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  1. Article ; Online: Myocardial ischemia/reperfusion: Translational pathophysiology of ischemic heart disease.

    Heusch, Gerd

    Med (New York, N.Y.)

    2024  Volume 5, Issue 1, Page(s) 10–31

    Abstract: Ischemic heart disease is the greatest health burden and most frequent cause of death worldwide. Myocardial ischemia/reperfusion is the pathophysiological substrate of ischemic heart disease. Improvements in prevention and treatment of ischemic heart ... ...

    Abstract Ischemic heart disease is the greatest health burden and most frequent cause of death worldwide. Myocardial ischemia/reperfusion is the pathophysiological substrate of ischemic heart disease. Improvements in prevention and treatment of ischemic heart disease have reduced mortality in developed countries over the last decades, but further progress is now stagnant, and morbidity and mortality from ischemic heart disease in developing countries are increasing. Significant problems remain to be resolved and require a better pathophysiological understanding. The present review attempts to briefly summarize the state of the art in myocardial ischemia/reperfusion research, with a view on both its coronary vascular and myocardial aspects, and to define the cutting edges where further mechanistic knowledge is needed to facilitate translation to clinical practice.
    MeSH term(s) Humans ; Myocardial Reperfusion Injury/etiology ; Myocardial Reperfusion Injury/prevention & control ; Myocardial Ischemia/prevention & control ; Myocardial Reperfusion/adverse effects ; Myocardium
    Language English
    Publishing date 2024-01-13
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2666-6340
    ISSN (online) 2666-6340
    DOI 10.1016/j.medj.2023.12.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book ; Conference proceedings: Der akute Herzinfarkt

    Heusch, Gerd

    Symposium der Nordrhein-Westfälischen Akademie der Wissenschaften und der Künste ; [Symposium am 12. März 2014 in Düsseldorf]

    (S / Nordrhein-Westfälische Akademie der Wissenschaften und der Künste ; 11)

    2015  

    Author's details Gerd Heusch (Hg.)
    Series title S / Nordrhein-Westfälische Akademie der Wissenschaften und der Künste ; 11
    S
    Collection S
    Keywords Herzinfarkt ; Akute Krankheit
    Subject Akutstadium ; Akutphase ; Akuter Schub ; Krankheit ; Koronarinfarkt ; Myokardinfarkt ; Myocardinfarkt
    Language German
    Size 172 S. : Ill., graph. Darst.
    Publisher Schöningh
    Publishing place Paderborn
    Publishing country Germany
    Document type Book ; Conference proceedings
    Note Literaturangaben
    HBZ-ID HT018654286
    ISBN 978-3-506-78190-1 ; 3-506-78190-1
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2015 A 3142 available for loan (reading room) Lesesaal EG

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  3. Article ; Online: Cardioprotection and its Translation: A Need for New Paradigms? Or for New Pragmatism? An Opinionated Retro- and Perspective.

    Heusch, Gerd

    Journal of cardiovascular pharmacology and therapeutics

    2023  Volume 28, Page(s) 10742484231179613

    Abstract: The dawn of cardioprotection by infarct size reduction originated from the idea to favourably alter the oxygen demand-supply balance of the ischaemic/infarcting myocardium by reducing the contractile determinants of its oxygen consumption. This idea is ... ...

    Abstract The dawn of cardioprotection by infarct size reduction originated from the idea to favourably alter the oxygen demand-supply balance of the ischaemic/infarcting myocardium by reducing the contractile determinants of its oxygen consumption. This idea is probably not correct, since the ischaemic/infarcting myocardium does not contract anyway. None of the successful initial preclinical attempts of infarct size reduction translated into clinical practice, except for timely reperfusion which has become and still is the backbone of all clinical infarct therapy up today. The idea of cardioprotection gained momentum again with the recognition of ischaemic conditioning, and a myriad of preclinical studies have identified molecules and mechanisms of such self-defence mechanism. Although there are positive clinical proof-of-concept studies, ischaemic conditioning strategies and drugs related to its signal transduction have not translated into clinical practice. We are currently trying to understand the obstacles to translation from successful preclinical studies on cardioprotection to clinical practice, but are also waiting for an innovative mechanistic breakthrough.
    MeSH term(s) Humans ; Myocardial Infarction/prevention & control ; Myocardial Reperfusion Injury/prevention & control ; Ischemic Preconditioning, Myocardial ; Signal Transduction ; Myocardium
    Language English
    Publishing date 2023-05-31
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1329372-2
    ISSN 1940-4034 ; 1074-2484
    ISSN (online) 1940-4034
    ISSN 1074-2484
    DOI 10.1177/10742484231179613
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Cardioprotection in cardio-oncology: a case for concern?

    Heusch, Gerd

    Cardiovascular research

    2023  Volume 119, Issue 12, Page(s) e144–e145

    Language English
    Publishing date 2023-08-16
    Publishing country England
    Document type Journal Article
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvad111
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    Zs.A 565: Show issues Location:
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  5. Article ; Online: Coronary blood flow in heart failure: cause, consequence and bystander.

    Heusch, Gerd

    Basic research in cardiology

    2022  Volume 117, Issue 1, Page(s) 1

    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 ... ...

    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.
    MeSH term(s) Coronary Circulation ; Heart ; Heart Diseases ; Heart Failure ; Hemodynamics ; Humans ; Stroke Volume
    Language English
    Publishing date 2022-01-13
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 189755-x
    ISSN 1435-1803 ; 0300-8428 ; 0175-9418
    ISSN (online) 1435-1803
    ISSN 0300-8428 ; 0175-9418
    DOI 10.1007/s00395-022-00909-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Myocardial stunning and hibernation revisited.

    Heusch, Gerd

    Nature reviews. Cardiology

    2021  Volume 18, Issue 7, Page(s) 522–536

    Abstract: Unlike acute myocardial infarction with reperfusion, in which infarct size is the end point reflecting irreversible injury, myocardial stunning and hibernation result from reversible myocardial ischaemia-reperfusion injury, and contractile dysfunction is ...

    Abstract Unlike acute myocardial infarction with reperfusion, in which infarct size is the end point reflecting irreversible injury, myocardial stunning and hibernation result from reversible myocardial ischaemia-reperfusion injury, and contractile dysfunction is the obvious end point. Stunned myocardium is characterized by a disproportionately long-lasting, yet fully reversible, contractile dysfunction that follows brief bouts of myocardial ischaemia. Reperfusion precipitates a burst of reactive oxygen species formation and alterations in excitation-contraction coupling, which interact and cause the contractile dysfunction. Hibernating myocardium is characterized by reduced regional contractile function and blood flow, which both recover after reperfusion or revascularization. Short-term myocardial hibernation is an adaptation of contractile function to the reduced blood flow such that energy and substrate metabolism recover during the ongoing ischaemia. Chronic myocardial hibernation is characterized by severe morphological alterations and altered expression of metabolic and pro-survival proteins. Myocardial stunning is observed clinically and must be recognized but is rarely haemodynamically compromising and does not require treatment. Myocardial hibernation is clinically identified with the use of imaging techniques, and the myocardium recovers after revascularization. Several trials in the past two decades have challenged the superiority of revascularization over medical therapy for symptomatic relief and prognosis in patients with chronic coronary syndromes. A better understanding of the pathophysiology of myocardial stunning and hibernation is important for a more precise indication of revascularization and its consequences. Therefore, this Review summarizes the current knowledge of the pathophysiology of these characteristic reperfusion phenomena and highlights their clinical implications.
    MeSH term(s) Humans ; Myocardial Stunning/physiopathology
    Language English
    Publishing date 2021-02-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2490375-9
    ISSN 1759-5010 ; 1759-5002
    ISSN (online) 1759-5010
    ISSN 1759-5002
    DOI 10.1038/s41569-021-00506-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Cardioprotection research has left its comfort zone.

    Heusch, Gerd / Kleinbongard, Petra

    European heart journal

    2024  

    Language English
    Publishing date 2024-03-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 603098-1
    ISSN 1522-9645 ; 0195-668X
    ISSN (online) 1522-9645
    ISSN 0195-668X
    DOI 10.1093/eurheartj/ehae079
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  8. Article ; Online: Myocardial ischaemia-reperfusion injury and cardioprotection in perspective.

    Heusch, Gerd

    Nature reviews. Cardiology

    2020  Volume 17, Issue 12, Page(s) 773–789

    Abstract: Despite the increasing use and success of interventional coronary reperfusion strategies, morbidity and mortality from acute myocardial infarction are still substantial. Myocardial infarct size is a major determinant of prognosis in these patients. ... ...

    Abstract Despite the increasing use and success of interventional coronary reperfusion strategies, morbidity and mortality from acute myocardial infarction are still substantial. Myocardial infarct size is a major determinant of prognosis in these patients. Therefore, cardioprotective strategies aim to reduce infarct size. However, a perplexing gap exists between the many preclinical studies reporting infarct size reduction with mechanical and pharmacological interventions and the poor translation into better clinical outcomes in patients. This Review revisits the pathophysiology of myocardial ischaemia-reperfusion injury, including the role of autophagy and forms of cell death such as necrosis, apoptosis, necroptosis and pyroptosis. Other cellular compartments in addition to cardiomyocytes are addressed, notably the coronary microcirculation. Preclinical and clinical research developments in mechanical and pharmacological approaches to induce cardioprotection, and their signal transduction pathways, are discussed. Additive cardioprotective interventions are advocated. For clinical translation into treatments for patients with acute myocardial infarction, who typically are of advanced age, have comorbidities and are receiving several medications, not only infarct size reduction but also attenuation of coronary microvascular obstruction, as well as longer-term targets including infarct repair and reverse remodelling, must be considered to improve patient outcomes. Future clinical trials must focus on patients who really need adjunct cardioprotection, that is, those with severe haemodynamic alterations.
    MeSH term(s) Humans ; Myocardial Reperfusion Injury/prevention & control
    Language English
    Publishing date 2020-07-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2490375-9
    ISSN 1759-5010 ; 1759-5002
    ISSN (online) 1759-5010
    ISSN 1759-5002
    DOI 10.1038/s41569-020-0403-y
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  9. Article ; Online: Shahbudin H. Rahimtoola: the scientific legacy.

    Heusch, Gerd

    European heart journal

    2019  Volume 40, Issue 11, Page(s) 866

    Language English
    Publishing date 2019-03-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 603098-1
    ISSN 1522-9645 ; 0195-668X
    ISSN (online) 1522-9645
    ISSN 0195-668X
    DOI 10.1093/eurheartj/ehz076
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  10. Article ; Online: Myocardial ischemia: lack of coronary blood flow, myocardial oxygen supply-demand imbalance, or what?

    Heusch, Gerd

    American journal of physiology. Heart and circulatory physiology

    2019  Volume 316, Issue 6, Page(s) H1439–H1446

    Abstract: This opinionated article reviews current concepts of myocardial ischemia. Specifically, the historical background is briefly presented. Then, the prevailing paradigm of myocardial oxygen-supply-demand imbalance is criticized since demand is a virtual ... ...

    Abstract This opinionated article reviews current concepts of myocardial ischemia. Specifically, the historical background is briefly presented. Then, the prevailing paradigm of myocardial oxygen-supply-demand imbalance is criticized since demand is a virtual parameter that cannot be measured and data on measurements of myocardial blood flow and contractile function rather support matching between flow and function. Finally, a concept of myocardial ischemia that focusses on the reduction of coronary blood flow to below 8-10 µl/g per beat with consequences for myocardial electrical, metabolic, contractile and morphological features is advocated.
    MeSH term(s) Animals ; Biomarkers/blood ; Coronary Circulation ; Coronary Vessels/physiopathology ; Humans ; Models, Cardiovascular ; Myocardial Contraction ; Myocardial Infarction/blood ; Myocardial Infarction/physiopathology ; Myocardial Ischemia/blood ; Myocardial Ischemia/physiopathology ; Myocardial Stunning/blood ; Myocardial Stunning/physiopathology ; Oxygen/blood ; Oxygen Consumption
    Chemical Substances Biomarkers ; Oxygen (S88TT14065)
    Language English
    Publishing date 2019-04-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00139.2019
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