title: Mitochondrial injury and autophagocytosis within the myocardial cell after the cold ischaemic anoxic asystole.
abstract: Right atrial myocardial biopsies were excised in the course of prosthetic aortic valve replacement operation from eight consecutive patients 1) before starting the extracorporeal circulation (controls) and 2) after the cold ischaemic anoxic asystole (aortic cross-clamping (50-70 min) during general hypothermia (30 degrees C) associated with local cardiac cooling with +4 degrees C saline solution and subsequent coronary reperfusion (20-30 min, until decannulation), and immediately processed for electron microscopy. In most cases no or only minimal changes were observed. These patients made a smooth recovery. In one case very severe damage was seen: extreme swelling, clearing and paling of the matrix, disruption of the inner and outer mitochondrial membranes, distortion, disruption and loss of the cristae and lamellar degeneration and vacuolization of the mitochondria. Huge amounts of large secondary lysosomal bodies in different stages of autodigestion were seen in company with the degenerating mitochondria. Also this patient ultimately recovered after a long-lasting low output syndrome. Pre- and intra-operatively until weaning from the cardiopulmonary bypass, nothing distinguished clinically this case with autophagocytosis from the other cases. The occurrence of autophagocytosis has been described earlier in relation to an irreversible lethal damage following extended normothermic ischaemia. Obviously this phenomenon may be associated also with sublethal myocardial injury occurring despite attempts to myocardial preservation by local cardiac cooling.
mesh_terms: D001021:Aortic Valve / Q000601:surgery; D001145:Arrhythmias, Cardiac / Q000150:complications*; D001343:Autophagy; D009202:Cardiomyopathies / Q000209:etiology* / Q000473:pathology; D006323:Heart Arrest / Q000150:complications*; D006324:Heart Arrest, Induced; D006350:Heart Valve Prosthesis; D006801:Humans; D007036:Hypothermia, Induced; D000860:Hypoxia; D008929:Mitochondria, Heart / Q000648:ultrastructure*; D010587:Phagocytosis