title: Circadian body temperature variability is an indicator of poor prognosis in cardiomyopathic hamsters.
abstract: BACKGROUND
  Low body temperature is an independent predictor of poor prognosis in patients with congestive heart failure. The cardiomyopathic hamster develops progressive biventricular dysfunction, resulting in heart failure death at 9 months to 1 year of life. Our goal was to use cardiomyopathic hamsters to examine the relationship between body temperature and heart failure decompensation and death.
  
  
  RESULTS
  To this end, we implanted temperature and activity transducers with telemetry into the peritoneal space of 46 male Bio-TO-2 Syrian cardiomyopathic hamsters. Multiple techniques, including computing mean temperature, frequency domain analysis, and nonlinear analysis, were used to determine the most useful method for predicting poor prognosis. Data from 44 hamsters were included in our final analysis. We detected a decline in core body temperature in 98% of the hamsters 8+/-4 days before death (P < .001). We examined the dominant frequency of temperature variation (ie, the circadian rhythm) by using cosinor analysis, which revealed a significant decrease in the amplitude of the body temperature circadian rhythm 8 weeks before death (0.28 degrees C; 95% CI, 0.26-0.31) compared to baseline (0.36 degrees C; 95% CI, 0.34-0.39; P=.005). The decline in the circadian temperature variation preceded all other evidence of decompensation.
  
  
  CONCLUSIONS
  We conclude that a decrease in the amplitude of the body temperature circadian rhythm precedes fatal decompensation in cardiomyopathic hamsters. Continuous temperature monitoring may be useful in predicting preclinical decompensation in patients with heart failure and in identifying opportunities for therapeutic intervention.
authors.affiliation: Texas Heart Institute at St. Luke's Episcopal Hospital, 6770Bertner Avenue, Houston, TX 77030, USA. Amany.H.Ahmed@uth.tmc.edu
authors.forename: Amany
authors.initials: A
authors.lastname: Ahmed
authors.forename: Sreedevi
authors.initials: S
authors.lastname: Gondi
authors.forename: Casey
authors.initials: C
authors.lastname: Cox
authors.forename: Suwei
authors.initials: S
authors.lastname: Wang
authors.forename: Igor V
authors.initials: IV
authors.lastname: Stupin
authors.forename: K J
authors.initials: KJ
authors.lastname: Shankar
authors.forename: Shahzeb M
authors.initials: SM
authors.lastname: Munir
authors.forename: Ed
authors.initials: E
authors.lastname: Sobash
authors.forename: Alan
authors.initials: A
authors.lastname: Brewer
authors.forename: James J
authors.initials: JJ
authors.lastname: Ferguson
authors.forename: Macarthur A
authors.initials: MA
authors.lastname: Elayda
authors.forename: S Ward
authors.initials: SW
authors.lastname: Casscells
authors.forename: James M
authors.initials: JM
authors.lastname: Wilson
mesh_terms: D000818:Animals; D001831:Body Temperature / Q000502:physiology*; D009202:Cardiomyopathies / Q000401:mortality / Q000503:physiopathology; D002423:Cause of Death; D002940:Circadian Rhythm; D006224:Cricetinae; D004195:Disease Models, Animal; D018450:Disease Progression; D006333:Heart Failure / Q000401:mortality* / Q000503:physiopathology*; D008297:Male; D008991:Monitoring, Physiologic / Q000379:methods; D011336:Probability; D012680:Sensitivity and Specificity; D016019:Survival Analysis; D018487:Ventricular Dysfunction, Left / Q000401:mortality / Q000503:physiopathology; D018497:Ventricular Dysfunction, Right / Q000401:mortality / Q000503:physiopathology