The pathophysiology of heart failure

The classical definition of heart failure (HF) is fundamentally a pathophysiological one. It is the ‘inability of the heart to provide sufficient oxygen to the metabolizing tissues despite an adequate filling pressure’. Initially, the abnormalities found in the HF syndrome were described in terms of their haemodynamic effects. However, as the relationship between the pathophysiology of HF and its therapy has emerged over the last 20 years, it is now clear that the pathophysiology of HF is highly complex. It also involves neurohormonal and inflammatory adaptations which initially help the situation but chronically contribute to progression of the HF syndrome and adversely affect the structure and function of the heart itself. This chapter reviews the pathophysiology of HF by outlining what is known about its key players: haemodynamic abnormalities, ventricular remodelling, neurohormonal activation, and inflammatory responses. Although any cardiac pathology can ultimately lead to HF, most is known about the pathophysiology of HF due to myocardial failure leading to left ventricular systolic dysfunction (LVSD), which concerns most of this chapter. Much work is needed to elucidate further the pathophysiology of HF when it occurs in the presence of normal systolic function.