<p>Obesity is a recognized risk factor for cardiovascular morbidity and mortality, however its impact on survival following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) remains controversial. Therefore, the aim of this study was to evaluate the feasibility of a preclinical model of CA/CPR in obese rats as well as 72-hour (h) survival, and investigate the effect of obesity on myocardial dysfunction post-CA/CPR. Rats were subjected to 6&#xa0;min of untreated ventricular fibrillation and to 6&#xa0;min of CPR. Hemodynamic parameters were continuously recorded up to 4&#xa0;h, serial blood samples were collected and echocardiography was performed at 2 and 4&#xa0;h after resuscitation. Rats were sacrificed 72 and 4&#xa0;h after resuscitation. After CA, no obese rats survived up to 72&#xa0;h compared to controls whereas each rat developed marked post- return of spontaneous circulation hemodynamic impairment during the 4&#xa0;h observation; obese rats showed an impairment in diastolic function as well as a significant increase in troponin T plasma concentration compared to controls. This could support that obesity negatively impacts survival, hemodynamic stability and left ventricular function after CA.</p>

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Impact of obesity on myocardial function and survival after cardiac arrest and cardiopulmonary resuscitation in a rat model

  • Marianna Cerrato,
  • Daria De Giorgio,
  • Aurora Magliocca,
  • Elisa Roncati Zanier,
  • Giuseppe Ristagno,
  • Francesca Fumagalli

摘要

Obesity is a recognized risk factor for cardiovascular morbidity and mortality, however its impact on survival following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) remains controversial. Therefore, the aim of this study was to evaluate the feasibility of a preclinical model of CA/CPR in obese rats as well as 72-hour (h) survival, and investigate the effect of obesity on myocardial dysfunction post-CA/CPR. Rats were subjected to 6 min of untreated ventricular fibrillation and to 6 min of CPR. Hemodynamic parameters were continuously recorded up to 4 h, serial blood samples were collected and echocardiography was performed at 2 and 4 h after resuscitation. Rats were sacrificed 72 and 4 h after resuscitation. After CA, no obese rats survived up to 72 h compared to controls whereas each rat developed marked post- return of spontaneous circulation hemodynamic impairment during the 4 h observation; obese rats showed an impairment in diastolic function as well as a significant increase in troponin T plasma concentration compared to controls. This could support that obesity negatively impacts survival, hemodynamic stability and left ventricular function after CA.