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Aortic input impedance in mild to moderate chronic congestive heart failure: lack of interrelation with neurohormonal
1Medizinische Klinik II, Universität Regensburg, Germany.
Insights
In early congestive heart failure (CHF), activated neurohormonal systems do not significantly increase left ventricular (LV) pulsatile load. Arterial properties remain largely unchanged in mild to moderate CHF patients.
Area of Science:
- Cardiology
- Vascular Physiology
- Hemodynamics
Background:
- Chronic heart failure (CHF) involves activated neurohormonal systems.
- These systems may cause vasoconstriction and alter arterial properties.
- This could potentially increase left ventricular (LV) pulsatile load.
Purpose of the Study:
- To investigate LV pulsatile load and neurohormonal activation in patients with mild to moderate chronic CHF.
- To measure aortic input impedance as an indicator of LV pulsatile load.
Main Methods:
- Studied 20 patients with mild to moderate chronic CHF.
- Measured aortic input impedance to assess LV pulsatile load.
- Assessed plasma levels of norepinephrine, renin, atrial natriuretic peptide, and arginine vasopressin.
Main Results:
- Patients exhibited reduced cardiac index and LV ejection fraction, with elevated pulmonary wedge pressure.
- Increased plasma levels of norepinephrine, renin, atrial natriuretic peptide, and arginine vasopressin were observed.
- Characteristic impedance (Zc) was normal and did not correlate with neurohormonal activation levels.
Conclusions:
- Early-stage CHF neurohormonal activation does not significantly elevate LV pulsatile load.
- The physical properties of the great arteries are not substantially altered in these early stages.
Unlabelled:
Patients with chronic congestive heart failure (CHF) have activated neurohormonal systems, which may induce vasoconstriction. In addition, the arterial wall sodium content may increase and could have direct trophic effects on vascular smooth muscle cells. These mechanisms might elevate left ventricular (LV) pulsatile load. We measured aortic input impedance to find out the LV pulsatile load and neurohormonal activation in 20 patients with mild to moderate chronic CHF. Cardiac index (2.2 +/- 0.3 l.min-1 x m-2) and LV ejection fraction (38 +/- 4%) were reduced, pulmonary wedge pressure was elevated (21 +/- 2 mmHg). Plasma norepinephrine levels (462 +/- 62 pg.ml-1), plasma renin concentration (12 +/- 4 ng.AI.ml-1h-1), plasma levels of atrial natriuretic peptide (408 +/- 64 pg.ml-1) and, to a slight degree, plasma arginine vasopressin (1.1 +/- 0.3 pg.ml-1) were increased. Characteristic impedance, Zc, was within the normal range (80 +/- 6 dyn.s.cm-5) and showed no significant correlation with the degree of neurohormonal activation (r-values: -0.05 to -0.35).
Conclusions:
Our data demonstrate that in early stages of CHF stimulation of the neurohormonal systems does not significantly elevate LV pulsatile load; therefore there is no substantial alteration in the physical properties of the great arteries.
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