Bernhard J Haubner1, Johanna Schneider1, Ulrich Schweigmann1, Thomas Schuetz1, Wolfgang Dichtl1, Corinna Velik-Salchner1, Joerg-I Stein2, Josef M Penninger2. 1. From the IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria (B.J.H., J.M.P.); and Department of Pediatrics III-Cardiology, Pulmonology, Allergology, Cystic Fibrosis (J.S., U.S., J.-I.S.), Department of Internal Medicine III (Cardiology and Angiology) (B.J.H., T.S., W.D.), and Department of Anesthesia and Intensive Care (C.V.-S.), Medical University of Innsbruck, Innsbruck, Austria. 2. From the IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria (B.J.H., J.M.P.); and Department of Pediatrics III-Cardiology, Pulmonology, Allergology, Cystic Fibrosis (J.S., U.S., J.-I.S.), Department of Internal Medicine III (Cardiology and Angiology) (B.J.H., T.S., W.D.), and Department of Anesthesia and Intensive Care (C.V.-S.), Medical University of Innsbruck, Innsbruck, Austria. Joerg.Stein@i-med.ac.at josef.penninger@imba.oeaw.ac.at.
Abstract
RATIONALE: Cardiac remodeling and subsequent heart failure remain critical issues after myocardial infarction despite improved treatment and reperfusion strategies. Recently, cardiac regeneration has been demonstrated in fish and newborn mice after apex resection or cardiac infarctions. Two key issues remain to translate findings in model organisms to future therapies in humans: what is the mechanism and can cardiac regeneration indeed occur in newborn humans? OBJECTIVE: To assess whether human neonatal hearts can functionally recover after myocardial infarction. METHODS AND RESULTS: Here, we report the case of a newborn child having a severe myocardial infarction due to coronary artery occlusion. The child developed massive cardiac damage as defined by serum markers for cardiomyocyte cell death, electrocardiograms, echocardiography, and cardiac angiography. Remarkably, within weeks after the initial ischemic insult, we observed functional cardiac recovery, which translated into long-term normal heart function. CONCLUSIONS: These data indicate that, similar to neonatal rodents, newborn humans might have the intrinsic capacity to repair myocardial damage and completely recover cardiac function.
RATIONALE: Cardiac remodeling and subsequent heart failure remain critical issues after myocardial infarction despite improved treatment and reperfusion strategies. Recently, cardiac regeneration has been demonstrated in fish and newborn mice after apex resection or cardiac infarctions. Two key issues remain to translate findings in model organisms to future therapies in humans: what is the mechanism and can cardiac regeneration indeed occur in newborn humans? OBJECTIVE: To assess whether human neonatal hearts can functionally recover after myocardial infarction. METHODS AND RESULTS: Here, we report the case of a newborn child having a severe myocardial infarction due to coronary artery occlusion. The child developed massive cardiac damage as defined by serum markers for cardiomyocyte cell death, electrocardiograms, echocardiography, and cardiac angiography. Remarkably, within weeks after the initial ischemic insult, we observed functional cardiac recovery, which translated into long-term normal heart function. CONCLUSIONS: These data indicate that, similar to neonatal rodents, newborn humans might have the intrinsic capacity to repair myocardial damage and completely recover cardiac function.
Authors: Martin Zschirnt; Christian Jux; Halvard Boenig; Andreas Zeiher; Birgit Assmus; Markus Khalil; Thomas Kriebel; Stefan Rupp Journal: Clin Res Cardiol Date: 2019-04-26 Impact factor: 5.460