Septal ventricular pacing in the immature canine heart: a new perspective.

Cardiac pacing initiated from epicardial or transvenous apical right ventricular electrodes causes asynchronous ventricular contraction. This alters myocardial stress vectors and results in adverse cellular and subcellular changes in the experimental animal. Clinically, such changes may contribute to the adverse hemodynamics reported with long-term ventricular pacing. To determine the feasibility of direct stimulation of the ventricular specialized conduction systems and therefore the potential for maintenance of normalized depolarization patterns, 13 beagle puppies were studied. Baseline ventricular activation and contraction patterns were obtained using intracardiac electrograms and multigated nuclear acquisition (MUGA) imaging. Septal electrode insertion from the aortoatrial groove was accomplished by use of two-dimensional echocardiography and continuous electrocardiographic (ECG) monitoring of the surface ECG during pacemaker implantation in five puppies. Standard right ventricular epicardial electrodes were implanted in five additional animals, with three remaining as age-matched non-paced controls. After 4 months of observation, repeat MUGA imaging and intracardiac electrograms demonstrated nearly normal biventricular activation and contraction patterns among the septal-paced group. Histopathologic examination illustrated normal cellular morphology in the septal-paced animals. This study demonstrates that pacing electrode insertion into the proximal interventricular septum is feasible and results in utilization of the normal ventricular conduction pathway. Such an approach to initiation of ventricular stimulation may attenuate the adverse effects of long-term ventricular pacing.

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.

A new low threshold platinized epicardial pacing electrode: comparative evaluation in immature canines.

A prospective comparison of pacing and sensing capabilities between the conventional Medtronic Model 4951 platinum-iridium epicardial pacing electrode and a new modified "platinized" version of the same electrode was performed in immature canines to determine if the new electrode design improves pacing in the immature myocardium. The conventional electrode was modified by electroplating platinum black particles onto the surface to increase the effective or true microscopic surface area, yet essentially maintain the same overall geometric electrode size. Both epicardial electrodes were inserted into the right ventricular myocardium with the lead pad sutured to the epicardium, and externalized to the scruff in five puppies (age 3 months). An additional left ventricular lead was implanted to permit chronic pacing following epicardially-induced atrioventricular block. Acute and chronic sensing and pacing capabilities of each externalized electrode were performed at implant and weekly up to 4 months. Histologic examination of each electrode implant site was performed at the end of the study period. At implant, both electrodes exhibited comparable values for sensed R waves, lead impedances, and pacing thresholds. During the study, the platinized electrode exhibited lower pacing thresholds. Analysis of all postimplant data demonstrated this threshold difference to be significantly lower (P less than .01) for the platinized version. Lead impedance and sensing capabilities remained comparable between the two designs. Histologic study demonstrated less fibrotic infiltration at the platinized electrode site. This preliminary evaluation indicates that for the duration of the postimplant study period, the platinized epicardial electrode design was associated with significantly lower thresholds and less fibrosis as a function of time compared to the conventional smooth electrode surface design. The new platinized electrode limits exit block in the developing immature myocardium and permits safe pacing at lower pulse widths and voltages to increase battery life.