HF is among the most serious symptom of heart disease, killing about two-thirds of all patients within five years of diagnosis. Patients are treated with mediations such as ACE inhibitors and digitalis so that the heart does not have to work so strenuously to pump blood. HF has other effects as well.
High sympathetic and decreased parasympathetic activities are characteristic of HF and are manifested as blunted baroreceptor activity, diminished parasympathetic effects on the sinoatrial node, increased norepinephrine, decreased heart rate variability, and diminished responsiveness and number of 1-receptors. These characteristics may result from peripheral or central aberrations. The parasympathetic alterations may derive from reduced cardiac muscarinic receptors; however, they also may result from central nervous system (CNS) dysfunction.
The cognitive deficits also suggest CNS dysfunction, possibly developing from ischemic damage as a consequence of HF. The principal neurological deficit of HF patients appears to be delayed recall. This memory dysfunction suggests specific neural damage related to the hippocampus or frontal lobe or associated circuitry, rather than generalized deficits over the entire brain.
Approximately one-half of chronic HF patients exhibit obstructive sleep apnea (OSA) or Cheyne-Stokes breathing during sleep. OSA cases show significant gray matter loss in cerebellar, insular, and cortical areas, which may contribute to abe
Contact: Donna Krupa
American Physiological Society