Developmental sequelae of fixed-rate ventricular pacing in the immature canine heart: an electrophysiologic, hemodynamic, and histopathologic evaluation.

Permanent, fixed-rate ventricular pacing (VVI) is associated with hemodynamic deterioration in the adult with compromised myocardial function. The effects of this pacing mode on the intact, immature heart, however, are largely unknown. Twelve beagle puppies (age 3 to 4 months) were equally divided into paced and age-matched control groups. All underwent identical hemodynamic and electrophysiologic evaluations. Transepicardial atrioventricular block and pacemaker insertion were additionally carried out in the paced group. After 4 months of observation, repeat hemodynamic and electrophysiologic measurements followed by histopathologic examinations were done in all puppies. The paced group exhibited significant (p less than 0.05) elevations of right atrial and pulmonary artery pressures, alterations in sinus node function, and prolongation of ventricular refractory periods compared with the control group. Initiation of dysrhythmias by programmed electrical stimulation was observed only among the paced group of puppies. Histologic examination demonstrated myofibrillar cellular disarray, dystrophic calcifications, prominent subendocardial Purkinje cells, and an increase in variable-sized, disorganized mitochondria only in the paced specimens. These findings indicate that permanent, apically-initiated VVI pacing ultimately predisposes to adverse cellular changes associated with hemodynamic and electrophysiologic deterioration in the intact, developing immature canine heart.