INCREASED AORTIC IMPEDANCE PRECEDES PERIPHERAL VASOCONSTRICTION AT THE EARLY-STAGE OF VENTRICULAR FAILURE IN THE PACED CANINE MODEL

Background. Aortic input impedance is altered in patients with congest ive heart failure. However, little is known about whether this vascula r response is an early change or a late manifestation of left ventricu lar dysfunction. Methods and Results. This investigation used a paced canine model of congestive heart failure to demonstrate that abnormal aortic input impedance does evolve in the setting of ventricular systo lic dysfunction and to prospectively define the time course of change in aortic input impedance and conduit vessel compliance. Studies were performed in closed-chest conditioned beagles aged 1 to 2 years that u nderwent hemodynamic evaluation at baseline and after induction of lef t ventricular dysfunction by rapid ventricular pacing. Within 48 hours of the onset of rapid ventricular pacing, we observed mild left ventr icular systolic dysfunction with an echocardiographically derived left ventricular ejection fraction of 37% (P<.001 compared with baseline) measured during interruption of rapid ventricular pacing. Concomitant with this reduction in left ventricular systolic function, the aortic input impedance spectrum was shifted above baseline in all dogs studie d. Characteristic impedance of the aorta significantly increased from 121+/-65 dynes.s/cm(5) to 186+/-114 dynes.s/cm(5) (P<.02), and a signi ficant increase in the first modulus of impedance from 137+/-43 dynes. s/cm(5) to 228+/-139 dynes.s/cm(5) was observed (P<.05). Although char acteristic aortic impedance increased by 50%, there was at this point no change in peripheral vascular resistance. Therefore, these abnormal ities in aortic input impedance are representative of an early vascula r change that evolves in response to ventricular systolic dysfunction. Conclusions. Considering the early appearance of these findings, the resultant impaired power transfer and reduced conduit vessel complianc e likely contribute to the progression of abnormal myocardial energeti cs and systolic dysfunction characteristic of ventricular failure.