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Glob Heart. Author manuscript; available in PMC 2018 June 01.
Published in final edited form as:
Glob Heart. 2017 June ; 12(2): 99–105. doi:10.1016/j.gheart.2017.01.002.
Prevalence and Prognostic features of Electrocardiographic 
Abnormalities in Acute Stroke among Africans: Findings from 
SIREN
A full list of authors and affiliations appears at the end of the article.
Abstract
Background—Africa has a growing burden of stroke with associated high morbidity and a 3-
year fatality rate of 84%. Cardiac disease contributes to stroke occurrence and outcomes, but the 
precise relationship of abnormalities as noted on a cheap and widely available test, the 
electrocardiogram (ECG), and acute stroke outcomes has not been previously characterized in 
Africans. We assessed the prevalence and prognoses of various ECG abnormalities among African 
acute stroke patients encountered in a multisite, cross-national epidemiologic study.
Methods—We included 890 patients from Nigeria and Ghana with acute stroke who had 12-lead 
ECG recording within first 24 hours of admission and stroke classified based on brain CT scan or 
MRI. Stroke severity at baseline was assessed using the Stroke levity scale (SLS), while one-
month outcome was assessed using the modified Rankin scale (mRS).
Results—Patients mean age was 58.4 (±13.4) years, 490 were male (55%) and 400(45%) 
females, 65.5% had ischemic stroke, and 85.4% had at least one ECG abnormality. Women were 
significantly more likely to have atrial fibrillation, or left ventricular hypertrophy (LVH) with or 
without strain pattern. Compared to ischemic stroke patients, hemorrhagic stroke patients were 
less likely to have atrial fibrillation (1.0% vs. 6.7%, p=0.002), but more likely to have LVH (64.4% 
vs. 51.4%, p=0.004). Odds of severe disability or death at one month was higher with severe stroke 
(AOR: 2.25; 95% CI :1.44–3.50), or atrial enlargement (AOR: 1.45; CI:1.04–2.02).
Conclusions—About four in five acute stroke patients in this African cohort had evidence of a 
baseline ECG abnormality, but presence of any atrial enlargement was the only independent ECG 
predictor of death or disability.
INTRODUCTION
Stroke is a common neurologic condition in all regions of the world. Of the 14.1 million 
people who died of cardiovascular diseases (CVD) in 2012 in the world, stroke accounted 
for 6.7 million deaths. (1) Many people who suffer acute stroke have underlying CVD such 
as hypertension, atrial fibrillation, and ischaemic heart disease. (2) These underlying CVD 
*Corresponding Author: Mayowa O. Owolabi, MBBS, MSc, DM, FMCP, Department of Medicine, University College Hospital, 
Ibadan, Nigeria, West Africa., Phone : + 234 802 077 5595, mayowaowolabi@yahoo.com. 
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Adeoye et al. Page 2
are associated with several pre-existing electrocardiographic (ECG) anomalies such as 
rhythm and conduction abnormalities, and left ventricular hypertrophy (LVH) with or 
without ST-T changes.
However, several researchers have postulated the existence of a ‘brain-heart axis’ whereby 
structural brain lesions by themselves result in electrocardiographic changes. (3) The precise 
mechanism that leads to the development of these ECG changes is still uncertain, though 
increasing evidence suggests that it is mainly due to autonomic nervous system 
dysregulation.(3, 4) Whereas some authors attribute these ECG changes in acute stroke to 
underlying CVD, others have demonstrated their presence in acute stroke patients without 
underlying CVD. (5, 6)
Irrespective of preexisting cardiac diseases or not, observing an abnormal ECG in an acute 
stroke patients more than doubled their mortality rate at 6 months (5) and these abnormal 
ECG changes have not been shown to be perfect predictive tool for stroke subtypes.(6, 7) 
While cardiac arrhythmia such as atrial fibrillation, and LVH has been linked with the 
occurrence and prognosis of acute stroke, the prognostic value of repolarization changes 
commonly seen after stroke such as ST segment depression, T-wave and U-wave 
abnormalities still remains unclear.(8, 9).
Despite the common occurrence of stroke in Africa, there is sparse data on the prevalence 
and prognostic significance of ECG abnormalities in acute stroke in the region. In addition, 
there is inadequate data on the contributions of cardiac arrhythmias, conduction 
abnormalities, LVH, QTc prolongation and QRS prolongation on one-month case fatality in 
acute stroke especially in the African context. Understanding these interactions will help 
develop interventions to reduce the morbidity and mortality associated with acute stroke.
We investigated the prevalence of specific baseline ECG abnormalities in Africans with 
acute stroke and their prognostic effect on severe disability or death at one-month after 
stroke.
METHODS
Study design
Design of the SIREN study has been described elsewhere.(10) It is a multicenter case-
control study involving several sites in Nigeria and Ghana, which has been running since 
August 2014. Ethical approval was obtained from the institutional ethical committees of all 
study sites and written informed consent was obtained from all subjects.
Cases included consecutively consenting adults (aged 18 years or older) with first clinical 
stroke within 8 days of current symptom onset, or ‘last seen without deficit’ with cranial CT 
or MRI scan performed to confirm diagnosis within 10 days of symptom onset. We excluded 
those with stroke mimics, primary subarachnoid hemorrhage and previous strokes that were 
not radiologically ascertained. Stroke severity was assessed at baseline using the stroke 
levity scale (SLS). (11) One-month outcome was assessed using the modified Rankin scale 
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(mRS).(11) Other clinical and laboratory information were obtained according to the SIREN 
protocol. (10)
Electrocardiography
A standard (resting) 12-lead ECG was performed in each subject using a commercially 
available ECG machine at 25 mm/s and 1mV/cm calibration. All the 12-lead ECGs were 
obtained within 24-hours after the onset of stroke. The ECG tracings were independently 
analyzed by the cardiologists who were unaware of the details of the clinical status of the 
patients. Abnormalities obtained from the ECGs were defined according to standard criteria 
as shown in Table 1.(12, 13) Left ventricular hypertrophy was diagnosed using the following 
criteria: Sokolow-Lyon voltage (sum of the amplitudes of S wave in V1 and R wave in V5 or 
V6 ≥3.5 mV), sex-specific Cornell voltage (sum of the amplitudes of S wave in V3 and R 
wave in aVL.2.0 mV in women and .2.8 mV in men). Cornell’s product (CP) was calculated 
as the product of Cornell voltage times QRS duration. Repolarization abnormalities in leads 
V5 and/or V6 indicated typical strain when there was down- sloping convex ST segment 
with an inverted asymmetrical T-wave opposite to the QRS axis. (14, 15) QT interval was 
determined using the tangent method.(16) The measured QT interval was corrected for heart 
rate using the Bazett’s formula. Prolonged QT interval was considered present when the 
QTc was >450milliseconds and >440 milliseconds in females and males respectively. 
Presence of other ST-T changes were documented according to standard criteria.(12) ECG 
definitions of criteria are in Table 1.
Data management and analysis
Quantitative variables were summarized using mean (SD) for normally distributed and 
median for asymmetric variables. Frequency and percentage was computed for categorical 
variables. To investigate the statistical significance of the difference in continuous variables 
according to gender and stroke type, independent samples t-test was employed. For 
categorical variables, the Chi-square test for the comparison of proportions was employed.
Total mRS scores 0–3 and 4–6 were categorized as good and poor respectively. Association 
between selected demographic, clinical characteristics and ECG findings was investigated at 
bivariate and multivariate levels. For bivariate analysis, chi square test was used while binary 
logistic regression was used for multivariate. Criteria for inclusion of variables in the logistic 
regression model was a p-value <0.05 in the bivariate or previous report in literature or basic 
demographic factors (age and sex). Goodness of fit was assessed using the Hosmer-
Lemeshow test.
RESULTS
The 12-lead ECGs of eight hundred and ninety subjects were analyzed. There were 490 men 
(55.1%) and 400 (44.9%) women. The overall mean age of all patients was 58.4±13.4 years 
with women showing a non-statistically significant trend towards being older (p=0.057). 
Variables with statistically significant gender difference included BMI, diastolic blood 
pressure, and heart rate. These are shown in table 2. Men were less likely to have atrial 
fibrillation. The four cases of ventricular tachycardia occurred only in women. Women also 
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had non-significant longer QT intervals and were more likely to have LVH diagnosed by 
Cornel voltage or product criteria. Atrial enlargement was significantly more common in 
men. (Tables 3 and 4)
Tables 5 and 6 depict the comparison of demographic and clinical as well as ECG 
abnormalities according to stroke types. Subjects with hemorrhagic stroke were significantly 
younger (by about 7 years) than those with ischemic stroke. They also had higher blood 
pressures (SBP, DBP, MAP, and PP). In terms of ECG abnormalities, atrial fibrillation was 
significantly more common in those with ischemic stroke, while LVH was significant in 
hemorrhagic stroke by any of the ECG-LVH criteria. LVH with strain, QTc duration, QRS 
duration and axis were comparable across stroke types.
Table 6 shows the demographic and some clinical characteristics of the subjects according to 
one-month disability status. The presence of sinus rhythm was associated with good mRS. 
Severe SLS and atrial enlargement on the 12-lead ECG was associated with poor mRS.
In a multivariate logistic regression analysis (Table 7), only severe SLS and presence of 
atrial enlargement were the independent predictors of one-month outcome.
DISCUSSION
In this ongoing African stroke study, women with stroke appeared older than their male 
counterpart with higher frequencies of tachycardia, atrial fibrillation and ventricular 
tachycardia. Men with stroke had higher mean diastolic blood pressure. ECG LVH was more 
common in women and in those with hemorrhagic stroke. There was no significant 
difference in the occurrence of conduction abnormalities or QT abnormalities according to 
gender or stroke type.(13, 17) The pathologic mechanism by which acute stroke generates 
various ECG abnormalities is still not clear. However, autonomic dysregulation due to 
sympathetic overactivity have been proposed. Some authors have implicated insular 
irritation to be responsible for the abnormal cardiac function in acute stroke.(18–23) This is 
thought to be mediated by impaired inhibition of the sympathetic nervous system leading to 
increased release of cathecholamines.(20, 23)
The management of patients with an acute stroke demands assessment of risk for morbidity 
and mortality, of which hypertension is major determinant. Studies have shown that elevated 
BP in acute stroke is associated with poor prognosis.(24) Increased blood pressure increase 
the risk of bleeding in thrombolytic treatment(25) and increases the bleeding tendency in 
hemorrhagic stroke. (26) In our study, both systolic and diastolic blood pressures were 
elevated. The subjects with hemorrhagic stroke had higher mean blood pressure parameter 
compared with ischemic stroke. This is similar to the findings by Quresh et.al. (26)
While the studies on the pathophysiology of “acute hypertensive response” in stroke have 
not been exhaustive, severely high blood pressure irrespective of mechanism is associated 
with poor outcome. (27) Whether the high blood pressure reported in the current study was 
“acute hypertensive response” or poorly controlled chronic blood pressure was difficult to 
decipher since pre morbid cardiac state was not known. The same explanation may go for 
high rate of abnormal ECG findings reported in our study. About four out of five stroke 
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Adeoye et al. Page 5
patients studied had at least one abnormal ECG finding. Irrespective of mechanism, 
abnormal ECG findings is associated with poor outcome.
Over 20% of our stroke subjects had prolonged QTc. This is not different in men and women 
and according to stroke type. Previous studies in patients with hypertensive heart diseases or 
diabetes mellitus have shown that QTc prolongation and QT interval dispersion are related 
to increased risk of all-cause and cardiovascular mortality through malignant arrhythmias. In 
a study, it was shown that idiopathic abnormal QTc prolongation was associated with a five-
fold increase in the probability of sudden cardiac death.(28)
Except for four cases of ventricular tachycardia (all occurred in women), no case of 
polymorphic tachycardia especially torsade’s de pointes were recorded. This is similar to 
previous reports.(13) However, this may not have been picked up because continuous ECG 
monitoring was not carried out in our subjects. Atrial fibrillation is the most common 
sustained cardiac arrhythmia (29) and its presence increases stroke risk by 5-folds.(30) 
Interestingly, the prevalence of atrial fibrillation in our study was low. This is in contrast to 
earlier studies that reported high prevalence of atrial fibrillation especially in ischemic stroke 
among non-African populations (30, 31). The lower prevalence of atrial fibrillation in 
African stroke patients may be due to their relatively younger age, or genetic influences. 
Certain genetic variants have been associated with occurrence of atrial fibrillation especially 
the familiar type.(32) Also earlier studies have shown a paradoxical relationship between 
established AF risk factors and AF incidence in people of African descent compared with 
those of European ancestry. Despite a higher prevalence of many traditional risk factors for 
AF, including hypertension, diabetes mellitus, heart failure, and larger BMI in African 
Americans, people of European ancestry had higher incidence of atrial fibrillation.(33) 
These discrepancies allows for further genomic studies in atrial fibrillation among 
indigenous African populations which SIREN will explore.
Furthermore, in this study more than half of the patients had LVH. LVH is a well-recognized 
independent risk factor for hypertensive target organ damage including stroke.(34–36) and 
when found with stroke it doubles the risk of repeat stroke.(37). In acute stroke therefore, it 
may not be a new development as it takes long period of blood pressure elevation for clinical 
LVH to develop; more so that more than half of the stroke patients had atrial enlargement. 
This suggests that probably more of our subjects had preexisting cardiac anomalies. Our 
findings are similar to a study by Familoni et.al who found 63% preexisting cardiac disorder 
in stroke patients with higher prevalence of long QT interval and reported more mortality in 
patients with preexisting cardiac conditions.(38)
In our study atrial enlargement and severity of stroke were major predictors of one month 
severe disability or death. While stroke severity is a recognized predictor of stroke outcome 
with more severe strokes recovering more slowly, atrial enlargement may indicate pre-
existing cardiovascular morbidity which impairs stroke recovery at one-month.
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Adeoye et al. Page 6
Strengths and Limitations
This is the largest study so far of the prognostic implication of ECG abnormalities among 
indigenous African stroke patients. We provided evidence that any atrial enlargement on 
baseline ECG is an independent predictor of one-month outcome in this population.
It is not clear if the ECG abnormalities observed in our cohort were related to the acute 
stroke event since we did not have access to their ECGs prior to the stroke event. Follow up 
ECG was also not obtained in order to document whether the abnormalities were transient.
Conclusion
Various ECG abnormalities were observed in our stroke subjects. However, only atrial 
enlargement was an independent ECG predictor of one month stroke outcome. We 
recommend baseline ECG not only as a tool for detecting cardiac abnormalities in acute 
stroke patients but also to prognosticate one-month outcome. We will explore this and other 
ECG variables further when data collection is complete in the SIREN study.
Authors 
Moshood Abiodun Adeoye, FWACP1, Okechukwu S. Ogah, FWACP1, Bruce 
Ovbiagele, MSc, MD2, Rufus Akinyemi, MD3, Vincent Shidali, FMCP4, Francis 
Agyekum, FWACP5, Akinyemi Aje, FMCP1, Oladimeji Adebayo, MB; BS1, Joshua O. 
Akinyemi, PhD1, Philip Kolo, FMCP6, Lambert Tetteh Appiah, FWACP7, Henry 
Iheonye, MWACP4, Uwanuruochi Kelechukwu8, Amusa Ganiyu, FWACI9, Taiwo O. 
Olunuga, FMCP3, Onoja Akpa, PhD1, Ojo Olakanmi Olagoke, MWACP1, Fred 
Stephen Sarfo, MBChB, PhD7, Kolawole Wahab, FMCP6, Samuel Olowookere6, 
Adekunle Fakunle, MPH1, Albert Akpalu, MD5, Philip B. Adebayo, FWACP10, 
Kwadwo Nkromah, MD5, Joseph Yaria, MB, BS1, Philip Ibinaiye, FICS4, Godwin 
Ogbole, FMCR1, Aridegbe Olumayowa, B. Tech11, Sulaiman Lakoh, MWACP1, 
Benedict Calys-Tagoe, MD5, Paul Olowoyo, FWACP12, Chukwuonye Innocent, 
FMCP8, Hemant K. Tiwari, PhD13, Donna Arnett, PhD14, Osaigbovo Godwin, 
FWACP9, Ayotunde Bisi, MWACP1, Josephine Akpalu, FWACP5, Okeke Obiora, 
FWACS8, Odo Joseph, MWACS1, Adeleye Omisore, FMCR15, Carolyn Jenkins, 
DrPH2, Daniel Lackland, DrPH2, Lukman Owolabi, MBBS, Ph.D16, Isah Suleiman, 
B.MLS16, Abdu H. Dambatta, FMCP, FWACS16, Morenikeji Komolafe, FWACP15, 
Andrew Bock-Oruma17, Ezinne Sylvia Melikam, MSc1, Lucius Chidiebere Imoh, 
FMCP8, Taofiki Sunmonu, FMCP18, Mulugeta Gebregziabher, PhD2, Oluyemisi 
Olabisi, MBBS15, Kevin Armstrong, BS2, Ugochukwu U. Onyeonoro, FMCPH8, 
Emmanuel Sanya, FWACP6, Atinuke M Agunloye, FMCR1, Luqman Ogunjimi, 
MWACP1, Oyedunni Arulogun, PhD1, Temitope H. Farombi, FMCP1, Olugbo 
Obiabo, FMCP17, Reginald Obiako, FMCP4, and Mayowa Owolabi, MSc, Dr.M1,* on 
behalf of SIREN Team as part of H3Africa Consortium
Affiliations
1University of Ibadan, Ibadan, Nigeria
2Medical University of South Carolina, South Carolina, USA
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Adeoye et al. Page 7
3Federal Medical Centre, Abeokuta, Nigeria
4Ahmadu Bello University, Zaria, Nigeria
5University of Ghana Medical School, Accra, Ghana
6University of Ilorin Teaching Hospital, Nigeria
7Komfo Anokye Teaching Hospital, Kumasi, Ghana
8Federal Medical Center, Umuahia, Abia State
9Jos University Teaching Hospital Jos, Nigeria
10Ladoke Akintola University of Technology, Ogbomoso, Nigeria
11Sacred Heart Hospital, Abeokuta, Nigeria
12Federal University Teaching Hospital, Ido-Ekiti, Nigeria
13University of Alabama at Birmingham, Birmingham, USA
14University of Kentucky at Lexington, USA
15Obafemi Awolowo University Teaching Hospital, Ile-Ife, Nigeria
16Aminu Kano Teaching Hospital, Nigeria
17Delta State University Teaching Hospital, Ogara, Nigeria
18Federal Medical Centre, Owo, Nigeria
Acknowledgments
Funding
This work is supported by the National Institutes of Health (NIH) and National Institute of Neurological Disorders 
and Stroke (NINDS) (Grant 1U54HG007479)
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Highlights
• Four in five acute stroke patients in this African cohort had at least one ECG 
abnormality
• Atrial fibrillation was rare in the cohort occurring in <5% overall.
• Atrial fibrillation was more common in female stroke patients.
• Presence of any atrial enlargement was the only independent ECG predictor 
of death or disability.
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Table 1
Definitions of Electro-cardiographic (ECG) variables
ECG variables Definitions
Rhythm Atrial Absent P waves and an irregular ventricular
Fibrillation rate
Atrial Flutter Rate more than 100/minutes and saw tooth
appearance of the p waves
Sinus Rhythm Regular p-wave with rate less between 60–100/minutes
Sinus Bradycardia Regular p-wave with rate less than 60/minutes
Sinus Tachycardia Regular p-wave with rate more than
100/minutes
Sinus Arrhythmia Beat-to-beat variation in normal P-P interval
Atrial Right atrial P wave amplitude > 2.5 millimeters in lead
enlargement enlargement II and duration less than 120mseconds
Left atrial Bifid P wave in lead II with duration more
enlargement than 120mseconds and amplitude less than >
2.5 millimeters in lead II
Bi-atrial P wave amplitude > 2.5 millimeters in lead
enlargement II + Bifid P wave with duration more than
120ms in lead II
Indeterminate None of above evidence of atrial
enlargement
Presence of other Premature QRS > 120mseconds and bizarre QRS
arrhythmias ventricular shapes
contraction
Supraventricular Evidences of sinus tachycardia, AV Nodal
tachycardia re-entry tachycardia(AVNRT) complexes,
Atrial fibrillation, Atrial flutter, Multifocal
atrial tachycardia, Accelerated junctional
tachycardia, atrial tachycardia
Ventricular Sustained (5 or more consecutive beats) or
tachycardia non-sustained tachycardia (less than 5
consecutive beats)
None None of above other arrthymias
Presence of First degree AV PR duration > 0.20secs with normal P and
conduction block QRS waves
abnormalities
Second degree AV Progressive PR interval prolongation (>
block 200msecs) with intermittent failed P wave
conduction or wide QRS(greater than
120mses) with dropped QRS no prior PR
prolongation or evidence of advanced block
Right bundle branch Deep S in lead I and V6 and tall late R wave
block(RBBB) in VI
Left bundle branch Tall R in lead I and V6 and deep S wave in
block(LBBB) VI
Left anterior hemi- QRS<120mseconds, left axis deviation, qR
block pattern in lead I and aVL, rS pattern in lead
II, III, aVF and R wave peak time in aVL
Left posterior QRS<120mseconds, right axis deviation, qR
hemiblock pattern in lead I and aVL, rS pattern in lead
II, III, aVF and R wave peak time in aVL
Bi-fascicular block RBBB with left anterior hemiblock
Tri-fascicular block RBBB, left anterior hemiblock withprimary
AV block(or RBBB + Left anterior hemi-
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ECG variables Definitions
block+ left posterior hemiblock)
Complete AV block Evidence of AV dissociation
Indeterminate intra- >110mseconds with absence of RBBB
ventricular block and LBBB
None None of the above conduction
abnormalities
QT dispersion QTC interval Prolonged, if duration is greater than >
440ms in men or > 460ms in women
Left ventricular Cornell Product V3-S +AVL-R>2440 mms (men)
hypertrophy Criteria V3-S + AVL-R + 8mm > 2440 mms
(women)
Sokolow Lyon V1-S + RV-5 or RV 6 if addition ≥
Criteria 35mm (whether male or female) there is
LVH
Cornell voltage V3-S +AVL-R if addition
criteria ≥20mm(Women) ≥28mm(men) there is
LVH
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Table 2
Demographic and clinical characteristics according to gender
Variable Total Males Females(n=400) p value
(n=890) (n=490)
Mean (SD) Mean (SD)
Age (years) 58.4 (13.4) 57.6 (12.0) 59.3 (14.9) 0.057
Height (m) 164.7 (7.8) 167.7 (7.2) 160.9 (6.8) <0.0001
Weight (kg) 72.4 (14.3) 72.7 (13.6) 72.1 (15.1) 0.678
Body Mass Index (kg/m2) 26.7 (5.3) 25.7 (4.7) 27.8 (5.7) <0.0001
Systolic Blood Pressure (mmHg) 162.3 (32.6) 163.1 (31.3) 161.2 (34.1) 0.413
Diastolic Blood Pressure (mmHg) 97.2 (19.2) 98.9 (19.5) 95.1 (18.6) 0.004
Heart Rate 91.3 (27.4) 89.3 (23.9) 93.7 (30.8) 0.042
Mean Arterial Pressure (mmHg) 97.4 (24.6) 97.1 (23.6) 97.8 (25.9) 0.682
Pulse Pressure (mmHg) 65.0 (22.4) 64.1 (21.7) 66.2 (23.3) 0.205
Stroke type: Ischaemic 403 (65.5) 216 (63.3) 187 (68.3)
  Haemorrhagic 212 (35.5) 125 (36.7) 87 (31.8) 0.203
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Table 3
ECG abnormalities according to gender
Variable Total (n=890) Males Females p value
frequency(%) 490 (55.1%) 400 (44.9%)
Atrial fibrillation 36 (4.2) 12 (2.5) 24 (6.2) 0.009
Atrial flutter 4 (0.5) 2 (0.4) 2 (0.5) 0.846
Other Arrhythmias 75 (8.9) 38 (8.2) 37 (9.6) 0.466
Conduction abnormality 106 (12.7) 55 (12.0) 51 (13.5) 0.539
Atrial enlargement 466 (55.1) 273 (59.1) 193 (50.4) 0.011
LVH* 397 (54.8) 192 (48.7) 205 (61.9) <0.001
LVH with ST-T changes 219 (25.5) 124 (26.2) 95 (24.7) 0.607
Prolonged QTC interval 235 (28.6) 138 (30.3) 97 (26.5) 0.228
Short QTC interval 49 (6.0) 26 (5.7) 23 (6.3) 0.732
Any ECG abnormality 708 (85.4) 381 (84.5) 327 (86.5) 0.410
*
either Sokolow, Cornell voltage or product. LVH: Left ventricular hypertrophy
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Table 4
Demographic and clinical characteristics according to stroke type
Variables Total Ischaemic Haemorrhagic p value
Mean (SD) Mean (SD) Mean (SD)
Age (years) 58.3 (13.2) 60.7 (13.1) 53.7 (12.2) <0.001
Height (m) 164.9 (7.8) 165.1 (8.0) 164.4 (7.4) 0.405
Weight (kg) 73.1 (14.2) 73.2 (14.7) 72.8 (13.1) 0.795
Body Mass Index (kg/m2) 26.7 (5.3) 26.7 (5.3) 26.9 (5.2) 0.768
Systolic Blood Pressure (mmHg) 161.0 (19.7) 154.1 (30.3) 173.6 (34.1) <0.001
Diastolic Blood Pressure (mmHg) 96.8 (19.7) 92.6 (18.4) 104.5 (19.8) <0.001
Heart Rate 92.1 (28.7) 90.6 (27.5) 94.8 (30.6) 0.118
Mean Arterial Pressure (mmHg) 96.5 (25.0) 92.4 (23.2) 103.9 (26.5) <0.001
Pulse Pressure (mmHg) 64.2 (22.9) 61.5 (21.5) 69.1 (24.6) <0.001
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Table 5
ECG abnormalities according to stroke type
Variables Total Ischaemic Hemorrhagic p value
Atrial Fibrillation 28 (4.7) 26 (6.7) 2 (1.0) 0.002
Atrial Flutter 4 (0.7) 4 (1.0) 0 (0.0) 0.304f
Other Arrhythmias 46 (7.8) 34 (8.8) 12 (5.9) 0.222
Conduction abnormality 71 (12.3) 47 (12.4) 24 (12.1) 0.906
Atrial enlargement(any) 340 (58.0) 228 (58.9) 112 (56.3) 0.541
LVH* 297 (55.8) 181 (51.4) 116 (64.4) 0.004
LVH with strain 156 (26.2) 94 (24.0) 62 (30.2) 0.102
Prolonged QTC 171 (29.6) 118 (31.3) 53 (26.4) 0.216
Short QTC 34 (5.9) 19 (5.0) 15 (7.5) 0.238
QRS duration (median) 84.0 84.0 84.0 0.672
Median QRS Axis 24.0 25.0 23.6 0.321
Any ECG abnormality 488(84.7) 316 (83.9) 172 (87.3) 0.213
f
Fisher’s exact test
*
either Sokolow-Lyon, Cornell voltage or product criteria
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Table 6
Demographic and selected clinical characteristics according to one-month disability status.
Good mRS Poor mRS Test
Variables (n= 254) (n= 421) statistic p-value
Age (years, Mean (SD)) 58.1 (12.1) 58.8 (14.0) 0.746 0.456
Male gender 161 (59.2) 288 (54.5) 1.574 0.21
Hypertension 255 (93.8) 496 (93.9) 0.011 0.916
Diabetes 106 (38.9) 187 (35.4) 0.977 0.323
Severe SLS 105 (45.5) 294 (60.6) 20.946 0.001
Sinus rhythm 239 (87.9) 427 (80.9) 6.302 0.012
Atrial fibrillation 8 (3.1) 24 (4.7) 1.147 0.284
Other Arrhythmias 24 (9.2) 45 (9.0) 0.013 0.961
Conduction abnormality 33 (13.3) 66 (13.1) 0.003 0.960
Atrial enlargement 101 (38.7) 243 (48.8) 7.046 0.008
LVH 138 (52.9) 276 (53.2) 0.007 0.936
LVH with strain 70 (26.9) 119 (23.3) 1.231 0.267
Prolong QTC 72 (27.6) 139 (29.0) 0.17 0.68
Short QTC 13 (5.0) 27 (5.6) 0.142 0.706
Any ECG abnormality 212 (83.5) 421 (86.5) 1.193 0.275
mRS: modified Rankin Scale. SLS: Stroke levity scale
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Table 7
Independent factors associated with one-month disability
Variables AOR (95% CI) p-value
Age(years) 1.01 (0.99–1.02) 0.471
Male gender 1.04 (0.75–1.44) 0.806
Hypertension 1.24 (0.62–2.48) 0.549
Diabetes 0.86 (0.61–1.20) 0.377
Stroke severity (SLS)
Mild 1.00
Moderate 1.17 (0.73–1.87) 0.506
Severe 2.25 (1.44–3.50) 0.001
Atrial enlargement 1.45 (1.04–2.02) 0.030
SLS: Stroke levity scale
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