neuro - cardiogenic interaction has been known for many years.1)2 ) an excessive release of catecholamines , known as a trigger of takotsubo cardiomyopathy ( tc ) , is developed when sympathetic nervous system is hyperactivated in stressful conditions including cerebral seizure .
cerebral seizure has been reported as a cause of tc internationally , and cardiac complications are one of the main causes of mortality in epilepsy.3)4 ) biventricular tc is associated with more hemodynamic instability than isolated left ventricular tc .
therefore , in that case , medical treatment should be more invasive and the course of hospitalization is longer.5 ) but , there has been no case report describing biventricular tc after cerebral seizure in korea . here ,
we report a case of a patient who presented with initial echocardiography showing biventricular apical ballooning after status epilepticus .
an 83-year - old female presented to our emergency room with 2 episodes of 10 minute - duration of generalized tonic - clonic seizures at home and in the ambulance .
blood pressure ( bp ) was 160/100 mm hg , pulse rate was 105/min , respiration rate was 22/min , and body temperature was 37.0. peripheral oxygen saturation was 96% with oxygen flow of 6 l / min via facial mask .
she had an epilepsy 7 years prior to this attack after cerebral hemorrhage on left parietal and right temporal lobe .
she was on donepezil 10 mg , methylphenidate 10 mg , choline alfoscerate 400 mg , acetyl l - carnitine 500 mg , trifrusal 300 mg because of her vascular dementia .
she was independent in her activities of daily living and had never complained about chest pain or dyspnea before the admission .
when she was admitted , there was another 5-minute duration of generalized tonic - clonic seizure with conjugate deviation of the eyes to the right .
status epilepticus was terminated after intravenous lorazepam 4 mg injection and phenytoin 750 mg infusion .
but bp was dropped from 160/100 mm hg to 70/40 mm hg and her consciousness was impaired .
chest x - ray showed cardiomegaly and patchy increased opacities in right upper and lower lobes ( fig .
1 ) . arterial blood gas analysis showed a metabolic acidosis ( ph : 7.24 , pao2 : 70 mm hg , paco2 : 39 mm hg , hco3- : 16.7 mmol / l ) .
a diffusion - weighted magnetic resonance brain imaging showed localized encephalomalacic lesions in left parietal lobe and right temporal pole region with peripheral old blood product deposition .
division of cardiology was called for suspecting st elevation myocardial infarction ( stemi ) since an electrocardiogram ( ecg ) showed precordial v2 - 4 st segment elevation and she was found to have elevated cardiac enzymes on serial measurements ( troponin i levels 0.62
2 ) . there was no evidence of pericarditis or pheochromocytoma from her history , clinical symptoms , laboratory findings and echocardiographical features .
an emergency transthoracic echocardiography ( tte ) showed an apical ballooning of the left ventricle ( lv ) with severe systolic dysfunction ( lv ejection fraction = 23% by simpsons methods ) and focal hypokinesia of right ventricular ( rv ) apex with decreased rv systolic function .
fractional area change ( fac ) , [ ( rv end diastolic area - rv end systolic area ) / rv end diastolic area  100 ] was 22 % , tricuspid annular plane systolic excursion was 20 mm .
despite tte finding was accordant with tc , emergency coronary angiography was done since we suspected stemi .
there was no significant stenosis in left anterior descending artery , left circumflex artery and right coronary artery .
however , hypokinesia of the mid to apical lv and rv from tte were discordant with coronary artery lesion .
she had no further epileptic seizures during hospitalization with sodium valproate 300 mg every 12 hours and initial metabolic acidosis was resolved .
after supportive care with standard heart failure therapy ( aspirin ,  - blocker , angiotensin converting enzyme inhibitor , 3-hydroxy-3-methylglutaryl - coenzyme a reductase inhibitor , diuretics and anti - convulsant ) , her clinical condition was getting better and moved from intensive care unit to a general ward . when patient was hospitalized for 10 days ,
mid to apical wall motion of lv was almost improved except for apico - anterior wall and apical rv wall motion abnormality was not observed any more ( fig . 5 ) .
tc , also known as left apical ballooning syndrome or stress - induced cardiomyopathy , is named for ventricle which seems similar in appearance to a japanese octopus trap on ventriculography scan.6 ) tc is becoming well recognized as a cause of acute , reversible , and transient lv systolic dysfunction . in some cases , it would not be simple to make difference between acute coronary syndrome and tc since ecg abnormalities , elevated cardiac enzyme and symptoms mimicking stemi are common findings in tc .
st - segment elevation is the most common ecg abnormality , reported in about 82% of patients , and t - wave inversion in 64%.7 ) generally in tc , there is no identifiable coronary culprit lesion explaining the wall - motion abnormality .
but , as in our case , several cases of tc with coronary atherosclerotic lesion were reported.8 ) even though coronary atherosclerotic lesion was present , it was discordant with echocardiographic findings and affected regions were reversibly recovered without primary coronary intervention.9 ) in our case , there was a significant stenosis in ramus intermedius artery , however , wall motion abnormality was seen in mid to apical lv and apical rv in tte .
those regional wall motion abnormalities extend beyond a single epicardial vascular distribution and discordant with coronary atherosclerotic lesion . as a result of this
when seizure begins , it rises quickly within 30 min and decreases within few hours.10)11 ) a similar catecholamine release was observed in a case of tc associated with epilepsy.12 ) therefore , we can assume that seizure may trigger a condition inducing tc . in tc associated with epilepsy
, complications were frequent and severe : heart failure , apical thrombus , cardiogenic shock , and left ventricular rupture were found in previous studies.13 ) although there is no hard data , it could be hypothesized that tc may be related to sudden unexpected death in epilepsy ( sudep ) .
mechanisms of sudep are not clearly understood , it may include cardiac arrhythmia , myocardial ischemia , dysfunction of autonomic nervous system to the heart .
cardiac abnormalities are found in up to 33% at autopsy of sudep.14 ) in our patient , apical rv hypokinesia was accompanied with lv involvement .
isolated lv involvement is the most common variant , but rv involvement is becoming well recognized .
it has been reported that rv involvement affects approximately 25% to 42% of patients with tc.15 ) daoko et al.5 ) said that most patients with biventricular tc are elderly women and presenting symptoms are similar to those of acute myocardial infarction . and
it is known that rv involvement is associated with increasing hemodynamic instability and the risk of complications . in conclusion
, tc should form a part of the differential diagnoses of cardiac event in patient with seizure . in high risk patients , such as elevated plasma troponin level and hemodynamic instability
is accompanied , ecg and tte should be taken as soon as possible to detect tc and identify rv involvement . in a biventricular tc associated with epilepsy ,
 we describe a case of takotsubo cardiomyopathy in an elderly woman after status epilepticus . in an emergency echocardiography , not only left ventricular apical ballooning but also right ventricular apical hypokinesia was observed . after a medical management , 
 the patient 's condition was improved and a follow - up echocardiography showed substantial recovery of left and right ventricular apical ballooning . 
Introduction
Case
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