SLOW CONDUCTION IN THE INFARCTED HUMAN HEART - ZIGZAG COURSE OF ACTIVATION

Background. Ventricular tachycardias occurring in the chronic phase of myocardial infarction are caused by reentry. Areas of slow conduction , facilitating reentry, are often found in the infarcted zone. The pur pose of this study was to elucidate the mechanism of slow conduction i n the chronic infarcted human heart. Methods and Results. Spread of ac tivation was studied in infarcted papillary muscles from hearts of pat ients who underwent heart transplantation because of infarction. Recor dings were carried out on 10 papillary muscles that were superfused in a tissue bath. High-resolution mapping was performed in areas reveali ng slow conduction. Activation delay between sites perpendicular to th e fiber direction and 1.4 mm apart could be as long as 45 milliseconds . Analysis of activation times revealed that activation spread in trac ts parallel to the fiber direction. Conduction velocity in the tracts was between 0.6 and 1 m/s. Although tracts were separated from each ot her over distances up to 8 mm, they often connected with each other at one or more sites, forming a complex network of connected tracts. In this network, wave fronts could travel perpendicular to the fiber dire ction. Separation of tracts was due to collagenous septa. At sites whe re tracts were interconnected, the collagenous barriers were interrupt ed. Conclusions. Slow conduction perpendicular to the fiber direction in infarcted myocardial tissue is caused by a ''zigzag'' course of act ivation at high speed. Activation proceeds along pathways lengthened b y branching and merging bundles of surviving myocytes ensheathed by co llagenous septa.