title: Postresuscitation myocardial diastolic dysfunction following prolonged ventricular fibrillation and cardiopulmonary resuscitation.
abstract: OBJECTIVE
  Postresuscitation myocardial dysfunction is one of the leading causes of early death after successful resuscitation from sudden death. However, the diastolic characteristics of postresuscitation myocardial dysfunction are not well defined. We therefore investigated the postresuscitation left ventricular diastolic function following prolonged cardiac arrest and subsequent cardiopulmonary resuscitation.
  
  
  METHODS
  Prospective, observational animal study.
  
  
  METHODS
  Medical research laboratory in a university-affiliated research and educational institute.
  
  
  METHODS
  Domestic pigs.
  
  
  METHODS
  Seven anesthetized pigs (40 +/- 4 kg) were studied before and after 7 mins of untreated occlusive ventricular fibrillation induced cardiac arrest. Ejection fraction, early and atrial peak transmitral flow velocities, deceleration time of early transmitral flow velocity, myocardial performance index, peak Emax and Amax mitral annulus velocities by Doppler tissue imaging, and early diastolic left ventricular flow propagation velocity were measured at baseline; 60, 120, 180, and 240 mins; and 72 hrs after resuscitation.
  
  
  RESULTS
  Five animals were successfully resuscitated. Left ventricular ejection fraction, E(m)/A(m) ratio, and propagation velocity were significantly decreased, and myocardial performance index was significantly increased compared with baseline measurements. Left ventricular diastolic and systolic function returned to baseline level at 72 hrs postresuscitation.
  
  
  CONCLUSIONS
  Left ventricular systolic dysfunction was significantly impaired after cardiac arrest and cardiopulmonary resuscitation, as previously demonstrated. This was associated with a profound left ventricular diastolic dysfunction. However, this postresuscitation left ventricular systolic and diastolic myocardial dysfunction was reversible after 72 hrs in this experimental model of ventricular fibrillation cardiac arrest.
authors: Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA.
authors: Tingyan
authors: T
authors: Xu
authors: Wanchun
authors: W
authors: Tang
authors: Giuseppe
authors: G
authors: Ristagno
authors: Hao
authors: H
authors: Wang
authors: Shijie
authors: S
authors: Sun
authors: Max Harry
authors: MH
authors: Weil
mesh_terms: D000818:Animals; D016887:Cardiopulmonary Resuscitation / Q000009:adverse effects*; D004195:Disease Models, Animal; D054144:Heart Failure, Diastolic / Q000209:etiology*; D013318:Stroke Volume; D034421:Sus scrofa; D018487:Ventricular Dysfunction, Left / Q000209:etiology; D014693:Ventricular Fibrillation / Q000150:complications* / Q000628:therapy*