Takotsubo cardiomyopathy is the main explanation for ischemic electrocardiographic changes in near drowning

Abstract

We thank Dr Madias for his interest in our article regarding the causes of ischemic electrocardiographic (ECG) changes in near drowning [1]. We are both in agreement that the cause of these ECG changes is likely due to Takotsubo cardiomyopathy (TC) but not due to myocardial infarction from classic occlusive coronary artery disease (CAD). We also agree that given the consequences of missing the diagnosis of STsegment elevation myocardial infarction (STEMI), the diagnostic accuracy of the ECG criteria is insufficient to reliably differentiate TC from STEMI; and lack of occlusive CAD is crucial. Indeed, we have recommended that in subjects with chest pain and ST-segment elevation (STE)—which occurs in approximately half the cases of TC [2]— who present to hospitals equipped with catheterization suites, a higher pretest probability of TC should still provoke coronary angiography as the sole management modality not only to confirm the diagnosis but also to avert the use of thrombolytic therapy, which is not beneficial in TC and maybe harmful [3]. This is especially important in countries using thrombolytic therapy as the main management for STEMI. When analyzing causes of these ischemic ECG changes in near drowning, we have taken into consideration the patients’ age, sex, ECG features, echocardiography, and coronary angiogram—if available—in addition to the diagnosis provided by the authors. Five (50%) of the 10 cases with underwater events that we evaluated had confirmed diagnosis of TC by lack of occlusive CAD on angiogram in addition to ECG features that may favor TC; 4 of these 5 cases were women. When the 2 cases with underwater events but no evidence of water aspiration were excluded, 3 of 8 cases had confirmed TC. Among the remaining 5 of 8 cases, we have also questioned the provided diagnosis of myocardial infarction in 2 cases because of minimal troponin leak. Therefore, TC was felt to be the main pathology in near drowning cases. Nonetheless, we have provided a different explanation for ischemic ECG changes that occurred in the 2 young cases based on patients’ demographics, presentation, and the provided ECGs; and therefore, we disagree that TC can be an explanation for all cases. In these 2 adolescents, we speculated that the likely underlying pathophysiology for the ECG changes is coronary artery spasm and hypothermia, and have therefore included these 2 entities in the differential diagnosis of ischemic ECG changes in near drowning (following TC, which is the major cause). The first case was a 16-year-old gentleman reported by our team [4] who had an initial ECG showing STE in leads II, III, aVF, V5, and V6; a tall R wave with ST-segment depression in V2; and reciprocal ST-segment depression in leads I and aVL conforming to acute inferoposterolateral STEMI. The patient was transferred to the cardiac catheterization suite; however, a repeat ECG immediately before the procedure revealed resolution of STE with appearance of pathological Q waves in the inferolateral leads. Although STE in TC usually occurs in the anterior leads because of involvement of the apical myocardium, it islessfrequentlyencounteredintheinferiorleadsbecauseofaffection of the apical inferior myocardium. However, the classic territorial affection, the presence of reciprocal ST-segment depression, and the development of Q waves favor that a coronary occlusive process rather than TC is the likely etiology for these findings. Moreover, this patient had significant troponin elevation of greater than 50 ng/mL (reference range, 0-0.08); and TC patients rarely have significantly elevated troponin. In the second 16-year-old gentleman, ECG showed classic Osborn waves with saddleback STE in leads V4 through V6 recorded at a temperature of 28°C (without reciprocal ECG changes and not followed by Q waves) that resolved after temperature normalization [5]. Transient STE during hypothermia that subsides with rewarming was also reported by others [6,7]. In fact, this saddleback STE during hypothermia was similarly reported several times and was attributed to hypothermia