Does Obesity Influence the Outcome of the Patients Following a Cardiac Arrest?

INTRODUCTION

Out-of-hospital cardiac arrest is a leading cause of death, with an estimated 15,000 people suffering a cardiac arrest in Australia every year.¹ Between 12% and 25% of out-of-hospital cardiac arrest, victims in Australia survive to hospital discharge.¹ Recent Australian observational study by ANZ-CODE investigators showed that 26.3% of in-hospital cardiac arrest patients survive hospital discharge.² Older age, cardiac arrest occurring at home, initial rhythm other than ventricular fibrillation and ventricular tachycardia, longer duration of no flow, longer duration of low flow, and treatment with adrenaline are known independent predictors of poor outcome after cardiac arrest.³

In recent times, obesity has emerged as one of the biggest health issues involving all age groups worldwide. It is one of the major risk factors for cardiovascular and peripheral vascular disease. However, obesity is associated with a lower mortality risk after cardiac surgery⁴ and with heart failure patients.⁵

Studies examining obese patients who suffered cardiac arrest provided conflicting results.^6–10 The American Heart Association National Registry of Cardiopulmonary Resuscitation (NRCPR) demonstrated a higher rate of survival to discharge for overweight and obese patients compared with underweight and normal-weight patients with cardiac arrest caused by shockable rhythms.⁸ In contrast, body mass index (BMI) was not associated with in-hospital mortality in those who underwent extracorporeal cardiopulmonary resuscitation (ECPR).⁹ Body mass index ≥30 kg/m² was shown to be a significant risk factor for mortality post-therapeutic hypothermia following cardiac arrest.¹⁰ Moreover, there is a lack of research on this topic from Australia. Therefore, we conducted this study to understand the association between obesity and mortality in patients following cardiac arrest.

MATERIALS AND METHODS

RESULTS

A total of 126 patients were admitted to the ICU following in-hospital (38) or out-of-hospital (74) cardiac arrest, from which 14 patients were excluded because of missing BMI data. Out of 112 patients, 76 patients had calculated BMI <30 and 36 patients had BMI ≥30.

The demographic characteristics of patients are summarized in Table 1. The mean age was similar between the two groups (61.7 vs 61.1 years). Both groups had more males than females. The obese (BMI ≥30) group more commonly had diabetes (47 vs 32%) and hypertension (61 vs 36%).

There was no difference in the primary outcome of survival to hospital discharge between obese (BMI ≥30) and non-obese (BMI <30) groups (52.8 vs 59.2%, p = 0.52, OR = 0.77, 95% CI 0.35–1.71; Table 2 and Fig. 1). There was no difference between non-obese and obese patients in ICU length of stay (76.0 vs 81.5 hours, p = 0.42; Table 3), hospital length of stay (10 vs 9 days, p = 0.63; Table 3), and duration of mechanical ventilation (43 vs 55 hours, p = 0.30; Table 3).

On subgroup analysis, there was a trend toward better survival in non-obese patients who had initial shockable rhythm (OR = 0.39, 95% CI 0.11–1.38, p = 0.15; Table 4).

In the logistical regression analysis, BMI was not associated with improved survival (OR = 0.97, 95% CI 0.92–1.03, p = 0.23, Table 5). There was a better survival with in-hospital cardiac arrest (OR = 2.94, 95% CI 1.02–8.49, p = 0.05) and initial shockable rhythm (OR = 3.74, 95% CI 0.94–14.82, p = 0.06) independent of BMI.

DISCUSSION

We could not show that obesity improves survival to hospital discharge among the patients admitted to the ICU following a cardiac arrest. Moreover, we found that obesity does not affect hospital or ICU length of stay or duration of mechanical ventilation.

There is an impression that obesity confers some survival advantages in heart failure and cardiac surgery.^4–6,12 This inverse correlation between BMI and mortality is known as the obesity paradox. Greater metabolic reserve, younger age, and better cardioprotective medical therapy to obese patients are some hypotheses postulated for this phenomenon. Saba et al. showed that higher BMI is associated with lower all-cause mortality in the survivor of sudden cardiac arrest, suggesting the obesity paradox also applies to the post-cardiac arrest population.⁶ In contrast, a single-center trial by Breathett et al. demonstrated BMI <30 compared with BMI ≥30 was associated with better survival post-hypothermia for cardiac arrest.⁹

In our study, we could not demonstrate that obesity confers survival benefit to patients who suffer cardiac arrest. We noted better survival to hospital discharge for the non-obese group. Although this difference was statistically non-significant, a 6.4% absolute difference in mortality in favor of non-obese can be clinically important. Possible explanations behind this observation of statistical non-significance include unequal distribution of patient population between two groups, inadequate sample size, or the absence of any protective effect associated with obesity.

There are possible reasons which may account for reduced survival in patients with a high BMI following cardiac arrest. There is a potential role of visceral adipose tissue as a source of inflammation and promoter of atherosclerosis.¹³ The intra-abdominal and epicardial space are two compartments that contain visceral fats which are metabolically active and are the source of humoral and cellular inflammation in obese patients. These visceral fats secrete large numbers of cytokines and free fatty acids which have been associated with arrhythmias and sudden cardiac death. Moreover, it has been reported that sagittal abdominal diameter and waist-hip ratio are associated with an increased risk of sudden cardiac death independent of BMI.^10,14

This study is the first trial from Australia to our knowledge which has explored the association between obesity and outcome following a cardiac arrest. This retrospective study was conducted in a major tertiary university teaching hospital that serves a large heterogeneous group of patients. We included all consecutive cardiac arrest patients without any selection to minimize bias and used objective clinical endpoints, such as, survival to hospital discharge, length of stay, and duration of mechanical ventilation as an outcome for our study.

There are several limitations to our study. It is a single-center and retrospective study. We excluded 14 (11%) patients due to a lack of available measurements for either height or weight or both. We did not follow-up patients for a functional outcome, so it remains unknown whether the patient’s BMI at the time of their cardiac arrest impacts their neurological or another recovery. In addition, given the retrospective nature of this study other anthropology measurements like sagittal abdominal diameter and waist-hip ratio were not collected.

Our study provides baseline data from an Australian center regarding outcomes following cardiac arrest in obese patients. Although our sample size was small and the difference between the two groups for the primary outcome was statistically non-significant, a 6.4% absolute difference in primary outcome in favor of non-obese can be important. If this difference is present, any future study would need approximately 1,880 patients (considering 80% study power and α = 0.05) and multicenter participation. Our study may inform future investigators who seek to undertake prospective studies in this area regarding the effects of obesity on hospital survival, length of stay, or duration of mechanical ventilation with regards to sample size determinations.

CONCLUSION

We could not show that obesity (BMI ≥ 30) contributes to either a protective or harmful effect among the patients following either an in-hospital or out-of-hospital cardiac arrest. Further larger studies would be required to determine the impact of obesity on the outcome of patients following cardiac arrest.

REFERENCES

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