..................................................................................................................... The year in cardiology 2018: heart failure John G.F. Cleland1,2*, Dirk J. van Veldhuisen3, and Piotr Ponikowski4 1Robertson Centre for Biostatistics & Clinical Trials, University of Glasgow, Glasgow, UK; 2National Heart & Lung Institute, Royal Brompton & Harefield Hospitals, Imperial College, London, UK; 3Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands; and 4Department of Heart Diseases, Wroclaw Medical University, Centre for heart diseases, Military Hospital, ul.Weigla 5, 50-981 Wroclaw, Poland Received 4 December 2018; revised 2 January 2019; editorial decision 8 January 2019; accepted 8 January 2019 Introduction Doctors pour drugs of which they know little, to cure diseases of which they know less, into patients of whom they know nothing. Jean-Baptiste Poquelin (aka Molie`re) 1622–1673. This article summarizes some of the research highlights on heart failure published in the previous year. Hopefully, it will show that Moliere’s perception of doctors is no longer quite as true as it once may have been. A key emerging theme in the science and medicine of heart failure is the need to identify and target specific causes of heart failure, defined by phenotype or genotype, which will respond to a particular intervention (Take home figure). QRS duration (a marker of cardiac dyssynchrony),1,2 mitral regurgitation,3,4 iron deficiency,5,6 and amyloidosis7 each identifies patients that will respond to a specific intervention. Just as for that other large cluster of malignant diseases called cancer, the ‘war’ on heart failure will be won one ‘battle’ at a time. The outcome of many large clinical trials is determined neither by universal failure nor universal success but rather the proportions of patients that obtained benefit or harm compared with those for whom the intervention had little effect. For instance, the success of trials of beta-blockers may be because they did not enrol too many patients that respond poorly to these agents, including those with atrial fibrillation, a pacemaker or with a left ventricular ejection fraction (LVEF) >50%.8,9 Had the trials been less selective they might have been neutral. Had they been more selective, the trials would have been smaller and shown an even larger benefit. Conversely, many interventions for heart failure with a preserved LVEF (>_50%; HFpEF) probably benefited some patients within this phenotype but not a large enough proportion to drive the overall result. We should take care that we do not reject effective treatments due to misunderstanding the results of trials that required a huge investment from patients, clinicians, academics, clinical research organizations, and funders. Of course, a phenotype only really matters to a patient and a clinician when it informs management. This last year has seen an explosion of data on a variety of ‘therapeutic phenotypes’ that matter. Epidemiology There is a paucity of contemporary data on the incidence and prevalence of heart failure, with few new useful sources of data. Conrad et al.,10 using administrative data from both primary and secondary care health records of four million adults in England and Wales, provide some estimates. The age-adjusted incidence of heart failure appears to be declining but both the overall incidence and prevalence are increasing due to the growing proportion of the population aged >70 years (Figure 1). More affluent regions had a lower age-adjusted incidence of heart failure, implying that we already have the means to modify risk. Most patients had three or more comorbid conditions, most commonly hypertension, ischaemic heart disease, and osteoarthritis but 25% also had cancer. The National Audit of Heart Failure in England and Wales is probably the world’s largest, with >500 000 individual patients now enrolled.11 This shows a steady increase in hospital admissions with a primary diagnosis of heart failure over the last decade. The median age at admission is 80 years, with men being, on average, 4 years younger than women. At the time of admission, most patients were not breathless at rest, at least when sitting upright but often had moderate or severe peripheral oedema. For those aged <75 years, the inpatient mortality is about 5% and the 3-year mortality of those surviving to discharge about 30%. For those aged >75 years, inpatient mortality is 12% and 3-year mortality about 60%. Overall, inpatient mortality appears to be much higher in the UK than in the USA. However, after correcting for risk profile, mortality appears similar suggesting a lower threshold for admission in the USA rather than better treatment.12,13 The prognosis of patients admitted with heart failure in Japan is better than for either the UK or USA and is only partially explained by differences in risk profile or plasma concentrations of natriuretic peptides.14 Heart failure aetiology, phenotype, presentation, and outcome varies by world region as shown by global registries (REPORT-HF: https://clinicaltrials.gov/ ct2/show/NCT02595814) and a growing number of reports from sub-Saharan Africa, China, and South-East Asia.15–18 There is a growing interest in prevention of heart failure. Cohort studies show that the common risk factors are, predictably, the presence of cardiovascular disease and risk-factors, including age.19 There The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology. * Corresponding author. Tel:- þ44 (0) 141-330-4744, Fax: þ44 (0) 141 357 5588, Email: [email protected] Published on behalf of the European Society of Cardiology. All rights reserved. VC The Author(s) 2019. For permissions, please email: [email protected]. European Heart Journal (2019) 00, 1–18 CURRENT OPINION doi:10.1093/eurheartj/ehz010 Heart failure/cardiomyopathy Downloaded from https://academic.oup.com/eurheartj/advance-article-abstract/doi/10.1093/eurheartj/ehz010/5333120 by Tarrant County College user on 19 February 2019 ...................................................................................................... have already been notable therapeutic successes with thiazide-like diuretics and angiotensin-converting enzyme (ACE) inhibitors for the prevention of heart failure in older patients with hypertension20 and, more recently and tentatively, sodium/glucose cotransporter-2 (SGLT2) inhibitors for Type-2 diabetes mellitus (T2DM).21 A key problem with epidemiological research in heart failure is the lack of criteria that are both sensitive and specific.22 Too often, sensitivity is sacrificed for specificity, which may lead to a serious underestimate of the disease burden associated with heart failure not only epidemiologically but also as endpoints in clinical trials. For instance, for every admission due primarily to heart failure there are probably three to four admissions for other reasons that are complicated or prolonged by heart failure.23 These patients have a poorer prognosis than patients with a primary diagnosis of heart failure24 but are no less in need of expert review; an opportunity that hospitalization provides.
HOME | BOOKSTORE | SHARE Hypertension and Stroke Alert Surprising Findings on Alcohol and Stroke Risk Results of a large international study, published in 2018 in The Lancet, challenge some long-held notions about alcohol and health. It found that overall, the standard definition of moderate drinking—one to two drinks per day—was linked to increased risk of certain cardiovascular diseases. And people who had more than one drink per day had a somewhat shortened life expectancy. The findings come from an analysis of 83 studies in 19 countries, including nearly 600,000 current drinkers. Over 7.5 years, 40,310 study participants died. The risk was lowest among people who drank less than 100 grams of alcohol each week—or about one standard drink per day. Under U.S. guidelines, that's the limit recommended for women, while men are advised to have no more than two drinks per day. As for the storied cardiovascular benefits of alcohol, the study found that the more people drank—even at moderate levels—the higher their risks of stroke, heart failure, and other cardiovascular ills. The one exception was heart attack risk, which declined. But on balance, that potential benefit did not seem worthwhile. The researchers estimate that if middle-aged men reduced their intake from two drinks per day to just one, they could add one or two years to their life expectancy. The bottom line: If you have more than one drink per day, consider cutting down.
