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      Coronary blood flow in heart failure: cause, consequence and bystander

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          Abstract

          Heart failure is a clinical syndrome where cardiac output is not sufficient to sustain adequate perfusion and normal bodily functions, initially during exercise and in more severe forms also at rest. The two most frequent forms are heart failure of ischemic origin and of non-ischemic origin. In heart failure of ischemic origin, reduced coronary blood flow is causal to cardiac contractile dysfunction, and this is true for stunned and hibernating myocardium, coronary microembolization, myocardial infarction and post-infarct remodeling, possibly also for the takotsubo syndrome. The most frequent form of non-ischemic heart failure is dilated cardiomyopathy, caused by genetic mutations, myocarditis, toxic agents or sustained tachyarrhythmias, where alterations in coronary blood flow result from and contribute to cardiac contractile dysfunction. Hypertrophic cardiomyopathy is caused by genetic mutations but can also result from increased pressure and volume overload (hypertension, valve disease). Heart failure with preserved ejection fraction is characterized by pronounced coronary microvascular dysfunction, the causal contribution of which is however not clear. The present review characterizes the alterations of coronary blood flow which are causes or consequences of heart failure in its different manifestations. Apart from any potentially accompanying coronary atherosclerosis, all heart failure entities share common features of impaired coronary blood flow, but to a different extent: enhanced extravascular compression, impaired nitric oxide-mediated, endothelium-dependent vasodilation and enhanced vasoconstriction to mediators of neurohumoral activation. Impaired coronary blood flow contributes to the progression of heart failure and is thus a valid target for established and novel treatment regimens.

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          Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction

          In patients with type 2 diabetes, inhibitors of sodium-glucose cotransporter 2 (SGLT2) reduce the risk of a first hospitalization for heart failure, possibly through glucose-independent mechanisms. More data are needed regarding the effects of SGLT2 inhibitors in patients with established heart failure and a reduced ejection fraction, regardless of the presence or absence of type 2 diabetes.
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            Cardiovascular and Renal Outcomes with Empagliflozin in Heart Failure

            Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of hospitalization for heart failure in patients regardless of the presence or absence of diabetes. More evidence is needed regarding the effects of these drugs in patients across the broad spectrum of heart failure, including those with a markedly reduced ejection fraction.
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              Empagliflozin in Heart Failure with a Preserved Ejection Fraction

              Sodium-glucose cotransporter 2 inhibitors reduce the risk of hospitalization for heart failure in patients with heart failure and a reduced ejection fraction, but their effects in patients with heart failure and a preserved ejection fraction are uncertain.
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                Author and article information

                Contributors
                gerd.heusch@uk-essen.de
                Journal
                Basic Res Cardiol
                Basic Res Cardiol
                Basic Research in Cardiology
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                0300-8428
                1435-1803
                13 January 2022
                13 January 2022
                2022
                : 117
                : 1
                : 1
                Affiliations
                GRID grid.5718.b, ISNI 0000 0001 2187 5445, Institute for Pathophysiology, West German Heart and Vascular Center, University of Essen Medical School, , University of Duisburg-Essen, ; Hufelandstr. 55, 45147 Essen, Germany
                Author information
                http://orcid.org/0000-0001-7078-4160
                Article
                909
                10.1007/s00395-022-00909-8
                8758654
                35024969
                de14bb2f-bf98-4ea3-a5a8-af22cef84d8b
                © The Author(s) 2022

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 3 December 2021
                : 20 December 2021
                : 21 December 2021
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001659, Deutsche Forschungsgemeinschaft;
                Award ID: SFB 1116 B8
                Award Recipient :
                Funded by: European Union COST ACTION
                Award ID: CA 16225
                Award Recipient :
                Funded by: Universitätsklinikum Essen (8912)
                Categories
                Review
                Custom metadata
                © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany 2022

                Cardiovascular Medicine
                coronary blood flow,coronary microcirculation,coronary reserve,extravascular compression,heart failure

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