title: Evaluation of Cardiovascular Risk Factors in the Wistar Audiogenic Rat (WAR) Strain.
abstract: BACKGROUND
  Risk factors for life-threatening cardiovascular events were evaluated in an experimental model of epilepsy, the Wistar Audiogenic Rat (WAR) strain.
  
  
  METHODS
  We used long-term ECG recordings in conscious, one year old, WAR and Wistar control counterparts to evaluate spontaneous arrhythmias and heart rate variability, a tool to assess autonomic cardiac control. Ventricular function was also evaluated using the pressure-volume conductance system in anesthetized rats.
  
  
  RESULTS
  Basal RR interval (RRi) was similar between WAR and Wistar rats (188 ± 5 vs 199 ± 6 ms). RRi variability strongly suggests that WAR present an autonomic imbalance with sympathetic overactivity, which is an isolated risk factor for cardiovascular events. Anesthetized WAR showed lower arterial pressure (92 ± 3 vs 115 ± 5 mmHg) and exhibited indices of systolic dysfunction, such as higher ventricle end-diastolic pressure (9.2 ± 0.6 vs 5.6 ± 1 mmHg) and volume (137 ± 9 vs 68 ± 9 μL) as well as lower rate of increase in ventricular pressure (5266 ± 602 vs 7320 ± 538 mmHg.s-1). Indices of diastolic cardiac function, such as lower rate of decrease in ventricular pressure (-5014 ± 780 vs -7766 ± 998 mmHg.s-1) and a higher slope of the linear relationship between end-diastolic pressure and volume (0.078 ± 0.011 vs 0.036 ± 0.011 mmHg.μL), were also found in WAR as compared to Wistar control rats. Moreover, Wistar rats had 3 to 6 ventricular ectopic beats, whereas WAR showed 15 to 30 ectopic beats out of the 20,000 beats analyzed in each rat.
  
  
  CONCLUSIONS
  The autonomic imbalance observed previously at younger age is also present in aged WAR and, additionally, a cardiac dysfunction was also observed in the rats. These findings make this experimental model of epilepsy a valuable tool to study risk factors for cardiovascular events in epilepsy.
authors.affiliation: Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
authors.forename: Rubens
authors.initials: R
authors.lastname: Fazan
authors.affiliation: Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
authors.forename: Carlos Alberto A
authors.initials: CA
authors.lastname: Silva
authors.affiliation: Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
authors.forename: José Antônio Cortes
authors.initials: JA
authors.lastname: Oliveira
authors.affiliation: Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
authors.forename: Helio Cesar
authors.initials: HC
authors.lastname: Salgado
authors.affiliation: Department of Clinical Sciences "Luigi Sacco", University of Milan, Milan, Italy.
authors.forename: Nicola
authors.initials: N
authors.lastname: Montano
authors.affiliation: Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
authors.forename: Norberto
authors.initials: N
authors.lastname: Garcia-Cairasco
mesh_terms: D000161:Acoustic Stimulation / Q000009:adverse effects*; D000818:Animals; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000473:pathology; D004195:Disease Models, Animal; D004562:Electrocardiography; D020195:Epilepsy, Reflex / Q000150:complications* / Q000473:pathology; D006339:Heart Rate; D008297:Male; D051381:Rats; D011922:Rats, Mutant Strains; D017208:Rats, Wistar; D012307:Risk Factors; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000473:pathology