REVIEW ARTICLE

Cardiac Arrhythmias and Abnormal

Electrocardiograms After Acute Stroke
Doungporn Ruthirago, MD, Parunyou Julayanont, MD,
Pakpoom Tantrachoti, MD, Jongyeol Kim, MD and Kenneth Nugent, MD

ABSTRACT
Cardiac arrhythmias and electrocardiogram (ECG) abnormalities occur frequently but are often underrecognized after
strokes. Acute ischemic and hemorrhagic strokes in some particular area of brain can disrupt central autonomic control of
the heart, precipitating cardiac arrhythmias, ECG abnormalities, myocardial injury and sometimes sudden death. Identification
of high-risk patients after acute stroke is important to arrange appropriate cardiac monitoring and effective management of
arrhythmias, and to prevent cardiac morbidity and mortality. More studies are needed to better clarify pathogenesis,
localization of areas associated with arrhythmias and practical management of arrhythmias and abnormal ECGs after acute
stroke.
Key Indexing Terms: Stroke; Arrhythmia; Abnormal electrocardiogram; Sudden death. [Am J Med Sci 2016;351(1):112–118.]

INTRODUCTION cardiac arrhythmias (ventricular tachycardia, ventricular

C
ardiac complications are common after acute
stroke. Since 1947, there have been several
studies on abnormal electrocardiograms (ECGs)
and arrhythmias after ischemic and hemorrhagic strokes.
Byer et al1 first reported a patient with intracerebral
hemorrhage, who had marked QT prolongation and
large T and U waves on ECG in 1947.2 Abnormal ECGs
and cardiac arrhythmias are identified in 50-70% of
patients with acute stroke.2,3 The patterns of abnor-
malities vary from abnormal T waves, to QT prolongation,
to fatal arrhythmias, such as ventricular fibrillation that
cause sudden cardiac death. The explanations for the
high frequency of cardiac arrhythmias in patients with
stroke include elevated catecholamine levels, cardiac
autonomic imbalance and underlying or undetected car-
diac problems without a direct relationship to stroke.
It is important to determine whether there is any
cause and effect relationship between abnormal ECGs,
arrhythmias and acute stroke, or whether they are simply
coincidences. However, this is often difficult to differ-
entiate because of the high prevalence of cardiac
diseases and risk factors for coronary artery disease
(CAD) in patients with stroke. New observational and
experimental studies on arrhythmias and abnormal
ECGs in acute stroke are reported every year. The aim
of this article is to provide the up-to-date information
about clinical importance, pathophysiology, classifica-
tion, anatomical localization, management of cardiac
arrhythmias and abnormal ECGs after acute stroke.
CARDIAC MORBIDITY AND MORTALITY
Sudden cardiac death is important but is often not
recognized as a possibility in patients with acute stroke.
It can be caused by fatal myocardial infarction (MI), fatal
congestive heart failure or cardiomyopathy, serious
fibrillation and cardiac arrest), inherited arrhythmogenic
disorder such as long-QT or short-QT syndromes and
Brugada syndrome and metabolic disorders, such as
hypokalemia.4 In addition, acute stroke can disturb
central autonomic control, resulting in mechanical and
electrical cardiac abnormalities. Underlying cardiovas-
cular comorbidities also increase the risk of cardiac
morbidity and mortality after stroke. It is possible that
an interaction between the cardiovascular and neuro-
logical systems contributes to sudden cardiac death
after acute stroke.
A meta-analysis that included 67,000 patients fol-
lowed for a mean of 3.5 years after acute stroke found
that the annual risk of MI was about 2%. It also reported
linear relationship of accumulative risk, suggesting that
risk of MI at 10 years after acute stroke was approx-
imately 20%.5 A prospective study monitored 501
patients with acute neurovascular syndrome during the
first 72 hours after admission and found that the risk for
significant cardiac arrhythmia is highest during the first
24 hours and subsequently declines. As higher National
Institutes of Health Stroke Scale (NIHSS) correlates with
impaired cardiovascular autonomic control, the NIHSS
can be used to stratify risk of serious cardiac event.
Higher NIHSS correlates with impaired cardiovascular
autonomic control, which is measured by lower para-
sympathetic tone and impaired baroreceptor reflex sen-
sitivity (BRS).6 Another study that followed 846 patients
during the first 3 months after acute stroke reported that
cardiac death and serious cardiac events occurred in
4% and 19% of patients, respectively. A history of heart
failure, high baseline serum creatinine (41.3 mg/dL),
stroke severity and long corrected QT interval (QTc) or
ventricular extrasystole, were independent risk factors
for serious cardiac events.

112 THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES

VOLUME 351 NUMBER 1 January 2016

TYPES AND INCIDENCE OF ARRHYTHMIA
The incidence of arrhythmias of any type is higher in
patients admitted to hospital with stroke than without
stroke. The numbers vary among studies and depend on
the type of stroke, namely ischemic and hemorrhagic
stroke. In a prospective cohort of 501 patients in whom
92% had ischemic stroke, serious arrhythmias were
detected in 25.1% in the first 72 hours after acute stroke.
Atrial fibrillation was the most common arrhythmia found
in this study, accounting for 16%. Ventricular arrhyth-
mias accounted for 2.6%. The incidence of arrhythmia
was highest in the first 24 hours. Several types of
tachyarrhythmia were detected in this cohort, including
atrial fibrillation (11%), focal atrial tachycardia (3%),
undetermined supraventricular tachycardia (2%), ven-
tricular ectopy, nonsustained ventricular tachycardia and
atrial flutter (1% on each type). Several types of bradyar-
rhythmia were detected, including atrial fibrillation with
slow ventricular response (5%), Mobitz type II second-
degree atrioventricular block (2%), asystole or sinoatrial
block(2%) and complete atrioventricular block (o1%).
Another study included both hemorrhagic and ische-
mic stroke and reported a 39% incidence of arrhythmias
in patients with stroke without previous cardiac disease.
The incidence went up to 71% in patients with hemor-
rhagic stroke.7
Goldstein2 reported a significantly higher frequency
of new QT prolongation and arrhythmia of any type (25%
versus 3%) in patients with stroke compared with those
of controls. Atrial fibrillation was the most common
arrhythmia, followed by ventricular arrhythmias. New
atrial fibrillation was more common in cardioembolic
than nonembolic stroke. QT prolongation was more
common in subarachnoid hemorrhage than other types
of stroke (71% versus 39%).
Using appropriate equipment for adequate duration
for cardiac monitoring after acute stroke is important for
detecting abnormal ECGs and significant arrhythmias. In
a study using 24-hour Holter monitoring, arrhythmias
occurred in 90% of their patients with subarachnoid
hemorrhage.8 In another study, 572 patients who had
cryptogenic ischemic stroke or transient ischemic attack
within 6 months were randomly assigned to be equipped
with either a 30-day event-triggered recorder (interven-
tion group) or a conventional 24-hour monitor (control
group). Noninvasive ambulatory ECG monitoring in
intervention group improved detection of atrial fibrillation
by a factor of more than 5 and doubled the rate of
treatment with anticoagulants.9
PATHOPHYSIOLOGY OF ARRHYTHMOGENESIS
AFTER STROKE
Several studies have reported that acute stroke
leads to imbalance of central autonomic control; stroke
can cause overactivity of sympathetic or parasympa-
thetic control, myocardial injury, ECG abnormalities,
cardiac arrhythmias and even sudden death. Although
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Cardiac Rhythm and Acute Stroke
the prevalence of CAD and CAD risk factors in patients
with acute stroke is high, it is unlikely that underlying or
undetected cardiac diseases are the only cause of
arrhythmia and cardiac damage after an acute stroke.
The pattern of ST changes in patients with acute stroke
that appear and disappear rapidly is not typical for
cardiac causes and may suggest neurologic causes
(Figure 1).10
Autonomic Imbalance
Autonomic dysfunction is common after acute
stroke. This is evident by impairment of physiological
regulation of heart rate and blood pressure, namely
decreased heart rate variability (HRV) and impaired
BRS, and increased catecholamine11 and cortisol lev-
els.12 The variability in heart rate is indicative of the
heart's ability to adjust to circulatory changes. Several
studies have reported decreased HRV in patients with
stroke, not only in acute phase but also at 1 and 6
months after stroke.13,14 The baroreceptor reflex stabil-
izes heart rate and blood pressure when body position
changes and was decreased in patients with acute
stroke in a study.15 Catecholamine excess can alter
electrical properties of cardiomyocytes and can increase
the likelihood of arrhythmia.16 Advanced age and
severity of neurologic deficits lead to increased auto-
nomic instability and increased sympathetic tone and
are associated with arrhythmias.6
Neurogenic Cardiac Damage
After acute stroke, overactivation of β-adrenergic
receptors by catecholamine excess can lead to tonic
opening of calcium channels, causing impaired seques-
tration of intracellular calcium ions, which is a necessary
process for relaxation of cardiac muscles.17 The pro-
longed contraction of cardiac muscles can lead to cell
damage or death.
Cardiac myofibrillar degeneration and contraction
band necrosis are characteristic lesions found in
patients dying from acute stroke and are histologically
similar to lesions occurring during catecholamine infu-
sion, hypothalamic stimulation or reperfusion injury of
cardiac muscle.18 Contraction band necrosis is found in
the distribution of cardiac nerves, instead of macro-
vascular distribution as in CAD.18,19 This lesion is
predominantly located at subendocardium and could
possibly involve the cardiac conduction system, increas-
ing the risk of arrhythmia. In a study, transient coronary
vasospasm from increased sympathetic tone after right-
hemispheric ischemic stroke caused “cardiac stunning”
or transient decrease in cardiac function with segmental
hypokinesis and ST-segment and Q-wave abnormalities.
This condition usually resolves in a few days after the
onset of stroke.20 Catecholamine surges after stroke can
precipitate takotsubo cardiomyopathy (TC), which pos-
sibly serves as substrate for ventricular arrhythmia.17
Overall, 1.2% of patients with ischemic stroke develop
113
Ruthirago et al
FIGURE 1. Schematic overview of the pathophysiology of cardiac arrhythmias after an acute stroke.
TC.21 This condition also occurs in patients with aneur-
ysmal subarachnoid hemorrhage. Sympathetic surge
and characteristic myocytolysis seen in patients with
subarachnoid hemorrhage also develop in patients with
TC.
Insular Stroke and Adverse Cardiac Outcomes
The insular cortex is an interconnecting part of
cerebral cortex located within the lateral sulcus of the
brain. Lesions in the insular cortex can alter autonomic
regulation of heart. A study, including 62 patients after
insular stroke, found that the patients had a higher
incidence of arrhythmias and decreased HRV than
age- and sex-matched controls.22 An animal study
showed that electrical stimulation of insular cortex could
cause significant arrhythmias, similar to what occurred
after acute stroke.23 This study also reported a relation-
ship among insular cortex, autonomic changes and
arrhythmias. Several studies in patients without CAD
have suggested that sympathetic overactivity can pro-
long repolarization period, decrease BRS and electrical
restoration and increase the chance of arrhythmogen-
esis.24,25
Elevated Cardiac Biomarkers After Acute Stroke
Elevation of several cardiac enzymes after acute
stroke supports the theory of stroke-related autonomic
imbalance that leads to cardiac dysfunction; it does not
necessarily indicate that myocardial injury occurs. In a
study, including patients with first episodes of acute
ischemic stroke, creatine kinase, creatine kinase-MB
and myoglobin were elevated for more than 3 days
114
and then returned to normal on the fourth day. Troponin
T that is more sensitive and specific for myocardial injury
was in the reference range. However, a larger study that
included 730 patients with acute ischemic stroke without
known heart or renal disease and no clinical, ECG or
echocardiographic changes suggestive of CAD found
that 7% of patients had troponin T level of 0.1 ng/mL or
higher. A meta-analysis of 15 studies, including patients
with acute ischemic or hemorrhagic stroke, found that
18% of these patients had elevated troponin T or
troponin I levels. Several studies have reported that
elevated troponin T level predicts morbidity and mortality
after acute stroke at 30 days and 6 months.26 A recent
study monitored the level of high-sensitivity cardiac troponin
(cTn) in patients with acute ischemic stroke and recom-
mended that the pattern of acute or chronic elevation of cTn
level, with clinical conditions, can help to classify the
different causes of elevated cTn level, such as MI, non-
coronary causes and neurogenic-heart syndrome.27 How-
ever, the clinical significance of elevated cardiac biomarkers
after acute stroke is inconclusive at this time.
LOCALIZATION AND LATERALIZATION OF
AREAS ASSOCIATED WITH ARRHYTHMIA
The middle cerebral artery (MCA) territory is the most
commonly affected area in ischemic stroke. This area
involves insular cortex and its subcortical white matter.
Autonomic imbalance from insular lesions can cause
arrhythmia after acute stroke.4 There is evidence indicat-
ing that lesion in some specific areas of brain that
involve central control of autonomic nervous system
can contribute to arrhythmogenesis.
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Insular Cortex
In a study, stimulation of human insular cortex
resulted in cardiovascular effects with some lateraliza-
tion. Stimulation of right insular cortex more frequently
produced sympathetic effects and stimulation of left side
more frequently produced parasympathetic effects.28 A
small number of case reports of isolated insular lesions
have suggested that right insular ischemic or hemor-
rhagic stroke results in bradycardia and sometimes
asystole. This can be explained by decreased sympa-
thetic tone from right insular lesion and relative para-
sympathetic overactivity. On the contrary, isolated left
insular lesion results in decreased HRV, possibly
because of the loss of parasympathetic tone and
increased basal cardiac sympathetic activity.29 However,
assuming that there is complete lateralization of auto-
nomic control from insular cortex is inappropriate
because the literature report conflicting results on this
topic. Some studies support lateralization,29 whereas
other argue against this theory. This can be explained by
the fact that most insular lesions are part of larger infarct
in the MCA territory and by the presence of interhemi-
spheric connections between the insular tracts.17
Left Parietal Lobe
A large prospective cohort study followed 655
patients with first ischemic stroke and found that left
parietal lobe infarction was an independent predictor of
cardiac death and MI at 4 years in 447 patients with
positive result on CT or MRI.30 However, the study did
not find any association between frontal, temporal or
insular stroke and fatal cardiac outcomes.
Right-Hemispheric Lesions
A recent study using voxel-based lesion-symptom
mapping in patients with acute ischemic stroke during
the first 72 hours found significant association between
the occurrence of clinically relevant severe arrhythmias
and lesions in right insular, frontal and parietal cortex,
right basal ganglia, thalamus and amygdala.31
The Anterior Cingulate Cortex
The anterior cingulate cortex is also a major compo-
nent of central autonomic control. However, it does not
attract significant clinical attention in studies because of
lower prevalence of ischemic stroke in anterior cerebral
artery territory when compared with MCA territory.4
ECG AND REPOLARIZATION ABNORMALITIES
ECG changes occur frequently in patients with
stroke, even in those without history or signs of under-
lying heart disease. An early study reported the preva-
lence of abnormal ECGs in patients with acute stroke as
high as 92%.2 The incidence and prevalence of ECG
abnormalities may vary among studies according to
criteria used to determine abnormal ECGs, the equip-
ment used for cardiac monitoring and duration after the
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Cardiac Rhythm and Acute Stroke
onset of stroke. A retrospective study in 2011, including
361 patients with ischemic stroke or intracerebral hem-
orrhage or subarachnoid hemorrhage, found that QT
prolongation and pathological Q waves occurred more
frequently in subarachnoid hemorrhage than other types
of stroke. The study did not find any relationship
between the frequency of other ECG abnormalities and
the types of stroke.32 ECG abnormalities were more
common in patients with stroke with history of cardio-
vascular diseases and hypertension. However, other
studies have demonstrated that ECG and repolarization
abnormalities did not exist before the stroke, suggesting
a neurologic cause of abnormal ECG.2 Repolarization
abnormalities increase the vulnerable time, in which
extrasystoles are more likely to cause ventricular tachy-
cardia and ventricular fibrillation resulting in sudden
cardiac death.33 QTc dispersion, or difference between
maximal and minimal QTc, was used as a marker of
abnormal cardiac repolarization. Huang et al34reported
significantly increased QTc dispersion in patients who
died after acute intracerebral hemorrhage compared
with the survivors. A study in 2008 found significantly
increased prevalence of early repolarization in subjects
who have idiopathic ventricular fibrillation than in control
subjects. These studies may support the possible cor-
relation between acute stroke and increased risk of
repolarization abnormalities, leading to significant arrhy-
thmias such as ventricular fibrillation.35
QT prolongation was reported in 38% of patients
with ischemic stroke, in 64% of patients with intra-
cerebral hemorrhage and in 71% of patients with sub-
arachnoid hemorrhage.33,36 In the absence of electrolyte
disturbance and underlying cardiac diseases, an abnor-
mal QT is likely due to stroke. New T-wave abnormalities
were found in 15% of patients with acute stroke.2 Both
prominent upright T waves known as “cerebral T
waves,” and inverted T waves were reported. Inverted
T wave was found 4 times more common in patients
after acute stroke than in age-matched controls in a
study. ST-segment changes occurred in 22% of patients
with stroke.37 Approximately 35% of patients had new
ischemic pattern ST changes after stroke. However,
coexisting MI was found in 5-11% of patients with
acute stroke.7 Patterns of appearance and disappear-
ance of cardiac biomarkers, other ECG characteristics
and CAD risk factors should be considered in determin-
ing the need to work up for coexisting MI in patients with
acute stroke. Some studies have found that inverted T
waves and ST-segment alterations may normalize after
brain death.38 This supports theory of neurally induced
cardiac abnormalities after stroke. New abnormal Q
waves were described in approximately 10% of patients
with acute ischemic or hemorrhagic stroke. As the
prevalence of acute MI in patients with stroke is lower
than the incidence of pathologic Q waves, ischemic
changes of Q waves cannot entirely be explained by
coexisting cardiac events. New U waves were found in
13% of patients with acute stroke.2 Studies have
115
Ruthirago et al
reported both isolated U waves and U waves in combi-
nation with abnormal T waves and QT prolongation. In
the absence of abnormal electrolytes, this change is
likely related to stroke.
MANAGEMENT
Cardiac arrhythmias and abnormal ECGs are known
to be more common in patients with acute stroke. Some
current guidelines recommend cardiac monitoring and
checking cardiac enzymes, but still rarely include spe-
cific advice on the management of this problem. Alth-
ough most patients with acute stroke are admitted to
intensive care units, but how long should they need to
be on cardiac monitoring, which equipment is appropri-
ate for detecting arrhythmias and when the patients with
abnormal ECGs or arrhythmias should be treated with
medication or surgical operation are still unclear in cur-
rent recommendations. This article provides some rec-
ommendations on management of arrhythmias after
acute stroke based on evidence from our literature
review (Figure 2).
 Risk stratification and cardiac monitoring: Data from a
prospective study reported that risk of serious cardiac
arrhythmia after an acute stroke is highest during the
first 24 hours of admission and declines over time
during the first 3 days.6 Current evidence suggests
FIGURE 2. Schematic overview of the management of cardiac arrhythmias after an acute stroke.
116
that the longer the duration of cardiac monitoring, the
higher the sensitivity to detect abnormal ECGs and
cardiac arrhythmias after acute stroke. Using non-
invasive cardiac monitoring for adequate duration
significantly improved rate of detection of arrhythmias.
Holter monitoring and event-triggered recorders
increase the detection of arrhythmias, especially atrial
fibrillation after acute stroke.9
Arrhythmia after acute stroke was independently
related to increased age and severity of neurologic
deficits, measured by NIHSS on admission.6 Elevated
troponin T level was found to be a poor prognostic
factor after acute stroke. Identification of patients with
high-risk stroke, such as patients with advanced age,
several comorbidities, elevated cardiac biomarkers
and high NIHSS, is important. Based on the current
evidences, ECG monitoring of at least 24 hours after
admission is recommended. Extended monitoring dur-
ing the first 72 hours of acute stroke would increase
the possibility of detecting arrhythmias if applicable.
For patients with high-risk stroke, use of prolonged
cardiac monitoring is important to detect severe
cardiac arrhythmias and to prevent sudden cardiac
death.6
 Supportive care and correction of electrolyte abnor-
malities: Abnormal level of electrolytes, especially
potassium, magnesium and calcium, can cause car-
diac arrhythmias and QT abnormalities. Patients with
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VOLUME 351 NUMBER 1 January 2016

stroke frequently have comorbidities and often take
medications that can cause electrolyte imbalance,
such as diuretics, insulin and angiotensin-converting
enzyme inhibitors. Correction of these electrolyte
abnormalities and monitoring of their level during acute
phase of stroke, as well as general supportive care,
including blood pressure control and monitoring of
vital signs, are important to prevent serious cardiac
arrhythmias and sudden death.
 Specific treatment for cardiac arrhythmias: Some
abnormal ECGs and arrhythmias after acute stroke
are transient and do not increase morbidity and
mortality, but some require urgent management. A
large study reported therapeutic consequences of
detected arrhythmia in 501 patients with acute neuro-
vascular syndrome. During median monitoring time of
73 hours, 25% of patients developed serious arrhyth-
mias. Antiarrhythmic treatment was given to 77.7% of
patients; 1 patient developed asystole and required
cardiopulmonary resuscitation, 11 patients underwent
implantation of permanent pacemaker, 2 patients
received cardioverter-defibrillator implantation and 2
patients required urgent coronary angiography.6 A
study has suggested that beta blockers may reduce
sympathetic tone and possibly prevent cardiac
arrhythmias and further cardiac damage following
stroke.10 Animal studies have shown that blockade of
autonomic activity by administering propranolol, atro-
pine and performing vagotomy, partially prevents
cardiac damage and arrhythmias after experimental
brain lesions or electrical stimulation.39 However, more
studies are needed before these strategies can be
used as a standard treatment of arrhythmia after
stroke.
 Prevention of recurrent stroke: Determining whether
ECG abnormalities and arrhythmias antedate or post-
date acute stroke is sometimes difficult. In cardioem-
bolic stroke, detection of atrial fibrillation needs
adequate duration of cardiac monitoring. Furthermore,
implementing different strategies such as continuous
telemetry, Holter monitoring and implantable event
recorder, can help improve sensitivity in detecting
arrhythmias. However, once they are detected, initia-
tion of anticoagulant is important to prevent recurrence
of stroke, no matter which occurred first. Management
of comorbidities by controlling blood pressure, main-
taining normoglycemic level, using lipid-lowering
agents and treating coexisting cardiac diseases, are
important to prevent stroke recurrence and also to
prevent cardiac arrhythmias and sudden death after
stroke.
CONCLUSIONS
Cardiac arrhythmias and ECG abnormalities occur
frequently in patients with acute stroke, either with or
without coexisting cardiac diseases. The incidence and
prevalence of arrhythmias and significantly abnormal
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Cardiac Rhythm and Acute Stroke
ECGs depend on the types and onset of stroke, the
duration and equipment used for cardiac monitoring and
criteria used for determination and classification of
arrhythmias. Ischemic and hemorrhagic lesions in some
particular areas of brain, such as the insular cortex, can
cause imbalances in central autonomic control of the
heart, can disrupt the heart's ability to adjust during
stress, can increase hormones of the sympathoadrenal
system and can cause characteristic damage of cardiac
tissue that is similar to histopathology found in sympa-
thetic overactivity. Identification of high-risk patients
after stroke is important, because appropriate cardiac
monitoring for early detection of ECG abnormalities
and arrhythmias and effective management, including
supportive and specific treatment of arrhythmias, can
prevent cardiac morbidity and mortality after acute
stroke.
Appendix
Definitions
Cardiac arrhythmias are abnormalities of cardiac
electrical activation that manifest as abnormalities in
the rate and rhythm of contraction. They can be broadly
classified into 2 categories—bradyarrhythmias and
tachyarrhythmias.
Abnormal electrocardiograms (ECGs) are abnormal-
ities of each component of cardiac electrical activities,
namely P waves, QRS complex, T waves and U waves,
in terms of duration, interval and characteristics. Some
common ECG abnormalities are defined according to
the following criteria:2,32
 ST-segment depression: ST-segment depression
(either flat or down sloping) of 1 mm or more.
 ST-segment elevation: Elevated ST segment of 1 mm
or more, in extremity and precordial leads (but eleva-
tion of 2 mm or more in lead V1 and V2).
 Q waves are considered significant (unless it confined
to lead III) if they are greater than 0.04 seconds in
duration or more than 25% of the height of R wave in
the same lead.
 T-wave abnormalities include T waves that have low
voltage or are flat or are inverted in leads that are usually
upright or T waves that are abnormally tall and peaked.
 Abnormal U waves are negative U waves with more than
0.1 mV depth or positive U waves that are higher than
25% of T wave in the same lead. U waves are considered
significant if they are visible in more than 2 leads.
 QT interval is interval measured from the beginning of
QRS complex to the end of T wave.
 Corrected QT interval is defined as QT interval divided
by the square root of the RR interval (Bazett's formula)
from an average of 3 complexes in lead II and
is considered prolonged if corrected QT interval is
longer than 0.45 seconds in men and longer than
0.46 seconds in women.
117
Ruthirago et al
Q-wave and T-wave abnormalities are assessed in
leads I, II, aVL, aVF and V2-V6.
Stroke is an acute episode of neurologic deficit of
presumed vascular origin, which persists 24 h or
more.40 It can be further classified into ischemic stroke
(large artery atherosclerosis, cardioembolic and small
vessel disease), hemorrhagic stroke and subarachnoid
hemorrhage.
The National Institutes of Health Stroke Scale is a
systematic tool, which provides a quantitative measure
of stroke-related neurologic deficit. The higher score
correlates with the more severe neurologic deficit of
patients with stroke.
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From the Department of Neurology (DR, PJ, JK), Texas Tech University
Health Sciences Center, Lubbock, Texas; Department of Internal Medicine
(PT, KN), Texas Tech University Health Sciences Center, Lubbock, Texas.
Submitted June 26, 2015; accepted September 4, 2015.
The authors have no financial or other conflicts of interest to disclose.
Correspondence: Doungporn Ruthirago, MD, Department of
Neurology, Texas Tech University, 3601 4th Street, Lubbock, TX 79430.
(E-mail: druthirago@gmail.com, doungporn.ruthirago@ttuhsc.edu).
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
VOLUME 351 NUMBER 1 January 2016