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Published in: Critical Care 1/2020

01-12-2020 | Central Nervous System Trauma | Research Letter

A longitudinal cohort of stress cardiomyopathy assessed with speckle-tracking echocardiography after moderate to severe traumatic brain injury

Authors: Raphaël Cinotti, Thierry Le Tourneau, Kalyane Bach-Ngohou, Maxime Le Courtois du Manoir, Bertrand Rozec, Karim Asehnoune

Published in: Critical Care | Issue 1/2020

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Excerpt

Stress cardiomyopathy is common after subarachnoid haemorrhage (SAH): 36% of patients display stress cardiomyopathy patterns assessed with speckle-tracking echography [1], which is a gold standard in the evaluation of left ventricular longitudinal systolic function. After traumatic brain injury (TBI), stress cardiomyopathy has been little described [2]. We performed a monocentric longitudinal study in moderate to severe TBI patients (Glasgow coma score ≤ 12). Consecutive patients were included. This study was approved by the local ethics committee (Groupe Nantais d’Ethique dans le Domaine de la Santé – IRB No. 6.02.2014). We a priori decided to include 100 patients in order to potentially detect 30 patients with sub-clinical stress cardiomyopathy [1]. The primary goal was to assess the incidence of stress cardiomyopathy with speckle-tracking echocardiography and the evolution of the global longitudinal strain (GLS) at day 1, day 3, and day 7. The secondary outcomes were the evolution of 2-dimensional echocardiographic parameters (LVEF, mitral E/A and E/E’ ratio, mitral S wave, TAPSE). Since stress cardiomyopathy is due to a major catecholamine increase in plasma [3], we explored the adrenergic response by comparing baseline blood levels of metanephrine and normetanephrine in patients with TBI and SAH admitted in our institution, matched on age and baseline GCS (biocollection IBIS – NCT 02426255). We included 100 patients from March 2014 to August 2017. The mean age was 42.6 (± 19.6) years and the baseline Glasgow coma score was 7 [4–10]. We included 75 (75%) male and 25 (25%) female patients. Twenty (20%) patients died in the ICU. At day 1, GLS (− 20.3 [± 3.6]%) and LVEF (66 [± 11]%) were preserved. The mean GLS was preserved at day 3 (− 22.2 [± 3.6] %) and at day 7 (− 20.7 [± 3.3] %). Nine (9%) patients displayed impaired GLS (− 13.3[− 14.5; − 11.6]%) at baseline. In these patients, there was a significant improvement at day 3 (− 22.2 [− 25.1; − 18.7]%) and day 7 (− 21.1 [− 23.2; − 18.1]%) (p < 0.0001), compatible with stress cardiomyopathy. These 9 patients had the same age (32 [23–48] vs 46 [23–60], p = 0.4), had a non-significant baseline ultra-sensitive troponin increase (16 [8–229] vs 9 [5–29] ng/mL−1, p = 0.1), and had similar Glasgow (10 [3–12] vs 7 [4–9], p = 0.3) and Marshall scores (p = 0.8) compared to the rest of the cohort. Three patients suffered from isolated TBI, and two from TBI associated with mild abdominal trauma or vertebral fracture, all due to road traffic accidents. The remaining four patients suffered from isolated TBI after a fall. These mechanisms did not seem to differ from the rest of the cohort. …
Literature
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go back to reference Cinotti R, Piriou N, Launey Y, Le Tourneau T, Lamer M, Delater A, et al. Speckle tracking analysis allows sensitive detection of stress cardiomyopathy in severe aneurysmal subarachnoid hemorrhage patients. Intensive Care Med. 2016;42:173–82.CrossRef Cinotti R, Piriou N, Launey Y, Le Tourneau T, Lamer M, Delater A, et al. Speckle tracking analysis allows sensitive detection of stress cardiomyopathy in severe aneurysmal subarachnoid hemorrhage patients. Intensive Care Med. 2016;42:173–82.CrossRef
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go back to reference Krishnamoorthy V, Rowhani-Rahbar A, Gibbons EF, Rivara FP, Temkin NR, Pontius C, et al. Early systolic dysfunction following traumatic brain injury. Crit Care Med. 2017;45:1028–36.CrossRef Krishnamoorthy V, Rowhani-Rahbar A, Gibbons EF, Rivara FP, Temkin NR, Pontius C, et al. Early systolic dysfunction following traumatic brain injury. Crit Care Med. 2017;45:1028–36.CrossRef
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go back to reference Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE. Stress (Takotsubo) cardiomyopathy—a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med. 2008;5:22–9.CrossRef Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE. Stress (Takotsubo) cardiomyopathy—a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med. 2008;5:22–9.CrossRef
Metadata
Title
A longitudinal cohort of stress cardiomyopathy assessed with speckle-tracking echocardiography after moderate to severe traumatic brain injury
Authors
Raphaël Cinotti
Thierry Le Tourneau
Kalyane Bach-Ngohou
Maxime Le Courtois du Manoir
Bertrand Rozec
Karim Asehnoune
Publication date
01-12-2020
Publisher
BioMed Central
Published in
Critical Care / Issue 1/2020
Electronic ISSN: 1364-8535
DOI
https://doi.org/10.1186/s13054-020-02935-1

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