Search

Background: The Surprise Question: 'would you be surprised if this patient were to die within the next year?' has been shown to predict mortality in patients with chronic kidney disease and cancer. This prospective study aimed to determine whether the Surprise Question could identify heart failure patients with a prognosis of less than 1 year, and whether the Surprise Question can be used by different healthcare professionals., Methods and Results: Overall, 129 consecutive patients admitted with decompensated heart failure were included. Doctors and nurses were asked to provide a 'surprised' or 'not surprised' response to the Surprise Question for each patient. Patients were followed up until death or 1 year following study inclusion. The sensitivity, specificity, positive predictive value and negative predictive value of the Surprise Question were assessed. Cox regression was used to determine covariates significantly associated with survival. The Surprise Question showed excellent sensitivity (0.85) and negative predictive value (0.88) but only fair specificity (0.59) and positive predictive value (0.52) when asked of cardiologists. There were similar levels of accuracy between doctors and specialist nurses. The Surprise Question was significantly associated with all-cause mortality in multivariate regression analysis (hazard ratio 2.8, 95% confidence interval 1.0-7.9, P = 0.046)., Conclusion: This study demonstrates that the Surprise Question can identify heart failure patients within the last year of life. Despite over-classification of patients into the 'not surprised' category, the Surprise Question identified nearly all patients who were within the last year of life, whilst also accurately identifying those unlikely to die., (© 2018 The Authors. European Journal of Heart Failure © 2018 European Society of Cardiology.)

Objective: Acute heart failure syndrome (AHFS) is a major cause of hospitalisation and imparts a substantial burden on patients and healthcare systems. Tools to define risk of AHFS hospitalisation are lacking., Methods: A prospective cohort study (n=628) of patients with stable chronic heart failure (CHF) secondary to left ventricular systolic dysfunction was used to derive an AHFS prediction model which was then assessed in a prospectively recruited validation cohort (n=462)., Results: Within the derivation cohort, 44 (7%) patients were hospitalised as a result of AHFS during 1 year of follow-up. Predictors of AHFS hospitalisation included furosemide equivalent dose, the presence of type 2 diabetes mellitus, AHFS hospitalisation within the previous year and pulmonary congestion on chest radiograph, all assessed at baseline. A multivariable model containing these four variables exhibited good calibration (Hosmer-Lemeshow p=0.38) and discrimination (C-statistic 0.77; 95% CI 0.71 to 0.84). Using a 2.5% risk cut-off for predicted AHFS, the model defined 38.5% of patients as low risk, with negative predictive value of 99.1%; this low risk cohort exhibited <1% excess all-cause mortality per annum when compared with contemporaneous actuarial data. Within the validation cohort, an identically applied model derived comparable performance parameters (C-statistic 0.81 (95% CI 0.74 to 0.87), Hosmer-Lemeshow p=0.15, negative predictive value 100%)., Conclusions: A prospectively derived and validated model using simply obtained clinical data can identify patients with CHF at low risk of hospitalisation due to AHFS in the year following assessment. This may guide the design of future strategies allocating resources to the management of CHF., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

Diabetes mellitus is a risk factor for the development of coronary artery disease and chronic heart failure. When carefully screened for, diabetes or prediabetic disorders, are present in the majority of patients with clinically manifest ischaemic heart disease, and confer a major adverse impact upon morbidity and mortality. Important therapeutic modifications are required in the management of coronary artery disease and chronic heart failure associated with diabetes, and vice versa. However, despite optimal management, aided by recent landmark trials solely recruiting patients with diabetes, outcomes for patients with diabetes and heart disease remain poor. This review outlines the epidemiology, pathogenesis and management of diabetic heart disease, along with highlighting the many gaps in the evidence-base and suggesting future research priorities., (© 2012 Blackwell Publishing Ltd.)

Background: Reduced diaphragm contractility occurs in some healthy subjects when they exercise to exhaustion. This indicates low frequency fatigue, which may contribute to task failure. We hypothesised that patients with congestive heart failure (CHF) might be especially vulnerable to the development of low frequency diaphragm fatigue after exhaustive exercise., Aims: To study the effect of exhaustive incremental cycle exercise on diaphragm contractility in patients with CHF., Methods: 12 patients with CHF with an ejection fraction of 36.5 +/- 7.3% and 12 healthy age-matched control subjects performed an incremental cycle test to exhaustion. The unpotentiated twitch transdiaphragmatic pressure (twitch Pdi) in response to bilateral anterolateral magnetic phrenic nerve stimulation (BAMPS) was measured before and after exercise., Results: Twitch Pdi at baseline was 20.2 +/- 6.7 cm H2O in the CHF group and 20.3 +/- .3 cm H2O in the controls (p = 0.957). 25 and 35 min post exercise the values were 19.9+/-5.4 and 20.0+/-5.1 cm H2O in the CHF group and 20.6 +/- 4.3 and 21.2 +/- 3.4 cm H2O in the control group; neither change was significant (F(2,27) = 0.007, p = 0.993; F(2,33) = 0.144, p = 0.866, respectively)., Conclusion: When patients with CHF cycle to exhaustion, low frequency fatigue of the diaphragm does not occur, and this is unlikely to be an important factor limiting exercise capacity of such patients.

Objectives: To explore the relation between non-invasive measures of cardiac function and sudden cardiac death, as well as the development and utility of an index integrating these variables to identify patients at increased risk of this mode of death., Design: UK-HEART (United Kingdom-heart failure evaluation and assessment of risk trial) was a prospective study conducted between December 1993 and April 2000. The study was specifically designed to identify non-invasive markers of death and mode of death among patients with chronic heart failure., Setting: 8 UK general hospitals., Main Outcome Measures: Death and mode of death., Results: 553 patients aged a mean (SD) of 63 (10) years, in New York Heart Association functional class 2.3 (0.02), recruited prospectively. After 2365 patient-years' follow up, 201 patients had died (67 suddenly). Predictors of sudden death were greater cardiothoracic ratio, QRS dispersion, QT dispersion corrected for rate (QTc) across leads V1-V6 on the 12 lead ECG, and the presence of non-sustained ventricular tachycardia. The hazard ratio and 95% confidence intervals (CI) of sudden death for a 10% increase in cardiothoracic ratio was 1.43 (95% CI 1.20 to 1.71), for a 10% increase in QRS dispersion 1.11 (95% CI 1.04 to 1.19), for the presence of non-sustained ventricular tachycardia 2.03 (95% CI 1.27 to 3.25), and for a 10% increase in QTc dispersion across leads V1-V6 1.03 (95% CI 1.00 to 1.07) (all p < 0.04). An index derived from these four factors performed well in identifying patients specifically at increased risk of sudden death., Conclusions: Results show that an index derived from three widely available non-invasive investigations has the potential to identify ambulant patients with chronic heart failure at increased risk of sudden death. This predictive tool could be used to target more sophisticated investigations or interventions aimed at preventing sudden death.

Background: Although breathlessness is common in chronic heart failure (CHF), the role of inspiratory muscle dysfunction remains unclear. We hypothesised that inspiratory muscle endurance, expressed as a function of endurance time (Tlim) adjusted for inspiratory muscle load and inspiratory muscle capacity, would be reduced in CHF., Methods: Endurance was measured in 10 healthy controls and 10 patients with CHF using threshold loading at 40% maximal oesophageal pressure (Poes(max)). Oesophageal pressure-time product (PTPoes per cycle) and Poes(max) were used as indices of inspiratory muscle load and capacity, respectively., Results: Although Poes(max) was slightly less in the CHF group (-117.7 (23.6) v -100.0 (18.3) cm H(2)O; 95% CI -37.5 to 2.2 cm H(2)O, p = 0.1), Tlim was greatly reduced (1800 v 306 (190) s; 95% CI 1368 to 1620 s, p<0.0001) and the observed PTPoes per cycle/Poes(max) was increased (0.13 (0.05) v 0.21 (0.04); 95% CI -0.11 to -0.03, p = 0.001). Most of this increased inspiratory muscle load was due to a maladaptive breathing pattern, with a reduction in expiratory time (3.0 (5.8) v 1.1 (0.3) s; 95% CI 0.3 to 3.5 s, p = 0.03) accompanied by an increased inspiratory time relative to total respiratory cycle (Ti/Ttot) (0.43 (0.14) v 0.62 (0.07); 95% CI -0.3 to -0.1, p = 0.001). However, log Tlim, which incorporates the higher inspiratory muscle load to capacity ratio caused by this altered breathing pattern, was >/=85% predicted in seven of 10 patients., Conclusions: Although a marked reduction in endurance time was observed in CHF, much of this reduction was explained by the increased inspiratory muscle load to capacity ratio, suggesting that the major contributor to task failure was a maladaptive breathing pattern rather than impaired inspiratory muscle endurance.

There is good evidence that nitric oxide has important autocrine/paracrine effects in the myocardium, serving to optimise and fine tune cardiac function

Heart failure is an increasingly common problem in the UK, particularly in older patients. This article reviews the available information is available on heart failure in the older population, and provides clinically useful guidelines on the investigation and treatment of patients with this condition.

Viral infection of the heart is relatively common and usually of little consequence. It can, however, lead to substantial cardiac damage and severe acute heart failure. It can also evolve into the progressive syndrome of chronic heart failure. Recent studies have gone some way towards unravelling the complex mechanisms underlying the heart muscle damage that occurs after viral infection. These studies have lent support to both immune and viral mediated (independent of an immune response) cardiac damage. Acute myocarditis can present in various ways, and it may be a cause of sudden death in an otherwise healthy young adult. New treatments for viral heart disease are awaited. In the meanwhile, the haemodynamic support of patients with acute left ventricular failure caused by myocarditis should be aggressive, to allow for the possibility of spontaneous recovery. Contemporary trials of treatment in chronic heart failure secondary to dilated cardiomyopathy support the use of angiotensin converting enzyme inhibitors, beta adrenoceptor blockers, and spironolactone in such patients. [ABSTRACT FROM AUTHOR]

An abstract of the study "Race and the Response to Treatment in Patients With Advanced Heart Failure," by J. Byrne et al. is presented.

An abstract of the study "An Audit of the First Year of Supplementary Prescribing Within a Multi-disciplinary Specialist Heart Failure Service in the United Kingdom," by H. Williams and colleagues is presented.

This article focuses on a study related to HRV spectral power and mortality in chronic heart failure (CHF) with 5 year results on Great Britain heart study. CHF is associated with progressive autonomic dysfunction. This alteration is believed to have a direct role in the pathophysiological process of deteriorating cardiac function and by implication may be related to the timing of cardiac death. All the frequency domain indices were significantly associated with all cause and progressive cardiac death but not sudden cardiac death.