ABSTRACT
The incidence and progression of heart failure are associated with an increasing severity of autonomic derangements, specically a compensatory increase in activity of the sympathetic nervous system and a decrease in activity of the parasympathetic nervous system (Floras, 2009; Binkley et al., 1991). In this simplistic model, left ventricular (LV) systolic dysfunction elicits an increase in sympathetic out¬ow directed at the entire vascular system. From this perspective, increasing sympathetic activity is mediated by re¬exes associated with arterial baroreceptors, which respond to decreased systolic and pulse pressures and decreased functioning of cardiopulmonary baroreceptors due to prior myocardial infarction (MI), receptor down-regulation or ventricular dilatation. If this simplistic description were sufcient, more severe heart failure should always be associated with a decrease in both global measures of heart rate variability (HRV) and in those that specically re¬ect parasympathetic activity. In reality, abnormalities in HRV among patients with heart failure have heterogeneous characteristics despite similar degrees of cardiac dysfunction, indicating that changes in the autonomic function of such patients are complex.
