Response letter to the editor. “Troponin I elevations and organophosphate poisoning: direct cardiac injury or demand ischemia?”

To the Editor:

Above all, thank you for your great interest in our paper. We were worried about comments of Dr. Repplinger et al., when we analyzed data. We wanted to know why troponin I was elevated. Of course, we thought about the possibility of troponin I elevation as secondary change (hypoxia, hypotension, atropine use, adrenergic drug use, sepsis, etc.). In organophosphate poisoning, even though it is possible to develop sepsis mostly due to pneumonia later, sepsis or sepsis-like syndrome in early phase directly caused by organophosphate poisoning is unknown. Therefore, we have assumed that elevation of troponin I was not caused by sepsis or sepsis-like syndrome.¹ The elevation of troponin I might be caused by other secondary effect of the poisoning. However, we thought that troponin I elevation cannot be explained by only secondary effects. Therefore, we analyzed to exclude the effect of initial shock, hypoxia, and atropine dosage for 48 h among myocardial injury patients. We also only included the troponin I within 48 h after arrival at ED to minimize possible occurrence of delayed conditions after admission that might increase troponin I.

As we have shown in discussion, in non-shock and non-hypoxia patients, myocardial injury was 31.3% and 34.3%, respectively; this result was similar to the total myocardial injury percent (34.3%). There was no statistical difference between the two groups in terms of atropine dosage for 48 h. Therefore, we thought that the secondary elevation of troponin I may be due to another mechanism which might cause direct myocardial injury. In other words, we would suggest the possibility of direct myocardial injury in severe organophosphate poisoning.

We used high-sensitivity TnI (Siemens Healthcare Diagnostics Inc., Newark, DE, USA) and reference range was less than 0.046 ng/ml. The median maximum of TnI level in this study was about 6.6 times the reference range. Of course, as per your comments, the median maximum of TnI level (0.305 ng/mL) was relatively low compared with that in other myocardial injuries, such as myocardial infarction and myocarditis.² Even though BNP was higher in patients with elevated TnI, there was no statistical difference between the two groups (p = 0.052) and BNP values of both groups were within the normal range (< 100 pg/mL). This may mean that myocardial injury related to OP is not enough to cause ventricular dysfunction. Therefore, I think that further studies should be required to clarify these results as per your comments and we have been studying about transthoracic echocardiography to investigate cardiac dysfunction in organophosphate-poisoned patient with elevated troponin I.

I hope that this short explanation will help to better understand our study. We thank you for your concern once again.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.