Download Effect of Definition on Incidence of Postinfarction

1537
Effect of Definition on Incidence
of Postinfarction Pericarditis
Is It Time to Redefine Postinfarction Pericarditis?
Philip B. Oliva, MD; Stephen C. Hammill, MD; James V. Talano, MD
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P ericarditis is possibly the most common cause of
chest pain after an acute transmural myocardial
infarction without reperfusion.' It occurs in
approximately 28% to 40% of fatal transmural infarctions,2-8 and a pericardial effusion is detectable by
serial echocardiograms in 28% to 63% of patients with
a nonfatal transmural infarction.9-12 Yet the clinically
reported frequency of postinfarction pericarditis
ranges between 7%13 and 41%.1 Such a wide range
seems inconsistent with the narrower frequency range
determined by pathological examination2-8 and serial
echocardiograms.9-12
Assuming that the wide frequency range of clinically
diagnosed postinfarction pericarditis is due to a difference in the clinical definition among various studies,
whereas the pathological and echocardiographic frequencies of postinfarction pericarditis and postinfarction pericardial effusion, respectively, are due to more
precise, objective diagnostic criteria and observations,
the present report reviews the clinical frequency of
postinfarction pericarditis according to its definition
(see below) and compares it with the available pathological and echocardiographic data.
Types of Postinfarction Pericarditis
Between 1936 and 1941, four articles14-'7 emphasized
an 80% to 85% incidence of acute localized - ie, regional-postinfarction pericarditis, in contrast to a 15% to
20% incidence of the diffuse variety. Both types occurred during the first week after an acute myocardial
infarction. In 1956, Dressler18 described a form of
postinfarction pericarditis characterized by prolonged
or recurrent positional pleuritic chest pain, pulmonary
infiltrates, fever, an increased erythrocyte sedimentation rate, and/or a pericardial friction rub. This syndrome usually occurs 2 to 11 weeks after the infarction,19 although occasionally it is recognized during the
first week.'8'20'21 Although some authors22,23 subsequently have questioned the existence of Dressler's
Received February 8, 1994; revision accepted April 18, 1994.
From the Heart Research and Education Association of Colorado, Rose Medical Center, Denver (P.B.O.); the Electrocardiography and Electrophysiology Laboratories, Mayo Clinic and Foundation, Rochester, Minn (S.C.H.); and the Cardiac Graphics
Laboratory, Division of Cardiology, Northwestern Memorial Hospital, Chicago, Ill (J.V.T.).
Correspondence to Philip B. Oliva, MD, Heart Research and
Education Association of Colorado, Rose Medical Center, Cardiology Division, 4567 E Ninth Ave, Denver, CO 80220.
X 1994 American Heart Association, Inc.
syndrome, despite a 12% incidence of postinfarction
heart muscle antibodies,24 general experience has established its incidence as 5%20 or less,21'25 a much lower
incidence than the accepted, consistently earlier form.
Definition of Pericarditis
During the pre-World War II years, when a three- or
four-lead ECG was standard, interest was focused on
the ECG alterations associated with pericarditis.26-34
The diagnosis of pericarditis was based on the presence
of a pericardial friction rub, a pericardial effusion, or
autopsy evidence of pericardial injury.26-34 Symptoms
were not used. Evolutionary changes of the ST segment
and T waves were recognized26-34 and shown to be due
to subepicardial inflammation and/or injury.28-32 It remained for Spodick35 to formally establish the characteristic four phases of repolarization changes due to
pericarditis.
After World War II, a spate of reports36-42 appeared
describing the clinical characteristics of acute rheumatic
or nonspecific pericarditis. These articles emphasized
the importance of recognizing positional pleuritic chest
pain as evidence of pericarditis. Whereas 92% to 100%
of patients with pericarditis had typical chest pain, only
47% to 74% had a pericardial friction rub.36-42
With regard to postinfarction pericarditis, authors of
late 20th-century textbooks on cardiology also advised
avoiding reliance on a friction rub as the sole indicator
of pericarditis. In 1966, Dr Charles K. Friedberg43
stated that "even when no rub is heard a highly probable diagnosis of acute pericarditis can be made on the
basis of the typical pleuropericardial pain." Six years
later he added that positional pleuritic chest pain is
"adequate to diagnose pericarditis whether or not a rub
is audible."44 In 1978, Dr J. Willis Hurst et a145 wrote
that "pericarditis secondary to transmural infarction is
much more common than the 15% incidence customarily quoted (by rub)." Moreover, they noted that if an
"observer demands the presence of a pericardial friction rub," the diagnosis of pericarditis may be "unrecognized in spite of typical pain." Others46 warned that
requiring a friction rub to diagnose postinfarction pericarditis will result in a "gross underestimate" of its
incidence since "many patients have classic symptoms,
but the friction rub does not occur or is missed because
of its fleeting nature." Gersh et all further state that
"pericarditis is possibly the commonest cause of recurring chest pain after admission to the hospital" for an
acute myocardial infarction, but the clinical diagnosis of
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Circulation Vol 90, No 3 September 1994
TABLE 1. Relation of Incidence of Postinfarction Pericarditis to Definition of Condition
Definition
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No. of Cases
With AMI
62
100
145
200
NS
109
41
176
208
NS
779
195
1284
305
338
554
300
1505
400
261
196
80
43
1264
121
423
46
703
No. (%)
With Per
8 (13)
Year
Author
White47
1926
7 (7)
1928
Parkinson and Bedford48
1929
Levine and Brown49
20 (14)
1931
White and Bland50
20 (10)
1935
Master and Jaffe51
2
Blumer14
1936
32 (29)
1936
Vander Veer and Brown52
7 (17)
1938
Bean53
24 (14)
1941
Rosenbaum and Levine54
33 (16)
1968
Wood55
(1 0)
1971
Thadani et a156
52 (7)
1973
22 (11)
Niarchos and McKendrick57
1973
Barman et a158
106 (8.25)
1974
31 (10)
Lichstein et a159
1974
Yan60
41 (10.6)
Toole and Silverman13
1975
40 (7)
1975
Liem et ai61
44 (15)
1975
McLean et a162
224 (14.9)
1976
Guillevin and Valere63 64
64 (16)
1980
38 (14.5)
Sawaya et a165
1981
Hutter et al66
28 (14)
1984
Northcote et a120
23 (28)
1985
12 (28)
Kaplan et a19
1985
Dubois et a167
297 (23.4)
1986
Galve et al10
35 (29)
1985
Krainin et a168
31 (7.3)
Somolinos et alll
1987
19 (41)
Tofier et al69
141 (20)
1989
Oliva et a170
1993
26 (30)
85t
AMI indicates acute myocardial infarction; Peri, postinfarction pericarditis;
*AII five patients with symptoms also had a friction rub.
tExclusive of 1 15 patients who received lytic therapy.
pericarditis is "likely underestimated" because pericardial friction rubs are often evanescent or overlooked or
because the pain may be "attributed to recurrent ischemia." Despite these recommendations by textbook
authors to accept the diagnosis of postinfarction pericarditis if typical symptoms exist without a friction rub,
authors publishing in medical journals have frequently
required a pericardial friction rub to establish the
diagnosis. Table 1 (References 47 through 69) discloses
that all published articles in the English-language literature from 1926 through 1973 based the diagnosis of
postinfarction pericarditis on a rub only. Not until
1974 was an article published that accepted typical
pericardial pain and/or a pericardial friction rub to
diagnose postinfarction pericarditis. From 1974 to
1993, 7 of 14 peer-reviewed articles9-1120,60,62,70 and two
letters to the Editor6364 accepted classic symptoms
and/or a friction rub.
Q-Wave
Non-Q-Wave
AMI, %
AMI, %
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
100
0
100
0
100
0
93
7
NS
NS
70
30
83
17
NS
NS
100
0
86
14
NS
NS
79
21
14
86
91
9
90
10
100
0
70
30
89
11
and NS, not stated.
Rub
NS
Symptoms
NS
+
NS
NS
+
+
+
+
+
+
+
+
+
+
+
+
_
+
5*
+
+
+
+
+
+
If a friction rub alone is used to diagnose postinfarction pericarditis, the mean incidence of this condition
among patients not receiving lytic therapy is 14%. If
classic symptoms or a friction rub or both are used as
diagnostic criteria, the mean incidence rises to 25%
(Table 1). This frequency approximates the autopsyobserved frequency of postinfarction pericarditis of
28% to 40%.2-8
Sensitivity of ECG Criteria for Regional
Postinfarction Pericarditis and Relation of
ECG Criteria to Definition of the Condition
Recently, through an autopsy examination of 70 patients with fatal left ventricular free-wall rupture, we
learned that regional postinfarction pericarditis accompanied rupture in 94% of instances and was consistently
associated with an atypical form of postinfarction
Oliva et al Definition of Postinfarction Pericarditis
TABLE 2. Effect of Lytic Therapy on Frequency of
Postinfarction Pericarditis
Incidence of Postinfarction
Pericarditis
Non-Lytic Therapy Lytic Therapy
Year
Author
Group, %
Group, %
17
7
Simoons et at75 1985
12
6.4
GISS176
1986
11
ECS77
1988
6.3
7
1990
15
AIMS71
30
Oliva et at74
1993
15
GISSI indicates Gruppo Italiano per lo Studio delta Streptochinasi nett'tnfarto Miocardico; ECS, European Cooperative Study
Group; and AIMS, Anistreplase in Acute Myocardial tnfarction
Study.
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T-wave evolution during the day, or more often several
days, before rupture.71 These T-wave changes were
similar to those recorded in dogs with localized postinfarction pericarditis in 1939.72 Two types of atypical
T-wave evolution were observed clinically. Either the T
waves remained persistently positive for 48 hours or
longer after the onset of an acute myocardial infarction
(type I), or initially inverted T waves gradually became
positive deflections (type II). The sensitivity and specificity, as defined previously, of these atypical T-wave
changes were 100% and 77%, respectively.70 The specificity rose to 96% if patients who had reinfarction,
underwent cardiopulmonary resuscitation, or sustained
a very small initial infarct as a consequence of early lytic
therapy were excluded. The frequency of postinfarction
pericarditis defined by classic symptoms and/or a rub
was 30% in those patients who did not receive lytic
therapy. There was a 2.5% frequency of unexplained
atypical T-wave evolution ("false-positives"). One explanation for this 2.5% incidence of false-positives is
that those patients may have had painless and acoustically silent postinfarction pericarditis. If so, the actual
incidence of postinfarction pericarditis would be 32.5%
in patients not receiving lytic therapy, in harmony with
the autopsy range of 28% to 40%.
The sensitivity of these ECG alterations for postinfarction pericarditis was recently confirmed by an investigation performed at Northwestern University.73 We
reviewed the serial ECGs of all patients from that
institution with clinically recognized (by typical positional pleuritic chest pain and/or a friction rub) postinfarction pericarditis reported by Kaplan et al.9 All
patients had one of the two types of atypical T-wave
evolution,73 affirming the 100% sensitivity of these ECG
changes to diagnose postinfarction pericarditis and also
justifying the use of typical symptoms and/or a friction
rub to diagnose this condition.
Effect of Lytic Therapy on the Incidence of
Postinfarction Pericarditis
Since 1985, five reports74-78 have addressed the effect
of lytic therapy on the incidence of postinfarction
pericarditis (Table 2). All agree that the incidence is
halved by lytic therapy, whether typical symptoms
and/or a friction rub or a rub alone is used to define
postinfarction pericarditis. We found that the incidence
1539
of postinfarction pericarditis as defined by typical symptoms and/or a rub was reduced from 30% to 15% by
lytic therapy.74 Other reports75-78 using a rub alone
found an incidence reduction from between 11% and
17% without lytic therapy to between 6% and 7% with
lytic therapy. The absolute numbers are, of course,
lower when a rub alone is used to define postinfarction
pericarditis, for reasons discussed earlier. However,
regardless of the definition, a 50% reduction of the
incidence of postinfarction pericarditis by lytic therapy
is observed.
Conclusions
Postinfarction pericarditis can be diagnosed when an
accurate history is elicited by an informed cardiologist
from an observant, articulate. patient. The requirement
of a friction rub leads to a significant underestimation of
the incidence of postinfarction pericarditis. Postinfarction pericarditis occurs in an average of 25% of instances of acute transmural myocardial infarction not
treated with lytic therapy when typical symptoms and a
pericardial friction rub are accepted as indicative of
pericarditis, whereas the average incidence is only 14%
when a friction rub alone is required.
Atypical T-wave evolution appears to be a very
sensitive and reasonably specific ECG sign of regional
postinfarction pericarditis. It is more sensitive than a
friction rub and, when observed in a patient with chest
pain after an acute myocardial infarction, provides an
objective method of differentiating among the three
causes of postinfarction chest pain.
Lytic therapy reduces the frequency of postinfarction
pericarditis by 50% whether classic symptoms and a
friction rub or a rub alone is used to define the
condition. Since postinfarction pericarditis is almost
always the consequence of a transmural infarction,7879
its reduction by lytic therapy implies sparing of the
pericardium and subjacent myocardium.
Acknowledgments
This work was supported, in part, by research grants from
the Rose Medical Foundation, Denver, Colo, and Marquette
Electronics, Inc, Milwaukee, Wis. The assistance of Marty
Bender at the Heart Research and Education Association of
Colorado, Marlene Ploetz at the Mayo Clinic, and Sharon
Baruch and Michell Parker, RN, at Northwestern University is
appreciated.
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Effect of definition on incidence of postinfarction pericarditis. It is time to redefine
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Circulation. 1994;90:1537-1541
doi: 10.1161/01.CIR.90.3.1537
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