Fragmented QRS may predict new onset atrial fibrillation in patients with
ST-segment elevation myocardial infarction

Mahmut Yesin MD, Macit Kalçık MD, Metin Çağdaş MD, Yavuz Karabağ
MD, İbrahim Rencüzoğulları MD, Mustafa Ozan Gürsoy MD, Süleyman
Çağan Efe MD, Süleyman Karakoyun MD

PII: S0022-0736(17)30255-8
DOI: doi: 10.1016/j.jelectrocard.2017.08.014
Reference: YJELC 52474

To appear in: Journal of Electrocardiology

Please cite this article as: Yesin Mahmut, Kalçık Macit, Çağdaş Metin, Karabağ
Yavuz, Rencüzoğulları İbrahim, Gürsoy Mustafa Ozan, Efe Süleyman Çağan, Karakoyun
Süleyman, Fragmented QRS may predict new onset atrial fibrillation in patients with
ST-segment elevation myocardial infarction, Journal of Electrocardiology (2017), doi:
10.1016/j.jelectrocard.2017.08.014

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 ACCEPTED MANUSCRIPT

Full Title: Fragmented QRS may predict new onset atrial fibrillation in patients with ST-

segment elevation myocardial infarction

Running Title: Fragmented QRS and atrial fibrillation

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Mahmut Yesin, MD1, Macit Kalçık, MD2, Metin Çağdaş, MD3, Yavuz Karabağ, MD3,

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İbrahim Rencüzoğulları, MD3, Mustafa Ozan Gürsoy, MD4, Süleyman Çağan Efe, MD5,

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Süleyman Karakoyun, MD3

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1. Department of Cardiology, Kars Harakani State Hospital, Kars, Turkey

2. Department of Cardiology, Hitit University Faculty of Medicine, Çorum, Turkey

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3. Department of Cardiology, Kars Kafkas University, Faculty of Medicine, Kars, Turkey
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4. Department of Cardiology, Gaziemir State Hospital, İzmir, Turkey

5. Department of Cardiology, Ağrı State Hospital, Ağrı, Turkey

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Competing interests: All of the authors have no conflict of interest.

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Funding: No funding.
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Correspondence author and address:

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Mahmut Yesin, MD. (Corresponding author)

Örnek mah. Hastane cad. Temel apt. No:32 Kars /TURKEY

e-mail: mahmutyesin@yahoo.com
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ABSTRACT
Background: Fragmented QRS (fQRS) has been shown to be a marker of local myocardial

conduction abnormalities, cardiac fibrosis in previous studies. It was also reported to be a

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predictor of sudden cardiac death and increased morbidity and mortality in selected

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populations. However, there is no study investigating the role of fQRS in the development of

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atrial fibrillation in patients with ST segment elevation myocardial infarction (STEMI). In this

study we aimed to investigate the relationship between the presence of fQRS after primary

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percutaneous coronary intervention (pPCI) and in-hospital development of new-onset atrial

fibrilation (AF) in patients with STEMI.

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Material and methods: This study enrolled 171 patients undergoing pPCI for STEMI.
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Among these patients 24 patients developed AF and the remaining 147 patients were

designated as the controls. All clinical, demographical and labaratory parameters were entered
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into a dataset and compared between AF group and the controls.

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Results: The presence of fQRS was higher in the AF group than in the controls (p = 0.001).

Diabetes Mellitus and fQRS was significantly more common in the AF group (p = 0.003 and
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p=0.001 respectively) Logistic regression analysis demonstrated that the presence of fQRS
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was the independent determinant of AF (OR: 3.243, 95% CI 1.016-10.251, P=0.042).

Conclusions: Increased atrial fibrillation was observed more frequently in STEMI patients

with fQRS than in patients without fQRS. fQRS is an important determinant of AF in STEMI

after pPCI.

Key words: Coronary artery disease, New Onset Atrial Fibrillation, Fragmented QRS, ST-
elevation myocardial infarction

INTRODUCTION
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New-onset atrial fibrillation (AF) is a frequent complication of ST segment elevation

myocardial infarction (STEMI) and its incidence varies between 2.3 % and 21 % according to

type of study group, diagnostic method and treatment modality used (1). Previous studies

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revealed that AF development in patients with STEMI was associated with worsened

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short/long-term prognosis (2-3). Several clinical parametres were found to be associated with

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AF development including older age, female gender, history of diabetes mellitus (DM),

increased heart rate (HR), decreased systolic blood pressure, number of diseased vessels and

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impaired left ventricular ejection fraction (LVEF) (2-4). Fragmented QRS complexes (fQRS)

are defined as various RSR’ patterns with or without Q waves on a 12-lead resting
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electrocardiography (ECG). The presence of fQRS on ECG is a sign of delay in ventricular

conduction, associated with myocardial scarring, ischemia, and fibrosis (5). These

fragmentations on surface ECG were associated with increased morbidity and mortality,
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sudden cardiac death and adverse cardiovascular events in previous studies (6-8). Elevated
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ventricular filling pressure due to abnormal LV diastolic and systolic functions after

myocardial infarction may be a potential pathophysiological mechanism for left atrial

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enlargement. These changes in the ventricles may influence the atria and cause atrial
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arrhythmias. Çetin et al. reported that the presence of fQRS was associated with NOAF after

coronary bypass graft surgery (9). But there is limited data regarding the relationship between

fQRS and AF development in the setting of STEMI. In the present study, we aimed to

investigate the relationship between the presence of fQRS after primary percutaneous

coronary intervention (pPCI) and in-hospital development of new-onset atrial fibrilation (AF)

in patients with STEMI.

MATERIAL AND METHODS

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Study patients
A total of 171 consequtive STEMI patients (142 males, mean age: 63±11) who underwent

pPCI between January 2016 and January 2017 were enrolled in the study. The patients with

end stage liver and renal disorders, coagulopathy, intolerance to dual anti-platelet drugs and

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malignancies were excluded from the study. The ECGs with QRS morphology indicating

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typical bundle branch block, pace rhythm, or any kind of significant conducting abnormalities

were also excluded from the study. Furthermore, patients who were admitted with cardiogenic

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shock and received inotropic agents (catecholamines) which may induce atrial fibrillation

were excluded from the study. All patients provided a written or oral-witnessed informed
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consent at emergency department and the protocol of study was approved by the local ethics
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committee of the hospital in accordance with the Declaration of Helsinki and Good Clinical

Practice guidelines.
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Definitions and laboratory measurements

Admission blood samples were used for laboratory assesment. The baseline clinical
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characteristics and risk factors for coronary artery disease including age, sex, smoking history,
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hypertension and diabetes mellitus were collected. Transthoracic echocardiography (Vivid

3,GE) was performed to all participants in the first month of admission with measurements of
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the left ventricular ejection fraction (EF) by using the Simpson method and left atrial

dimensions (LAD). AF was defined as any episode of atrial fibrillation during the hospital

stay after myocardial infarction. STEMI was defined in the presence of following criteria;

symptoms of myocadial ischemia with persistent ST segment changes and increase in

biomarkers of myocardial ischemia (10).

Angiographic analysis
Coronary angiography was performed via transfemoral approach to all patients. Seldinger

method with a 7 french catheter was used. Patients received 600 mg clopidogrel (p.o) and

300 mg acetylsalicylic acid (p.o) and 70 IU/kg intravenous unfractionated heparin before
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pPCI. Successful pPCI was defined as a post-procedural residual-diameter stenosis <30 %,

with TIMI 3 flow in the infarct-related artery and no procedural complications. Acute

transient or persistent coronary flow reduction (final thrombolysis in myocardial infarction

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(TIMI) flow grade <3 at the target vessel lesion in the absence of spasm, trombus, dissection

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and/or significant residual stenosis was defined as epicardial no-reflow (11). After the

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interventions, all patients were monitored in the coronary care unit until they were stabilized.

Electrocardiogram

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The standard 12-lead ECGs were obtained at a paper speed of 25 mm/s, amplitude of 10

mm/mv, and a filter range 0.04 to 40 Hz from all patients after pPCI. fQRS was defined as the
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presence of an additional R wave (R’), notching of the R or S wave, or the presence of
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fragmentation (more than one R’) in two contiguous leads corresponding to a major coronary

artery (Figure 1) (12). The ECGs were analyzed by 2 independent and experienced
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cardiologists, who were blinded to all data. In case of disagreement, the final decision was
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made by consensus.

Patients were divided into 2 groups as the AF group and the controls. All clinical,
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demographical and labaratory parameters were entered into a dataset and compared between
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AF group and the controls. Patients were also grouped regarding the presence of fQRS

complexes. All clinical, demographical and labaratory parameters were also compared

between patients with and without fQRS.

Statistical analysis

Continuous variables are expressed as mean ± standard deviation, whereas categorical

variables are expressed as percentage. Chi-square or Fisher exact test were used for

comparison of categorical data. The normality distribution of continuous variables was tested

with Kolmogorov-Smirnov test. Correlation of continuous variables was assessed by Pearson

correlation test and non-continous variables was assesed by Spearman test. Student t test or
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Mann- Whitney U test was used to compare continuous variables between the 2 groups. In

order to identify the independent predictors of arial fibrillation multivariate logistic regression

analysis was performed. A 2-sided P value of < 0.05 was considered as significant. Data were

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analyzed by using SPSS 15.0 version (SPSS Inc, Chicago, Illinois).

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RESULTS
A total of 171 patients (142 males (83%) and 29 females (17%)) with a mean age of 63±11

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years were included in the study. The baseline clinical and laboratory characteristics of the

patients are shown in Table 1.

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The infarct related coronary artery was left anterior descending artery in 78 (45.6%) and other
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coronary arteries in 93 (54.4%) patients. During the follow up after pPCI, AF was observed in

24 (%14) patients. The majority of the NOAF population (83.3%) were the patients who
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admitted with acute anterior wall STEMI.

Gender, diabetes mellitus frequency, white blood cell (WBC) count, C-reactive protein
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(CRP), fasting blood glucose (FBG), total cholesterol, no-reflow frequency, SYNTAX score,
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left ventricular ejection fraction, QRS durations before and after revascularization were

significantly different between patient groups with and without AF (Table 1 and 2). Morever,
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AF existence was significantly related to the presence and number of fQRS. On the other

hand, left atrial diameters were similar between two groups (p=0.114), and there was no

significant difference in terms of age, smoking status, hypertension frequency, heart rate,

serum creatinine, hemoglobine and platelet counts (Table 1 and 2).

There were fQRS complexes on electrocardiography in 87 (50.8%) patients. There was no

significant difference between the patients with and without fQRS in terms of hypertension

frequency, systolic blood pressure, serum creatinine, hemoglobine, smoking status and total

cholesterol (Table 3). Diabetes mellitus frequency, age, WBC count, CRP, no-reflow

frequency, FBG, multivessel disease frequency, SYNTAX score and creatine kinase
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myocardial band (CKMB) peak levels were significantly higher in patients with fQRS

complexes (Table 3 and 4). Furthermore the AF frequency were significantly higher in

patients with fQRS complexes [20 (23%) vs. 4(4.8%); p=0.001]. The clinical, angiographic

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and laboratory characteristics of the patient groups according to the presence of fQRS are

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shown in Table 3 and 4.

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Multiple logistic regression analysis provided that the CRP (OR: 1.412, 95% CI 1.086-1.723,
P=0.012), CKMB peak level (OR: 1.028, 95% CI 1.013-1.048, P=0.004), FBG (OR: 1.018,

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95% CI 1.008-1.029, P<001), SYNTAX Score (OR: 1.113, 95% CI 1.025-1.373, P=0.025),
fQRS (OR: 3.243, 95% CI 1.016-10.251, P=0.042) and P wave dispersion (OR: 1.023, 95%
CI 1.011-1.034, P=0.032) were the independent predictors of AF (Table 5).
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DISCUSSION
In this study, we focused on the potential relationship between fQRS and the development of
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AF in patients undergoing pPCI for STEMI. Our results indicate that presence of fQRS is

independently associated with AF and may be a useful marker to predict AF in patients

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undergoing pPCI for STEMI. To our knowledge, this is the first report demonstrating the
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potential role of fQRS for the development AF in patients undergoing pPCI for STEMI.

Fragmentation of QRS complex is an easy and non-invasive electrocardiographic parameter

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associated with inhomogeneous activation of the ventricles and myocardial conduction delays

due to myocardial scar and/or ischaemia, which could predict arrhythmic events as well as

death. Myocardial scar and/or ischemia have been implicated in the formation of

fragmentation of the QRS complex, leading to inhomogeneous ventricular activations.

Different fQRS morphologies are caused by shifting QRS vector during depolarization in and

around scars or myocardial ischemic areas, depending on their extent and ventricular locations

(13-15). It has been reported previously that myocardial fibrosis and scar formation lead to

abnormalities of impulse conduction (16). Pietrasik et al. have reported the sensitivity of

fQRS for determining myocardial scar, and postulated that the presence of fQRS can be a
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good predictor of cardiac events (5). . The presence of fQRS complexes was associated with

AF after coronary by-pass graft surgery (8). In the present study, AF was observed

significantly more common in patients with fQRS complexes after pPCI for STEMI. Çetin et

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al. reported that the presence of fQRS may be related to inflammation in patients with acute

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coronary syndromes (17). Similarly in our study, CRP and WBC counts were significantly

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higher in fQRS group. In another study by Bekler et al., it was reported that the presence of

fQRS complexes may be related to the complexity of coronary artery disease (18). In our

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study, the frequency of multivessel disease and SYNTAX score were also significantly

higher in fQRS group.

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Atrial fibrillation is the most common supraventricular arrhythmia following STEMI (19).

Previous studies demonstrated that AF development in the setting of acute myocardial

infarction during hospitalization is associated with a worse short and long-term prognosis in
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patients undergoing pPCI (2-4). There are many factors such as left or right ventricular
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dysfunction, atrial ischemia, pericarditis, excessive catecholamine release, drugs, acute

hypoxia, and hypopotassemia that are associated with development of atrial fibrillation after
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myocardial infarction (20). The AF in the acute phase of myocardial infarction are now well
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known; those found most frequently are indicators of left ventricular (LV) dysfunction and

increased heart rate on admission. The reduced LVEF could explain the frequent episodes of

heart failure following the onset of AF, and was found in association with increased LV

diastolic pressure and increased left atrial (LA) volume (21). In our study, gender, diabetes

mellitus, WBC count, CRP, FBG, total cholesterol, no-reflow frequency, SYNTAX score,

reduced left ventricular ejection fraction, QRS duration before and after revascularization,

number fragmented derivations on electrocardiography and the presence of fQRS were found

to be predictors of AF. In a similar study, it was reported that the number fragmented
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derivations on electrocardiography may be associated with AF development after coronary

by-pass graft surgery (8).

In a recent study that evaluated the prognostic effect of AF after STEMI treated with primary

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angioplasty, the reported incidence of AF was 6.4% (22). In a different study, the incidence of

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silent atrial fibrillation after acute myocardial infarction and in-hospital mortality in AF

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patients were reported as 16% and 17.8%, respectively (23). In our study, AF development

was observed in 24 (%14) patients after revascularization. Despite similar left atrial diameters

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between the groups with and without AF development, fQRS frequency was significantly

higher in AF group. Consequently, the presence of fQRS complexes in electrocardiograms of

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patients who underwent pPCI for STEMI may help and guide clinicians to identify the

patients with high risk of AF development and to begin preventive therapies.

The present study has some limitations. Firstly the sample size is quite small. Myocardial
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fibrosis was not investigated with advanced imaging modalities or histopathological

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examination. Furthermore, it is a nonrandomized retrospective study which has been

conducted in a single center.

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CONCLUSION

The major finding of the present study is that the presence of fQRS may predict AF

development in patients undergoing pPCI for STEMI. Fragmented QRS is a simple, cheap

and non-invasive modality that could be a valuable tool for predicting cardiac arrhythmias.

Future studies with larger sample size will be needed to confirm the results of the present

study.

Conflict of Interests
The authors declare that there is no conflict of interests regarding the publication of this
paper.
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Figure Legends:
Figure 1: Electrocardiography revealing fragmented QRS complexes in three contiguous

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leads (II, III and aVF) corresponding to right coronary artery in patient with acute inferior

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wall ST-segment elevation myocardial infarction.

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Table 1: The baseline characteristics and laboratory findings of study patients

Atrial Fibrillation

Total (n:171) -(n:147) +(n:24) P value

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Age (years) 63±11 64±11 63±8 .682

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Female Gender, n(%) 29 (17) 21 (14.3) 8 (33.3) .021

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Diabetes mellitus, (%) 61 (35.70) 46 (31.3) 15 (62.5) .003

Hypertension, (%) 89 (52) 75 (51) 14 (58.3) .506

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Smoking, n(%) 110 (64.3) 97 (66) 13 (54.2) .262

Family history, n(%) 44 (25.7) 35 (23.8) 9 (37.5) .155

SBP, (mmHg) 138.28±23.29

N 138.85±24.21 134.83±16.54 .312
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FBG, (g/dL) 120.40±43.14 113.04±34.07 165.50±62.59 .000

Baseline creatinine, (mg/dl) 0.90±0.17 0.90±0.17 0.93±0.18 .534

Haemoglobin, (g/dL) 14.95±1.64 14.91±1.64 15.17±1.67 .482

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PLT Count, (10*3/µl) 209.92±60.03 207.24±60.26 226.33±57.10 .149

WBC Count, (10*3/µl) 11.39±3.17 11.12±3.26 13.04±1.90 .006

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TC, (mg/dL) 179.12±48.43 174.41±40.13 207.97±78.12 .001

C-Reactive protein, (mg/dl) 1.25±2.36 0.98±1.20 2.90±5.36 .000

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Peak CK-MB, (U/L) 236.94±147.14 204.60±122.08 435.02±133.33 .000

Sodium (mEq/L) 138.2±4.94 138.3±4.7 137.4±6.01 .370

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Potassium (mEq/L) 4.1±0.5 4.1±0.5 3.92±0.38 .060

Abbreviations: CKMB: Creatine kinase-myocardial band, FBG: Fasting Blood Glucose, PLT:Platelets Count,SBP: Systolic Blood
Pressure, TC:Total Cholesterol, WBC:White Blood Cell (Continuous variables with normal distribution were expessed as mean ± standard
deviation and continuous variables without normal distribution were expressed as median (25 th -75th percentiles))
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Table 2: The electrocardiographic and angiographic findings of study patients

Atrial Fibrillation

Total (n:171) -(n:147) +(n:24) P value

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Electrocardiographic

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characteristics

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P-min (msec) 67.27±10.6 67.3±10.3 66.9±12.2 .859

P-max (msec) 105±14.5 103.9±14 113.9±14.89 .002

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P-dispersion (msec) 38.06±9.88 36.59±8.99 47.05±10.45 .000

fQRS in infarct related 76 (44.4)

N 60 (40.8) 16 (66.7) .018
derivations, n(%)
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Number of Fqrs 1.42±2.20 1.05±1.93 3.6±2.48 .000

Q wave 1.13±1.48 1.07±1.50 1.59±1.29 .052

QRS Duration before RV, (msec) 95.21±14.42 94.12±15.04 101.90±6.83 .014

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QRS Duration after RV, (msec) 91.95±16.44 89.98±16.59 104.0±8.55 .000

fQRS, n(%) 87 (50.9) 67 (45.60) 20 (83.30) .001

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Number of FD after RV 2.44±2.92 1.99±2.65 5.25±3.00 .000

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Angiographic characteristics
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Symptom onset to balloon time, 2.66±0.92 2.61±0.96 2.93±0.55 .116

hours

IRA LAD, n (%) 78 (45.60) 58 (39.50) 20 (83.30) .000

SYNTAX score 18.57±7.60 17.93±7.66 22.50±5.96 .004

No-reflow, n(%) 77(45) 57 (38.80) 20 (83.30) .000

LVEF, % 44.18±7.38 45.37±6.71 36.83±7.16 .000

LAD, cm 37.73±2.44 37.85±2.36 37.00±2.83 .114

Abbreviations: RV: Revascularization, FD: Fragmented Derivation, IRA:Infarcted Related Artery, LAD: Left Anterior Descending
Artery, LV EF: Left Ventricular Ejection Fraction, LAD:Left Atrial Diameter (Continuous variables with normal distribution were expessed
as mean ± standard deviation and continuous variables without normal distribution were expressed as median (25 th -75th percentiles))
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Table 4: The baseline electrocardiographic and angiographic characteristics of study patients

Fragmented QRS complexes

Total (n:171) - (n:84) + (n:87) p Value

Age (years) 63±11 61±10 66±11 0.007

T
Female, n (%) 29 (17) 4 (4.8) 25 (28.7) <0.001

IP
DM, n (%) 61 (35.7) 20 (23.8) 41 (47.1) 0.001

CR
HT, n (%) 89 (52) 40 (47.6) 49 (56.3) 0.255

Smoking, n (%) 110 (64.3) 54 (64.3) 56 (64.4) 0.991

Family History, n (%) 44 (25.7) 24 (28.6) 20 (23.0) 0.404

US
Heart Rate, (bpm) 72.37±17.12 71.46±19.41 73.25±14.63 0.496

SBP, (mmHg) 138.29±23.29 N 135.90±28.33 140.59±16.93 0.190

FBG, (g/dL) 120.40±43.14 108.76±34.43 131.64±47.69 <0.001

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Creatinine, (mg/d)l 0.90±0.17 0.93±0.17 0.88±0.17 0.087

Haemoglobin, (g/dL) 14.95±1.64 15.12±1.63 14.78±1.65 0.168

PLT Count, (10*3/µl) 209.92±60.03 198.00±45.37 221.43±69.75 0.174

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WBC Count, (10*3/µl) 11.38±3.17 10.85±3.59 11.91±2.62 0.03

TC, (mg/dL) 179.12±48.43 180.38±40.86 177.90±54.97 0.738

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CRP, (mg/dl) 1.25±2.36 0.79±0.89 1.69±3.14 0.012

Peak CK-MB, (U/L) 236.94±147.14 166.55±94.83 304.90±156.86 <0.001

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Abbreviations: IRA:Infarcted Related Artery, LAD:Left Anterior Descending Artery, MVD: Multi Vessel Disease, LV EF: Left
Ventricular Ejection Fraction, LA: Left Atrium, RV: Revascularization, AF: Atrial fibrillation (Continuous variables with normal
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distribution were expessed as mean ± standard deviation and continuous variables without normal distribution were expressed as median (25
th
-75th percentiles))
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Table 4: The baseline electrocardiographic and angiographic characteristics of study patients

Fragmented QRS complexes

Total (n:171) - (n:84) + (n:87) p Value

T
Symtom to balloon
2.66±0.92 2.30±0.74 3.01±0.95 <0.001
time

IP
IRA (LAD) 78 (45.6) 16 (19) 62 (71.3) <0.001

CR
SYNTAX 18.57±7.60 15.67±6.61 21.38±7.47 <0.001

No-reflow, n(%) 77 (45) 12 (14.3) 65 (74.7) <0.001

MVD, n(%) 20 (11.7) 4 (4.8) 16 (18.4) 0.006

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LV EF, (%) 44.18±7.38 48.05±4.12 40.44±7.90 <0.001

LA Diameter, (cm) 37.73±2.44 N 37.33±2.69 38.11±2.11 0.037

ST elevation before
9.52±6.67 8.27±5.65 12.20±7.28 0.01
RV
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ST elevation after RV 2.50±1.42 1.88±1.03 5.42±3.08 <0.001

% change in ST 64.86±20.86 78.20±13.17 51.97±18.73 <0.001

70% ST resolution 77 (45) 60 (71.4) 17 (19.5) <0.001

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QRS Duration before

95.21±14.42 90.58±15.21 99.69±12.10 <0.001
RV
QRS Duration after
91.95±16.44 83.35±14.73 100.25±13.53 <0.001
RV
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Q Wave 1.13±1.48 0.62±1.10 1.63±1.62 <0.001

AF 24 (14) 4 (4.8) 20 (23) 0.001

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Pmin 67.27±10.6 68.37±10.9 66.2±10.2 0.186

Pmax 105.3±14.5 100.4±14.33 110±13.1 <0.001

AC

Pdispersion 38.06±9.88 32.07±6.61 43.8±9 <0.001

Abbreviations: IRA:Infarcted Related Artery, LAD:Left Anterior Descending Artery, MVD: Multi Vessel Disease, LV EF: Left
Ventricular Ejection Fraction, LA: Left Atrium, RV: Revascularization, AF: Atrial fibrillation (Continuous variables with normal
distribution were expessed as mean ± standard deviation and continuous variables without normal distribution were expressed as median (25
th
-75th percentiles))
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Table 5: Independent Predictors of Atrial Fibrillation in Multivariate Logistic Regression

Analysis.
Variables Univariate OR, 95% CI Univariate P Value Multivariate OR,95% CI Multivariate P value

T
CRP 1.110 (1.065-1.157) <0.001 1.412 (1.086-1.723) .012

IP
Peak CK-MB 1.201 (1.138-1.268) <0.001 1.028 (1.013-1.048) .004

CR
FBG 0.829 (0.773-0.888) <0.001 1.018 (1.008-1.029) .000

SYNTAX Score 11.570 (4.885-27.402) <0.001 1.113 (1.025-1.373) .025

US
fQRS 2.296 (1.069-4.933) 0.030 3.243 (1.016-10.251) .042

PWD 1,112(1.060-1,166) <0.001 1.023 (1.011-1.034) .032

Abbreviations: CRP: C-Reactive Protein, CK-MB: Creatinin Kinase , FBG: Fasting Blood Glucose, PWD: P
N
Wave Dispersion
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Highlights
• The major finding of the present study is that the presence of fQRS may predict
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NOAF development in patients undergoing pPCI for STEMI.

• Fragmented QRS is a simple and cheap

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• Fragmented QRS is a non-invasive modality that could be a valuable tool for

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predicting cardiac arrhythmias.

AC