To the Editor,
We have read with interest the study by Y.S. Cha and colleagues investigating organophosphate (OP) poisoning and myocardial injury.Citation1 The authors conclude that OP poisoning can cause direct myocardial injury during the acute phase of poisoning as well as that trending serum troponin I concentration may be needed in severe OP poisoning. However, these data presented from this retrospective study raise some questions as to the author's interpretation.
Based on 34% of their subjects having elevated troponin I concentration, the authors conclude that severe OP poisoning can cause direct myocardial injury. The highest troponin I level reached was 2.33 ng/ml and the mean elevation was only 0.305 ng/ml. These seemingly trivial elevations make it difficult to determine the relationship of OP poisoning as a cause of direct myocardial injury. Rather, these elevations could be related to demand ischemia and “troponin leak” in severely poisoned patients. Furthermore, were there any overt signs of cardiac injury or clinical significance to this troponin elevation? Only 26% of these patients with elevated troponins experienced hypotension, and there was no statistical difference in B-type natriuretic peptide (BNP) concentrations, suggesting that the patients did not have acute heart failure.
The patients found to have troponin I elevations were different in a number of pertinent demographic variables. Namely, those patients with troponin I elevations were older, had a lower initial Glasgow Coma Scale (GCS), higher Namba classification, a higher incidence of mechanical ventilation, and higher rates of pneumonia. These patient discrepancies would simply indicate that a more severely ill patient population is more likely to have elevations in troponin I.
Multiple studies have demonstrated elevated troponin I levels in critically ill patients without acute coronary syndromes (ACS), suggesting that sepsis and other systemic inflammatory response syndrome (SIRS)-related disease processes account for these elevations.Citation2–4 Here, the authors found no statistical significance in the difference between the two groups with respect to sepsis; however, they did not discuss how they controlled for this specific variable. Also, only 18.2% of patients had troponin I elevations on initial presentation suggesting that other confounding variables while in hospital may have attributed to the remainder of troponin I elevations. Moreover, previous studies have shown that mechanical ventilation alone increases mortality in critically ill patients with suggested myocardial injury.Citation5
Mechanical ventilation was required for 91.2% of their cohort. Could this be attributed to the observed troponin I elevations?
We commend the author's efforts in identifying troponin I elevations in patients with OP poisoning. However, based on these data, it seems more plausible that the troponin I elevations are likely due to some other physiologic process rather than direct cardiac injury. An interesting question for future investigation would be evaluating the prognostic value of troponin I elevation in this setting with regard to morbidity and mortality.
Declaration of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
- Cha YS, Kim H, Go J, Kim TH, Kim OH, Cha KC, et al. Features of myocardial injury in severe organophosphate poisoning. Clin Toxicol (Phila) 2014; 52:873–879.
- Favory R, Neviere R. Significance and interpretation of elevated troponin in septic patients. Crit Care 2006; 10:224.
- Ammann P, Maggiorini M, Bertel O, Haenseler E, Joller-Jemelka HI, Oechslin E, et al. Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes. J Am Coll Cardiol 2003; 41:2004–2009.
- Roongsritong C, Warraich I, Bradley C. Common causes of troponin elevations in the absence of acute myocardial infarction: incidence and clinical significance. Chest 2004; 125:1877–1884.
- Frazier SK, Brom H, Widener J, Pender L, Stone KS, Moser DK. The prevalence of myocardial ischemia during mechanical ventilation and weaning and its effects on weaning success. Heart Lung 2006; 35:363–373.