Stone heart syndrome after prolonged cardioplegia induced cardiac arrest in open-heart surgery – a pilot study on pigs

• Published in: Cardiovascular pathology 2022-09, Vol.60, p.107427-107427, Article 107427
• Main Authors: Krasniqi, Lytfi, Ipsen, Marie Hvid, Schrøder, Henrik Daa, Hejbøl, Eva Kildall, Rojek, Aleksandra Maria, Kjeldsen, Bo Juel, Riber, Lars Peter
• Format: Article
• Language: English
• Subjects: Aortic cross clamp; Cardioplegia; Myocytes; Pig; Stone heart syndrome
• ISSN: 1054-8807; 1879-1336
• DOI: 10.1016/j.carpath.2022.107427

•Additional cases of Stone Heart were reported the last decade with fatal outcome•Stone Heart developed in pigs after 180 minutes of aortic cross-clamp time•Early morphologically damage of cardiomyocyte must be studied with electron microscopy•The transition state should be further researched for improvement of cardioplegic regime in cardiac surgery To investigate Stone Heart Syndrome (SHS) as consequence of prolonged ischemic arrest in an experimental study on pigs in regards to onset of SHS and pathological changes. Outcomes defined as aortic cross clamp (ACC) time until onset of SHS and cellular changes characterized by SHS. Eight pigs were included to undergo normothermic cardioplegia induced cardiac arrest ranging from 80 to 240 minutes of ACC. Duration of ACC was defined as time from initiation of aortic cross clamping until cessation. Normothermic, cardioplegic solution administered directly into the arterial system, though in a reduced dose compared to clinical practice. Myocardial contracture evaluated by palpation of the myocardium. Biopsies were collected from the left ventricle just after the induction of cardiac arrest and after reperfusion. Biopsies were evaluated for pathological changes indicative of SHS by electron microscopy. Six pigs completed the full trial, while two were lost to bleeding. Pigs undergoing 80 to 120 minutes of ACC regained heart rhythm either spontaneously or after defibrillation. Pigs undergoing more than 180 minutes of ACC had contracted hearts with no electrocardiographic response indicating the development of SHS. Electron microscopy findings after ACC of 80 to 120 minutes showed no or low degrees of cellular changes, whereas pig hearts with more than 180 minutes of ACC showed severe mitochondrial changes, endothelial damage, and shortening of sarcomeres consistent with SHS. Development of SHS in pigs was ACC time dependent and solely avoided when ACC was limited to a maximum of 120 minutes.