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Heart Failure II: Pathophysiology

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Related Experiment Video

Updated: Jun 12, 2026

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion

Published on: March 20, 2017

Complement activation, endothelial dysfunction, insulin resistance and chronic heart failure.

Mette Bjerre¹, Caroline Kistorp, Troels Krarup Hansen

¹Medical Research Laboratories, Clinical Institute & Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Denmark. mette.bjerre@ki.au.dk

Scandinavian Cardiovascular Journal : SCJ

|June 8, 2010

Summary

Insulin resistance is linked to complement activation and endothelial dysfunction in chronic heart failure (CHF) patients. This study explores these connections, finding independent associations between soluble membrane attack complex (sMAC), soluble E-selectin (sEsel), and insulin resistance (IR).

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Area of Science:

Cardiovascular Medicine
Immunology
Metabolic Syndrome

Background:

Patients with chronic heart failure (CHF) exhibit heightened immune responses, endothelial damage, and a greater risk of diabetes mellitus (DM).
The interplay between complement activation (sMAC), inflammation (hsCRP), endothelial activation (sEsel), endothelial damage (vWf), and insulin resistance (IR) in CHF prognosis is not well understood.

Purpose of the Study:

To investigate the associations between plasma biomarkers of complement activation, inflammation, endothelial activation/damage, and insulin resistance in CHF patients.
To determine if elevated levels of these biomarkers impact the prognosis of CHF.

Main Methods:

A prospective study involving 193 CHF patients and 100 age-matched controls.
Plasma levels of soluble membrane attack complex (sMAC), high-sensitivity C-reactive protein (hsCRP), soluble E-selectin (sEsel), and von Willebrand factor (vWf) were measured.
Insulin resistance (IR) was assessed using the homeostatic model assessment (HOMA).

Main Results:

sMAC levels were higher in CHF patients with ischemic heart disease compared to non-ischemic etiology.
No significant prognostic impact of high biomarker levels on survival or CHF progression was observed.
A significant association was found between sMAC and sEsel, independent of IR and DM.
Insulin resistance (IR) independently predicted sMAC levels in the CHF group.

Conclusions:

Independent associations exist between sMAC, sEsel, and IR in CHF patients.
A hypothesis is proposed where IR drives endothelial activation, leading to complement system activation and subsequent heart tissue damage.