Physiological mechanisms associated with cognitive impairment in heart failure patients

  • Ms Christina Kure, Brain Sciences Institute, Swinburne University of Technology, Australia
  • Prof Franklin Rosenfeldt, Department of Cardiothoracic Surgery, Alfred Hospital, Australia
  • Prof Con Stough, Brain Sciences Institute, Swinburne University of Technology, Australia
  • Prof Andrew Scholey, Brain Sciences Institute, Swinburne University of Technology, Australia
  • Dr Andrew Pipingas, Brain Sciences Institute, Swinburne University of Technology, Australia
  • Prof David Kaye, Heart Failure Research Group, Baker IDI Heart and Diabetes Institute, Australia
  • Dr Peter Bergin, Heart Centre, Alfred Hospital, Australia
  • Prof Stephen Myers, School of Health and Human Sciences, Southern Cross University, Australia

Background: Cognitive impairment (CI) is common in heart failure (HF), especially in older patients. CI may reduce the patient’s ability to understand and comply with therapeutic regimes, increase hospital readmissions and mortality rates. Understanding the mechanisms associated with CI in HF may facilitate development of interventions to potentially preserve cognitive function at various stages of the condition. Previous research indicates that CI may be underpinned by changes in cerebral blood flow (CBF), however the effects of inflammation and oxidative-stress have not been investigated.
Objective: To investigate whether inflammation and oxidative-stress are associated with CI in older HF patients.
Methods: Well established measures of memory, attention and mood were administered to HF patients and a healthy control group matched for age, sex and IQ. Biochemical measures included high sensitive C-reactive protein (hsCRP), biological antioxidant potential (BAP), determinable reactive oxygen metabolites (d-ROM), CBF and arterial stiffness.
Results: To date 20 of a projected 30 HF patients (67.10±6.34 years; 70% male; NYHA class II-III) and 38 healthy controls (67.13±5.29 years; 53% male) have completed the study. Preliminary results show that in patients hsCRP was significantly correlated with the following subscales of Profile of Mood States: depression/dejection (r=.595, p=.005); vigour (r=-.550; p<.001) but not in controls: depression/dejection (r=.079, p=.360), vigour (r=-.321; p=.068). d-ROM, BAP, CBF, arterial stiffness and further cognitive data are currently being analysed. Enrolment is continuing to a projected total of 30 HF patients.
Conclusions: Inflammation may contribute to depression and reduced vigour in HF potentially leading to novel therapeutic regimes.