COMPENSATED CARDIAC-HYPERTROPHY - ARRHYTHMOGENICITY AND THE NEW MYOCARDIAL PHENOTYPE .1. FIBROSIS

The high incidence of arrhythmias in compensated cardiac hypertrophy i s related to two independently regulated components-fibrosis and the a daptational phenotypic changes in membrane proteins linked to cardiac hypertrophy, and fibrosis. During the regression of hypertensive cardi opathy in middle-aged spontaneously hypertensive rats, the roles of ca rdiac hypertrophy and fibrosis can be analysed separately, revealing t hat both correlate independently with arrhythmias. In an experimental model of myocardial infarction it is possible to prevent arrhythmias w ith propranolol at the same time as cardiac hypertrophy, despite ventr icular fibrosis. Fibrosis would appear to create arrhythmias both by a natomical uncoupling and by a re-entry mechanism generated by the zig- zag propagation of the transverse waveform. Triggered activity and aut omaticity depend on the membrane phenotype of the cardiocyte. They als o play an important role, which is aggravated by myocardial heterogene ity.