Chronic supraventricular tachycardia causes ventricular dysfunction and subendocardial injury in swine.

摘要: Chronic supraventricular tachycardia has been associated with ventricular dysfunction in humans and animals. However, this failure is poorly characterized, the ultrastructural consequences of are unknown. We serially examined right left function, endomyocardial ultrastructure, creatine kinase activity eight pigs at base line again 1, 2, 3 wk following rapid atrial pacing. Left ejection fractions fell significantly from after 1 chronic tachycardia. Three weeks pacing resulted further deterioration fractions. Significant biventricular chamber dilatation developed was a reduction end-diastolic wall thickness 2 Mitochondrial injury diminished mitochondrial cytochrome oxidase staining subendocardial myocytes were observed Endomyocardial control levels Postmortem examination revealed compared 14 Fibrosis occurred along layer paced animals, glycogen content also reduced. In summary, severe pump that alterations reduced enzyme myocytes. These metabolic changes may be potential mechanisms responsible for model.