Increased Aortic Impedance Precedes Peripheral Vasoconstriction at the Early Stage of Ventricular Failure in the Paced Canine Model

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Abstract

Background.

Aortic input impedance is altered in patients with congestive heart failure. However, little is known about whether this vascular response is an early change or a late manifestation of left ventricular 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 systolic 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 underwent hemodynamic evaluation at baseline and after induction of left ventricular dysfunction by rapid ventricular pacing. Within 48 hours of the onset of rapid ventricular pacing, we observed mild left ventricular 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 studied. Characteristic impedance of the aorta significantly increased from 121±65 dynes • s/cm5 to 186±114 dynes • s/cm5 (P<.02), and a significant increase in the first modulus of impedance from 137±43 dynes • s/cm5 to 228±139 dynes • s/cm5 was observed (P<.05). Although characteristic aortic impedance increased by 50%, there was at this point no change in peripheral vascular resistance. Therefore, these abnormalities in aortic input impedance are representative of an early vascular 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 compliance likely contribute to the progression of abnormal myocardial energetics and systolic dysfunction characteristic of ventricular failure. (Circulation.1993;88:2714–2721.)

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