ABSTRACT

In response to myocardial damage, activation of neurohormonal systems, pro-inflammatory cytokines and various second messenger systems contribute to progression of left ventricular remodelling and subsequent cardiac decompensation. Heart failure is thus the clinical endpoint for a number of complex patho-physiological processes. However, the severity and time course of the disease is influenced also by the presence and control of known comorbid disease factors, which themselves are modified by different gender-specific, genetic and environmental backgrounds.