Abstract
We read with interest the article by Libersa et al. (2023) reporting on a 41-year-old woman who presented with mid-ventricular Takotsubo syndrome (TTS) after complete avalanche burial. Glasgow Coma Scale at extrication was 3. On admission she was tachypneic, tachycardic, hypothermic, and hypotensive. Electrocardiography (ECG) showed atrial fibrillation. There was lactic acidosis with a pH of 7.16 and a serum lactate of 11.8 mM. She recovered completely and was discharged after 5 days. The study is compelling but has limitations that should be discussed.
We disagree with the statement that the ECG did not contain evidence of acute ischemia. The ECG showed inverted T-waves in aVR, aVL, V1–V3, and Q-waves in aVR, V1, and V2 after spontaneous resolution of atrial fibrillation, suggesting myocardial ischemia. Another argument for myocardial ischemia is the greatly increased troponin T. Creatine-kinase values are missing. They could be high not only due to myocardial ischemia but also due to rhabdomyolysis or crush syndrome.
A limitation of the study is that no coronary angiography was performed. Because TTS is typically diagnosed using the revised Mayo Clinic criteria, it is imperative to rule out obstructive coronary artery disease or acute plaque rupture before diagnosing TTS (Boyd and Solh, 2020). A pheochromocytoma and myocarditis must also be ruled out according to these criteria (Boyd and Solh, 2020). The exclusion of myocardial ischemia is particularly important since the high-sensitive troponin T was elevated to 241 ng/l (normal <5 ng/l). According to the revised Mayo Clinic criteria, troponin T should only be slightly elevated in TTS (Boyd and Solh, 2020). It is not reported whether the index patient was a smoker or an alcoholic.
Another limitation is that no pro-brain natriuretic peptide (proBNP) was determined. Since the ejection fraction was reduced to 41% and TTS can be complicated by heart failure (Matta and Carrie, 2023), it is imperative to measure proBNP to assess the degree of heart failure.
Since the patient was initially unconscious, it would have been crucial to perform not only cerebral computed tomography but also magnetic resonance imaging to determine if hypoxia caused structural damage, particularly of the cortex and the basal ganglia (Muttikkal and Wintermark, 2013). In addition, it would have been interesting to perform neuropsychological tests after recovery to determine whether cerebral hypoxia resulted in long-term cognitive deficits. It would have been also crucial to record an electroencephalogram to determine whether coma was due to nonconvulsive status epilepticus.
Another limitation is that she did not undergo electrophysiological studies after recovery to determine if there was a predisposition to supraventricular or ventricular arrhythmias. In addition to physical and psychological stress, TTS could also be due to atrial fibrillation, lactic acidosis, hypoxia, or hypothermia.
In summary, this interesting study has limitations that put the results and their interpretation into question. Addressing these issues would strengthen the conclusions and could improve the status of the study. Before the diagnosis of TTS, coronary artery disease must be ruled out by coronary angiography, especially in patients with severely elevated troponin T.