differential was also explained by the finding that the most deprived experienced a higher number of admissions per person. Finally, the population attributable risk associated with SED is comparable to that of other traditional cardiovascular risk factors. In conclusion, I have found that the risk of CVD in the most deprived is higher even after adjustment for a number of cardiovascular risk factors. The numbers of hospitalisations, costs and mortality are also highest in the most deprived. Efforts are required to redress this imbalance. This can be achieved at the level of the individual through health care interventions to reduce the absolute burden of cardiovascular risk factors and to treat disease. However, societal level interventions are also required to tackle this problem as SED exerts complex effects on health that seem to also be independent of risk factors

Analysing registries in heart failure: the case of angiotensin receptor blockers in Asians with heart failure with reduced ejection fraction

No abstract available

Improving recruitment for clinical trials: the human touch

No abstract available

Declining risk of sudden death in heart failure

No abstract available

Contemporary management of heart failure in the elderly

The foundation of the treatment of heart failure with reduced ejection fraction is a number of pharmacotherapies shown to reduce morbidity and mortality in large randomised multinational clinical trials. These include angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, mineralocorticoid receptor antagonists, and more recently, a combined angiotensin receptor blocker neprilysin inhibitor, sacubitril/valsartan. In select cases, digoxin, ivabradine and hydralazine with isosorbide dinitrate have a role to play in the treatment of heart failure with reduced ejection fraction. On this foundation, other more advanced treatments such as implantable cardioverter defibrillators and cardiac resynchronisation therapy are recommended in guidelines for the treatment of heart failure with reduced ejection fraction (i.e. an ejection fraction of ≤ 40%) and for a select few there remains the option of mechanical circulatory support and cardiac transplantation. The efficacy of pharmacotherapy does not vary by age and each of these therapies should be considered in all patients, irrespective of age. Other factors such as co-morbidities like renal dysfunction may limit the use of some of these drugs in the elderly. Decision making with regard to device therapy is more complex; the likelihood of competing non-cardiovascular causes of death and life expectancy need to be considered. Despite multiple treatment options for heart failure with reduced ejection fraction, the options for heart failure with preserved ejection fraction are limited. In the absence of robust outcomes data from a large randomised trial, a mineralocorticoid receptor antagonist is a reasonable therapy to reduce the risk of hospitalisation for heart failure in patients with heart failure with preserved ejection fraction

Early use of mineralocorticoid receptor antagonists in ST-elevation myocardial infarction: is it ever too early?

No abstract available

The recurring problem of heart failure hospitalisations

No abstract available

Catheter ablation for atrial fibrillation with heart failure

No abstract available

Non-ischaemic cardiomyopathy, sudden death and implantable defibrillators: a review and meta-analysis

Objective: The recent Danish Study to Assess the Efficacy of ICDs in Patients with Non-ischemic Systolic Heart Failure on Mortality (DANISH) trial suggested that implantable cardioverter defibrillators (ICDs) do not reduce overall mortality in patients with non-ischaemic cardiomyopathy (NICM), despite reducing sudden cardiac death. We performed an updated meta-analysis to examine the impact of ICD therapy on mortality in NICM patients. Methods: A systematic search for studies that examined the effect of ICDs on outcomes in NICM was performed. Our analysis compared patients randomised to an ICD with those randomised to no ICD, and examined the endpoint of overall mortality. Results: Six primary prevention trials and two secondary prevention trials were identified that met the pre-specified search criteria. Using a fixed-effects model, analysis of primary prevention trials revealed a reduction in overall mortality with ICD therapy (RR 0.76, 95% CI 0.65 to 0.91). Conclusions: Although our updated meta-analysis demonstrates a survival benefit of ICD therapy, the effect is substantively weakened by the inclusion of the DANISH trial—which is both the largest and most recent of the analysed trials—indicating that the residual pooled benefit of ICDs may reflect the risk of sudden death in older trials which included patients treated sub-optimally by contemporary standards. As such, these data must be interpreted cautiously. The results of the DANISH trial emphasise that there is no ‘one size fits all’ indication for primary prevention ICDs in NICM patients, and clinicians must consider age and comorbidity on an individual basis when determining whether a defibrillator is appropriate