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. 2021 Feb 15;6(1):239-243.
doi: 10.1002/epi4.12452. eCollection 2021 Mar.

Takotsubo stress cardiomyopathy following explantation of sEEG electrodes

Pamela Sarkar  1   2 , John Graby  1 , Paul Walker  1 , Leyla Osman  1 , Marcus Bradley  1 , Marcus Likeman  1 , David R Sandeman  1 , Kasia A Sieradzan  1 , Claire M Rice  1   3
Affiliations

Takotsubo stress cardiomyopathy following explantation of sEEG electrodes

Pamela Sarkar et al. Epilepsia Open. .

Abstract

Objective: Takotsubo stress cardiomyopathy is characterized by dysfunction of the left ventricle of the heart including apical ballooning and focal wall-motion abnormalities. Although reported in association with seizures and intracerebral hemorrhage, there are no studies reporting its occurrence in patients having stereoelectroencephalography (sEEG).

Methods: A 38-year-old lady with no prior history of cardiac disease experienced sudden onset chest pain and acute left ventricular failure 4 hours following explantation of stereoelectroencephalogram electrodes.

Results: A small parenchymal hematoma related to the right posterior temporal electrode had been noted postelectrode insertion but was asymptomatic. Focal-onset seizures from nondominant mesial temporal structures were recorded during sEEG. Following the presentation with LVF, new-onset anterolateral T-wave inversion with reciprocal changes in leads II, III, and aVF was noted on electrocardiogram (ECG) and the chest X-ray findings were consistent with pulmonary edema. Echocardiography demonstrated hypokinesis of the cardiac apex and septum consistent with Takotsubo stress cardiomyopathy.

Significance: Awareness of the possible complication of Takotsubo stress cardiomyopathy is required in an epilepsy surgery program.

Keywords: Takotsubo stress cardiomyopathy; intracerebral hemorrhage; stereoelectroencephalography.

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Conflict of interest statement

None of the authors has any conflict of interest to declare. We confirm that we have read the Journal's position of issues involved in ethical publication and affirm that this report is consistent with those guidelines.

Figures

FIGURE 1
FIGURE 1
sEEG electrode placement and representative seizure. sEEG electrode placement was as illustrated (A and B): A‐R superior temporal 1 (deep contacts abnormal area insula)—8 contacts; B‐R superior temporal 2 (caudal, deep contacts post insula)—10 contacts; C‐R temporal pole (via T2, deep contacts in mesial ant temporal cortex)—8 contacts; D‐R amygdala (via T2 into amygdala)—12 contacts; E‐R hippocampus anterior (via T2 into R hippocampus ant)—12 contacts; F‐R temporal post (via posterior T2 into basal temporal lobe (fusiform)—12 contacts; G‐R temporal basal 1 (via T3, rostral exploring basal temp lobe)—10 contacts; H‐R temporal basal 2 (via T3, caudal exploring basal temp lobe)—10 contacts; I‐R frontal oblique 1 (rostral margin of lesion R middle frontal gyrus)—10 contacts; J‐R frontal oblique 2 (caudal margin of lesion R middle frontal gyrus)—10 contacts; K‐R frontal below the margin of scarring in F2, deep contact ant cingulate—10 contacts; L‐R orbitofrontal orthogonal—15 contacts; M‐R orbitofrontal oblique—into R gyrus rectus—15 contacts; N‐L orbitofrontal—(orthogonal or oblique targeting L gliosis in L gyrus rectus)—15 contacts; sEEG (C) demonstrates evolving mesial temporal discharge in the amygdala and anterior hippocampus spreading to the basal temporal and orbitofrontal cortices
FIGURE 2
FIGURE 2
ECG changes and chest X‐ray during presentation with acute chest pain. ECGs on admission (A) and during the acute episode (B) demonstrate new antero‐lateral T wave inversion with reciprocal changes in leads II, III and aVF. The chest X‐ray (C) appearances are consistent with pulmonary edema
FIGURE 3
FIGURE 3
Neuroimaging changes consistent with intracranial hemorrhage. T2 MRI (A) and FLAIR (B) of the brain demonstrate a hematoma in the right temporal lobe
See this image and copyright information in PMC

Comment in

References

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