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Increased aortic impedance precedes peripheral vasoconstriction at the early stage of ventricular failure in the
G M Eaton1, R J Cody, P F Binkley
1Ohio State University, Department of Medicine, Columbus 43210.
Insights
Abnormal aortic input impedance is an early vascular change in heart failure, developing rapidly with left ventricular systolic dysfunction. This impedance shift precedes changes in peripheral resistance, impacting energetics and disease progression.
Area of Science:
- Cardiovascular Physiology
- Hemodynamics
- Heart Failure Pathophysiology
Background:
- Aortic input impedance alterations are noted in heart failure.
- The timing of these vascular changes relative to left ventricular dysfunction is unclear.
Purpose of the Study:
- To investigate if abnormal aortic input impedance is an early or late manifestation of left ventricular dysfunction.
- To define the time course of changes in aortic input impedance and conduit vessel compliance.
Main Methods:
- Utilized a paced canine model of congestive heart failure.
- Hemodynamic evaluation in beagles before and after inducing left ventricular dysfunction via rapid ventricular pacing.
- Measured left ventricular ejection fraction and aortic input impedance spectrum.
Main Results:
- Within 48 hours of pacing, left ventricular systolic dysfunction (ejection fraction 37%) was observed.
- Aortic input impedance spectrum shifted significantly upward.
- Characteristic impedance increased by 50% without concurrent changes in peripheral vascular resistance.
Conclusions:
- Abnormalities in aortic input impedance represent an early vascular change in response to ventricular systolic dysfunction.
- Early impedance changes likely impair power transfer and reduce conduit vessel compliance.
- These factors contribute to the progression of myocardial energetics and systolic dysfunction in heart failure.
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.