Is cardiac contraction and relaxation in heart failure modulated by the systemic inflammatory response?
There is overwhelming evidence that inflammatory biomarkers predict worse outcome in acute and chronic heart failure.
Despite the wealth of evidence, clinical trials in this area have either not been completed, failed, or provided inconclusive results.
The questions that remain are:
1) Is inflammation a mechanism of disease in acute or chronic heart failure?
2) Are there viable targets in the inflammatory cascade that can modulate cardiac contraction and relaxation? and can this be achieved without deleterious off-target effects?
3) Can inflammatory biomarkers serve as surrogate endpoints in patients with heart failure?