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High-degree atrioventricular block

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infarction in the...

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DOI: 10.1136/heartjnl-2015-308260

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Coronary artery disease

ORIGINAL ARTICLE

High-degree atrioventricular block complicating

ST segment elevation myocardial infarction
in the contemporary era
Vincent Auffret,1,2,3 Aurélie Loirat,1,2,3 Guillaume Leurent,1,2,3 Raphael P Martins,1,2,3
Emmanuelle Filippi,4 Isabelle Coudert,5 Jean Philippe Hacot,6 Martine Gilard,7,8
Philippe Castellant,7,8 Antoine Rialan,9 Régis Delaunay,10 Gilles Rouault,11
Philippe Druelles,12 Bertrand Boulanger,13 Josiane Treuil,14 Bertrand Avez,15
Marc Bedossa,1,2,3 Dominique Boulmier,1,2,3 Marielle Le Guellec,1,2,3
Jean-Claude Daubert,1,2,3 Hervé Le Breton1,2,3

▸ Additional material is
published online only. To view
this file please visit the journal
online (http://dx.doi.org/10.
1136/heartjnl-2015-308260).
For numbered affiliations see
end of article.
Correspondence to
Dr Vincent Auffret, Service
de Cardiologie et Maladies
Vasculaires, CHU de Rennes,
2 rue Henri Le Guilloux,
Rennes 35000, France;
v.auffret@gmail.com
VA and AL contributed equally.
Received 12 June 2015
Revised 21 July 2015
Accepted 15 October 2015
To cite: Auffret V, Loirat A,
Leurent G, et al. Heart
2016;102:40–49.
40
ABSTRACT
Background High-degree atrioventricular block (HAVB)
is a common complication of ST segment elevation
myocardial infarction (STEMI). HAVB in STEMI is
historically considered as a marker of worse outcome but
overall data about HAVB in the contemporary era of
mechanical reperfusion and potent antiplatelet therapies
are scarce.
Aim Analysing incidence, clinical correlates and impact
on inhospital outcomes of HAVB in a large prospective
registry (Observatoire Régional Breton sur l’Infarctus,
ORBI) of modern management of STEMI with a special
focus on potential differences between patients with
HAVB on admission and those who developed HAVB
during hospitalisation.
Methods All patients enrolled in ORBI between June
2006 and December 2013 were included in the present
analysis and were divided into 3 groups: patients
without HAVB at any time, patients with HAVB on
admission and those who developed HAVB during
hospitalisation.
Results A total of 6662 patients (age: 62.0 (52.0–
74.0) years; male: 76.3%) were included in the present
analysis. HAVB was documented in 3.5% of patients,
present on admission in 63.7% of patients and
occurring during hospitalisation in 36.3%. Patients with
HAVB on admission or occurring during the first 24 h of
hospitalisation had higher inhospital mortality rates
(18.1% and 28.6%, respectively) than patients without
(4.5%) or with HAVB occurring beyond the first 24 h of
hospitalisation (8.0%). However by multivariable
analysis, HAVB was not independently associated with
inhospital mortality contrarily to age, presentation as
cardiac arrest, anterior STEMI location, reperfusion
therapy, cardiogenic shock, mechanical ventilation and
occurrence of sustained ventricular tachyarrhythmias or
mechanical complication.
Conclusions Patients with HAVB had a higher
mortality rate than patients without. However HAVB is
not an independent predictor of inhospital mortality.
INTRODUCTION
Complications and mortality rates of ST segment
elevation myocardial infarction (STEMI) markedly
Auffret V, et al. Heart 2016;102:40–49. doi:10.1136/heartjnl-2015-308260
declined over the past 20 years owing to widespread
use of reperfusion therapies, modern antithrombo-
tic treatments and recommended prevention
drugs.1 2 High-degree atrioventricular block
(HAVB) is a common complication of STEMI that
is reported in 2.7% to 14% of patients3–7 according
to definitions of HAVB and location of wall-
necrosis in previous studies. Similarly to other
complications, rate of HAVB has been shown to be
decreasing over time,8 however the presence of
HAVB in the acute phase of STEMI is known to be
associated with an increased inhospital mortality
regardless of reperfusion therapy.6 9–11
Primary percutaneous coronary intervention
(p-PCI), especially when performed in a timely
fashion, is currently the treatment of choice of
STEMI.12 To date, only few studies specifically
reported the incidence, predictors and outcomes of
patients with HAVB complicating STEMI in the
contemporary era of emergent mechanical reperfu-
sion and potent antithrombotic drugs.5–7 11 13
These studies reached conflicting results about the
independent relationship between HAVB and short-
term mortality.
Therefore, this work aimed at analysing inci-
dence, clinical correlates and impact on inhospital
outcomes of HAVB in a large registry of modern
management of STEMI with a special focus on
potential differences between patients with HAVB
on admission and those who developed HAVB
during hospitalisation.
METHODS
Data collection
This retrospective observational study used data
from the Brittany Regional Infarction Observatory
(Observatoire Régional Breton sur l’Infarctus,
ORBI) that prospectively includes from 2006 all
patients admitted to any of the 9 participating
interventional cardiology centres (list in online
supplementary appendix 1) for STEMI (final diag-
nosis), within 24 h of symptom onset. The centra-
lised database used for the present study contains
demographic information and comprehensive
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Coronary artery disease

clinical, ECG, procedural and inhospital data concerning
patients with STEMI.
Patients
All patients enrolled in ORBI between June 2006 and
December 2013 were included in the present analysis and
divided into three groups: patients without HAVB at any time,
patients with HAVB on admission and those who developed
HAVB during hospitalisation.
admitted in emergency departments. HAVB was considered as
occurring inhospital in other cases.
First medical contact (FMC) was defined according to the
2008 European Society of Cardiology STEMI guidelines.15
Total ischaemic time and FMC-to-treatment delay were defined
respectively as the time between symptom onset or FMC and
initiation of reperfusion: balloon inflation, in the case of p-PCI,
or administration of fibrinolytic treatment.
Patients with atypical symptoms were defined as patients who
presented without typical chest pain or cardiac arrest.

Definitions Statistical analysis

STEMI was defined according to guidelines as ST segment eleva-
tion, measured at the J point, ≥1 mm in two contiguous leads
or new left bundle branch block, accompanied by one or more
positive cardiac biomarkers confirming cardiac necrosis.14
HAVB was defined as third-degree or second-degree type 2
atrioventricular blocks. HAVB on admission was defined as the
presence of presumed new-onset HAVB on any ECG before hos-
pital admission in patients managed by mobile intensive care
units or on the first ECG on admission in patients directly
Data are summarised as number ( percentages) for categorical
variables. Quantitative variables are expressed as mean±SD if
normally distributed and median (IQR) if non-normally distrib-
uted. Qualitative data were compared using χ2 test or Fisher’s
exact test while quantitative data were compared using unpaired
t test, Kruskal-Wallis test or Mann-Whitney test. Inhospital all-
cause mortality was analysed as a binary and time-dependent
outcome using stepwise logistic and Cox regression analyses,
respectively. ORs, HRs and 95% CIs were calculated for

Table 1 Baseline characteristics of patients according to the occurrence of HAVB

HAVB on HAVB during
All patients No HAVB admission hospitalisation Overall p Value p Value p Value
(n=6662) (n=6428)a (n=149)b (n=85)c p value a vs b a vs c b vs c

Age, years 62.0 (52.0–74.0) 62.0 (52.0–73.0) 69.0 (58.0–79.5) 74.0 (62.5–81.0) <0.001 <0.001 <0.001 0.061
Male sex 5080 (76.3) 4931 (76.7) 95 (63.8) 54 (63.5) <0.001 <0.001 0.006 1.000
Hypertension 2680 (40.2) 2543 (39.6) 82 (55.0) 55 (64.7) <0.001 <0.001 <0.001 0.169
Diabetes mellitus 640 (9.6) 621 (9.7) 9 (6.0) 10 (11.8) 0.259 0.159 0.578 0.140
Dyslipidaemia 3102 (46.6) 2993 (46.6) 64 (43.0) 45 (52.9) 0.336 0.407 0.274 0.173
Current smoker 2550 (38.3) 2481 (38.6) 54 (36.2) 15 (17.6) <0.001 0.610 <0.001 0.003
Body mass index ≥30 kg/m2 1221 (18.3) 1175 (18.3) 26 (17.4) 20 (23.5) 0.338 1.000 0.148 0.300
Previous myocardial infarction 521 (7.8) 506 (7.9) 11 (7.4) 4 (4.7) 0.543 0.880 0.320 0.581
Previous coronary artery bypass 87 (1.3) 76 (1.2) 8 (5.4) 3 (3.5) <0.001 0.001 0.084 0.750
graft
Chronic obstructive pulmonary 345 (5.2) 331 (5.1) 13 (8.7) 1 (1.2) 0.039 0.061 0.131 0.020
disease
Previous stroke 232 (3.5) 224 (3.5) 6 (4.0) 2 (2.4) 0.839 0.820 1.000 0.714
Peripheral artery disease 305 (4.6) 282 (4.4) 13 (8.7) 10 (11.8) 0.001 0.017 0.004 0.497
Chronic kidney disease 122 (1.8) 112 (1.7) 7 (4.7) 3 (3.5) 0.015 0.018 0.189 0.751
Symptoms <0.001 <0.001 <0.001 0.187
Typical chest pain 6093 (91.5) 5911 (91.9) 117 (78.5) 65 (76.5)
Sudden cardiac death 147 (2.2) 140 (2.2) 3 (2.0) 4 (4.7)
Angina pectoris before index 1427 (21.4) 1386 (21.6) 29 (19.5) 12 (14.1) 0.212 0.549 0.110 0.372
event
ECG on admission
Q wave 2226 (33.4) 2156 (33.5) 42 (28.2) 28 (32.9) 0.480 0.234 0.910 0.554
ST segment elevation 6412 (96.2) 6185 (96.2) 144 (96.6) 83 (97.6) 0.842 0.536 0.782 1.000
Left bundle branch block 141 (2.1) 132 (2.1) 6 (4.0) 3 (3.5) 0.105 0.132 0.256 1.000
Time delays (minutes)
Symptoms onset-to-first 97.0 (55.0–192.0) 96.0 (54.0–190.0) 92.5 (50.0–195.0) 146.5 (75.0–378.75) 0.002 0.870 <0.001 0.003
medical contact
First medical 90.0 (68.0–121.25) 90.0 (68.0–120.0) 103.0 (79.5–156.5) 110.0 (70.0–149.0) <0.001 <0.001 0.012 0.969
contact-to-treatment
Total ischaemic time 191.0 (137.0–300.0) 190 (135.0–298.0) 214.0 (158.0–385.0) 238.0 (163.0–325.0) 0.006 0.018 0.026 0.620
Haemodynamic on admission
Cardiogenic shock 216 (3.2) 168 (2.6) 39 (26.2) 9 (10.6) <0.001 <0.001 <0.001 0.004
Heart rate (bpm) 75.0 (64.0–88.0) 75.0 (65.0–88.0) 51.0 (40.0–72.0) 65.0 (55.0–85.5) <0.001 <0.001 <0.001 <0.001
Systolic blood pressure 130.0 (115.0–150.0) 130.5 (116.0–150.0) 110.0 (83.0–127.0) 119.0 (100.0–143.0) <0.001 <0.001 <0.001 0.004
(mm Hg)
Quantitative data are expressed as median (IQR). Categorical variables are expressed as number (percentage).
a
no HAVB group, bHAVB on admission group, cHAVB during hospitalisation group.
HAVB, high-degree atrioventricular block.

Auffret V, et al. Heart 2016;102:40–49. doi:10.1136/heartjnl-2015-308260 41

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Coronary artery disease

inhospital mortality. To assess the independent nature of the

Figure 1 Number of patients who developed HAVB during
hospitalisation according to time from admission. HAVB, high-degree
atrioventricular block.
relationship between HAVB and inhospital mortality, a model
adjusting for the following clinically relevant baseline, proced-
ural and inhospital variables was constructed: age, sex, diabetes
mellitus, presentation as cardiac arrest, anterior STEMI location,
use of any reperfusion therapy, cardiogenic shock, need for
mechanical ventilation and occurrence of sustained ventricular
tachyarrhythmias or any mechanical complication of STEMI.
Subsequently, analysis was restricted to the subgroup of patients
treated by p-PCI. To account for a potential ‘healthy survivor
bias’, analysis was also performed censoring patients who died
before the median time of occurrence of inhospital HAVB. OR
and 95% CI were calculated for HAVB according to its time of
occurrence. The prognostic relevance of different characteristics
on HAVB according to its time of occurrence was assessed in
univariable and multivariable fashion using stepwise logistic
regression analysis. Variables with a p≤0.05 in univariable ana-
lysis were used for multivariable analysis and were removed in a

Table 2 Management and procedural characteristics of patients according to the occurrence of HAVB
All HAVB on HAVB during
patients No HAVB admission hospitalisation Overall p Value p Value p Value
(n=6662) (n=6428)a (n=149)b (n=85)c p value a vs b a vs c b vs c

Thrombolysis 0.008 0.034 0.073 0.797

Prehospital 397 (6.0) 385 (6.0) 9 (6.0) 3 (3.5)
Inhospital 426 (6.4) 423 (6.6) 2 (1.3) 1 (1.2)
Primary percutaneous coronary intervention 4931 (74.0) 4759 (74.0) 115 (77.2) 57 (67.1) 0.236 0.397 0.170 0.123
Angiography*
Angiography performed 6542 (98.2) 6326 (98.4) 141 (94.6) 75 (88.2) <0.001 0.003 <0.001 0.123
Radial access 2881 (54.7) 2814 (55.2) 44 (37.6) 23 (39.7) <0.001 <0.001 0.023 0.869
Infarct related coronary artery
Left anterior descending 2707 (41.4) 2671 (42.2) 11 (7.8) 25 (33.3) <0.001 <0.001 0.126 <0.001
Left circumflex 981 (15.0) 963 (15.2) 12 (8.5) 6 (8.0) 0.020 0.031 0.104 1.000
Right 2732 (41.8) 2572 (40.7) 115 (81.6) 45 (60.0) <0.001 <0.001 <0.001 <0.001
Left main 64 (1.0) 62 (1.0) 1 (0.7) 1 (1.3) 0.835 1.000 0.529 1.000
Three-vessel disease 1138 (17.4) 1085 (17.2) 36 (25.5) 17 (22.7) 0.052 0.021 0.466 0.518
TIMI flow grade at initial angiography† <0.001 <0.001 0.168 0.412
0 3482 (54.1) 3335 (53.6) 98 (71.0) 49 (66.2)
1 512 (8.0) 492 (7.9) 15 (10.9) 5 (6.8)
2 833 (12.9) 814 (13.1) 11 (8.0) 8 (10.8)
3 1607 (25.0) 1581 (25.4) 14 (10.1) 12 (16.2)
Percutaneous coronary intervention (PCI)‡
PCI performed 5895 (90.1) 5698 (90.1) 130 (92.2) 67 (89.3) 0.693 0.601 0.007 0.097
Thromboaspiration 2949 (50.0) 2838 (49.8) 80 (61.5) 31 (46.3) 0.024 0.010 0.624 0.049
Stent implantation 5364 (90.9) 5192 (91.1) 113 (86.9) 59 (88.0) 0.125 0.056 0.656 0.655
Drug-eluting stent 1013 (18.9) 999 (19.2) 10 (7.7) 4 (6.0) 0.002 0.004 0.047 0.809
Multivessel PCI 245 (4.2) 236 (4.1) 4 (3.1) 5 (7.5) 0.305 0.661 0.193 0.159
Complete revascularisation 2952 (50.1) 2877 (50.5) 53 (40.8) 22 (32.8) 0.002 0.033 0.006 0.353
TIMI flow grade after PCI† <0.001 <0.001 <0.001 0.851
0 122 (2.1) 103 (1.8) 11 (8.5) 8 (12.1)
1 44 (0.8) 40 (0.7) 3 (2.3) 1 (1.5)
2 171 (2.9) 160 (2.8) 7 (5.4) 4 (6.1)
3 5491 (94.2) 5330 (94.6) 108 (83.7) 53 (80.3)
Quantitative data are expressed as median (IQR). Categorical variables are expressed as number (percentage).
*For radial access, n=5270 with data about vascular access. For infarct-related artery, percentages are of patients who underwent angiography.
†n=6434 patients with data about TIMI flow at initial angiography and n=5828 patients with data about TIMI flow grade after PCI.
‡For PCI performed, percentages are of patients who underwent angiography. For thromboaspiration, stent implantation, multivessel PCI and complete revascularisation, percentages
are of patients who underwent PCI. For drug-eluting stent, percentages are of patients who underwent stent implantation.
a
no HAVB group, bHAVB on admission group, cHAVB during hospitalisation group.
HAVB, high-degree atrioventricular block; TIMI, thrombolysis in myocardial infarction.

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Coronary artery disease

stepwise selection process on the basis of a significance level of
0.10. All tests were two-sided at the 0.05 significance level.
Statistical analysis was performed with the use of Statistical
Package for Social Sciences, V.21 (SPSS, IBM, Chicago, Illinois,
USA).
RESULTS
Patients
From June 2006 to December 2013, 6662 patients (age: 62.0
(52.0–74.0) years; male sex: 76.3%) were registered in ORBI
and included in the present analysis. Overall, HAVB was docu-
mented in 3.5% of patients. Among these patients, HAVB was
present on admission in 63.7% of patients and occurred during
hospitalisation in 36.3%. Among patients treated by p-PCI
(n=4931) or fibrinolysis (n=823), rates of HAVB occurring
during hospitalisation were only of 1.2% and 0.5%, respectively,
( p=0.097) as compared with 2.6% in patients who did not
benefit from any reperfusion strategy at the acute phase
( p=0.001 vs p-PCI and <0.001 vs fibrinolysis).
Baseline characteristics of patients according to the occur-
rence of HAVB are listed in table 1 and figure 1 shows the
cumulative rate of HAVB according to time from admission in
patients with inhospital HAVB.
patients with HAVB (68.7%) with the highest rate in patients
with HAVB on admission. In case of anterior STEMI, HAVB
was more frequent in patients with a significant lesion (≥50%
diameter stenosis) of the RCA (2.5% vs 0.9%, p=0.002) with
a non-significant trend towards more HAVB in patients
presenting with an occlusion of the RCA (3.3% vs 1.3%,
p=0.077). Contrarily, in case of non-anterior STEMI, rates of
HAVB were non-significantly different between patients with
and without a significant left anterior descending artery (LAD)
lesion (5.4% vs 4.4%, p=0.184). Table 2 summarises manage-
ment and procedural characteristics.
Inhospital treatments and outcomes
Usage rates of guidelines-recommended therapies at discharge,
especially β-blockers were lower in patients with HAVB (table 3).
Overall, inhospital death occurred in 329 patients (4.9%) and
was mainly attributed to cardiovascular causes. Patients with
HAVB had a higher inhospital mortality rate (17.5%) than
patients without (4.5%, p<0.001). In patients with HAVB, the
rate of inhospital mortality was numerically higher in patients
who received than in patients who did not receive temporary
pacemaker (23.1% vs 16.4%) however this difference did not
reach statistical significance ( p=0.356) (table 4).

Procedures Predictors of inhospital mortality

Coronary angiography was performed less frequently in Results of stepwise multivariable logistic and Cox regression ana-
patients with HAVB (98.4% vs 92.3%). Unsurprisingly, the lyses are shown in figure 2. In both models, HAVB was not inde-
right coronary artery (RCA) was the culprit artery in most pendently associated with inhospital mortality ( p=0.977 and

Table 3 Inhospital treatments according to the occurrence of HAVB

HAVB on HAVB during
All patients No HAVB admission hospitalisation Overall p Value p Value p Value
(n=6662) (n=6428)a (n=149)b (n=85)c p value a vs b a vs c b vs c

Treatments of the first 48 h

Glycoprotein IIb/IIIa inhibitors 3413 (51.2) 3296 (51.3) 80 (53.7) 37 (43.5) 0.306 0.563 0.190 0.174
Aspirin 6621 (99.4) 6389 (99.4) 148 (99.3) 84 (98.8) 1.000 0.601 0.410 1.000
P2Y12 receptor antagonists <0.001 0.209 <0.001 0.022
Clopidogrel 4994 (74.9) 4806 (74.8) 113 (75.8) 75 (88.2)
Prasugrel 1396 (21.0) 1366 (21.3) 25 (16.8) 5 (5.9)
Ticagrelor 172 (2.6) 168 (2.6) 4 (2.7) 0 (0.0)
Anticoagulants 0.382 0.103 0.965 0.446
Unfractionated heparin 3114 (46.7) 2996 (46.6) 79 (53.0) 39 (45.9)
Low molecular weight heparin 3398 (51.0) 3289 (51.2) 65 (43.6) 44 (51.8)
Bivalirudin 36 (0.5) 34 (0.5) 2 (1.3) 0 (0.0)
Inotropic agents/vasopressors 406 (6.1) 343 (5.3) 42 (28.2) 21 (24.7) <0.001 <0.001 <0.001 0.646
Diuretics 1216 (18.3) 1154 (18.0) 33 (22.1) 29 (34.1) <0.001 0.196 <0.001 0.064
β-blockers 5389 (80.9) 5284 (82.2) 67 (45.0) 38 (44.7) <0.001 <0.001 <0.001 1.000
ACE inhibitors/ARB 3174 (47.6) 3122 (48.6) 26 (17.4) 26 (30.6) <0.001 <0.001 0.001 0.023
Statins 5878 (88.2) 5697 (88.6) 110 (73.8) 71 (83.5) <0.001 <0.001 0.167 0.105
Treatments at discharge (n=6333) (n=6140) (n=122) (n=71)
Aspirin 6119 (96.6) 5932 (96.6) 118 (96.7) 69 (97.2) 1.000 1.000 1.000 1.000
P2Y12 receptor antagonists <0.001 0.017 0.002 0.007
Clopidogrel 4316 (68.2) 4174 (67.9) 80 (65.5) 62 (87.3)
Prasugrel 1558 (24.6) 1525 (24.8) 27 (22.1) 6 (8.5)
Ticagrelor 185 (2.9) 183 (3.0) 2 (1.6) 0 (0.0)
Diuretics 897 (14.2) 854 (13.9) 22 (18.0) 21 (29.6) 0.003 0.204 0.002 0.074
β-blockers 5768 (91.1) 5631 (91.7) 93 (76.2) 44 (62.0) <0.001 <0.001 <0.001 0.048
ACE inhibitors/ARB 4417 (69.8) 4296 (70.0) 73 (59.8) 48 (67.6) 0.051 0.017 0.696 0.355
Statins 5989 (94.6) 5814 (94.7) 110 (90.2) 65 (91.5) 0.047 0.031 0.277 0.804
Categorical variables are expressed as number (percentage).
a
no HAVB group, bHAVB on admission group, cHAVB during hospitalisation group.
ARB, angiotensin receptor blocker; HAVB, high-degree atrioventricular block.

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Coronary artery disease

Table 4 Inhospital outcomes according to the occurrence of HAVB

HAVB on HAVB during
No HAVB All HAVB admission hospitalisation Overall p Value p Value p Value
(n=6428)a (n=234) (n=149)b (n=85)c p value a vs b a vs c b vs c

Length of hospitalisation (days)

Intensive care unit 4.0 (3.0–5.0) 4.0 (3.0–7.0) 4.0 (3.0–6.0) 6.0 (3.5–9.0) <0.001 0.264 <0.001 <0.001
Total 6.0 (5.0–7.0) 8.0 (5.0–12.0) 7.0 (5.0–10.0) 10.0 (6.0–15.5) <0.001 0.001 <0.001 <0.001
Echocardiographic LVEF (%) 50.0 (45.0–60.0) 50.0 (40.0–58.0) 50.0 (45.0–60.0) 45.0 (39.5–53.5) <0.001 0.782 <0.001 0.001
LVEF <40% 728 (11.3) 39 (16.7) 19 (12.8) 20 (23.5) 0.003 0.502 0.002 0.070
Additional devices/techniques
Temporary pacemaker 7 (0.1) 39 (16.7) 25 (16.8) 14 (16.5) <0.001 <0.001 <0.001 1.000
Mechanical circulatory assistance <0.001 <0.001 0.022 0.409
Intra-aortic balloon pump 231 (3.6) 23 (9.8) 16 (10.7) 7 (8.2)
Other devices 17 (0.3) 7 (3.0) 6 (4.0) 1 (1.2)
Mechanical ventilation 234 (3.6) 24 (10.3) 16 (10.7) 8 (9.4) <0.001 <0.001 0.013 0.826
Outcomes
All-cause mortality 288 (4.5) 41 (17.5) 27 (18.1) 14 (16.5) <0.001 <0.001 <0.001 0.859
Cardiovascular mortality 264 (4.1) 40 (17.1) 27 (18.1) 13 (15.3) <0.001 <0.001 <0.001 0.596
Reinfarction 50 (0.8) 3 (1.3) 1 (0.7) 2 (2.4) 0.202 1.000 0.147 0.299
Recurrent ischaemia 63 (1.0) 4 (1.7) 1 (0.7) 3 (3.5) 0.076 1.000 0.055 0.138
Stent thrombosis 43 (0.7) 9 (3.8) 5 (3.4) 4 (4.7) <0.001 0.004 0.003 0.727
Ventricular arrhythmia <0.001 <0.001 <0.001 0.841
Sustained ventricular tachycardia 152 (2.4) 15 (6.4) 10 (6.7) 5 (5.9)
Ventricular fibrillation 211 (3.3) 31 (13.2) 21 (14.1) 10 (11.8)
Atrial fibrillation/flutter 320 (5.0) 30 (12.8) 20 (13.4) 10 (11.8) <0.001 <0.001 0.010 0.840
Asystole/electromechanical dissociation 112 (1.7) 20 (8.5) 15 (10.1) 5 (5.9) <0.001 <0.001 0.018 0.336
Cardiogenic shock 246 (3.8) 31 (13.2) 18 (12.1) 13 (15.3) <0.001 <0.001 <0.001 0.549
Mechanical complications <0.001 <0.001 <0.001 0.044
Pseudoaneurysm 21 (0.3) 3 (1.3) 3 (2.0) 0 (0.0)
Mitral regurgitation 127 (2.0) 5 (2.1) 4 (2.7) 1 (1.2)
Pericardial effusion 116 (1.8) 5 (2.1) 0 (0.0) 5 (5.9)
Ventricular septal rupture 57 (0.9) 4 (1.7) 3 (2.0) 1 (1.2)
Right ventricular infarction 68 (1.1) 49 (20.9) 31 (20.8) 18 (21.2) <0.001 <0.001 <0.001 1.000
Stroke 27 (0.4) 3 (1.3) 3 (2.0) 0 (0.0) 0.057 0.030 1.000 0.555
Quantitative data are expressed as median (IQR). Categorical variables are expressed as number (percentage).
a
no HAVB group, bHAVB on admission group, cHAVB during hospitalisation group.
HAVB, high-degree atrioventricular block; LVEF, left ventricular ejection fraction.

0.907, respectively) contrary to other well known high-risk fea-
tures. Restricting analysis to patients treated by p-PCI yielded the
same results (OR=1.162, 95% CI (0.641 to 2.106), p=0.622
and HR=1.088, 95% CI (0.678 to 1.744), p=0.727) as did cen-
soring patients who died before the median time of occurrence
of inhospital HAVB (OR=1.419, 95% CI (0.738 to 2.727),
p=0.294 and HR=1.221, 95% CI (0.714 to 2.090), p=0.466).
Comparison between patients with HAVB on admission and
HAVB occurring during hospitalisation
Baseline characteristics of patients with HAVB on admission and
those with inhospital HAVB were largely comparable (table 1)
and their inhospital outcomes were similar (table 4).
The LAD artery was the culprit lesion in a third of patients
who developed HAVB during hospitalisation compared with
7.8% of patients with HAVB on admission and was associated
with a 27.8% inhospital mortality rate among patients with
HAVB compared with 16.7% for the left circumflex coronary
artery and 11.9% for the RCA ( p=0.048).
When further separating patients with inhospital occurrence
of HAVB in two groups according to the occurrence of HAVB
during the first 24 h of hospitalisation, the highest mortality rate
was found in patients who developed HAVB during the first 24 h
44
of hospitalisation (28.6%) followed by patients with HAVB on
admission (18.1%) whereas mortality rates in patients who
developed HAVB beyond 24 h of hospitalisation (8.0%) and
patients without HAVB (4.5%) were not significantly different
(figure 3). Cardiogenic shock on admission and right ventricular
infarction were more common in patients who developed HAVB
during the first 24 h of hospitalisation than in patients who
developed HAVB beyond the first 24 h of hospitalisation (20.0%
vs 4.0%, p=0.029 and 37.1% vs 10.0%, p=0.003, respectively).
Predictors of HAVB according to time of occurrence
To identify independent predictors of HAVB on admission, ana-
lysis was restricted to baseline and angiographic (before percu-
taneous coronary intervention) characteristics.
All (baseline, procedural and inhospital) variables were
assessed for association with HAVB occurring during hospitalisa-
tion. Results of multivariable analyses are shown in table 5.
Regarding time-dependent variables, inhospital HAVB occurred
before ventricular fibrillation in 10% of patients (n=1/10);
before right ventricular infarction in 16.7% of patients (n=3/18)
but never occurred before stent thrombosis (n=0/4). When
excluding these patients from the analysis, ventricular
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Coronary artery disease

Figure 2 Results of stepwise multivariable logistic regression (A) and Cox regression (B) analyses for inhospital all-cause mortality. HAVB,
high-degree atrioventricular block; STEMI, ST elevation myocardial infarction.

Auffret V, et al. Heart 2016;102:40–49. doi:10.1136/heartjnl-2015-308260 45

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Coronary artery disease

Figure 3 Kaplan Meier (KM) time-to-event curves showing cumulative rates of inhospital all-cause mortality according to the occurrence and
timing of high-degree atrioventricular block (HAVB). Grey full line: no HAVB; black dotted line: HAVB on admission; black full line: inhospital HAVB
occurring in the first 24 h of hospitalisation (≤24 h); grey dotted line: inhospital HAVB occurring beyond the first 24 h of hospitalisation (>24 h).
STEMI, ST elevation myocardial infarction.

fibrillation, right ventricular infarction and stent thrombosis
remained strong correlates of inhospital HAVB.
DISCUSSION
The main findings of the present study are as follows: HAVB (1)
remains a common complication of STEMI which occurred in
3.5% of cases in our study, (2) is associated with other high-risk
complications and a higher inhospital mortality rate, (3) does
not represent an independent predictor of inhospital mortality
but is rather a surrogate marker of more severe STEMI.
Incidence and prognosis implication of HAVB in STEMI
As for all other complications of STEMI, rates of HAVB
decreased in recent years.8 However, it remains a common com-
plication after STEMI as it occurred in 3.5% of our study
cohort of 6662 patients. Over the 8 years of this study period,
no decline in the rates of HAVB was observed. These data are
overall consistent with previous studies5 6 8 10 11 16 although
slight differences exist according to the inclusion criteria of
these studies especially location, type of myocardial infarction
(STEMI or non-STEMI) or population.
It was shown that early reperfusion by decreasing infarct size
and attenuating additional complications could have an impact
upon the incidence of HAVB.11 13 Indeed, Harpaz et al demon-
strated a decrease of HAVB complicating STEMI in the thromb-
olysis versus prethrombolysis era (10). Studies in the p-PCI era
also showed a reduced rate of HAVB7 11 and in our study the
46
rate of HAVB occurring during hospitalisation after p-PCI was
only 1.2%. Moreover, most patients also recovered from HAVB
after revascularisation in the p-PCI era and permanent pace-
maker insertion is rarely needed.7 11 13 17 As previously specu-
lated some of the decrease in the incidence of HAVB may be
related to the continued development of reperfusion therapies,
especially p-PCI which rapidly mitigates the ischaemic insult to
the conduction system and reduces the total infarct size with a
low risk of subsequent reinfarction owing to low rates of stent
thrombosis with current devices.11
Patients with HAVB had poorer outcomes including a high
risk of cardiogenic shock, left ventricular dysfunction, right ven-
tricular infarction and ventricular fibrillation. Gómez-Talavera
et al6 also previously demonstrated the association between
HAVB and other complications of acute myocardial infarction
such as cardiogenic shock, reinfarction or cardiac arrest.
In our study, patients with HAVB had a higher inhospital all-
cause mortality rate than patients without, which was mainly
driven by cardiovascular mortality. Our findings are in line with
all published studies on the subject which showed a short-term
increase in mortality in patients with HAVB complicating
STEMI.5 6 8 9 16 18 19 However, in the present study, HAVB,
conversely to other well known mechanical, electrical and
haemodynamic parameters classically associated with instability,
was not an independent predictor of inhospital mortality which
has already been demonstrated by other authors.4 7 20
According to these authors, HAVB is not responsible for the
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Coronary artery disease

Table 5 Independent predictors of HAVB according to time of occurrence

Multivariable Multivariable
All patients Patients with primary PCI
HAVB on admission* OR (95% CI) p Value HAVB on admission† OR (95% CI) p Value

Age 1.017 (1.001 to 1.033) 0.040 Symptoms 0.024

Symptoms 0.041 Sudden cardiac death 0.264 (0.057 to 1.224) 0.089
Sudden cardiac death 0.279 (0.061 to 1.284) 0.101 Atypical symptoms 2.158 (0.998 to 4.670) 0.051
Atypical symptoms 1.947 (0.940 to 4.032) 0.073 FMC-to-balloon delay 1.002 (1.000 to 1.004) 0.011
Cardiogenic shock Cardiogenic shock
On admission 15.763 (8.889 to 27.954) <0.001 On admission 19.930 (11.165 to 35.576) <0.001
IRA IRA
RCA 9.035 (5.129 to 15.915) <0.001 RCA 8.033 (4.485 to 14.390) <0.001
TIMI flow grade of the IRA before PCI 0.037
0 2.696 (1.272 to 5.715) 0.010
1 3.678 (1.453 to 9.309) 0.006
2 2.191 (0.847 to 5.670) 0.106
HAVB during hospitalisation‡ HAVB during hospitalisation§
Age 1.043 (1.004 to 1.076) 0.009 Age 1.045 (1.011 to 1.079) 0.009
Hypertension 2.346 (1.095 to 5.029) 0.028 Hypertension 2.216 (1.002 to 4.902) 0.050
Heart rate on admission 0.978 (0.961 to 0.996) 0.018 Heart rate on admission 0.974 (0.956 to 0.993) 0.009
TIMI flow grade of the IRA after PCI <0.001 Angiography-to-PCI delay 1.049 (1.019 to 1.080) 0.001
TIMI flow grade of the IRA after PCI 0.001
0 24.776 (6.088 to 100.834) <0.001
1 – 0.998 0 8.257 (2.923 to 23.326) <0.001
2 2.957 (0.818 to 10.691) 0.098 1 – 0.998
Stent implantation 0.022 2 1.942 (0.409 to 9.207) 0.403
Bare-metal stent 10.189 (1.599 to 64.936) 0.014 Ventricular arrhythmias 0.036
Drug-eluting stent 3.831 (0.367 to 39.998) 0.262 Sustained VT 1.670 (0.309 to 9.019) 0.551
Ventricular arrhythmias <0.001 Ventricular fibrillation 3.943 (1.370 to 11.347) 0.011
Sustained VT 2.624 (0.604 to 11.393) 0.198 Right ventricular infarction 8.610 (2.773 to 26.734) <0.001
Ventricular fibrillation 6.266 (2.486 to 15.793) <0.001 Stent thrombosis 5.893 (1.254 to 27.698) 0.025
Right ventricular infarction 9.959 (3.655 to 27.140) <0.001
Stent thrombosis 7.015 (1.861 to 26.448) 0.004
Reference values are: per 1 year increase for age; per 1 beat per minute increase for heart rate on admission; per 1 min increase for every delay; typical chest pain for symptoms; TIMI
flow grade 3 for TIMI flow grade before/after PCI and absence/no for all other variables.
*Multivariable logistic regression model based on 5184 observations with complete covariate information.
†Multivariable logistic regression model based on 3895 observations with complete covariate information.
‡Multivariable logistic regression model based on 3837 observations with complete covariate information.
§Multivariable logistic regression model based on 3161 observations with complete covariate information.
FMC, first medical contact; HAVB, high-degree atrioventricular block; IRA, infarct related artery; PCI, percutaneous coronary intervention; RCA, right coronary artery; TIMI, thrombolysis
in myocardial infarction; VT, ventricular tachycardia.

increased mortality but is a surrogate marker of larger infarct
size. Our findings support this hypothesis as patients with
HAVB suffered more frequently from right and left ventricular
dysfunctions as demonstrated by a greater frequency of cardio-
genic shock and right ventricular infarction and for patients
who developed HAVB during hospitalisation, had lower left
ventricular ejection fraction. These features are markers of
severe STEMI with extensive transmural wall necrosis and thus
identify a subgroup of patients at high risk for inhospital
complications.21
Mechanism of HAVB in acute myocardial infarction and
differences between early versus late HAVB
Mechanisms of HAVB in STEMI are multifactorial and depend
on the location of the culprit lesion and delay of appearance
after acute myocardial infarction. Anatomy of the coronary
arteries explains the differences in mechanisms of HAVB in
STEMI. Indeed, in about 90% of cases, a branch of the RCA
supplies the atrioventricular node and the bundle of His.
Penetrating branches from the LAD coronary artery predomin-
antly supply the ventricular septum and the bundle branches.22
Auffret V, et al. Heart 2016;102:40–49. doi:10.1136/heartjnl-2015-308260
In inferior STEMI, the heart block is most often transient,
early and due to an increased parasympathetic tone via the
vagus nerve also known as the Bezold-Jarisch reflex4 23 or an
ischaemia of the atrioventricular node due to RCA occlusion
and impairment of collateral blood flow from concomitant LAD
disease.3 Contrarily, in anterior STEMI, HAVB is related to
interruption of septal perfusion associated with extensive myo-
cardial necrosis. This conduction disturbance occurs later during
hospitalisation and is frequently irreversible secondary to atrio-
ventricular node necrosis.9 11 23
Therefore, the location of wall necrosis in STEMI compli-
cated by HAVB has major prognostic implications. Poorer clin-
ical outcomes of HAVB in anterior STEMI than in inferior have
been demonstrated. For example, Nguyen et al8 showed in their
historical cohort that two-thirds of patients with HAVB died
after anterior STEMI compared with 37% after inferior STEMI.
As expected, in our cohort, HAVB complicating RCA-related
STEMI was more common than in cases of LAD or circumflex
artery involvement and a difference in inhospital mortality was
also obvious despite reduced event rates compared with previ-
ous studies.
47
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Coronary artery disease
Interestingly, the presence of HAVB on admission was mainly
associated with culprit lesions of the RCA, poorer blood supply
to the conduction system as assessed by thrombolysis in myocar-
dial infarction flow grade before p-PCI and haemodynamic
instability whereas the occurrence of HAVB during hospitalisa-
tion was primarily driven by p-PCI failure as assessed by post
p-PCI thrombolysis in myocardial infarction flow grade, p-PCI
complications (stent thrombosis) or complications of the STEMI
itself. These findings are consistent with the abovementioned
physiopathology of HAVB complicating STEMI.
In the present study, the highest mortality rate was found in
patients who developed HAVB during the first 24 h of hospital-
isation followed by patients with HAVB on admission. Strasberg
et al21 also showed this association between early blocks and a
higher mortality compared with late blocks. Nonetheless, it can
be hypothesised that the early time of occurrence of HAVB is
not solely responsible for this higher mortality which is prob-
ably related to an overall greater severity of STEMI as assessed
by the presence of cardiogenic shock on admission in 20–25%
of cases and the higher frequency of right ventricular infarction
in these subgroups.
Limitations
Retrospective observational studies are inherently vulnerable to
selection bias and unidentified confounders, thus our study has
some limitations that need to be acknowledged.
First, as in any registry, under-reporting of complications, even
clinically significant ones such as HAVB, cannot be ruled out.
Moreover, ORBI is, by definition, restricted to patients admitted
to an interventional cardiology centre, which may induce selec-
tion bias: STEMI cases managed medically in non-interventional
centres or patients who do not survive the prehospital phase are
not included. Another limitation of this study is the absence of
Key messages
What is already known on this subject?
High-degree atrioventricular block (HAVB) is a common
complication of ST segment elevation myocardial infarction
(STEMI) and is known to be associated with higher mortality
rates at the acute phase. Previous studies reached conflicting
results about the potential independent relationship between
HAVB and short-term mortality.
What might this study add?
Few studies have examined the incidence, correlates and
prognostic implication of HAVB in the modern era of primary
percutaneous coronary intervention ( p-PCI). This study reported
a 3.5% incidence of HAVB complicating STEMI in a large
prospective registry including more than 4900 patients treated
by p-PCI and identified predictors of HAVB according to its time
of occurrence. HAVB was not independently related to mortality
regardless of reperfusion therapy despite higher mortality rates
in patients with HAVB (17.5% vs 4.5%).
How might this impact on clinical practice?
In the contemporary era of emergent mechanical reperfusion
and potent antithrombotic therapies, HAVB still identifies a
subgroup of patients with larger and more severe STEMI at high
risk for inhospital complications.
48
exhaustive recording of permanent pacemaker implantation
during the course of hospitalisation; however previous studies
have already demonstrated the high reversibility rate of HAVB in
the setting of acute STEMI especially in the p-PCI era making
infrequent the need for permanent pacemaker implantation.
Finally, ORBI is limited to the inhospital phase and does not
include a long-term follow-up. Consequently, we were unable to
assess the long-term prognostic significance of HAVB according
to its time of occurrence. Nevertheless, our study also has several
strengths such as its large population with a cohort of 4931
patients treated with p-PCI which may add to the currently
limited knowledge about HAVB in this specific setting.
CONCLUSION
Despite the widespread use of modern and potent antithrombo-
tic therapies, HAVB remains a common complication of STEMI
as it occurred in 3.5% of patients overall. However, the rate of
HAVB occurring during hospitalisation after p-PCI was low at
1.2%. HAVB, when present on admission or occurring during
the first 24 h of hospitalisation, was associated with a higher
inhospital mortality rate. Multivariable analysis identified
several well known high-risk features but not HAVB as inde-
pendent predictors of inhospital mortality. Moreover, predictors
of HAVB differed according to its time of occurrence as HAVB
on admission was mainly associated with RCA culprit lesions,
cardiogenic shock and less culprit artery patency whereas HAVB
occurring during hospitalisation was associated with STEMI or
p-PCI complications and failure to achieve reperfusion of the
culprit lesion.
Author affiliations
1
CHU Rennes, Service de Cardiologie et Maladies Vasculaires, Rennes, France
2
Université de Rennes 1, LTSI, Rennes, France
3
INSERM, U1099, Rennes, France
4
CH de Vannes, Service de Cardiologie, Vannes, France
5
CH de Saint-Brieuc, SAMU, Saint Brieuc, France
6
CH de Lorient, Service de Cardiologie, Lorient, France
7
Département de Cardiologie, CHU de Brest, Brest, France
8
EA4324, Optimisation des Régulations Physiologiques (ORPhy), UFR Sciences et
Techniques, Brest, France
9
CH de Saint Malo, Service de Cardiologie, Saint Malo, France
10
CH de Saint Brieuc, Service de Cardiologie, Saint Brieuc, France
11
CH de Quimper, Service de Cardiologie, Quimper, France
12
Clinique Saint Laurent, Service de Cardiologie, Rennes, France
13
CH de Vannes, SAMU, Vannes, France
14
CHU de Brest, SAMU, Brest, France
15
CHU de Rennes, Service des Urgences médicales, Rennes, France
Acknowledgements The authors thank the team of clinical research assistants
who ensured data collection: Q Lepage (CHU de Rennes); P Héry (Clinique
Saint-Laurent, Rennes); F Langlais (Centre Hospitalier de Saint-Brieuc); P Dias and C
Kergoulay (CHU de Brest); and P Rameau and M Paquin (Centre Hospitalier de
Quimper). The authors also thank all cardiologists, emergency and SAMU staff who
collected the data.
Contributors VA, J-CD and HLB designed the study. MLG and VA performed the
statistical analysis. AL and VA wrote the first draft of the manuscript and are co-first
authors. J-CD and HLB were responsible for final approval of the manuscript. All
other contributors provided critical review for important intellectual matters.
Competing interests None declared.
Ethics approval The registry was approved by the Commission Nationale de
l’Informatique et des Libertés and this study was approved by the local ethics
committee.
Provenance and peer review Not commissioned; externally peer reviewed.
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High-degree atrioventricular block

complicating ST segment elevation
myocardial infarction in the contemporary era
Vincent Auffret, Aurélie Loirat, Guillaume Leurent, Raphael P Martins,
Emmanuelle Filippi, Isabelle Coudert, Jean Philippe Hacot, Martine
Gilard, Philippe Castellant, Antoine Rialan, Régis Delaunay, Gilles
Rouault, Philippe Druelles, Bertrand Boulanger, Josiane Treuil, Bertrand
Avez, Marc Bedossa, Dominique Boulmier, Marielle Le Guellec,
Jean-Claude Daubert and Hervé Le Breton

Heart 2016 102: 40-49

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