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      Identifying and Managing Hibernating Myocardium: What’s New and What Remains Unknown?

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          Abstract

          Purpose of Review

          Hibernation is an important and reversible cause of myocardial dysfunction in ischaemic heart failure.

          Recent Findings

          Hibernation is an adaptive process that promotes myocyte survival over maintaining contractile function. It is innate to mammalian physiology, sharing features with physiological hibernation in other species. Advanced imaging methods have reasonable accuracy in identifying hibernating myocardium. Novel superior hybrid methods may provide diagnostic potential. New evidence supports the role of surgical revascularisation in ischaemic heart failure, but the role of viability tests in planning such procedures remains unclear. Research to date has exclusively involved patients with ambulatory heart failure: Investigating the role of hibernation in ADHF is a key avenue for the future.

          Summary

          Whilst our understanding of hibernation pathophysiology has improved dramatically, the clinical utility of identifying and targeting hibernation remains unclear.

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          Most cited references46

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          Coronary-Artery Bypass Surgery in Patients with Ischemic Cardiomyopathy.

          The survival benefit of a strategy of coronary-artery bypass grafting (CABG) added to guideline-directed medical therapy, as compared with medical therapy alone, in patients with coronary artery disease, heart failure, and severe left ventricular systolic dysfunction remains unclear.
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            Systolic blood pressure at admission, clinical characteristics, and outcomes in patients hospitalized with acute heart failure.

            The association between systolic blood pressure (SBP) at admission, clinical characteristics, and outcomes in patients hospitalized for heart failure who have reduced or relatively preserved systolic function has not been well studied. To evaluate the relationship between SBP at admission, clinical profile, and outcomes in patients hospitalized for acute heart failure. Cohort study using data from the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) registry and performance-improvement program for patients hospitalized with heart failure at 259 US hospitals between March 2003 and December 2004. Patients were divided into quartiles by SBP at hospital admission ( 161 mm Hg). In-hospital outcomes were based on 48,612 patients aged 18 years or older with heart failure. Of the 41,267 patients with left ventricular function assessed, 21,149 (51%) had preserved left ventricular function. Postdischarge outcomes were based on a prespecified subgroup (n = 5791, 10% of patients) with follow-up data assessed between 60 and 90 days. In-hospital and postdischarge mortality. Patients with higher SBP were more likely to be female and black and to have preserved systolic function. Fifty percent of the patients had SBP higher than 140 mm Hg at admission. Patients with lower SBP at admission had higher in-hospital and postdischarge mortality rates. Higher SBP at admission was associated with lower in-hospital mortality rates: 7.2% ( 161 mm Hg) (P<.001 for overall difference). Postdischarge mortality rates in the follow-up cohort by SBP at admission were 14.0%, 8.4%, 6.0%, and 5.4%, respectively (P<.001 for overall difference). Systolic hypertension is common in patients hospitalized for heart failure. Systolic blood pressure is an independent predictor of morbidity and mortality in patients with heart failure with either reduced or relatively preserved systolic function. Low SBP (<120 mm Hg) at hospital admission identifies patients who have a poor prognosis despite medical therapy. These findings may have important therapeutic implications because characteristics and outcomes differ greatly among patients with heart failure with varying SBP.
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              Cardiac troponin and outcome in acute heart failure.

              Cardiac troponin provides diagnostic and prognostic information in acute coronary syndromes, but its role in acute decompensated heart failure is unclear. The purpose of our study was to describe the association between elevated cardiac troponin levels and adverse events in hospitalized patients with acute decompensated heart failure. We analyzed hospitalizations for acute decompensated heart failure between October 2001 and January 2004 that were recorded in the Acute Decompensated Heart Failure National Registry (ADHERE). Entry criteria included a troponin level that was obtained at the time of hospitalization in patients with a serum creatinine level of less than 2.0 mg per deciliter (177 micromol per liter). A positive troponin test was defined as a cardiac troponin I level of 1.0 microg per liter or higher or a cardiac troponin T level of 0.1 microg per liter or higher. Troponin was measured at the time of admission in 84,872 of 105,388 patients (80.5%) who were hospitalized for acute decompensated heart failure. Of these patients, 67,924 had a creatinine level of less than 2.0 mg per deciliter. Cardiac troponin I was measured in 61,379 patients, and cardiac troponin T in 7880 patients (both proteins were measured in 1335 patients). Overall, 4240 patients (6.2%) were positive for troponin. Patients who were positive for troponin had lower systolic blood pressure on admission, a lower ejection fraction, and higher in-hospital mortality (8.0% vs. 2.7%, P<0.001) than those who were negative for troponin. The adjusted odds ratio for death in the group of patients with a positive troponin test was 2.55 (95% confidence interval, 2.24 to 2.89; P<0.001 by the Wald test). In patients with acute decompensated heart failure, a positive cardiac troponin test is associated with higher in-hospital mortality, independently of other predictive variables. (ClinicalTrials.gov number, NCT00366639 [ClinicalTrials.gov].). Copyright 2008 Massachusetts Medical Society.
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                Author and article information

                Contributors
                divaka.perera@kcl.ac.uk
                Journal
                Curr Heart Fail Rep
                Curr Heart Fail Rep
                Current Heart Failure Reports
                Springer US (New York )
                1546-9530
                1546-9549
                29 June 2018
                29 June 2018
                2018
                : 15
                : 4
                : 214-223
                Affiliations
                [1 ]GRID grid.425213.3, The Rayne Institute, , St Thomas’ Hospital, ; 4th Floor Lambeth Wing, Westminster Bridge Road, London, SE1 7EH UK
                [2 ]ISNI 0000 0001 2322 6764, GRID grid.13097.3c, Cardiovascular Division, , King’s College London, ; London, UK
                Article
                396
                10.1007/s11897-018-0396-6
                6061160
                29959688
                7ea97e4c-6385-4b49-ad69-b18283c2e12e
                © The Author(s) 2018

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Funding
                Funded by: King's College London
                Categories
                Decompensated Heart Failure (P Banerjee, Section Editor)
                Custom metadata
                © Springer Science+Business Media, LLC, part of Springer Nature 2018

                Cardiovascular Medicine
                hibernation,viability,revascularisation,ischaemic heart failure,ischaemic cardiomyopathy,hfref

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