This literature review summarizes the clinical characteristics of myocardial stunning (neurogenic stunned myocardium or NSM) seen in patients after acute ischemic stroke. The review identified 7 case reports/series describing a total of 13 patients with NSM following stroke. Key findings include that NSM after stroke was more common in older females, with involvement of the left ventricle apex. Less than half of cases involved the insular cortex. Troponin levels and left ventricular dysfunction were typically mild. Most patients showed significant left ventricular recovery within 4 weeks, indicating a generally favorable prognosis. However, larger prospective studies are still needed.

1. Accepted Manuscript
Review
Clinical characteristics of myocardial stunning in acute stroke
Santosh B. Murthy, Shreyansh Shah, Chethan P. Venkatasubba Rao, Jose I.
Suarez, Eric M. Bershad
PII: S0967-5868(14)00049-6
DOI: http://dx.doi.org/10.1016/j.jocn.2013.11.022
Reference: YJOCN 5496
To appear in: Journal of Clinical Neuroscience
Received Date: 30 October 2012
Accepted Date: 10 November 2013
Please cite this article as: S.B. Murthy, S. Shah, C.P. Venkatasubba Rao, J.I. Suarez, E.M. Bershad, Clinical
characteristics of myocardial stunning in acute stroke, Journal of Clinical Neuroscience (2014), doi: http://
dx.doi.org/10.1016/j.jocn.2013.11.022
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2. D-12-01547
Review
Clinical characteristics of myocardial stunning in acute stroke
Santosh B. Murthy, Shreyansh Shah, Chethan P. Venkatasubba Rao, Jose I. Suarez, Eric
M. Bershad
Department of Neurology, Baylor College of Medicine, 6501 Fannin, NB 302
Houston, TX 77030, USA
*Corresponding author. Tel.: +1 713 798 8472; fax: +1 713 798 3091.
E-mail address: bershad@bcm.edu (E.M. Bershad).
Conflicts of Interest/Disclosures
The authors declare that they have no financial or other conflicts of interest in relation to
this research and its publication.

3. Abstract
Neurogenic stunned myocardium (NSM) after subarachnoid hemorrhage (SAH) is well
known, but there is a paucity of data regarding its occurrence following acute stroke. The
aim of this study is to study the clinical characteristics of NSM in acute non-hemorrhagic
stroke. We performed an electronic literature search with Medline and Google Scholar
for English-language articles using the terms “ischemic stroke” along with “stunned
myocardium” or “Takotsubo cardiomyopathy”. The search resulted in seven case
reports/series, but no prospective studies. The mean age of patients with myocardial
stunning following ischemic stroke was 72.5 years and 77% of these patients were
females. Insular cortex was involved in 38.4% of cases. Mean National Institutes of
Health Stroke Scale (NIHSS) score at admission was 12.6 and mean NIHSS at discharge
was 10.8. T-wave inversions and ST-segment elevations were noted in 84.6% and 69.2%
of patients, respectively. Mean troponin elevation was 0.64 mcg/dL and mean left
ventricular ejection fraction (LVEF) was 34.4%. In terms of outcomes, 84.6% of patients
had significant improvement in LVEF, mostly within 4 weeks of onset of symptoms. To
summarize, NSM was more common in females, with favorable prognosis. Less than half
the patients with NSM following stroke had insular involvement. The mean troponin
level in NSM after stroke was only half of that seen in SAH. While the lack of
prospective studies on NSM in stroke patients precludes drawing further conclusions,
more studies are warranted to study the risk factors for NSM and the effect on stroke
outcomes.

4. Keywords: Acute stroke; Neurogenic stunned myocardium; Takotsubo cardiomyopathy
1. Introduction
Left ventricular (LV) dysfunction following acute stress is a syndrome characterized by
transient wall-motion abnormalities mimicking ST-segment elevation myocardial
infarction.1
It is also referred to as “stress cardiomyopathy”,2
“Takotsubo
cardiomyopathy”,3
and more recently as “neurogenic stunned myocardium (NSM)”.4
The
diagnostic criteria include transient hypokinesis/akinesis beyond a single epicardial
vascular distribution, new ST-segment elevation or T-wave inversion, absence of
obstructive coronary disease, and absence of pheochromocytoma or myocarditis.5
The
typical triad of clinical findings include transient LV wall motion abnormalities,
electrocardiographic (ECG) changes and elevation in myocardial enzymes.6
NSM is well
described in subarachnoid hemorrhage (SAH). Autonomic dysfunction in the form of
cardiac arrhythmias, ECG changes and cardiac enzyme elevations are also commonly
seen after acute stroke (AS) but there is a paucity of data on the occurrence of this entity.7
Its incidence following AS is reported to be about 1%.8
Here we present a literature
review on the clinical characteristics and outcomes of NSM secondary to AS.

5. 2. Materials and methods
An electronic literature search was performed with Medline and Google Scholar for
English-language articles using the terms “acute stroke” along with “stunned
myocardium” or “Takotsubo cardiomyopathy”. The search returned 15 articles, of which
six were discarded since they were not in English. The remaining nine articles were
carefully screened to ensure that the AS preceded the myocardial stunning. Two of those
articles described patients where the stroke occurred as a consequence of thrombus
propagation from the depressed left ventricular apex, and were also excluded. The
bibliographies of identified articles were searched for additional studies, and this method
was repeated until no further articles were found. This resulted in seven case
reports/series. No prospective studies were identified.
2.1. Data extraction
Data extracted from the selected articles included demographics like age, sex, and prior
cardiac history like atrial fibrillation, congestive heart failure, and valvular heart disease.
Hypertension was not included in the cardiac history given its strong independent
association with stroke. Strokes were classified into small vessel, large vessel,
cardioembolic or cryptogenic based on the Trial of Org 10172 in Acute Stroke Treatment
(TOAST) criteria. The anatomic location of the stroke was also considered. Stroke
severity in terms of the National Institutes of Health Stroke Scale (NIHSS) was also
recorded. The cardiac parameters included ECG features such as T-wave inversion and
ST-segment elevation, maximum troponin elevation, left ventricular ejection fraction
(LVEF), and ventricular segments involved on echocardiography. The time to occurrence

6. of NSM following the acute stroke was also documented. An improved LVEF described
as “normal” was recorded as “>50%”.
3. Results
A total of 13 patients were included. The baseline and stroke characteristics are
summarized in Table 1. The mean age of patients with NSM from stroke was 72.5 years
and 77% were females. Three patients had a prior history of atrial fibrillation and two had
concomitant congestive heart failure. Two case reports did not mention prior cardiac
history.9,10
The most frequently encountered stroke subtypes were cardioembolic (five
patients), followed by cryptogenic (four patients) and large vessel territory (two patients).
Interestingly, both cases of large vessel stroke involved the basilar artery distribution. In
terms of location of the stroke, six out of 13 (38.4%) had involvement of the insular
cortex. Of these, four involved the left insular cortex and two patients had right insular
lesions. The cardiac parameters are described in Table 2. T-wave inversions and ST-
segment elevations were noted in 84.6% and 69.2% of patients respectively, with a mean
maximum troponin elevation of 0.64 mcg/L and mean LVEF of 34.4%. NIHSS data on
admission was available in seven patients and the mean NIHSS was 12.6. NIHSS data on
discharge was available in eight patients and the mean NIHSS was 10.8. Eleven patients
received therapeutic anticoagulation after being diagnosed with NSM. While all studies
commented on improvement in LVEF, there was no homogeneity in terms of what the

7. cut off was and when the follow-up LVEF was performed. We found that 84.6% of
patients had significant improvement in LVEF to >50%. This occurred in the first 4
weeks in a majority of patients.
4. Discussion
The main pathophysiologic mechanism by which NSM occurs is due to catecholamine
mediated damage to the myocardium.11,12
Plasma catecholamine levels can be up to 20
times higher in NSM patients compared to normal individuals.13
While catecholamines
have a positive inotropic effect on the myocardium of the ventricle, supraphysiologic
levels however result in negative inotropy resulting in myocardial stunning. 41
With this
background, we can interpret the results of our literature review.
A few observations are noteworthy. First, the mean age was 72.5 years in the stroke
patients, while that of NSM in SAH patients varied from 54–59 years.14-16
One cannot
read much into this since stroke and SAH are two different cerebrovascular disorders
with a complex interplay of risk factors, and tend to affect different age groups. One
common thing is that even in AS patients, there is a higher rate of NSM-related cardiac
damage in women.17
There is one plausible theory to explain this. To begin with basal
plasma epinephrine levels are lower in women.13
Estrogen is believed to reduce the stress
induced gene expression in the ventricular myocardium, as shown in rodent studies.18
It is

8. purported that the absence of this protective effect of estrogen in postmenopausal women
places them at risk for NSM with relatively milder catecholamine elevations.19
While the role of the insular cortex in central autonomic control has been extensively
studied,20
surprisingly less than half the stroke patients with NSM had involvement of the
insular cortex.21
This suggests that other subcortical and brainstem structures have a
larger role to play in the neuro-cardiac axis. Some of these structures include the lateral
nucleus of the hypothalamus, periaqueductal gray in the midbrain, nucleus of tractus
solitarius and parabrachial complex in the rostral brainstem, and rostral ventrolateral
medulla.22
Patients with brainstem stroke are shown to have substantially higher mean
plasma norepinephrine levels compared to patients with hemispheric infarction.23,24
This
could explain why two of the patients with strokes involving the basilar artery territory
had NSM (Table 1). The severity of myocardial involvement is believed to correlate with
the size of the stroke.8
Studies have also shown a cardiotropic organization of autonomic
function. In the rat model, stimulation of the right insula resulted in bradycardia and left
insular stimulation caused tachycardia.25
Similarly, patients with left insular lesions were
found to have a sympathetic predominance with 40% of them developing tachycardia, T-
wave inversion, and QTc prolongation.26
We observed that the majority of the patients
also had left insular lesions in our review, however, two patients had right insular lesions.
This suggests that there may be more factors at work in the causation of NSM following
AS.

9. NSM seen in AS patients is different from NSM seen in SAH patients in a few important
aspects. We found that the mean maximum cardiac troponin-I (cTI) elevation in AS
patients with NSM was 0.64 mcg/L. Contrast this with SAH patients, where the mean
maximum cTI level ranges from 1.2–2.7 mcg/L. This suggests that cardiac injury
following AS is of milder variety compared to the one following SAH. It is typically
believed that neurally mediated injury spares the apex of the ventricle.27
Accordingly,
NSM in SAH most commonly involves the mid ventricular and basal segments, and
rarely affects the apical segments.28,29
On the other hand, it is intriguing to note that all
the stroke patients in our review had involvement of the apex. The AS and SAH subsets
also differ in the arrhythmias that are encountered. For instance, atrial fibrillation is the
most common arrhythmia after AS, followed by ventricular arrhythmia30
, while SAH
patients have sinus bradycardia followed by sinus tachycardia and other arrhythmias like
atrial flutter, atrial fibrillation and supraventricular tachycardia.31,32
We speculate that
there may be a significant difference in the autonomic overactivity in stroke and SAH,
resulting in differences regarding involvement of the myocardial segments, occurrence of
arrhythmias, and cTI elevations. One may wonder, considering the above differences, if
the myocardial stunning in AS has a different underlying mechanism.
Despite the overall good prognosis of NSM, early recognition of this entity is of
paramount importance particularly in stroke patients. When permissive hypertension in
the AS setting is important to increase cerebral perfusion to the ischemic penumbra and
prevent progression,33
NSM can cause hypotension due to the depressed ventricular
myocardium, which can complicate the management.34
In addition, NSM can lead to LV

10. apical thrombus formation in about 5% of patients, which can result in embolic
complications.35
Embolic phenomena occur more frequently in NSM, as the improvement
of LV apical contraction may promote the discharge of LV apical thrombus, necessitating
anticoagulant therapy.35
In fact, most of the patients in this review received therapeutic
anticoagulation. However, it is unclear what the role of anticoagulation is in the setting of
a cardioembolic stroke like atrial fibrillation, which has a much greater likelihood of
hemorrhagic transformation. Moreover, the effect of NSM on stroke outcome is not
known. It would also be useful to know if certain variables like prior cardiac history,
degree of cTI elevation, and extent of LVEF depression at the time of admission can
affect the degree of improvement in LVEF.
Our study has a few limitations. First, the data on NSM in AS is very limited and only
available as case reports/series. The sample size is very small and hence any substantial
conclusions cannot be drawn at this time. Data were not available on NIHSS score at
admission or modified Rankin Scale score at discharge in nearly half the patients. We
also did not have information on the administration of intravenous thrombolysis
(recombinant tissue plasminogen activator) in many patients. Despite these shortcomings,
we can draw attention to a few differences in the clinical picture of NSM in stroke
compared to that in SAH. While patients with higher NIHSS scores are more likely to
have autonomic dysfunction,7
the risk factors promoting NSM remain to be elucidated.
5. Conclusion

11. Myocardial stunning in AS is an under-reported entity. While the pathophysiology is
believed to be the same as NSM following SAH, it does have a few distinct clinical
features that differ from NSM. The overall prognosis is good, but there are no data on the
effect of myocardial stunning on stroke outcomes. Future studies using case-control
methods may be useful to identify stroke patients who are at a higher risk of developing
NSM and the subsequent outcomes.
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17. Table 1 Baseline variables and stroke characteristics
Reference Age,
sex
Prior
cardia
c
histor
y
Stroke
subtype
Stroke
location
NIHSS at
admissio
n
NIHSS at
follow-up
IV r-tPA
Wang et al.9
2000
65,
F
NA NA R parieto-
temporal
NA NA No
Sadamatsu et
al.10
2000
65,
M
NA NA NA NA NA NA
Yoshimura et
al.8
2008
78,
F
None Cryptogeni
c
Hemisphe
ric
9 3 No
Yoshimura et
al.8
2008
90,
F
A.fib,
CHF
Cardioemb
olism
Hemisphe
ric
15 14 No
Yoshimura et
al.8
2008
78,
F
A.fib Cardioemb
olism
Hemisphe
ric
19 17 No
Yoshimura et
al.8
75,
F
A.fib Cardioemb
olism
Hemisphe
ric
3 0 No

18. 2008
Yoshimura et
al.8
2008
82,
F
A.fib,
CHF
Cryptogeni
c
Basal
ganglia
8 8 No
Yoshimura et
al.8
2008
80,
F
None Cryptogeni
c
Basal
ganglia
6 19 No
Yoshimura et
al.8
2008
47,
F
None Large
vessel,
basilar
artery
B/l pons,
cerebellu
m
28 25 Yes
(intra-
arterial)
Dias et al.36
2009
78,
M
None Cryptogeni
c
L
striatocap
sular
NA 0 Yes
Cho et al.37
2009
52,
M
None Cardioemb
olism
L fronto-
parietal
NA NA No
Kato et al.38
2009
70,
F
None Large
vessel,
basilar
artery
L
thalamus,
R
temporal
NA NA NA
Scheitz et al.39
2012
82,
F
None Cardioemb
olism
L insula NA NA NA

19. A.fib = atrial fibrillation, B/l = bilateral, CHF = congestive heart failure, F = female, IV =
intravenous, L = left, M = male, NA = not available, NIHSS = National Institutes of
Health Stroke Scale, R = right, r-tPA = recombinant tissue plasminogen activator.

20. Table 2 Characteristics of myocardial stunning with acute stroke

21. Referen
ce
T-
wave
invers
ion
ST-
elevati
on
Mean
max
cTI
Apical
segment
ECHO
LVEF
at
diagno
sis (%)
Time to
occurre
nce
Anti-
coagulati
on
LVEF
at
follow-
up (%)
Improv
ed
LVEF
Time to
LVEF
improv
ement
Wang et
al.9
2000
– + NA Severe
hypokin
esis
42 NA Heparin 60% +
(died)
5 days
Sadamat
su et
al.10
2000
+ + NA Akinesis 37 3 days NA >50% + 4 weeks
Yoshim
ura et
al.8
2008
+ + 0.01 Severe
hypokin
esis
40 5 hours Heparin >50% + Within 1
month
Yoshim
ura et
al.8
2008
+ – 0.01 Akinesis 12 9.5
hours
Heparin NA – NA
Yoshim
ura et
al.8
2008
+ + 0.3 Severe
hypokin
esis
34 8 hours Heparin >50% + Within 1
month
Yoshim + + 0.05 Akinesis 30 2.5 Heparin NA – NA

22. ura et
al.8
2008
hours
Yoshim
ura et
al.8
2008
+ + NA Akinesis 27 5 hours Argatrob
an
>50% + Within 1
month
Yoshim
ura et al8
2008
+ + NA Akinesis 45 6 days Argatrob
an
>50% + Within 1
month
Yoshim
ura et
al.8
2008
+ – 0.1 Severe
hypokin
esis
21 12 days Argatrob
an
>50% + Within 1
month
Dias et
al.36
2009
+ – 0.8 Hypokin
esis
38 13
minutes
LMW
heparin
>50% + 4
months
Cho et
al.37
2009
+ + 1.2 Severe
hypokin
esis
36 On
admissio
n
Heparin,
coumadin
>50% + 14 days
Kato et
al.38
2009
+ + 3.2 Akinesis NA NA Heparin >50% + 10 days

23. cTI = cardiac troponin I, ECHO = echocardiogram, LMW = low molecular weight,
LVEF = left ventricular ejection fraction, NA = not available, + = present, – = absent.
Scheitz
et al.39
2012
– – 0.1 Hypokin
esis
51 On
admissio
n
None 72% + 14 days