ABSTRACT
The interactions of the systemic and myocardial adaptations during and after rapid ventricular pacing, a model of heart failure, were assessed in conscious, unstressed dogs. Ultrasonic probes and vascular catheters were surgically implanted into dogs for measurements of blood flows and pressures during 3 weeks of pacing and after 2 months of recovery. Three weeks of tachycardia (260 beats/min) resulted in a marked reduction in hemodynamic parameters and left ventricular dilatation, with caudal wall thinning throughout the pacing period and 1 week of recovery. Sinus rhythm resumed after the pacer was turned off, with return toward normal in hemodynamic parameters; however, left ventricular dilatation and ventricular remodeling, with significant fibrosis, loss of myocytes, and hypertrophy of the surviving cells were still present after 2 months of recovery. In conclusion, even though hemodynamic parameters normalized during recovery, adaptive myocardial remodeling caused permanent ventricular fibrosis, hypertrophy, and increased cardiac filling pressures.
