coronary circulation in acute myocardial ischaemia/reperfusion injury: a target for cardioprotection.
acute coronary syndromes; blood capillaries; cardiac myocytes; cardiac vasculature; Cardioprotection; Coronary circulation; Coronary circulation; CYTOLOGY; edema; endothelium; erythrocytes; HEMORRHAGE; infarction; Ischaemia; ischemia; ischemia; ISCHEMIC preconditioning; leukocytes; MEDICAL sciences; Microvascular obstruction; midventricular obstruction; MYOCARDIAL reperfusion; personal integrity; pharmacology; physiologic reperfusion; PRASUGREL; Reperfusion; reperfusion injury; reperfusion injury; reperfusion therapy
The coronary circulation is both culprit and victim of acute myocardial infarction. The rupture of an epicardial atherosclerotic plaque with superimposed thrombosis causes coronary occlusion, and this occlusion must be removed to induce reperfusion. However, ischaemia and reperfusion cause damage not only in cardiomyocytes but also in the coronary circulation, including microembolization of debris and release of soluble factors from the culprit lesion, impairment of endothelial integrity with subsequently increased permeability and oedema formation, platelet activation and leucocyte adherence, erythrocyte stasis, a shift from vasodilation to vasoconstriction, and ultimately structural damage to the capillaries with eventual no-reflow, microvascular obstruction (MVO), and intramyocardial haemorrhage (IMH). Therefore, the coronary circulation is a valid target for cardioprotection, beyond protection of the cardiomyocyte. Virtually all of the above deleterious endpoints have been demonstrated to be favourably influenced by one or the other mechanical or pharmacological cardioprotective intervention. However, no-reflow is still a serious complication of reperfused myocardial infarction and carries, independently from infarct size, an unfavourable prognosis. MVO and IMH can be diagnosed by modern imaging technologies, but still await an effective therapy. The current review provides an overview of strategies to protect the coronary circulation from acute myocardial ischaemia/reperfusion injury. This article is part of a Cardiovascular Research Spotlight Issue entitled 'Cardioprotection Beyond the Cardiomyocyte', and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.
Hausenloy Derek J; Chilian William; Crea Filippo; Davidson Sean M; Ferdinandy Peter; Garcia-Dorado David; van Royen Niels; Schulz Rainer; Heusch Gerd
Cardiovascular Research
2019
1905-07
<a href="http://doi.org/10.1093/cvr/cvy286" target="_blank" rel="noreferrer noopener">10.1093/cvr/cvy286</a>
Myocardial ischemia: From disease to syndrome.
Angina; Chronic coronary syndromes; Coronary artery disease; Ischemic heart disease; Microvascular dysfunction
Although current guidelines on the management of stable coronary artery disease acknowledge that multiple mechanisms may precipitate myocardial ischemia, recommended diagnostic, prognostic and therapeutic algorithms are still focused on obstructive epicardial atherosclerotic lesions, and little progress has been made in identifying management strategies for non-atherosclerotic causes of myocardial ischemia. The purpose of this consensus paper is three-fold: 1) to marshal scientific evidence that obstructive atherosclerosis can co-exist with other mechanisms of ischemic heart disease (IHD); 2) to explore how the awareness of multiple precipitating mechanisms could impact on pre-test probability, provocative test results and treatment strategies; and 3) to stimulate a more comprehensive approach to chronic myocardial ischemic syndromes, consistent with the new understanding of this condition.
Marzilli Mario; Crea Filippo; Morrone Doralisa; Bonow Robert O; Brown David L; Camici Paolo G; Chilian William M; DeMaria Anthony; Guarini Giacinta; Huqi Alda; Merz C Noel Bairey; Pepine Carl; Scali Maria Chiara; Weintraub William S; Boden William E
International journal of cardiology
2020
2020-04-26
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
journalArticle
<a href="http://doi.org/10.1016/j.ijcard.2020.04.074" target="_blank" rel="noreferrer noopener">10.1016/j.ijcard.2020.04.074</a>
The coronary circulation in acute myocardial ischaemia/reperfusion injury - a target for cardioprotection.
The coronary circulation is both culprit and victim of acute myocardial infarction. The rupture of an epicardial atherosclerotic plaque with superimposed thrombosis causes coronary occlusion, and this occlusion must be removed to induce reperfusion. However, ischaemia and reperfusion cause damage not only in cardiomyocytes but also in the coronary circulation, including microembolisation of debris and release of soluble factors from the culprit lesion, impairment of endothelial integrity with subsequently increased permeability and oedema formation, platelet activation and leukocyte adherence, erythrocyte stasis, a shift from vasodilation to vasoconstriction, and ultimately structural damage to the capillaries with eventual no-reflow, microvascular obstruction and intramyocardial haemorrhage. Therefore, the coronary circulation is a valid target for cardioprotection, beyond protection of the cardiomyocyte. Virtually all of the above deleterious endpoints have been demonstrated to be favourably influenced by one or the other mechanical or pharmacological cardioprotective intervention. However, no-reflow is still a serious complication of reperfused myocardial infarction and carries, independently from infarct size, an unfavourable prognosis. Microvascular obstruction and intramyocardial haemorrhage can be diagnosed by modern imaging technologies, but still await an effective therapy. The current review provides an overview of strategies to protect the coronary circulation from acute myocardial ischaemia/reperfusion injury. This article is part of a Cardiovascular Research Spotlight Issue entitled 'Cardioprotection Beyond the Cardiomyocyte', and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.
Hausenloy Derek J; Chilian William; Crea Filippo; Davidson Sean M; Ferdinandy Peter; Garcia-Dorado David; van Royen Niels; Schulz Rainer; Heusch Gerd
Cardiovascular research
2018
2018-11
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1093/cvr/cvy286" target="_blank" rel="noreferrer noopener">10.1093/cvr/cvy286</a>