Download Hyperglycemia Increases New-Onset Atrial Fibrillation in Patients

Hyperglycemia Predicts AF in STEMIs
Original Article
Acta Cardiol Sin 2012;28:279-285
Arrhythmia and Electrophysiology
Hyperglycemia Increases New-Onset Atrial
Fibrillation in Patients with Acute ST-Elevation
Myocardial Infarction
Hong-Pin Hsu,1 Yu-Lan Jou,1 Tao-Cheng Wu,2,3 Ying-Hwa Chen,2,3 Shao-Song Huang,2,3 Yenn-Jiang Lin,2,3
Li-Wei Lo,2,3 Yu-Feng Hu,2,3 Ta-Chuan Tuan,3 Shih-Lin Chang2,3 and Shih-Ann Chen2,3
Background: Atrial fibrillation (AF) is a frequent complication of acute myocardial infarction, and is often
accompanied by an increased morbidity and mortality. The aim of this study was to investigate the predictors and
outcome of new-onset AF occurring after acute ST-elevation myocardial infarction (STEMI).
Methods: A total of 307 patients with acute STEMI from May 2007 to June 2009 were included in our study. Of
those patients, 57 patients experienced new-onset AF during their hospitalization in the coronary care unit with
continuous ECG monitoring. The primary endpoint was the occurrence of AF during the hospitalization. The
secondary endpoint was the all-cause mortality during a 12-month follow-up period.
Results: Two hundred eighty three patients (92.2%) received revascularization during the hospitalization. The
patients with new-onset AF after the acute STEMI were older, with lower diastolic blood pressure, higher initial
fasting glucose, lower lipid level, and a higher incidence of coronary artery disease history when compared to those
without new-onset AF. In a multivariable analysis, the initial fasting glucose level (p = 0.025, OR = 1.007, 95% CI =
1.001~1.012) was an independent predictor of the occurrence of new-onset AF after acute STEMI. New-onset AF
was associated with a higher all-cause mortality rate during the follow-up (p = 0.001).
Conclusion: A higher initial fasting glucose level was an independent predictor of the occurrence of AF in patients
with acute STEMI, which may be associated with a poor prognosis.
Key Words:
Atrial fibrillation · Hyperglycemia · Myocardial infarction
INTRODUCTION
and associated with an increased mortality and morbidity.1,2 Those patients with AMI who developed AF were
at a greater risk for an acute stroke and mortality during
their hospitalization than those without it.3 On the other
hand, ventricular tachyarrhythmias are also an important
cause of sudden cardiac death in patients with AMI. The
patients with ventricular tachyarrhythmias had higher
low-density lipoprotein cholesterol (LDL-C) levels and a
lower blood pressure on their initial arrival, suggesting
that dyslipidemia may impose a higher risk of developing tachyarrhythmias in the acute phase of ST-segment
elevation myocardial infarction (STEMI).4 However, the
relationship of new-onset AF to the clinical biochemical
markers and outcome in the patients with acute STEMI
is still not fully clarified. The purpose of this study was
Atrial fibrillation (AF) is the most frequently occurring supraventricular tachycardia during an acute myocardial infarction (AMI), with an incidence of 6-21%,
Received: June 9, 2011
Accepted: July 13, 2012
1
Division of Cardiology, Department of Internal Medicine, Taipei
City Hospital; 2Division of Cardiology, Taipei Veterans General
Hospital; 3Department of Medicine and Institute of Clinical Medicine,
Cardiovascular Research Center, National Yang-Ming University
School of Medicine, Taipei, Taiwan.
Address correspondence and reprint requests to: Dr. Shih-Lin Chang,
Division of Cardiology, Taipei Veterans General Hospital, No. 201,
Sec. 2, Shih-Pai Road, Taipei, Taiwan. Tel: 886-2-2875-7156; Fax:
886-2-2873-5656; E-mail: [email protected]
279
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Hong-Pin Hsu et al.
total creatine kinase (CK) level was < 200 IU/L.
AF was detected by the 12-lead ECGs recorded during the entire hospital course and the 24 hour continuous
ECG monitoring in the CCU. The ECG monitor automatically detected and recorded any non-sustained or
sustained supraventricular and ventricular arrhythmias
after the myocardial infarction, and the recording was
further confirmed by the CCU doctor. All of the 12-lead
ECGs acquired during the hospitalization were confirmed by the cardiologists. Patients who had AF episodes in the past were excluded from the study.
The serum lipids, including the total cholesterol
(TC), LDL-C, high-density lipoprotein cholesterol
(HDL-C), triglyceride (TG), and fasting glucose level
were sampled on the morning after the day of admission,
and all patients generally should fast for at least 8 hours
before checking those biochemical data. The C-reactive
protein (CRP) level was checked immediately upon the
patient’s arrival at our emergency room.
Hypertension was defined as a systolic blood pressure (SBP) of ³ 140 mmHg and/or diastolic pressure
(DBP) of ³ 90 mmHg with more than two readings during a resting state, according to the criteria of the Joint
National Committee-VII (JNC-VII),6 or those who had
taken antihypertensive medications during their daily
life. Diabetes mellitus (DM) was defined according to the
American Diabetes Association criteria,7 or as those who
used oral hypoglycemic agents or insulin for blood sugar
control. A past history of coronary artery disease (CAD)
was defined according to the results of the previous coronary angiography (CAG) or non-invasive stress imaging.
The left atrial (LA) diameter and left ventricular
ejection fraction (LVEF) were determined by echocardiography during the hospitalization. The culprit lesion
was identified by correlating the coronary angiography
with the ST-segment elevation on the admission ECG,
and the regional wall motion abnormality in the left
ventriculography. Coronary artery stenosis of > 50% in
diameter was regarded as significant. The number of diseased arteries was determined accordingly. The hemodynamic status included the SBP, DBP, and heart rate,
which were recorded immediately after arrival at the
emergency room.
to determine the predictors of the risk of developing
new-onset AF in the clinical setting of acute STEMI, and
to try to elucidate the relationship between new-onset
AF and the clinical outcome.
PATIENTS AND METHODS
A retrospective study was designed and we enrolled
those patients admitted to Taipei Veterans General Hospital of Taiwan due to acute STEMI from May 2007 to
June 2009. A total of 307 consecutive patients without
any documented AF prior to admission were included in
this study based on the registration of the coronary care
unit (CCU) of Taipei Veterans General Hospital. The
outcome within 12 months after discharge was acquired
by the medical records of the hospital and telephone
communication with family members.
The patients included in this study met the following
criteria for acute STEMI: (1) chest pain of ³ 30 minutes
in duration; (2) electrocardiograph (ECG) showing
ST-segment elevation of ³ 0.1 mV in two or more leads;
and (3) elevated creatine kinase-MB (CK-MB) isoenzymes or troponin-I within 24 hours of the chest pain.
Most of these patients were treated with a primary percutaneous coronary intervention (PCI), coronary artery
bypass graft (CABG) surgery, or medical control and
then an elective PCI according to the guidelines published by the American College of Cardiology/American
Heart Association (ACC/AHA).5 All the patients were
initially admitted to the CCU, with follow-up cardiac
enzyme tests and 12 lead ECGs taken every 6 hours to
trace the ST-T change after the acute STEMI. Continuous ECG, blood pressure and oximetry monitoring
were performed in all the study patients when they were
in the CCU. The medications used during the hospital
course, such as aspirin, clopidogrel, anticoagulants, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers, beta-antagonists, lipid-lowering agents, and intravenous or sublingual nitroglycerin
were all administered as recommended by the ACC/
AHA guidelines and were continued after discharge
from the hospital unless there was any contraindication
for the patients. The patients were transferred to an ordinary ward if they became hemodynamically stable, no
symptoms of ongoing ischemia were observed, and the
Acta Cardiol Sin 2012;28:279-285
Statistical analyses
Data are expressed as the mean ± standard deviation.
280
Hyperglycemia Predicts AF in STEMIs
CAD into the multivariable analysis, the initial fasting
glucose level [odds ratio (OR) = 1.007, confidence interval (CI) = 1.001~1.012, p = 0.025] was an independent
predictor of the occurrence of new-onset AF after acute
STEMI (Table 2).
After a follow-up of 12 months, the patients with
new-onset AF had a higher all-cause mortality rate
(39.1% vs. 16.0%, p = 0.001) (Figure 1) and a higher
rate of cardiovascular death (28.1% vs. 13.6%, p = 0.01)
than those without AF. The causes of cardiovascular
death included recurrent myocardial infarction (2 patients), decompensated heart failure (35 patients), and
ventricular arrhythmias (13 patients). The non-cardiovascular deaths included septic shock (5 patients) and
malignant neoplasms (2 patients). Because there was a
significant difference in the age between new-onset AF
and non-AF, the age was adjusted in a Cox regression
model to compare the mortality of these two groups. The
all-cause mortality rate of new-onset AF during 12
months was still higher than that for non-AF (Hazard
ratio = 1.851, 95% CI = 1.062~3.227, p = 0.03).
Chi-square and Fisher’s exact tests were used for categorical data. Student’s t tests were used for continuous
data. A univariate analysis of the various clinical variables was performed to determine the predictors of
new-onset AF occurring after acute STEMI. The variables selected to be tested in the multivariate analysis
(logistic regression) were those with p values of < 0.1 in
the univariate models. The survival rate and cumulative
survival curve between the two groups were analyzed by
a Kaplan-Meier method and log-rank test. The comparison of the all-cause mortality between the sinus rhythm
and AF groups was further adjusted by age with a Cox
regression analysis. A p value of < 0.05 was considered
statistically significant.
RESULTS
Among the 307 patients admitted due to an acute
STEMI, 83% were male and 17% were female. A total of
283 patients (92.2%) received revascularization (either a
primary PCI, elective PCI, or CABG), including a primary PCI in 250 patients (81%) during the hospitalization. Nearly half (45.3%) of the patients had a culprit lesion in the left anterior descending coronary artery, 12.1%
in the left circumflex coronary artery, 33.2% in the right
coronary artery, and 4.9% of those patients had left main
coronary disease. Fourteen patients had no definite culprit
lesion due to coronary spasms. There were 57 patients
(18.6%) that suffered from new-onset AF during the
hospital course, and all of them had paroxysmal AF.
The comparison of the clinical characteristics in the
patients with and without new-onset AF after acute
STEMI is shown in Table 1. Patients with new-onset AF
had a higher incidence of a CAD history than those without new-onset AF. There was no significant difference in
the culprit arteries between the patients with and without
new-onset AF. Patients with new-onset AF had a higher
mean fasting glucose level. There was a trend for the patients with a history of DM to be associated with a higher
occurrence of new-onset AF compared with those without
it. The patients with new-onset AF had a lower incidence
of a history of hyperlipidemia with a lower triglyceride
level and total cholesterol level compared to those without AF. After taking the fasting glucose, TG, and LDL-C
levels, age, diastolic BP, TIMI score, history of DM and
DISCUSSION
New onset of AF after an acute STEMI
A variant incidence of AF after an AMI has been reported in previous studies. Goldberg et al. reported that
the incidence of new-onset AF after AMI increased from
11.3% to 14.4% during the period 1999 to 2005.2 The
development of new-onset AF after AMI was associated
with an increase in the mortality and risk of stroke during the hospitalization. A discordant incidence of AF
after AMI has been demonstrated in previous studies.
Pederson et al. found that the incidence of paroxysmal
AF/atrial flutter after AMI was 21%.8 In the GUSTO-I
trial, the incidence of AF after AMI was 2.5% on admission and 7.9% after enrollment. In the GRACE trial, the
incidence of new-onset AF was 6.2%. In our study, the
incidence of new-onset AF after acute STEMI was about
18%, which was higher than that of some other studies
(5% to 15%).9-13 The different methodology in the AF
detection and varied severity of the disease may account
for the discrepancy in results. Continuous ECG monitoring was performed in all of our patients with acute
STEMI during the CCU admission, which differed from
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Hong-Pin Hsu et al.
Table 1. Clinical characteristics of the patients with/without AF
Age (years)
Male gender (%)
Heart rate (bpm)
Systolic pressure (mmHg)
Diastolic pressure (mmHg)
Killip Class
Class I, n (%)
Class II, n (%)
Class III, n (%)
Class IV, n (%)
TIMI score
Left atrial diameter (mm)
LV ejection fraction (%)
Body mass index (Kg/m2)
Smoking (%)
HbA1C (%)
Triglyceride (mg/dl)
Total cholesterol (mg/dl)
Fasting glucose (mg/dl)
HDL-cholesterol (mg/dl)
LDL-cholesterol (mg/dl)
C-reactive protein (mg/dl)
Primary PCI, n (%)
Revascularization, n (%)
Culprit lesion
LAD, n (%)
LCX, n (%)
RCA, n (%)
LM, n (%)
Hypertension, n (%)
Hyperlipidemia, n (%)
Diabetes mellitus, n (%)
Coronary artery disease history, n (%)
Cerebral vascular disease, n (%)
All-cause mortality, n (%)
CV death, n (%)
Sinus rhythm (n = 250)
AF (n = 57)
p value
067.3 ± 14.3
83.2
082.2 ± 21.0
130.9 ± 33.0
075.8 ± 18.0
75.2 ± 10.2
80.7
083.7 ± 32.0
121.9 ± 39.8
069.6 ± 19.7
< 0.001
0.80
0.77
0.11
0.04
0.11
107 (42.8%)0
57 (22.8%)
33 (13.2%)
53 (21.2%)
06 ± 3
39.2 ± 6.1
044.6 ± 12.7
25.0 ± 3.5
90 (36.0%)
07.0 ± 1.8
112.5 ± 96.7
164.3 ± 42.2
150.5 ± 80.4
040.4 ± 12.4
105.6 ± 35.6
01.9 ± 0.2
205 (82.0%)0
233 (93.2%)0
18 (31.6%)
11 (19.3%)
07 (12.3%)
21 (36.8%)
08 ± 3
41.1 ± 6.1
042.9 ± 16.3
24.1 ± 4.2
18 (31.6%)
06.9 ± 1.4
081.0 ± 55.7
146.3 ± 40.9
0197.6 ± 111.4
042.5 ± 13.3
093.0 ± 35.3
02.6 ± 0.7
45 (78.9%)
49 (86.0%)
118 (47.6%)0
33 (13.3%)
76 (30.6%)
13 (5.2%)0
161 (64.4%)0
86 (34.4%)
93 (37.2%)
44 (17.6%)
35 (14.4%)
36 (14.4%)
34 (13.6%)
21 (36.8%)
4 (7.0%)
26 (45.6%)
2 (3.5%)
42 (73.7%)
09 (15.8%)
29 (50.9%)
19 (33.3%)
4 (7.0%)
21 (36.8%)
16 (28.1%)
< 0.001
0.27
0.63
0.41
0.78
0.83
0.02
0.01
0.01
0.29
0.03
0.21
0.73
0.13
0.10
0.24
0.01
0.08
0.01
0.23
00.001
0.01
AF, atrial fibrillation; CV death, cardiovascular death; HDL, high-density lipoprotein; LAD, left anterior descending artery; LCX,
left circumflex artery; LDL, low-density lipoprotein; LM, left main coronary artery; LV, left ventricle; PCI, percutaneous coronary
intervention; RCA, right coronary artery.
low HDL-C, which are considered to be independent
risk factors of AMI, are not independent risk factors of
new-onset AF after AMI in our study.14 Previous studies
found an increased risk of AF in patients with DM.15-17
Koracevic et al. showed that hyperglycemia is associated
with an increased prevalence of AF and higher inhospital mortality in patients after AMI (either STelevation or non-ST elevation). 18 Our study further
the other studies, using only one episode of an ECG recording. Moreover, the exclusion of the patients at high
risk for AF (acute STEMI) may result in the lower incidence of AF observed in some clinical trials.
Metabolic disturbance leads to a new onset of
AF
Many risk factors, such as hypertension, DM, and
Acta Cardiol Sin 2012;28:279-285
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Hyperglycemia Predicts AF in STEMIs
Table 2. Univariate and multivariate analyses of the risk factors for AF
Risk factor
Age*
TIMI score*
Diastolic BP*
Fasting glucose*
LDL-cholesterol*
Total triglyceride*
Previous CAD history
Diabetes mellitus
Univariate p value
Multivariate p value
Odds ratio
95% CI
< 0.001
< 0.001
0.04
0.01
0.03
0.02
0.01
0.08
0.206
0.383
0.749
0.025
0.789
0.060
0.709
0.646
1.034
1.117
0.995
1.007
0.998
0.989
0.812
1.295
0.982~1.088
0.871~1.432
0.968~1.023
1.001~1.012
0.983~1.013
0.979~1.000
0.272~2.424
0.430~3.894
* Continuous variable.
BP, blood pressure; CAD, coronary artery disease; LDL, low-density lipoprotein; TIMI, Thrombolysis in Myocardial Infarction.
animal study, an increased diffuse fibrotic deposition
was revealed on histologic examination of diabetic
rats.20 Fibrosis in the left atrium plays an important role
in determining the dynamics of AF, which could present
as an anchor for reentrant circuits and alter the wavefront propagation, causing fractionated electrograms,
wave breaks, and conduction delays and thus promoting
AF perpetuation.21,22
In the present study, both the TC and TG levels exhibited a negative association with new-onset AF after
myocardial infarction. Although the real mechanism underlying this phenomenon remains unclear, it has been
suggested that hypolipidemia may cause electrophysiological changes that could increase the occurrence of AF.
Annoura et al. found that the TC, TG, and HDL-C were
inversely and linearly associated with the incidence of
AF in patients. 23 In an animal model study, a cholesterol-fed state led to a longer effective refractory period
and shortened the conduction time of the atrium, which
resulted in an antiarrhythmic state in rabbits. 23 This
could suggest that hypolipidemia may be associated with
the occurrence of AF. Although Dublin reported that
hyperlipidemia seemed to be more common among
new-onset AF,24 Funk found that hyperlipidemia was a
negative independent predictor of AF after cardiac surgery.25 Because lipid-lowering medications were often
prescribed to patients with hyperlipidemia or CAD at
other hospitals, even though they did not have elevated
lipid levels, this lipid profile obtained after admission
may not truly represent a condition of hyperlipidemia.
No previous studies have well defined the presence or
absence of hyperlipidemia as an independent predictor
of AF, and the real mechanism for the negative association between hyperlipidemia and AF remains unclear.
Figure 1. Cumulative survival (all-cause mortality) in patients with
and without new-onset atrial fibrillation (AF) during the 12 months
after an acute ST elevation myocardial infarction (STEMI).
demonstrated that hyperglycemia can predict the occurrence of new-onset AF following STEMI, with a 0.7%
increased risk of AF for an elevation in the blood glucose level of 1 mg/dl.
The reason why hyperglycemia correlates independently with AF after myocardial infarction is still unclear.
Chao et al. have found that patients with abnormal glucose metabolism, including those with DM and those
with an impaired fasting glucose, had a lower atrial
voltage and longer atrial activation time than those with
normal glucose metabolism. The AF recurrence rate after catheter ablation was greater in the abnormal glucose
metabolism group than in the normal glucose metabolism group.19 The study supports the hypothesis that
hyperglycemia results in damage to the atrial tissue, with
subsequent changes in the electrophysiologic properties,
which could lead to the genesis of AF.
Oxidative stress-related atrial fibrosis in patients
with hyperglycemia was a possible mechanism. In an
283
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Hong-Pin Hsu et al.
2. Saczynski JS, McManus D, Zhou Z, et al. Trends in atrial fibrillation complicating acute myocardial infarction. Am J Cardiol
2009;104:169-74.
3. Bhatia GS, Lip GY. Atrial fibrillation post-myocardial infarction:
frequency, consequences, and management. Curr Heart Fail Rep
2004;1:149-55.
4. Liu YB, Wu CC, Lee CM, et al. Dyslipidemia is associated with
ventricular tachyarrhythmia in patients with acute ST-segment
elevation myocardial infarction. J Formos Med Assoc 2006;
105:17-24.
5. Krumholz HM, Anderson JL, Bachelder BL, et al. ACCAHA
2008 performance measures for adults with ST-elevation and
non-ST-elevation myocardial infarction. Circulation 2008;118:
2596-648.
6. Chobanian AV, Bakris GL, Black HR, et al. and The National
High Blood Pressure Education Program Coordinating Committee. The seventh report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. JAMA 2003;289:2560-72.
7. James RG, Alberti KGMM, Mayer BD, et al. Report of the expert
committee on the diagnosis and classification of diabetes mellitus. Diabetes Care 2003;26:S5-20.
8. Pedersen OD, Bagger H, Kober L, et al. The occurrence and prognostic significance of atrial fibrillation/-flutter following acute
myocardial infarction. TRACE Study group. Trandolapril cardiac
evalution. Eur Heart J 1999;20:748-54.
9. Crenshaw BS, Ward SR, Granger CB, et al. Atrial fibrillation in
the setting of acute myocardial infarction: the GUSTO-I experience. Global utilization of streptokinase and TPA for occluded
coronary arteries. J Am Coll Cardiol 1997;30:406-13.
10. Wong CK, White HD, Wilcox RG, et al. Significance of atrial
fibrillation during acute myocardial infarction, and its current
management: insights from the GUSTO-3 trial. Card Electrophysiol Rev 2003;7:201-7.
11. Mehta RH, Dabbous OH, Granger CB, et al. Comparison of outcomes of patients with acute coronary syndromes with and without atrial fibrillation. Am J Cardiol 2003;92:1031-6.
12. Eldar M, Canetti M, Rotstein Z, et al. Significance of paroxysmal
atrial fibrillation complicating acute myocardial infarction in the
thrombolytic era. SPRINT and thrombolytic survey groups. Circulation 1998;97:965-70.
13. Goldberg RJ, Yarzebski J, Lessard D, et al. Recent trends in the
incidence rates of and death rates from atrial fibrillation complicating initial acute myocardial infarction: a community-wide
perspective. Am Heart J 2002;143:519-27.
14. Lin YC, Hsu LA, Ko YS, et al. Impact of conventional cardiovascular risk factors on acute myocardial infarction in young adult
Taiwanese. Acta Cardiol Sin 2010;26:228-34.
15. Barriales Alvarez V, Morís de la Tassa C, Sánchez Posada I, et al.
The etiology and associated risk factors in a sample of 300 patients with atrial fibrillation. Rev Esp Cardiol 1999;52:403-14.
16. Kalus JS, White CM, Caron MF, et al. Indicators of atrial fibrillation risk in cardiac surgery patients on prophylactic amiodarone.
Poor outcome in patients with new-onset AF
AF leads to progressive electrical and structural
changes to the atria, contributing to the initiation and
perpetuation of AF.26 Patients with AMI could have a reduced mortality rate after receiving primary PCI,27 but
patients with new-onset AF after an acute STEMI had a
higher all cause-mortality after 12 months of follow-up
in our study, similar to the findings of other studies.28-30
A new-onset AF can predict the occurrence of a stroke,
CHF, and mortality after acute STEMI.31-33
The optimal prevention of AF is to terminate it as
soon as possible and interrupt the remodeling of AF.26
Aggressive rhythm control of AF after an acute STEMI
may reduce the occurrence of AF after discharge. As
shown in this study, a higher initial fasting glucose level
could predict the occurrence of AF. Therefore, tight blood
sugar control may prevent the occurrence of AF and decrease the recurrence of AF during follow-up. More prospective studies are necessary to prove this hypothesis.
LIMITATION
In our study, the AF was acquired by both continuous ECG monitoring and the 12-lead ECG. Because continuous ECG monitoring was not routinely used in the
ordinary wards, some asymptomatic new-onset AF cases
occurring on the ordinary wards may have been undetected. Besides, the LA volume was not routinely measured in this study, which may provide more precise information than the LA diameter.
CONCLUSION
A higher initial fasting glucose level was an independent predictor of new-onset AF after acute STEMI.
In addition, patients with new-onset AF are associated
with a poor prognosis.
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