Erythropoietin in Patients With Acute ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Ott, Ilka; Schulz, Stefanie; Mehilli, Julinda; Fichtner, Stefanie; Hadamitzky, Martin; Hoppe, Katharina; Ibrahim, Tareq; Martinoff, Steffan; Maßberg, Steffen; Laugwitz, Karl‐Ludwig; Dirschinger, Josef; Schwaiger, Markus; Kastrati, Adnan; Schömig, Albert

doi:10.1161/circinterventions.109.904425

Cited by 119 publications

(81 citation statements)

References 21 publications

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“…234 Erythropoietin in patients with STsegment elevation myocardial infarction and interventional reperfusion neither reduced infarct size (creatine kinase and MRI) nor improved TIMI flow. 235 Two different mitochondria-targeting drugs 236,237 failed to reduce infarct size or to improve coronary microvascular function. Currently, only 4 drugs stand unchallenged to provide cardioprotection in term of infarct size reduction: atrial natriuretic peptide, 238 metoprolol, 32 esmolol, 239 and exenatide, [240][241][242] and no information on coronary microvascular function is available for these drugs.…”

Section: Clinical Studiesmentioning

confidence: 99%

The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

209

160

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Abstract:The atherosclerotic coronary vasculature is not only the culprit but also a victim of myocardial ischemia/ reperfusion injury. Manifestations of such injury are increased vascular permeability and edema, endothelial dysfunction and impaired vasomotion, microembolization of atherothrombotic debris, stasis with intravascular cell aggregates, and finally, in its most severe form, capillary destruction with hemorrhage. In animal experiments, local and remote ischemic pre-and postconditioning not only reduce infarct size but also these manifestations of coronary vascular injury, as do drugs which recruit signal transduction steps of conditioning. Clinically, no-reflow is frequently seen after interventional reperfusion, and it carries an adverse prognosis. The translation of cardioprotective interventions to clinical practice has been difficult to date. Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol) stand unchallenged to date in reducing infarct size in patients with reperfused acute myocardial infarction; unfortunately, for these drugs, no information on their impact on the ischemic/reperfused coronary circulation is available. (Circ Res.

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Section: Clinical Studiesmentioning

confidence: 99%

The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

209

160

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“…33 The safety and efficacy of EPO administration for patients with AMI is still controversial. 34,35 The limitation of EPO is possible tumor-angiogenic activity in cancer patients and its thrombopoietin (TPO)-like activity. 36 Bolus administration of EPO may cause cerebrovascular and cardiovascular events.…”

Section: Discussionmentioning

confidence: 99%

“…36 Bolus administration of EPO may cause cerebrovascular and cardiovascular events. 35 Moreover, there might be an optimal dose of EPO administration to treat coronary ischemia/reperfusion injury. 37 AEPO is one of the candidates to avoid platelet activation because the serum level of AEPO does not elevate while preserving their angiogenic (PCT Patent 2006/129755) and cardioprotective effects but not erythropoietic effects.…”

Section: Discussionmentioning

confidence: 99%

A novel synthetic derivative of human erythropoietin designed to bind to glycosaminoglycans

Matsushima¹,

Toba²,

Hanawa³

et al. 2012

Drug Delivery

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“…Ott et al 66 described a randomized, double-blind trial of 138 patients with STEMI who received epoetin-β (3.33×10 4 U) or placebo immediately after PCI and at 24 and 48 hours later. Primary end point was LVEF at 6 months, determined by MRI; secondary end point was myocardial infarct size at day 5 and 6 months.…”

Section: Other Older and Newer Pharmacological Approaches Erythropoietinmentioning

confidence: 99%

Current State of Clinical Translation of Cardioprotective Agents for Acute Myocardial Infarction

Kloner

2013

Circulation Research

138

112

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Abstract:There is continued interest in the concept of limiting myocardial infarct size with adjunctive agents administered along with reperfusion injury; however, there remains considerable controversy in the literature. The purpose of this article is to review the medical literature on clinical trials performed during the past 3 years that have attempted to reduce myocardial infarct size by administration of adjunctive therapies along with reperfusion therapy. A PubMed-driven literature search revealed a host of clinical trials focusing on the following prominent types of therapies: endogenous conditioning (postconditioning and remote ischemic conditioning); rapid cooling; pharmacological therapy (cyclosporine, abciximab, clopidogrel, tirofiban, erythropoietin, thrombus aspiration, adenosine, glucose-insulin-potassium, statins, antidiabetic agents, FX06, iron chelation, and ranolazine). Although there remains some controversy, quite a few of these studies showed that adjunctive therapy further reduced myocardial infarct size when coupled with reperfusion. Antiplatelet agents are emerging as some of the newest agents that seem to have cardioprotective capabilities. Postconditioning has become a bit more controversial in the clinical literature; remote conditioning, early and rapid cooling, adenosine, and ranolazine are intriguing therapies deserving of larger studies. Certain agents and maneuvers, such as erythropoietin, protein kinase C δ inhibitors, iron chelation, and intra-aortic balloon counterpulsation, perhaps should be retired. The correct adjunctive therapy administered along with reperfusion has the capability of further reducing myocardial injury during ST-segment-elevation myocardial infarction. ( infarct size reducing agents in clinical trials. Some of these disappointing agents included antibodies that prevent white blood cell adhesion to the endothelium; eniporide, a sodium/hydrogen exchange inhibitor; caldaret, an intracellular calcium-handling modulator; nicorandil, a potassium ATP channel opener/vasodilator; glucose-insulin-potassium (GIK); delcasertib (a protein kinase C δ inhibitor); and erythropoietin. 5 However, some agents and maneuvers that were observed to work in experimental models did show promise in clinical trials of MI under the right circumstances: postconditioning; remote conditioning; cyclosporine (maintains the mitochondrial permeability transition pore closed); intravenous adenosine infusions; atrial natriuretic peptide; mild hypothermia induced before reperfusion; supersaturated oxygen therapy and others. [4][5][6][7] The reasons for discrepancies between experimental findings and clinical trials have been reviewed in detail. 6,7 Since these reviews were written there have been a large number of new clinical trials recently published during the past 3 years, on the basis of literature searches through PubMed. These trials cover additional new studies on therapies, such as conditioning, abciximab, clopidogrel, erythropoietin, hypothermia, thrombectomy, intracoronary adenosine...

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Erythropoietin in Patients With Acute ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Cited by 119 publications

References 21 publications

The Coronary Circulation as a Target of Cardioprotection

The Coronary Circulation as a Target of Cardioprotection

A novel synthetic derivative of human erythropoietin designed to bind to glycosaminoglycans

Current State of Clinical Translation of Cardioprotective Agents for Acute Myocardial Infarction

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