Myocardial effects of repetitive episodes of rapid ventricular pacing in conscious dogs: surgical creation, echocardiographic evaluation, and morphometric analysis.
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.
Department of Veterinary Sciences, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, NJ 08543-4000.
D E
DE
Burkett
A A
AA
Seymour
D H
DH
Knight
C E
CE
Rabon
V M
VM
Lanoce
A F
AF
Clemons
F G
FG
Spinale
D000818:Animals; D002304:Cardiac Pacing, Artificial; D002404:Catheterization; D004195:Disease Models, Animal; D004285:Dogs / Q000601:surgery; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics; D008297:Male; D009200:Myocardial Contraction; D009929:Organ Size; D013610:Tachycardia; D014463:Ultrasonography