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Aortic input impedence and neurohormonal activation in patients with mild to moderate chronic congestive heart
E P Kromer1, D Elsner, S R Holmer
1II Medizinische Klinik, Universitätsklinikum Regensburg, Germany.
Insights
In chronic heart failure, increased neurohormonal activation does not correlate with altered pulsatile afterload. This suggests no impact on great artery properties in early stages of heart failure.
Area of Science:
- Cardiovascular Physiology
- Heart Failure Pathophysiology
Background:
- Chronic heart failure (CHF) is characterized by neurohormonal activation and altered hemodynamics.
- The relationship between pulsatile afterload and neurohormonal status in CHF requires further elucidation.
Purpose of the Study:
- To investigate the interrelation between pulsatile components of left ventricular afterload and neurohormonal activation in patients with mild to moderate chronic congestive heart failure.
Main Methods:
- Measured aortic input impedance, plasma noradrenaline, renin, atrial natriuretic factor, and arginine vasopressin in 20 CHF patients.
- Assessed cardiac index, left ventricular ejection fraction, and pulmonary wedge pressure.
Main Results:
- Patients exhibited reduced cardiac index and ejection fraction, with elevated pulmonary wedge pressure.
- Plasma levels of noradrenaline, renin, atrial natriuretic factor, and arginine vasopressin were significantly increased.
- Pulsatile components of left ventricular afterload (characteristic impedance and oscillatory pressure power) were within normal limits and showed no significant correlation with neurohormonal activation.
Conclusions:
- No interrelationship exists between neurohormonal activation and pulsatile afterload in mild to moderate chronic heart failure.
- This suggests that stimulated neurohormonal systems may not exert trophic effects on great artery properties in these early stages of heart failure.
Objective:
The aim was to investigate the interrelation between pulsatile components (assessed by determination of aortic input impedance) and neurohormonal activation in chronic congestive heart failure.
Methods:
Aortic input impedance, plasma noradrenaline, renin, atrial natriuretic factor, and arginine vasopressin were measured in 20 patients with mild to moderate chronic congestive heart failure (coronary artery disease n = 12, idiopathic dilated cardiomyopathy n = 8).
Results:
Cardiac index [2.2(SEM 0.3) litre.min-1.m-2] and left ventricular ejection fraction [38(4)%] were reduced, and pulmonary wedge pressure was increased [21(2) mmHg]. Plasma concentrations of noradrenaline [462(62) pg.ml-1], renin [12(4) ng AI.ml.h-1], atrial natriuretic factor [408(64) pg.ml-1], and--to a slight degree--arginine vasopressin [1.1(0.3) pg.ml-1] were increased. Characteristic impedance Zc [80(6) dyne.s.cm-5) and relative oscillatory aortic input pressure power [10(1)%]--both reflecting the pulsatile components of left ventricular afterload--were within the normal range. There was no significant correlation between these variables and the degree of neurohormonal activation (r values: -0.05 to -0.35).
Conclusions:
The data show that in patients with mild to moderate chronic congestive heart failure there is no interrelationship between the degree of neurohormonal activation and pulsatile components of left ventricular afterload. This may indicate that in these stages of heart failure there are no trophic effects of stimulated neurohormonal systems on the physical properties of the great arteries.