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Journal of Cardiology 71 (2018) 125–128

Contents lists available at ScienceDirect

Journal of Cardiology
journal homepage: www.elsevier.com/locate/jjcc

Original article

Clinical factors associated with the development of atrial fibrillation in


the year following STEMI treated by primary PCI
Hyo-In Rhyou (MD), Tae-Ho Park (MD)*, Young-Rak Cho (MD), Kyungil Park (MD),
Jong-Sung Park (MD), Moo-Hyun Kim (MD), Young-Dae Kim (MD)
Department of Cardiology, Dong-A University Hospital, Busan, Republic of Korea

A R T I C L E I N F O A B S T R A C T

Article history: Background: Advanced age, poor left ventricular function, and congestive heart failure are known
Received 16 May 2017 predictors of atrial fibrillation (AF) in acute myocardial infarction (AMI) patients. Recent advances in AMI
Received in revised form 26 July 2017 treatment may have changed the occurrence of new-onset AF. Thus, we investigated the factors
Accepted 24 August 2017
associated with the development of new-onset AF in ST elevation myocardial infarction (STEMI) patients.
Available online 29 September 2017
Methods: This study included 527 STEMI patients [mean age, 60.6  12.8 years; 102 (19.4%) women] who
underwent primary percutaneous coronary intervention (PCI) in the previous 7 years. New-onset AF was
Keywords:
evaluated following STEMI treated by primary PCI. Patients who developed AF during this follow-up
Cardiogenic shock
Atrial fibrillation
period were compared with those who did not develop AF to identify factors that were associated with
ST elevation myocardial infarction the development of AF.
Results: New-onset AF was documented in 81 patients (15.4%) at 1 year after STEMI. Patients with new-
onset AF (n = 81) tended to be older (p < 0.001); were more often female (p = 0.009); had more
congestive heart failure (p = 0.015); had less use of beta-blockers (p = 0.001); had more often used
antiarrhythmic drugs (p < 0.001); experienced cardiogenic shock more frequently (p = 0.038); had lower
left ventricular ejection fraction (p = 0.024); and had higher E velocity (p < 0.001), E/e0 (p = 0.011), and
left atrial volume index (LAVI; p = 0.029) than the 446 patients with no AF. Multivariate regression
analysis revealed that cardiogenic shock, LAVI, and age were predictors of new-onset AF in STEMI
patients (OR 2.823, 1.254, and 1.124; p = 0.005, <0.001, and 0.028, respectively).
Conclusion: Cardiogenic shock was a new predictor of new-onset AF in STEMI patients.
© 2017 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Introduction occurrence of AF in AMI [8]. Many predictors of AF after AMI such


as advanced age, female sex, left ventricular hypertrophy, and
Atrial fibrillation (AF) is one of the most common supraven- congestive heart failure (CHF) have been identified [10], but
tricular arrhythmias in acute myocardial infarction (AMI), with an predictors of AF in patients with ST elevation myocardial infarction
incidence of 5–18% in patients with AMI [1,2]. Its occurrence in AMI (STEMI) have yet to be clearly defined. Our aim was to identify
patients is important because AF increases the risk of cardiovas- factors that predict the development of AF in STEMI patients.
cular events [3]. Notably, structural heart disease, hypertension,
diabetes, and advanced age induce progressive structural remo-
Methods
deling in the atria, which leads to the development of AF
[4]. Dysfunctions of the sinoatrial (SA) and atrioventricular (AV)
STEMI patients who underwent primary percutaneous coro-
nodes also contribute to the development of AF. In AMI patients,
nary intervention (PCI) between January 2009 and December
acute ischemic insults to the atria and ventricles can induce AF [5–
2015 at Dong-A University Hospital (Busan, Korea) were screened.
9]. Moreover, the location of the culprit vessel also affects the
Of the 545 patients, we excluded 5 patients with a previous history
of AF, 10 patients who died during admission, and 3 patients who
did not complete the 1-year follow-up. Thus, a total of 527 patients
* Corresponding author at: Department of Cardiology, Dong-A University
with STEMI were enrolled in the study. The diagnosis of STEMI was
Hospital, Daeshingongwon-Ro 26, Seo-gu, Busan 602-715, Republic of Korea. based on typical chest pain symptoms, electrocardiographic (ECG)
E-mail address: thpark65@dau.ac.kr (T.-H. Park). changes, and serial elevation of serum cardiac enzymes. The ECG

http://dx.doi.org/10.1016/j.jjcc.2017.08.004
0914-5087/© 2017 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
126 H.-I. Rhyou et al. / Journal of Cardiology 71 (2018) 125–128

criterion for the diagnosis of STEMI was an ST-segment elevation of with STEMI. Variables with p-values 0.20 in univariate analyses
0.2 mV in 2 contiguous leads or new left bundle branch block. were candidates for the multivariable logistic regression model. A
AF was defined as the absence of P waves with irregular RR backward stepwise elimination algorithm reduced the variables
intervals. Cardiogenic shock was defined as a state of systolic blood until only significant variables (p < 0.05) remained in the
pressure less than 80 mmHg due to STEMI in the absence of multivariate model. All statistical comparisons were two-sided,
hypovolemia that was associated with clinical signs of hypoperfu- and the statistical significance was set at p < 0.05. The statistical
sion or CHF [11]. CHF was diagnosed based on a known history of analysis was performed using the Statistical Package for Social
CHF and/or Killip class 2 at any time during hospitalization with Science v. 20.0 (SPSS; IBM, Chicago, IL, USA).
the need for diuretics [12]. Dyslipidemia was defined by either
documentation of the diagnosis in the patient's history, current use
of lipid-modifying drugs, a fasting total cholesterol level 200 mg/ Results
dl, or a low-density lipoprotein cholesterol level of 130 mg/dl.
Hypertension and diabetes were defined based on documentation A total of 527 STEMI patients with primary PCI were enrolled in
of the clinical diagnosis. All patients received standard pharmaco- the study. The mean age was 60.6  12.8 years, and 102 patients
logical therapies [13] and revascularization, had continuous (19.4%) were female. New-onset AF was documented in 81 (15.4%)
ECG monitoring in the coronary care unit, and had 12-lead ECG at 1 year after STEMI. Early AF was identified in 67 patients (12.7%)
performed daily during their hospital admission. After hospital and late AF in 14 patients (2.7%). In the STEMI patients, the culprit
discharge, all patients were followed up with ECG check up within vessel was LAD in 271 patients (51.4%), RCA in 203 patients (38.5%),
1 month and every 2 or 3 months after. New-onset AF patients LCX in 50 patients (9.5%), and LMCA in 3 patients (0.6%). However,
were divided into two groups. Early AF was defined as AF in patients with new-onset AF, the most common culprit vessel
documented during admission, and late AF was defined as new- was the RCA (35 patients; 43.2%), followed by the LAD (34 patients;
onset AF within 1 year after discharge. This retrospective study was 42.0%), the LCX (10 patients; 12.3%), and the LMCA (2 patients;
approved by our institutional review board. 2.5%) (Table 1).
Patients with new-onset AF were older (65.9  12.4 years vs.
Echocardiography 59.7  12.7 years, p < 0.001), more often female (30.9% vs. 17.3%,
p = 0.009), and more often had cardiogenic shock (16.0% vs. 8.3%,
All patients underwent echocardiography within 48 h after p = 0.038). Patients with new-onset AF had less use of beta-
hospital admission. Echocardiography was performed using the blockers (86.7% vs. 53.6%, p = 0.001) and had more often used
iE33 ultrasound system with 2.5-MHz transducer (Philips, antiarrhythmic drugs (21.0% vs. 4.5%, p < 0.001) than patients with
Amsterdam, The Netherlands). Standard 2D and Doppler echocar- no AF. However, there was no significant difference with respect to
diography were performed according to the recommendations of the location of the culprit vessel between the AF group vs. the no AF
the American Society of Echocardiography [14,15]. Left ventricular group (Table 1). An implantable cardioverter defibrillator was
end-diastolic dimension (LVEDD) and left ventricular end-systolic implanted in one patient with no AF.
dimension (LVESD) were measured using 2D echocardiography.
Left ventricular ejection fraction (LVEF) was assessed semi- Echocardiographic characteristics
quantitatively with visual estimation and the wall-motion score
index. Left atrial (LA) volume was measured using the biplane In echocardiographic analysis, patients who developed new-
Simpson method at end-systole from apical 4- and 2-chamber views. onset AF had lower LVEF (46.0  8.6% vs. 48.4  8.8%, p = 0.024),
LA volume index (LAVI) was calculated as the LA volume divided higher E velocity (75.9  24.4 cm/s vs. 66.4  19.4 cm/s, p < 0.001),
by the body surface area. LV diastolic function was assessed by higher E/e0 (12.1  6.7 vs. 10.1  3.9, p = 0.011), and higher LAVI
conventional Doppler (mitral E, mitral A, and the E/A ratio) and by (34.4  13.1 ml/m2 vs. 29.4  8.6 ml/m2, p = 0.002) than the
tissue Doppler imaging (TDI). Peak systolic (s0 ), early diastolic (e0 ), and 446 patients without AF (Table 2). The incidence of AF develop-
late diastolic velocities (a0 ) were obtained at the lateral mitral annulus ment increased as LAVI increased (Fig. 1).
from the apical 4-chamber view. LV systolic and diastolic dysfunction
were defined as LVEF <40% and E/e0 ratio >15, respectively.
Table 1
Baseline clinical and angiographic characteristics.
Coronary angiography
All (n = 527) No AF (n = 446) AF (n = 81) p-value

Coronary angiography was performed in all patients. The culprit Age 60.6  12.8 59.7  12.7 65.9  12.4 <0.001
vessel was defined as a vessel with complete closure or the most Female sex 102 (19.4%) 77 (17.3%) 25 (30.9%) 0.009
Hypertension 265 (50.3%) 220 (49.3%) 45 (55.6%) 0.335
significant stenosis corresponding to ECG changes. Patients were Diabetes mellitus 153 (29.0%) 135 (30.3%) 18 (22.2%) 0.183
further classified by the site of occlusion: left anterior descending Dyslipidemia 399 (75.7%) 344 (77.1%) 55 (67.9%) 0.090
artery (LAD), left circumflex artery (LCX), right coronary artery DBT, min 61.5  68.9 60.7  67.9 66.0  74.7 0.530
(RCA), and left main coronary artery (LMCA). CHF 148 (28.0%) 114 (25.5%) 34 (42.0%) 0.015
Cardiogenic shock 50 (9.5%) 37 (8.3%) 13 (16.0%) 0.038
Culprit LAD 271 (51.4%) 237 (53.1%) 34 (42.0%) 0.070
Statistical analysis Culprit LCX 50 (9.5%) 40 (9.0%) 10 (12.3%) 0.310
Culprit RCA 203 (38.5%) 168 (37.7%) 35 (43.2%) 0.385
Baseline clinical, echocardiographic, and angiographic data Culprit LMCA 3 (0.6%) 1 (0.2%) 2 (2.5%) 0.063
were collected and analyzed. The data are presented as mean Aspirin 517 (98.1%) 438 (98.2%) 79 (97.5%) 0.821
Beta-blocker 432 (82.0%) 387 (86.7%) 45 (55.6%) 0.001
values with standard deviations for normally distributed continu-
ACEI/ARB 448 (85.0%) 380 (85.2%) 68 (84.0%) 0.732
ous variables and as numbers and percentages for categorical Statin 456 (86.5%) 387 (86.7%) 69 (85.2%) 0.634
variables. The differences between the two groups were assessed Antiarrhythmic drugs 37 (7.0%) 20 (4.5%) 17 (21.0%) <0.001
with the unpaired 2-tailed t-test for normally distributed AF, atrial fibrillation; CHF, congestive heart failure; DBT, door to balloon time;
continuous values and with the chi-square test for categorical LAD, left anterior descending artery; LCX, left circumflex artery; RCA, right
variables. Logistic regression analysis was used to identify coronary artery; LMCA, left main coronary artery; ACEI, angiotensin-converting
independent risk factors for the development of AF in patients enzyme inhibitor; ARB, angiotensin-receptor blocker.
H.-I. Rhyou et al. / Journal of Cardiology 71 (2018) 125–128 127

Table 2 volume was significantly associated with the development of new-


Baseline echocardiographic characteristics.
onset AF in this study. (iii) The location of the culprit vessel was not
All (n = 527) No AF (n = 446) AF (n = 81) p-value significantly related to the occurrence of new-onset AF in STEMI
LVEDD (mm) 49.7  5.4 49.8  5.2 48.9  6.1 0.156
patients.
LVPW (mm) 9.5 1.2 9.5  1.2 9.5 1.2 0.968 Structural remodeling, which is characterized by increased LA
LVSW (mm) 9.3  1.5 9.3  1.5 9.3  1.5 0.733 size and atrial fibrosis, is perhaps the most obvious mechanism of
LVEF (%) 48.0  8.8 48.4  8.8 46.0  8.6 0.024 AF, but it may not be the major effect in STEMI patients. In contrast,
Mitral E (cm/s) 67.8  20.5 66.4  19.4 75.9  24.4 <0.001
acute atrial ischemia and impaired atrial perfusion may directly
Mitral A (cm/s) 76.0  20.7 75.3  20.0 80.4  24.1 0.058
Mitral E/A 0.93  0.44 0.95  3.9 0.75  0.64 0.190 cause AF in STEMI patients. Cardiogenic shock in STEMI patients is
e0 (lateral) (cm/s) 7.0  2.2 7.1  2.2 6.9  2.1 0.398 a severe form of CHF that predisposes patients to AF. Patients with
E/e0 10.4  4.5 10.1 3.9 12.1 6.7 0.011 cardiogenic shock tend to have more severe myocardial ischemia,
LAVI (ml) 20.1 9.6 29.4  8.6 34.4  13.1 0.002 which can induce atrial ischemia and provoke new-onset AF.
LVEF <40% 60 (11.4%) 46 (10.5%) 13 (11.4%) 0.178
E/e0 >15 54 (10.2%) 36 (8.2%) 17 (21.5%) 0.001
Cardiogenic shock is the leading cause of death in AMI patients,
and mortality from cardiogenic shock is greater than 50%
LAVI, left atrial volume index; LVEDD, left ventricular end-diastolic dimension;
[16–18]. The incidence of AF is more common in patients who
LVPW, left ventricular posterior wall; LVEF, left ventricular ejection fraction;
LVSW, left ventricular septal wall. had cardiogenic shock after STEMI than in those who had no
cardiogenic shock [19]. In the present study, 50 STEMI patients had
cardiogenic shock, and 13 (26.0%) of them developed new-onset
AF, which was more common than in the total group of STEMI
patients (15.3%). Although Kinjo et al. reported that Killip class IV
(cardiogenic shock) was an independent predictor of new-onset AF
[20], cardiogenic shock was not highlighted in past studies. Rather,
previous studies showed that CHF is a predictor of new-onset AF in
AMI [1,10,21]. In this study, cardiogenic shock was the strongest
predictor of new-onset AF in STEMI patients. Thus, we speculate
that cardiogenic shock is a more potent risk factor than CHF for the
development of AF in STEMI patients.
AF can be secondary to structural remodeling of the LA, and
both LA pressure and LA remodeling may be increased in patients
with diastolic dysfunction. New-onset AF occurs more frequently
in patients with diastolic dysfunction [22,23]. Measurement of the
LA volume is helpful in evaluating LV diastolic function because it
often reflects the LV filling pressure as well as the chronicity of
diastolic dysfunction. Furthermore, LAVI 34 ml/m2 is an inde-
pendent predictor of AF [14]. Likewise, in this study, LAVI was an
independent index that predicted new-onset AF in STEMI patients.
Fig. 1. Incidence of AF according to LAVI. The incidence of AF increased as LAVI However, the cut-off value of LAVI for predicting new-onset AF was
increased. AF, atrial fibrillation; LAVI, left atrial volume index. 30 ml/m2, which is lower than the upper normal limit of 34 ml/m2
[24]. Accordingly, the sensitivity and specificity for using LAVI as a
predictor of new-onset AF was not high in this study, but our
Prediction of new-onset AF results may still indicate that upper normal size of LA can cause the
development of new-onset AF in STEMI.
Multivariate regression analysis revealed that cardiogenic Since acute atrial ischemia can be a mechanism underlying
shock, LAVI, and age were predictors of new-onset AF in STEMI new-onset AF in STEMI, we hypothesized that new-onset AF may
patients (OR 2.823, 1.254, and 1.124, p = 0.005, <0.001, and 0.028, be more related to the LCX or the RCA as the culprit vessel than to
respectively) (Table 3). In the early AF group, cardiogenic shock (OR LAD as the culprit vessel. Some studies have reported that new-
2.232, 95% CI 1.047–4.758, p = 0.038) was a predictor of new-onset onset AF is more frequent when RCA or LCX is the culprit vessel
AF, whereas, age (OR 1.059, 95% CI 0.010–1.108, p = 0.017) was a than when LAD is the culprit vessel [3,20,25]. In this study, out of
predictor in the late AF group. 81 STEMI patients with new-onset AF, the culprit vessel was RCA in
35 (43.2%) patients, LAD in 34 (42.0%), LCX in 10 (12.3%), and LMCA
in 2 (2.5%). However, when we grouped STEMI patients according
Discussion to the culprit vessel, excluding LMCA as the culprit vessel, the
incidence of new-onset AF was highest in the LCX group (20%),
The major findings of the present study were as follows: (i) followed by the RCA group (17.2%) and the LAD group (12.5%).
cardiogenic shock was a strong predictor of new-onset AF in STEMI Although new-onset AF was more common when the culprit vessel
patients, which was not highlighted in the past studies. (ii) LA was not the LAD than when it was the LAD, this did not reach
statistical significance in this study.
The mechanisms underlying new-onset AF in STEMI patients
Table 3 remain unclear, and multiple mechanisms may be involved.
Independent predictors of new-onset AF in STEMI patients. Although the use of beta-blockers was not an independent
OR 95% CI p-value predictor of new-onset AF, lower beta-blocker use affected the
development of new-onset AF in this study. Thus, an increased
Cardiogenic shock 2.823 1.372–5.808 0.005
LAVI 1.254 1.026–1.083 <0.001 catecholamine level is another mechanism underlying new-onset
Age 1.124 1.003–1.046 0.028 AF in STEMI patients. Our findings suggest that the predictors of
LAVI, left atrial volume index.
new-onset AF in STEMI patients are different between early and
late phase AF. For early phase AF, cardiogenic shock was the only
128 H.-I. Rhyou et al. / Journal of Cardiology 71 (2018) 125–128

predictor for new-onset AF in STEMI, implying that atrial ischemia [10] Schmitt J, Duray G, Gersh BJ, Hohnloser SH. Atrial fibrillation in acute myocar-
dial infarction: a systematic review of the incidence, clinical features and
and hemodynamic overload are main causes of AF. However, in late prognostic implications. Eur Heart J 2009;30:1038–45.
phase AF, atrial remodeling and fibrosis (due to advanced age) may [11] Goldberg RJ, Samad NA, Yarzebski J, Gurwitz J, Bigelow C, Gore JM. Temporal
lead to new-onset AF, even in STEMI. trends in cardiogenic shock complicating acute myocardial infarction. N Engl J
Med 1999;340:1162–8.
Advanced age, poor LV function, and CHF are common [12] Køber L, Torp-Pedersen C, Pedersen OD, Høiberg S, Camm AJ. Importance of
predictors of new-onset AF in AMI patients. However, this study congestive heart failure and interaction of congestive heart failure and left
found that cardiogenic shock, LAVI, and advanced age were ventricular systolic function on prognosis in patients with acute myocardial
infarction. Am J Cardiol 1996;78:1124–8.
predictors of the development of new AF in STEMI patients. Thus, [13] Hsieh MJ, Lee CH, Chen CC, Chang SH, Wang CY, Hsieh IC. Predictive
acute atrial ischemia due to cardiogenic shock, as well as performance of HAS-BLED risk score for long-term survival in patients with
structural remodeling of the LA due to advanced age and diastolic non-ST elevated myocardial infarction without atrial fibrillation. J Cardiol
2017;69:136–43.
dysfunction, might be related to AF development in STEMI
[14] Nagueh SF, Appleton CP, Gillebert TC, Marino PN, Oh JK, Smiseth OA, Waggoner
patients. AD, Flachskampf FA, Pellikka PA, Evangelista A. Recommendations for the
This study had limitations. First, it was a relatively small study evaluation of left ventricular diastolic function by echocardiography. J Am Soc
that was conducted at a single center. Second, new-onset AF was Echocardiogr 2009;22:107–33.
[15] Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, Picard
diagnosed by retrospective chart review with ECG, the actual MH, Roman MJ, Seward J, Shanewise JS, Solomon SD, Spencer KT, Sutton MS,
number of AF could have underestimated. Stewart WJ, Chamber Quantification Writing Group; American Society of
In conclusion, this study demonstrated that cardiogenic shock, Echocardiography's Guidelines and Standards Committee; European Associa-
tion of Echocardiography. Recommendations for chamber quantification: a
LAVI, and age were predictors of new-onset AF in STEMI patients. report from the American Society of Echocardiography's Guidelines and
Additional prospective studies in a larger population are needed to Standards Committee and the Chamber Quantification Writing Group, devel-
confirm and clarify our findings. oped in conjunction with the European Association of Echocardiography, a
branch of the European Society of Cardiology. J Am Soc Echocardiogr
2005;18:1440–63.
Funding [16] Califf RM, Bengtson JR. Cardiogenic shock. N Engl J Med 1994;330:1724–30.
[17] Dauerman HL, Goldberg RJ, White K, Gore JM, Sadiq I, Gurfinkel E, Budaj A,
None. Lopez de Sa E, Lopez-Sendon J, Global Registry of Acute Coronary Events.
GRACE Investigators. Revascularization, stenting, and outcomes of patients
with acute myocardial infarction complicated by cardiogenic shock. Am J
Conflict of interest Cardiol 2002;90:838–42.
[18] Thiele H, Zeymer U, Neumann F-J, Ferenc M, Olbrich HG, Hausleiter J, de
The authors declare that there is no conflict of interest. Waha A, Richardt G, Hennersdorf M, Empen K, Fuernau G, Desch S, Eitel I,
Hambrecht R, Lauer B, et al. Intra-aortic Balloon Pump in cardiogenic shock
II (IABP-SHOCK II) trial investigators. Intra-aortic balloon counterpulsation
References in acute myocardial infarction complicated by cardiogenic shock (IABP-
SHOCK II): final 12 month results of a randomised, open-label trial. Lancet
[1] Pizzetti F, Turazza FM, Franzosi MG, Barlera S, Ledda A, Maggioni AP, Santoro L, 2013;382:1638–45.
Tognoni G, GISSI-3 Investigators. Incidence and prognostic significance of [19] Awad HH, Anderson Jr FA, Gore JM, Goodman SG, Goldberg RJ. Cardiogenic
atrial fibrillation in acute myocardial infarction: the GISSI-3 data. Heart shock complicating acute coronary syndromes: insights from the Global
2001;86:527–32. Registry of Acute Coronary Events. Am Heart J 2012;163:963–71.
[2] Sugiura T, Iwasaka T, Ogawa A, Shiroyama Y, Tsuji H, Onoyama H, Inada M. [20] Kinjo K, Sato H, Sato H, Ohnishi Y, Hishida E, Nakatani D, Mizuno H, Fukunami
Atrial fibrillation in acute myocardial infarction. Am J Cardiol 1985;56:27–9. M, Koretsune Y, Takeda H, Hori M, Osaka Acute Coronary Insufficiency Study
[3] Sakata K, Kurihara H, Iwamori K, Maki A, Yoshino H, Yanagisawa A, Ishikawa K. (OACIS) Group. Prognostic significance of atrial fibrillation/atrial flutter in
Clinical and prognostic significance of atrial fibrillation in acute myocardial patients with acute myocardial infarction treated with percutaneous coronary
infarction. Am J Cardiol 1997;80:1522–7. intervention. Am J Cardiol 2003;92:1150–4.
[4] Wann LS, Curtis AB, Ellenbogen KA, Estes 3rd NA, Ezekowitz MD, Jackman WM, [21] Wong CK, White HD, Wilcox RG, Criger DA, Califf RM, Topol EJ, Ohman EM. New
January CT, Lowe JE, Page RL, Slotwiner DJ, Stevenson WG, Tracy CM. atrial fibrillation after acute myocardial infarction independently predicts
2011 ACCF/AHA/HRS focused update on the management of patients with death: the GUSTO-III experience. Am Heart J 2000;140:878–85.
atrial fibrillation (update on dabigatran): a report of the American College of [22] Abhayaratna WP, Seward JB, Appleton CP, Douglas PS, Oh JK, Tajik AJ, Tsang TS.
Cardiology Foundation/American Heart Association Task Force on practice Left atrial size: physiologic determinants and clinical applications. J Am Coll
guidelines. J Am Coll Cardiol 2011;57:1330–7. Cardiol 2006;47:2357–63.
[5] Kyriakidis M, Barbetseas J, Antonopoulos A, Skouros C, Tentolouris C, [23] Jons C, Joergensen RM, Hassager C, Gang UJ, Dixen U, Johannesen A, Olsen NT,
Toutouzas P. Early atrial arrhythmias in acute myocardial infarction. Role Hansen TF, Messier M, Huikuri HV, Thomsen PE. Diastolic dysfunction predicts
of the sinus node artery. Chest 1992;101:944–7. new-onset atrial fibrillation and cardiovascular events in patients with acute
[6] Sugiura T, Iwasaka T, Takahashi N, Yuasa F, Takeuchi M, Hasegawa T, Matsutani myocardial infarction and depressed left ventricular systolic function: a
M, Inada M. Factors associated with atrial fibrillation in Q-wave anterior CARISMA substudy. Eur J Echocardiogr 2010;11:602–7.
myocardial infarction. Am Heart J 1991;121:1409–12. [24] Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, Flachskampf
[7] Rechavia E, Strasberg B, Mager A, Zafrir N, Kusniec J, Sagie A, Sclarovsky S. FA, Foster E, Goldstein SA, Kuznetsova T, Lancellotti P, Muraru D, Picard MH,
The incidence of atrial arrhythmias during inferior wall myocardial infarction with Rietzschel ER, Rudski L, et al. Recommendations for cardiac chamber quanti-
and without right ventricular involvement. Am Heart J 1992;124:387–91. fication by echocardiography in adults: an update from the American Society
[8] Hod H, Lew AS, Keltai M, Cercek B, Geft IL, Shah PK, Ganz W. Early atrial of Echocardiography and the European Association of Cardiovascular Imaging.
fibrillation during myocardial infarction: a consequence of impaired left atrial J Am Soc Echocardiogr 2015;28:1–39.
perfusion. Circulation 1987;75:146–50. [25] Crenshaw BS, Ward SR, Granger CB, Stebbins AL, Topol EJ, Califf RM. Atrial
[9] ZoniBerisso M, Carratino L, Ferroni A, De Caro E, Mela GS, Vecchio C. The fibrillation in the setting of acute myocardial infarction: the GUSTO-I experience.
relation between supraventricular tachyarrhythmias and left ventricular dys- Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries. J Am
function after acute myocardial infarction. Acta Cardiol 1988;43:689–701. Coll Cardiol 1997;30:406–13.

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