Download The incidence of atrial arrhythmias during inferior wall myocardial

The incidence of atrial arrhythmias during
inferior wall myocardial infarction with and
without right ventricular
involvement
The atrial arrhythmia profile during inferior wall acute myocardial infarction (AMI) has not been
systematically
examined with respect to right ventricular (RV) involvement. To this end, 62
consecutive
patients with first inferior wall AMI and no other conditions known to increase
susceptibility
for rhythm disturbances
were studied by 24-hour Holter monitoring during the first
and tenth day of infarction. Based on radionuclear
ventriculography
performed on day 2 of
infarction, patients were allocated to two groups: group A-36 patients (56%) with right
ventricular ejection fraction (RVEF) ~40% (mean + SD, 31 I 6%) and group B-26 patients
(42%) with normal (>40%) RVEF (mean f SD, 47 ? 5%). There were no significant differences
between the two groups with respect to age, sex, or left ventricular (LV) function. In the group as
a whole, ectopic activity in the different categories of atrial arrhythmias was significantly
higher
during the first day than on the tenth day of infarction. Comparing the two groups, 33 patients
(92%) in group A had a mean hourly frequency of one or more atrial premature contractions
(APCs) during the first day of infarction compared with 16 patients (69%) in group B (p < 0.001).
Atrial and supraventricular
tachycardia were recorded more frequently in group A patients (16 of
36 [44%] versus 6 of 26 [31%]) as well as atrial fibrillation (AF) (7 of 36 [19%] versus 1 of 26
[4%]). Quantitative analysis showed a similar trend for a higher rate of ectopic events in group A
patients. Ectopic activity was neither influenced by LVEF nor by age or sex. Using stepwise
regression analysis, RVEF was independently
related to the prevalence of AF and APCs. The
data presented indicate that patients with inferior wall Ml accompanied
by RV dysfunction are
more prone to develop atrial rhythm disturbances
than patients with preserved RV function. Atrial
infarction or ischemia, atrial distension, and a raised right atrial pressure may account for this
trend. (AM HEART J 1992;124:367.)
Eldad Rechavia, MD, Boris Strasberg, MD, Aviv Mager, MD, Nili Zafrir, MD,
Jairo Kusniec, MD, Alex Sagie, MD, and Samuel Sclarovsky, MD
Petah-Tiqva and Tel-Aviv, Israel
The spectrum of atria1 arrhythmia ranges from a single atria1 premature contraction (APC) to atria1
fibrillation (AF). These were commonly observed in
patients with acute myocardial infarction (AMI)‘, 2
and have been reported to occur frequently in patients with atria1 infarction.3-6 The hemodynamic
hazards associated with right ventricular (RV) infarction are assuming progressively greater importance. In this respect, an excess prevalence of atria1
arrhythmias, especially during the evolutionary vulnerable phase, may have a considerable hemodyFrom the Cardiovascular
ical Center,
Petah-Tiqva;
Medicine.
Division
and Coronary
Care
and the Tel-Aviv
University
Received
Sept.
Reprint
Medical
4/l/38098
for publication
requests:
Center,
26. 1991;
accepted
Eldad Rechavia,
MD, Cardiovascular
Petah-Tiqva,
49100 Israel.
Unit, Beilinson
MedSackler
School
Of
Feb.
10, 1992.
Division,
Beilinson
namic impact. Although atria1 arrhythmias apparently do not carry the same prognostic implications
as ventricular arrhythmias, still the accompanying
loss of atrioventricular (AV) functional integrity and
its potential adverse effect on RV diastolic and systolic function may contribute to the development of
cardiogenic shock. 7,8 Despite widespread clinical
concern for RV infarction, the incidence of atria1 arrhythmias during inferior wall MI has not yet been
documented with respect to RV involvement. We
therefore undertook a prospective Holter monitoring
(HM) study to assessthe prevalence of early and late
atria1 arrhythmias during inferior wall MI.
METHODS
Study patients.
Seventy-five consecutive patients who
were admitted to the coronary care unit within 4 hours of
symptom onset of an inferior wall MI were consideredfor
inclusion in this prospective study. Patients wereineligible
367
388
Rechavia et al.
American
August 1992
Heart Journal
Table I. Prevalence and event rates of early (Holter I) versus late (Holter II) atria1 ectopic activity in 59 patients with
inferior wall MI
APCs
h4lhr
Holter I
Holter II
p Value
AT + SVT
No. of
patients (Cb1’
9 k 14
122
48 (81)
26 (44)
co.00
<0.001*
M/24 hr
4+7
1
0.04
AF, Atria1 fibrillation;
AF
No. of
patients (%lt
21 (36)
9 (15)
0.007
APCs, atria1 premature contractions; AT, atria1 tachycardia; M, mean number
significant; SVT, supraventricular
tachycardia.
*Number of patients with a mean hourly frequency of one or more atria1 premature contractions.
tNumber
of patients with one or more arrhythmic
episodes per 24 hours.
for inclusion if they had a history or electrocardiographic
evidence of previous MI, aortocoronary bypass surgery or
coronary angioplasty, chronic or paroxysmal atria1 arrhythmias, valvular or congenital heart disease,pericarditis, cardiomyopathy, preexisting heart failure, significant
obesity, chronic pulmonary diseaseor pulmonary hypertension, or if they were receiving digitalis or antiarrhythmic therapy. Thyrotoxicosis or pulmonary embolismwere
suspectedin none of the patients. An acute inferior wall MI
wasdefined by typical chest pain lasting for more than 30
minutes; by the appearanceof pathologic Q waves in the
correspondinginferior leads;and by the elevation of serum
cardiac enzymes(creatine kinasehad to be morethan twice
the upper limit of normal). There were 55 men and 20
women, aged 34 to 80 years (mean & SD, 60 f 10 years).
All patients had 24-hour HM during the first 24 hours of
admission.During normal AV conduction, gated equilibrium radionuclide ventriculography was performed in 71
patients on the following day (within 36 hours of admission).
Of the 75 patients entering this study, four died during
the first 24 hours of infarction. Nine others had to be excluded becauseof temporary pacemaker implantation or
right heart catheterization during the HM period (five patients) or becauseof technically unsatisfactory recording or
radionuclear analysis (four patients). From the remaining
62 patients who formed the definite study population, 59
had an additional HM study on the tenth day after infarction. One patient who died on the fifth day of MI and two
others who required aortocoronary bypass surgery were
eliminated from a secondstudy. All patients were treated
with intravenous heparin except for those in whom anticoagulants were contraindicated. Intravenous streptokinase
(1.5 million units) was given to 10 patients who were subsequently classifiedashaving RV dysfunction and to nine
others with no evidence of RV involvement.
Radionuclear ventriculography. First-pass ventriculographic studies (30-degree right anterior oblique view)
were performed at rest on day 2 of infarction, 24to 36 hours
after admission.A single-crystal digital camera (Apex 415,
Elscint, Inc., Hackensack, N.J.) and integrated computer
system with a high-efficiency low-resolution collimator
were used. A bolus of 15 mC; of technetium-99m pertech-
M/24 hr
2t1
1
NS
of ectopic events; MI, myocardial
No. of
patients i%)#
8 (14)
1 (2)
NS
infarction;
NS, not
netate wasinjected in a medial antecubital fossavein. Acquisition was performed on a 64 X 64 pixel matrix with a
frame rate varying from 20 to 32 frames for 30 seconds.
Data analysiswas accomplishedby nearly completely automated processing. Right ventricular ejection fraction
(RVEF) and left ventricular ejection fraction (LVEF) were
obtained, aswell asthe segmentalfunctional imagesutilizing end-diastolic and end-systolic perimeters. Significant
RV or LV dysfunction was considered to occur once the
correspondingEF fell below the standard deviation of the
normal values as determined in our radionuclear laboratory (RVEF = 46 F 5%; LVEF = 60 f 6% )-less than
40Sband 547, , respectively.
Basedon the radionuclear data, patients weregroupedas
follows: group A-36 patients (58%) with depressedRVEF
(mean -+ SD, 31 -+ 6%) and group B-26 patients (42%)
with normal RVEF (mean + SD, 47 + 5%).
Holter monitoring procedure. Sixty-two patients had
24-hour HM during the first 24hours following admission.
An additional recording was made in 59 patients 10 days
after infarction. No patient wasreceiving antiarrhythmic,
inotropic, or fl-adrenergic blocking agents at the time of the
studies.None of them had clinical signsof pericarditis. The
24-hour HM tapeswereinitially scannedby an experienced
technician, usinga dynamic electrocardioscanner(Innovator 500, Del Mar Avionics, Irvine, Calif.) capable of digital
ternplating of atria1 and ventricular ectopic events. At the
completion of the analysis, the computerized arrhythmic
scanner tabulates the frequency of each arrhythmia and
provides a digital printout of the total number of singleectopic beats and arrhythmias for eachhour of recording. In
addition to the computerized analysis, the scannerswere
scannedvisually and printouts were madefrom all definite
and questionable episodesof arrhythmias. All recordings
were interpreted by an experienced physician.
Grading of atrial arrhythmias. Atria1 arrhythmias were
graded from isolated APCs to complex atria1 arrhythmias.
For convenience, complex atria1 arrhythmias were separated into two categories(Tables I to III). The first category consisted of atria1 tachycardia and supraventricular
tachycardia, defined as three or more consecutive APCs
with an atria1 rate greater than lOO/min. Atria1 fibrillation
(AF) was considered as the second category of complex
Volume
124
Number
2
Atria1 arrhythmias
in inferior
AMI
389
Table II. Prevalence and event rates of atria1 ectopic activity during the early phaseof inferior wall MI in patients
with depressedversus normal RV function
APCs
RVEF
(%I)
Groul;
A (n =36)
N (n = 26)
61 + 11
60 k 9
62 ?z 10
62 +- 10
p Value
NS
NS
LVEF,
*Number
*Number
31 I 6
47 k 5
<O.OOl
Mlhr
13 + 17
6_t5
0.05
AT + SVT
No. of
patients (%,) *
33 (92)
18 (69)
0.01
No. of
patients (%i*
M/24 hr
5k8
1
NS
Left ventricular
ejection fraction; RVEF, right ventricular
ejection fraction;
01‘ patients with a mean hourly frequency of one or more atria1 premature
of’ patients with one or more arrhythmic
episodes per 24 hours.
AF
Ml24 hr
16 (44)
8 (31)
0.02
other abbreviations
contractions.
No. of
patients iS)f
311
1
NS
7 (19)
1 (4)
NS
as in Table I.
Table III. Prevalence and event rates of atria1 ectopic activity during the late phase (tenth day) of inferior wall MI in
patients with depressedversus normal RV function
APCs
--
Age
W)
LVEF
(“6)
RVEF
C’S)
61 5 11
60 k 9
62 k 10
63 zk 10
NS
NS
30 k 6
47 2 5
<O.OOl
Group
A (n = 34)
H (n = 25)
1-2
Value
Abbreviations
and footnote
AT + SVT
Mlhr
No. of
patients (%) *
M/24 hr
313
3*3
17 (50)
9 (36)
1
1
7 (21)
NS
NS
NS
NS
No. of
patients (%)r
2 (8)
symbols as in Tables I and II.
atria1 arrhythmias. Within each category the number of
ectopic episodeswas analyzed separately. Atria1 arrhythmias were diagnosedusing standard electrocardiographic
criteria.g
Statistical analyses. Clinical data are presentedas the
mean k SI). Clinical variables were compared between
patient groups usingthe t test. Inter- and intragroup comparisonsof the proportions of patients having a given arrhythmia and cumulative event rates of ectopic episodesin
each category during the first and tenth day of infarction
were basedon a t test for unpaired and paired data aswell
ason McNemar’s test, the chi squaretest (with Yates’ correction), and a proportion test as appropriate. For small
samplecomparison,Mann-Whitney and Wilcoxon nonparametric tests were used. Stepwise multiple regression
analysisand Pearson correlation were conducted to identify clinical variables (age,sex, RVEF, and LVEF) related
to atria1 rhythm disturbances.R-square and t values were
reported to delineate the relative importance of each factor selectedby the multiple regressionanalysis.Probability values less than 0.05 were considered statistically
significant..
RESULTS
For the entire group of patients, the incidence of
atria1 ectopic activity was significantly higher during
the first day of MI than on the tenth day (Table I).
Comparing the two groups, there were no significant
differences with respect to age, sex distribution, or
LVEF (mean _+SD, 62 i 10% for both groups). Of
the 36 patients in group A, 33 (92 %) had one or more
APCs per hour, compared with 18 patients (69 % ) in
group B (Table II). Atria1 and supraventricular
tachycardia were more often present in group A patients(16of36
[44%] versus8of26[31’%]).
However,
this trend was not as significant as the one observed
withrespect to AF (7 of 36 [19%] versus 1 of 26 [4%]).
Quantitative
analysis revealed a mean hourly frequency of APCs of 13 f 17 in group A patients compared with 6 k 5 in group B patients (p = 0.05). In
patients with complex atria1 arrhythmias,
arrhythmic episodes were recorded more frequently in group
A patients (p = 0.02). Episodes of AF were single in
two patients (one from each group) and multiple (two
to four episodes) in the remaining group A patients.
The prevalence of late rhythm disturbances (tenth
day after MI) was comparable among group A and B
subjects (Table III).
Stepwise multiple regression analysis revealed that
the prevalence of atria1 rhythm disturbances was unrelated to age, sex, or LVEF. After adjusting for the
other selected variables, RVEF was independently
related to the prevalence of APCs and AF (R
square = 7 ?-;I and 7.7% ; significance of t = 0.02 and
0.02, respectively). A weaker nonsignificant
association was observed between RV function and the
prevalence of atria1 and supraventricular
tachycardia. The correlation between RV function and rhythm
390
Rechavia et al.
disturbances was further explored using the Pearson
correlation. Likewise, RVEF was significantly related
to the prevalence of APCs (p = 0.019) and to the occurrence of AF @ = 0.014).
DISCUSSION
Atria1 rhythm disturbances, occurring in about
20 % to 45 % of MI patients13 2* lo usually disappear
within a few days unless significant ventricular dysfunction persists or pericarditis occurs.1o’ l1 In this
study, the prevalence of atria1 arrhythmias
was
investigated in a carefully preselected group of patients with first inferior wall MI. Stringent inclusion
criteria ensured selection of patients with no other
conditions
known to increase susceptibility
for
rhythm disturbances or that could impose a further
hemodynamic
burden on the RV. The major observations were: (1) The incidence of atria1 ectopic activity in patients with inferior wall MI is significantly
higher during the first than on the tenth day of infarction. (2) Patients with RV dysfunction have an
increased incidence of early atria1 arrhythmias when
compared with patients with an intact RV. (3) RVEF
is independently
related to the prevalence of APCs
and AF. In accordance with previously reported daour LVEF data for patients with inferior wall
ta, 1’2Y14
MI was comparable with the normal control values.
The prevalence of RV dysfunction was also in close
agreement with that in previous reports.15-I9
This study provides no information
about the naturally occurring trigger responsible for the higher
propensity toward atria1 rhythm disturbances among
patients with RV dysfunction. However, several precipitating factors alone or in combination
may be
important in accounting for this trend. These include
atria1 infarction, an increased right atria1 pressure,
atria1 distension, and autonomic factors. Their etiologic role as an arrhythmogenic
trigger and their
contribution
to the observed incidence of atria1
arrhythmias have not yet been determined.
It has been suggested that AF early in the course
of inferior wall MI is primarly related to left atria1 ischemia or infarction, induced by a proximal occlusion
of the circumflex coronary artery.3 However, in the
setting of inferior wall MI complicated by RV infarction, a circumflex artery occlusion is unlikely to be a
major ischemic cause of an increased prevalence of
atria1 ectopic activity, since the right coronary artery
is almost always the culprit vessel.i5a 2o In addition, as
the sinus node artery originates from t,he right coronary artery in 55% and from the AV nodal artery in
almost 90% of cases, one could not ignore their potential role in the genesis of atria1 arrhythmias during RV infarction.‘, 21 Bouts of tachycardia can be
American
August 1992
Heart Journal
precipitated by sinus node ischemia and dysfunction,
making AF, atria1 ectopic activity, and junctional
rhythms more likely, similar to sick sinus syndrome.
Role of atrial infarction
mias. In most published
in genesis
of atrial
arrhyth-
studies of atria1 infarction,
particular attention has been given to the occurrence
of atria1 arrhythmias.“*, 23 Of note is the study by
Soderstrom,”
in which 26 out of 47 patients with
atria1 infarction exhibited either paroxysmal or sustained AF. Consequently,
one difficuhy in truly
attributing
atria1 rhythm disturbances to RV infarction stems largely from its unreported association
with right atria1 infarction. In postmortem
studies,
the highest reported incidence of atria1 infarction
among autopsy-verified
cases of MI is 429; .24 The
hypothesis that right atria1 infarction might, be a
major determinant
of arrhythmogenesis
in patients
with RV infarction is gaining indirect support from
the consistently higher reported rate of right atria1 as
opposed to Ieft atria1 infarction.sT fi, 24 Cushing et al.‘j
reported that out of 31 autopsy-proven cases of atria1
infarction, 27 were right-sided. In an experimental
model of RV infarction,25 necropsy findings of right
atria1 necrosis, varying from 40% to 95(‘; of the atria1
mass, were apparent in all examined hearts.
Role of atrial pressure and enlargement
in genesis
atrial arrhythmias.
Maintaining
the contribution
of
of
atria1 contraction to diastolic filling is particularly
beneficial in patients with RV infarction, in whom
diastolic filling is a crucial determinant
of systolic
function. However, the infarcted RV imposes increased preload and afterload on the right atrium,
resulting in enhanced right atria1 pressure and subsequent enlargement. Under these circumstances, it
is likely that susceptibility
to atria1 rhythm disturbances is substantially aggravated, as demonstrated
by Legrand et a1.,“6 who noted a large RV infarct in
nearly all patients who experienced an episode of AF.
In addition, the study by Sugiura et al.27 has provided
an insight into the importance of right atria1 pressure
and its possible adverse arrhythmogenic
effect. Discriminant analysis in this study revealed that the rise
in right atria1 pressure identified a group of patients
who were much more likely to have AF. Another pertinent observation has emerged from the study of
Sanfilippo et al. 28 Once sinus rhythm is not maintained, atria1 enlargement can develop as a consequence of atria1 arrhythmias, contributing
to a selfperpetuating
anatomic-arrhythmogenic
interrelated
cycle. This vicious cycle would be expected to affect,
mainly the right atrium in cases of RV infarction.
Clinical implications.
The main implication
of this
study is that patients with inferior wall MI would be
expected to have a higher incidence of atria1 ectopic
Volume
Number
124
2
Atria1 arrhythmias
activity once RV dysfunction coexists. Whether the
hemodynamic
state and prognosis are adversely affected by the magnitude of difference in arrhythmic
events is a question to be addressed in further
studies.
We thank
Franc0
for
analyses.
Mrs. Silvia Shtein, Mrs.
assistance
in performing
Judith Sasdi, and Mrs. Yael
the Holter
and statistical
REFERENCES
1. DeSanctis
RW, Block P, Hutter
AD. Tachyarrhythmias
in
myocardial
infarction.
Circulation
1972;45:681-702.
2. Liherthson
RR, Salisbury
KW, Hutter
AM, DeSanctis
RW.
Atria1 tachyarrhythmias
in acute myocardial
infarction.
Am J
Med 1976;60:956-60.
3. Hod H, Lew AS, Keltai M, Cercek B, Geft IL, Shah PK, Ganz
W. Early atria1 fibrillation
during evolving
myocardial
infarction: a consequence
of impaired
left atria1 perfusion.
Circulation 1987;75:146-50.
4. Liu CK, Greenspan
G, Piccirillo
RT. Atria1 infarction
of the
heart. Circulation
1961;23:331-8.
5. Soderstrom
N. Myocardial
infarction
and mural thrombosis
in
the atria of the heart. Acta Med Stand 1948;217(suppl):l-114.
6. Cushing EH, Feil HS, Stanton
EJ, Wartman
WB. Infarction
of the cardiac auricles (atria): clinical, pathological
and experimental
studies. Br Heart J 1942;4:17-34.
7. Love JC, Hafferjee
CI, Gore JM, Alpert
JS. Reversibility
of
hypotension
and shock by atria1 or atrioventricular
sequential
pacing in patients with right ventricular
infarction.
AM HEART
d 1984;104:5-13.
8. Isner JM, Fisher GP, DelNegro
AA, Borer JS. Right ventricular infarction
with hemodynamic
decompensation
due to
transient
loss of active atria1 augmentation:
successful
treatment with atria1 pacing. AM HEART J 1981;4:931-9.
9. Criteria
Committee
of the New York
Heart
Association.
Nomeneclature
and criteria
for diagnosis
of diseases of the
heart and great vessels. 8th ed. Boston: Little,
Brown,
& Co,
1979:188-218.
IO. Cristal N, Szwarcherg
J, Gueron M. Supraventricular
arrhythmias in acute myocardial
infarction.
Ann Intern
Med 1975;
82:35-‘I.
11. Lofmack
R, Orinius
E. Supreventricular
tachyarrhythmias
in
acute myocardial
infarction.
Acta Med Stand 1978;60:956-60.
12. Shah PK, Maddahi
J, Berman
DS, Pichler
M, Swan HJC.
Scintigraphically
detected predominant
right ventricular
dysfunction
in acute myocardial
infarction:
clinical and hemodvnamic correlates
and implications
for therapy
and prognosis.
.J Am Co11 Cardiol
1985;6:1264-72.
13. Dell’Italia
LJ, Starling
MR, Crawford
MH, Boros BL, Chaudhuri TK, O’Rourke
RA. Right ventricular
infarction:
identification by hemodynamic
measurements
before and after volume loading and correlation
with noninvasive
techniques.
J
Am Co11 Cardiol
1984:4:931-g.
in inferior
AMI
391
14. Baigrie
RS, Haq A, Morgan
CD, Rakowski
H, Drobac
M,
McLaughlin
P. The spectrum
of right ventricular
involvement
in inferior waI1 myocardial
infarction:
a clinical, hemodynamic
and noninvasive
study. J Am Co11 Cardiol
1983;1:1396-404.
15. Verani MS, Tortoledo
FE, Batty JW, Raizner
AE. Effect of
coronary
artery recanalization
on right ventricular
function
in
patients
with acute myocardial
infarction.
J Am Co11 Cardiol
1985;5:1029-35.
16. Rodrigues
EA, Dewhurst
NG, Smart LM, Hannan
WJ, Muir
AL. Diagnosis
and prognosis
of right ventricular
infarction.
Br
Heart J 1986;56:19-26.
17. Candell-Riera
J, Figueras
J, Valle V, Alvarez
A, Gutierrez
L,
Cortadellas
J, Cinca J, Salas A, Rius J. Right ventricular
infarction:
relationship
between
ST segment
elevation
in Vqn
and hemodynamic,
scintigraphic
and echocardiographic
findings in patients
with acute inferior
myocardial
infarction.
AM
HEART J 1981;101:281-7.
18. Lopez Sendon J, Coma Canella I, Gamallo
C. Sensitivity
and
specificity
of hemodynamic
criteria
in the diagnosis
of acute
right ventricular
infarction.
Circulation
1981;64:515-25.
19. Strasberg
B, Pinchas A, Arditti
A, Lewin RF, Sclarovsky
S,
Hellman
C, Zafrir
N, Agmon
J. Left and right ventricular
function
in inferior
acute myocardial
infarction
and significance of advanced
atrioventricular
block. Am J Cardiol
1984;
54:985-7.
20. Andersen
HR, Falk E, Nielsen D. Right ventricular
infarction:
frequency,
size and topography
in coronary
heart disease. A
prospective
study comprising
107 consecutive
autopsies from
a coronary
care unit. J Am Co11 Cardiol
1985$X264-72.
21. James TN. Myocardial
infarction
and atria1 arrhythmias.
Circulation
1961;14:761-76.
22. Gardin JM, Singer DH. Atria1 infarction:
importance,
diagnosis and localization.
Arch Intern
Med 1981;141:1345-8.
23. Lazar EJ, Goldberger
J, Peled H, Sherman
M, Frishman
WH.
Atria1 infarction:
diagnosis
and management.
AM HEART J
1988;116:1058-63.
24. Wartman
WB, Sanders
JC. Localization
of myocardial
infarcts with respect to the muscle bundles of the heart. Arch
Path01 Lab Med 1950;50:321-64.
25. Goldstein
JA, Vlahakes
GJ, Verrier
ED, Schiller NB. Tyberg
JV, Ports TA, Parmley
WW, Chatterjee
K. The role of right,
ventricular
systolic dysfunction
and elevated intrapericardial
pressure
in the genesis of low output
in experimental
right
ventricular
infarction.
Circulation
1982;65:513-22.
26. Legrand
V, Rigo P, Smeets JP, Demoulin
JC. Collignon
P.
Kulbertus
HE. Right ventricular
myocardial
infarction
diagnosed by 99m technetium
pyrophosphate
scintigraphy:
clinical course and follow-up.
Eur Heart J 1983;4:9-19.
27. Sugiura T, Iwasaka
T, Ogawa A, Shiroyama
Y, Tsuji H, Onoyama H, Inada M. Atria1 fibrillation
in acute myocardial
infarction.
Am J Cardiol
1985;56:27-9.
28. Sanfilippo
AJ, Abascal VM, Sheehan M, Oertel LB, Harrigan
P, Hughes RA, Weyman
AE. Atria1 enlargement
as a consequence of atria1 fibrillation.
Circulation
1990;82:792-7.