Echocardiographic assessment of myocardial dysfunction in perinatal asphyxia

We thank Kumar and Yadav for their interest in our case— control study which aimed to assess myocardial dysfunction as a predictor of the severity andmortality of hypoxic ischaemic encephalopathy in severe perinatal asphyxia and their knowledgeable comments. We acknowledge that calculating the odds of having myocardial dysfunction in severe perinatal asphyxia and theodds ofmortality in neonates with myocardial dysfunction would have been more useful in prognostication, but our study reported myocardial dysfunction in all asphyxiated neonates so odds ratios cannot be calculated. One concern was demonstrating the association between the severity of myocardial dysfunction and mortality with various stages of hypoxic ischemic encephalopathy (HIE). This association is clearly mentioned in the article. In the asphyxia group, serum creatinine kinase total (p<0.001), creatinine kinase MB (p<0.001), troponin-T (p=0.002) level, electrocardiographic (ECG) changes (p<0.001) and echocardiographic (echo) parameters [left ventricular ejection fraction (LVEF) p<0.001, right ventricular ejection fraction (RVEF) p<0.001] and right cardiac wall motion abnormality (p=0.03) showed increasing abnormalities with increasing severity of HIE and the differences between different grades were significant (p<0.05). In addition, the mean serum levels of CK-T (p<0.001), CKMB (p<0.001) and troponin-T (p=0.002) were significantly higher in the non-survivors, and mean LVEF and RVEF values were higher in the survivors (p<0.001) [1]. Another concern was whether or not there was actual myocardial dysfunction (defined as LVEF <55% and RVEF <35%). Myocardial dysfunction was not defined solely on the basis of echo abnormalities. Asphyxiated neonates with elevated cardiac enzymes (CK-T >190 IU/L or CKMB >25 IU/L or troponinT-positive, >0.1 ng/ml) or having ECG abnormalities were considered to have myocardial involvement. In the asphyxia group, three (13%) neonates had cardiac involvement as per echo abnormalities [1]. We agree that the mean LVEF and RVEF values in the asphyxiated group were within the normal range. This can be explained by recovery of cardiac function in the first 24 h after vigorous resuscitation and clinical management as we performed echo within a predefined window of 24–72 h. Kanik et al. reported that echo abnormalities such as left ventricular dysfunction may be obscured by compensatory mechanisms in the early days of life in asphyxiated neonates [2]. Moller et al. also reported similar results and suggested that left ventricular dysfunction was a late change in severe perinatal asphyxia [3]. In addition, we took a low cut-off value of LVEF (<55%) and RVEF (<35%) to define myocardial dysfunction. Past studies have used a cut-off value of <60% to define LVEF dysfunction [2,4]. We agree with Kumar and Yadav that EF reflects only systolic function and is not a good marker of overall myocardial dysfunction. That diastolic dysfunction was not assessed is a limitation of the study. In summary, we believe that the study has a few limitations with respect to echo abnormalities and that the results would have been more accurate and useful if diastolic dysfunction in asphyxiated neonates had also been assessed.