Prediction, staging, and outcomes of ischaemic cardiogenic shock after STEMI: a complex clinical interplay

Prediction, staging, and outcomes of ischaemic cardiogenic shock after STEMI: a complex clinical... This editorial refers to ‘Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score’†, by V. Auffret et al., on page 2090. Despite the implementation of an early coronary reperfusion strategy with primary percutaneous coronary intervention (PCI), cardiogenic shock (CS) remains a persistent complication of ST-segment elevation myocardial infarction (STEMI), affecting a significant proportion of cases, with high in-hospital and short-term mortality.1,2 Until recently, few risk-scoring models of post-STEMI CS were available, and most had limitations such as absence of external validation, difficult to assess variables, or inclusion of causes of CS other than STEMI. Early coronary reperfusion (most frequently with PCI) and appropriate haemodynamic support remain the main treatment to avert CS complications or improve CS outcomes. A user-friendly model for CS risk stratification was introduced last year.3 A simple age-based stratification was associated with improved mid-term survival, as was demonstrated 18 years ago by the SHOCK trial investigators.4 Since then, additional pharmacological or mechanical strategies failed to improve outcomes significantly in the setting of ischaemic CS in several, mostly small sized, clinical trials. Two types of methodological bias have been raised for nearly all recent CS trials: (i) ‘sick’ patients may not be enrolled, but rather treated with maximum support for humanitarian reasons by the clinical site investigators; or (ii) on the other hand, there is no practical and objective way to screen out futile cases and therefore their inclusion may also impact the outcomes. Therefore, deriving risk factors of CS development and the recognition of different stages of CS with the understanding of their outcomes is a very relevant goal for proper clinical practice and clinical research. The extent of revascularization in CS has also been debated. Its application in non-culprit coronary lesions during the index procedure (for STEMI complicated by CS) was granted a class IIa level C recommendation by the European Society of Cardiology.1 However, this recommendation was recently challenged by the results of a prospective randomized trial: a culprit-lesion-only PCI strategy in CS patients was associated with lower rate of death or renal replacement at 30 days compared with immediate multivessel PCI.5 Additionally, routine intra-aortic balloon pump (IABP) support after PCI for STEMI with CS is no longer indicated in the absence of mechanical complications.1 Mechanical left ventricular assist devices correct haemodynamic parameters, but no adequately powered trials have so far demonstrated improved clinical outcomes.1,6,7 These devices are mainly used as a salvage strategy in the case of refractory CS.1,7 The development of a strategy to provide haemodynamic support before initiating PCI in such cases has recently stemmed from pre-clinical research.8 Only a small minority (<15%) of patients in a previous randomized trial1,2 were indeed given IABP support before the start of PCI, hence this proposal has never been adequately tested. A prospective randomized trial is ongoing on this subject (DanShock trial, NCT01633502) with use of a percutaneous left ventricular assist device. Regarding pharmacological therapeutics, inotropic agents such as dobutamine are used as first line-treatment in the case of low cardiac output with preserved systolic blood pressure, or norepinephrine instead of dopamine, in the case of severe hypotension.1,2 However, catecholamines are only symptomatic therapy for CS, with a lack of clear efficacy on survival.1,2,7 Quite complex pathophysiology is evolving in CS cases. Post-STEMI CS is the consequence of acute or subacute impairment of the entire circulatory system, driven by the initial depression of cardiac contractility and a sharp increase in intraventricular pressure, eventually leading to multiorgan dysfunction syndrome.2,7,9 The compensatory vasoconstriction and systemic inflammatory response subsequent to both STEMI-related haemodynamic instability and tissue hypoperfusion create a vicious circle leading to ensuing myocardial ischaemia and contractile dysfunction. In advanced stages, restoring cardiac power may not be sufficient to reverse the multiorgan dysfunction and systemic inflammatory response.7 The coronary revascularization alone may only address this complex process in part and generally too late due to imperfect methods for clinical discrimination of early/salvageable vs. futile/terminal cases. Various pathophysiological mechanisms may be present in different intensity in each patient, resulting in a wide range of clinical presentations of CS, from the so-called ‘pre-shock’ (or impending CS) to severe refractory CS status. Therefore, patients with impending CS may only present few of the clinical criteria of classic CS upon presentation, and subsequently progress into complete CS with multiorgan dysfunction syndrome, as their vicious pathophysiological circle deteriorates. In fact, nearly half of post-STEMI CS cases develop during the first 6 h of hospitalization and 75% of them within the first 24 h.1 These patients, if identified early, could benefit from an aggressive haemodynamic management strategy and intensive surveillance, including transfer to tertiary centres. In Figure 1, we introduce ideas to distinguish phases of ischaemic CS, and set them apart from the mere recognition of isolated, previously described risk factors of developing CS.1,2,10 A reliable and user-friendly predictive score remains an important goal for clinical investigation in this field of medicine. Figure 1 View largeDownload slide Proposed predictors and staging of ischaemic cardiogenic shock. NT-proBNP, N-terminal pro-brain natriuretic peptide blood level; HR, heart rate; SBP, systolic blood pressure; LVEF, left ventricular ejection fraction; CABG, coronary artery bypass graft; PCI, percutaneous coronary intervention; TIMI, Thrombolysis in Myocardial Infarction; Cardiac power, (mean arterial pressure × cardiac output)/451 (W); Cardiac index, cardiac output indexed on body surface area (L/min/m2); pulse pressure, difference between systolic and diastolic blood pressure (mmHg). Figure 1 View largeDownload slide Proposed predictors and staging of ischaemic cardiogenic shock. NT-proBNP, N-terminal pro-brain natriuretic peptide blood level; HR, heart rate; SBP, systolic blood pressure; LVEF, left ventricular ejection fraction; CABG, coronary artery bypass graft; PCI, percutaneous coronary intervention; TIMI, Thrombolysis in Myocardial Infarction; Cardiac power, (mean arterial pressure × cardiac output)/451 (W); Cardiac index, cardiac output indexed on body surface area (L/min/m2); pulse pressure, difference between systolic and diastolic blood pressure (mmHg). In this issue of the journal, Auffret et al. present such a CS score. Eleven easy to collect variables were determined to derive a risk score for development of CS, identifying four categories of incremental risk in STEMI-related CS after PCI.11 This score may help the clinician in early identification of such highest risk patients who could benefit from intensive surveillance and therapy, including transfer to tertiary centres and potentially early haemodynamic support. The inclusion of baseline patient characteristics, haemodynamic variables, tissue perfusion/inflammation markers, coronary anatomy parameters, and PCI success measures underscores the high level of complexity of CS assessment, and make its early identification and staging quite challenging. As in every new field, ‘the toughest step is always the first’ (traditional Chinese/Taoism teaching by Lao Tse). Future clinical trials may use this initial score (in whole or in part) and start defining subsets of ‘pre-shock’ patients for early intervention. Their results will help refine this score, as well as modify and improve its abilities. Conflict of interest: none declared. References 1 Ibanez B , James S , Agewall S , Antunes MJ , Bucciarelli-Ducci C , Bueno H , Caforio ALP , Crea F , Goudevenos JA , Halvorsen S , Hindricks G , Kastrati A , Lenzen MJ , Prescott E , Roffi M , Valgimigli M , Varenhorst C , Vranckx P , Widimský P , ESC Scientific Document Group . 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC) . Eur Heart J 2018 ; 39 : 119 – 177 . Google Scholar CrossRef Search ADS PubMed 2 Diepen S van , Katz JN , Albert NM , Henry TD , Jacobs AK , Kapur NK , Kilic A , Menon V , Ohman EM , Sweitzer NK , Thiele H , Washam JB , Cohen MG , American Heart Association Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Quality of Care and Outcomes Research; and Mission: Lifeline. Contemporary management of cardiogenic shock: a scientific statement from the American Heart Association . Circulation 2017 ; 136 : e232 – e268 . Google Scholar CrossRef Search ADS PubMed 3 Pöss J , Köster J , Fuernau G , Eitel I , Waha S de , Ouarrak T , Lassus J , Harjola V-P , Zeymer U , Thiele H , Desch S. Risk stratification for patients in cardiogenic shock after acute myocardial infarction . J Am Coll Cardiol 2017 ; 69 : 1913 – 1920 . Google Scholar CrossRef Search ADS PubMed 4 Hochman JS , Sleeper LA , Webb JG , Sanborn TA , White HD , Talley JD , Buller CE , Jacobs AK , Slater JN , Col J , McKinlay SM , LeJemtel TH. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock . N Engl J Med 1999 ; 341 : 625 – 634 . Google Scholar CrossRef Search ADS PubMed 5 Thiele H , Akin I , Sandri M , Fuernau G , Waha S de , Meyer-Saraei R , Nordbeck P , Geisler T , Landmesser U , Skurk C , Fach A , Lapp H , Piek JJ , Noc M , Goslar T , Felix SB , Maier LS , Stepinska J , Oldroyd K , Serpytis P , Montalescot G , Barthelemy O , Huber K , Windecker S , Savonitto S , Torremante P , Vrints C , Schneider S , Desch S , Zeymer U , CULPRIT-SHOCK Investigators . PCI strategies in patients with acute myocardial infarction and cardiogenic shock . N Engl J Med 2017 ; 377 : 2419 – 2432 . Google Scholar CrossRef Search ADS PubMed 6 Cheng JM , den Uil CA , Hoeks SE , van der Ent M , Jewbali LSD , van Domburg RT , Serruys PW. Percutaneous left ventricular assist devices vs. intra-aortic balloon pump counterpulsation for treatment of cardiogenic shock: a meta-analysis of controlled trials . Eur Heart J 2009 ; 30 : 2102 – 2108 . Google Scholar CrossRef Search ADS PubMed 7 Werdan K , Gielen S , Ebelt H , Hochman JS. Mechanical circulatory support in cardiogenic shock . Eur Heart J 2014 ; 35 : 156 – 167 . Google Scholar CrossRef Search ADS PubMed 8 Kapur NK , Qiao X , Paruchuri V , Morine KJ , Syed W , Dow S , Shah N , Pandian N , Karas RH. Mechanical pre-conditioning with acute circulatory support before reperfusion limits infarct size in acute myocardial infarction . JACC Heart Fail 2015 ; 3 : 873 – 882 . Google Scholar CrossRef Search ADS PubMed 9 Reynolds HR , Hochman JS. Cardiogenic shock: current concepts and improving outcomes . Circulation 2008 ; 117 : 686 – 697 . Google Scholar CrossRef Search ADS PubMed 10 Obling L , Frydland M , Hansen R , Møller-Helgestad OK , Lindholm MG , Holmvang L , Ravn HB , Wiberg S , Thomsen JH , Jensen LO , Kjærgaard J , Møller JE , Hassager C. Risk factors of late cardiogenic shock and mortality in ST-segment elevation myocardial infarction patients . Eur Heart J Acute Cardiovasc Care 2018 ; 7 : 7 – 15 . Google Scholar CrossRef Search ADS PubMed 11 Auffret V , Cottin Y , Leurent G , Gilard M , Beer JC , Zabalawi A , Chagué F , Filippi E , Brunet D , Hacot JP , Brunel P , Mejri M , Lorgis L , Rouault G , Druelles P , Cornily JC , Didier R , Bot E , Boulanger B , Coudert I , Loirat A , Bedossa M , Boulmier D , Maza M , Le Guellec M , Puri R , Zeller M , Le Breton H ; On behalf of the ORBI and RICO Working Groups . Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score . Eur Heart J 2018 ; 39 : 2090 – 2102 . Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Heart Journal Oxford University Press

Prediction, staging, and outcomes of ischaemic cardiogenic shock after STEMI: a complex clinical interplay

European Heart Journal , Volume Advance Article (22) – Apr 19, 2018

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Abstract

This editorial refers to ‘Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score’†, by V. Auffret et al., on page 2090. Despite the implementation of an early coronary reperfusion strategy with primary percutaneous coronary intervention (PCI), cardiogenic shock (CS) remains a persistent complication of ST-segment elevation myocardial infarction (STEMI), affecting a significant proportion of cases, with high in-hospital and short-term mortality.1,2 Until recently, few risk-scoring models of post-STEMI CS were available, and most had limitations such as absence of external validation, difficult to assess variables, or inclusion of causes of CS other than STEMI. Early coronary reperfusion (most frequently with PCI) and appropriate haemodynamic support remain the main treatment to avert CS complications or improve CS outcomes. A user-friendly model for CS risk stratification was introduced last year.3 A simple age-based stratification was associated with improved mid-term survival, as was demonstrated 18 years ago by the SHOCK trial investigators.4 Since then, additional pharmacological or mechanical strategies failed to improve outcomes significantly in the setting of ischaemic CS in several, mostly small sized, clinical trials. Two types of methodological bias have been raised for nearly all recent CS trials: (i) ‘sick’ patients may not be enrolled, but rather treated with maximum support for humanitarian reasons by the clinical site investigators; or (ii) on the other hand, there is no practical and objective way to screen out futile cases and therefore their inclusion may also impact the outcomes. Therefore, deriving risk factors of CS development and the recognition of different stages of CS with the understanding of their outcomes is a very relevant goal for proper clinical practice and clinical research. The extent of revascularization in CS has also been debated. Its application in non-culprit coronary lesions during the index procedure (for STEMI complicated by CS) was granted a class IIa level C recommendation by the European Society of Cardiology.1 However, this recommendation was recently challenged by the results of a prospective randomized trial: a culprit-lesion-only PCI strategy in CS patients was associated with lower rate of death or renal replacement at 30 days compared with immediate multivessel PCI.5 Additionally, routine intra-aortic balloon pump (IABP) support after PCI for STEMI with CS is no longer indicated in the absence of mechanical complications.1 Mechanical left ventricular assist devices correct haemodynamic parameters, but no adequately powered trials have so far demonstrated improved clinical outcomes.1,6,7 These devices are mainly used as a salvage strategy in the case of refractory CS.1,7 The development of a strategy to provide haemodynamic support before initiating PCI in such cases has recently stemmed from pre-clinical research.8 Only a small minority (<15%) of patients in a previous randomized trial1,2 were indeed given IABP support before the start of PCI, hence this proposal has never been adequately tested. A prospective randomized trial is ongoing on this subject (DanShock trial, NCT01633502) with use of a percutaneous left ventricular assist device. Regarding pharmacological therapeutics, inotropic agents such as dobutamine are used as first line-treatment in the case of low cardiac output with preserved systolic blood pressure, or norepinephrine instead of dopamine, in the case of severe hypotension.1,2 However, catecholamines are only symptomatic therapy for CS, with a lack of clear efficacy on survival.1,2,7 Quite complex pathophysiology is evolving in CS cases. Post-STEMI CS is the consequence of acute or subacute impairment of the entire circulatory system, driven by the initial depression of cardiac contractility and a sharp increase in intraventricular pressure, eventually leading to multiorgan dysfunction syndrome.2,7,9 The compensatory vasoconstriction and systemic inflammatory response subsequent to both STEMI-related haemodynamic instability and tissue hypoperfusion create a vicious circle leading to ensuing myocardial ischaemia and contractile dysfunction. In advanced stages, restoring cardiac power may not be sufficient to reverse the multiorgan dysfunction and systemic inflammatory response.7 The coronary revascularization alone may only address this complex process in part and generally too late due to imperfect methods for clinical discrimination of early/salvageable vs. futile/terminal cases. Various pathophysiological mechanisms may be present in different intensity in each patient, resulting in a wide range of clinical presentations of CS, from the so-called ‘pre-shock’ (or impending CS) to severe refractory CS status. Therefore, patients with impending CS may only present few of the clinical criteria of classic CS upon presentation, and subsequently progress into complete CS with multiorgan dysfunction syndrome, as their vicious pathophysiological circle deteriorates. In fact, nearly half of post-STEMI CS cases develop during the first 6 h of hospitalization and 75% of them within the first 24 h.1 These patients, if identified early, could benefit from an aggressive haemodynamic management strategy and intensive surveillance, including transfer to tertiary centres. In Figure 1, we introduce ideas to distinguish phases of ischaemic CS, and set them apart from the mere recognition of isolated, previously described risk factors of developing CS.1,2,10 A reliable and user-friendly predictive score remains an important goal for clinical investigation in this field of medicine. Figure 1 View largeDownload slide Proposed predictors and staging of ischaemic cardiogenic shock. NT-proBNP, N-terminal pro-brain natriuretic peptide blood level; HR, heart rate; SBP, systolic blood pressure; LVEF, left ventricular ejection fraction; CABG, coronary artery bypass graft; PCI, percutaneous coronary intervention; TIMI, Thrombolysis in Myocardial Infarction; Cardiac power, (mean arterial pressure × cardiac output)/451 (W); Cardiac index, cardiac output indexed on body surface area (L/min/m2); pulse pressure, difference between systolic and diastolic blood pressure (mmHg). Figure 1 View largeDownload slide Proposed predictors and staging of ischaemic cardiogenic shock. NT-proBNP, N-terminal pro-brain natriuretic peptide blood level; HR, heart rate; SBP, systolic blood pressure; LVEF, left ventricular ejection fraction; CABG, coronary artery bypass graft; PCI, percutaneous coronary intervention; TIMI, Thrombolysis in Myocardial Infarction; Cardiac power, (mean arterial pressure × cardiac output)/451 (W); Cardiac index, cardiac output indexed on body surface area (L/min/m2); pulse pressure, difference between systolic and diastolic blood pressure (mmHg). In this issue of the journal, Auffret et al. present such a CS score. Eleven easy to collect variables were determined to derive a risk score for development of CS, identifying four categories of incremental risk in STEMI-related CS after PCI.11 This score may help the clinician in early identification of such highest risk patients who could benefit from intensive surveillance and therapy, including transfer to tertiary centres and potentially early haemodynamic support. The inclusion of baseline patient characteristics, haemodynamic variables, tissue perfusion/inflammation markers, coronary anatomy parameters, and PCI success measures underscores the high level of complexity of CS assessment, and make its early identification and staging quite challenging. As in every new field, ‘the toughest step is always the first’ (traditional Chinese/Taoism teaching by Lao Tse). Future clinical trials may use this initial score (in whole or in part) and start defining subsets of ‘pre-shock’ patients for early intervention. Their results will help refine this score, as well as modify and improve its abilities. Conflict of interest: none declared. References 1 Ibanez B , James S , Agewall S , Antunes MJ , Bucciarelli-Ducci C , Bueno H , Caforio ALP , Crea F , Goudevenos JA , Halvorsen S , Hindricks G , Kastrati A , Lenzen MJ , Prescott E , Roffi M , Valgimigli M , Varenhorst C , Vranckx P , Widimský P , ESC Scientific Document Group . 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC) . Eur Heart J 2018 ; 39 : 119 – 177 . Google Scholar CrossRef Search ADS PubMed 2 Diepen S van , Katz JN , Albert NM , Henry TD , Jacobs AK , Kapur NK , Kilic A , Menon V , Ohman EM , Sweitzer NK , Thiele H , Washam JB , Cohen MG , American Heart Association Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Quality of Care and Outcomes Research; and Mission: Lifeline. Contemporary management of cardiogenic shock: a scientific statement from the American Heart Association . Circulation 2017 ; 136 : e232 – e268 . Google Scholar CrossRef Search ADS PubMed 3 Pöss J , Köster J , Fuernau G , Eitel I , Waha S de , Ouarrak T , Lassus J , Harjola V-P , Zeymer U , Thiele H , Desch S. Risk stratification for patients in cardiogenic shock after acute myocardial infarction . J Am Coll Cardiol 2017 ; 69 : 1913 – 1920 . Google Scholar CrossRef Search ADS PubMed 4 Hochman JS , Sleeper LA , Webb JG , Sanborn TA , White HD , Talley JD , Buller CE , Jacobs AK , Slater JN , Col J , McKinlay SM , LeJemtel TH. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock . N Engl J Med 1999 ; 341 : 625 – 634 . Google Scholar CrossRef Search ADS PubMed 5 Thiele H , Akin I , Sandri M , Fuernau G , Waha S de , Meyer-Saraei R , Nordbeck P , Geisler T , Landmesser U , Skurk C , Fach A , Lapp H , Piek JJ , Noc M , Goslar T , Felix SB , Maier LS , Stepinska J , Oldroyd K , Serpytis P , Montalescot G , Barthelemy O , Huber K , Windecker S , Savonitto S , Torremante P , Vrints C , Schneider S , Desch S , Zeymer U , CULPRIT-SHOCK Investigators . PCI strategies in patients with acute myocardial infarction and cardiogenic shock . N Engl J Med 2017 ; 377 : 2419 – 2432 . Google Scholar CrossRef Search ADS PubMed 6 Cheng JM , den Uil CA , Hoeks SE , van der Ent M , Jewbali LSD , van Domburg RT , Serruys PW. Percutaneous left ventricular assist devices vs. intra-aortic balloon pump counterpulsation for treatment of cardiogenic shock: a meta-analysis of controlled trials . Eur Heart J 2009 ; 30 : 2102 – 2108 . Google Scholar CrossRef Search ADS PubMed 7 Werdan K , Gielen S , Ebelt H , Hochman JS. Mechanical circulatory support in cardiogenic shock . Eur Heart J 2014 ; 35 : 156 – 167 . Google Scholar CrossRef Search ADS PubMed 8 Kapur NK , Qiao X , Paruchuri V , Morine KJ , Syed W , Dow S , Shah N , Pandian N , Karas RH. Mechanical pre-conditioning with acute circulatory support before reperfusion limits infarct size in acute myocardial infarction . JACC Heart Fail 2015 ; 3 : 873 – 882 . Google Scholar CrossRef Search ADS PubMed 9 Reynolds HR , Hochman JS. Cardiogenic shock: current concepts and improving outcomes . Circulation 2008 ; 117 : 686 – 697 . Google Scholar CrossRef Search ADS PubMed 10 Obling L , Frydland M , Hansen R , Møller-Helgestad OK , Lindholm MG , Holmvang L , Ravn HB , Wiberg S , Thomsen JH , Jensen LO , Kjærgaard J , Møller JE , Hassager C. Risk factors of late cardiogenic shock and mortality in ST-segment elevation myocardial infarction patients . Eur Heart J Acute Cardiovasc Care 2018 ; 7 : 7 – 15 . Google Scholar CrossRef Search ADS PubMed 11 Auffret V , Cottin Y , Leurent G , Gilard M , Beer JC , Zabalawi A , Chagué F , Filippi E , Brunet D , Hacot JP , Brunel P , Mejri M , Lorgis L , Rouault G , Druelles P , Cornily JC , Didier R , Bot E , Boulanger B , Coudert I , Loirat A , Bedossa M , Boulmier D , Maza M , Le Guellec M , Puri R , Zeller M , Le Breton H ; On behalf of the ORBI and RICO Working Groups . Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score . Eur Heart J 2018 ; 39 : 2090 – 2102 . Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Journal

European Heart JournalOxford University Press

Published: Apr 19, 2018

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