CASE REPORT
Acase of earl postmycardial 'infarct'ion syndrome
J.W. Beekhuis
A 65-year old woman was admitted with an inferior infarction. Six hours later she developed a pericarditis with specific ECG alterations in the anterior wall accompanied with pericardial and pleural effuision. This early form of true pericarditis after acute myocardial infarction can be explained as an exacerbation of a latent inflammation, whether or not triggered by the acute infarction. (Neth HeartJ2001;9:240-3.) Key words: pericardial effusion, postmyocardial infarction syndrome, virus infection n 1973, Kossowsky et al. reported on patients with * early postmyocardial infarction syndrome within one week after acute myocardial infarction. They based their diagnosis on the finding ofpencardial effiusion on chest X-ray, which they believed does not occur with pericarditis epistenocardica. None of these patients showed ECG changes characteristic of pericarditis.' Later on in 1986, when echocardiography became available, pericardial effusion was diagnosed in 28 of 138 patients (20.3%) with acute myocardial infarction.2 Consequently, the diagnosis of early postmyocardial infarction syndrome can only be made if, as well as pericardial effusion, changes in the ECG characteristic of pericarditis are also present.
Case report A 65-year-old woman was admitted in 1985 with an inferior infarction with a maximal aspartate aminotransferase (ASAT) of 134 u/l (normal (20) and a lactate dehydrogenase (LDH) of 933 u/l (normal (370). The creatinine phosphokinase (CPK) was not measured. Six weeks earlier, the patient had had a persistent pharyngitis with enlarged cervical lymph J.W. Beekhuls. Wilhelmina Hospital, Wilhelminastraat 27, 9401 NN Assen. Address for correspondence: J.W. Beekhuis.
E-mail:[email protected]
240
nodes and fever for ten days; there was no response to antibiotics. The patient remained tired until the infarction occurred. On admission, the ECG showed a total AV block, and she was hypotensive with a systolic pressure of 60 mmHg. When treated with dobutamine and isoprenaline, her heart rhythm soon became normal and there was an increase in systolic blood pressure to 100 mmHg. Central venous pressure remained slightly elevated for a long time. Six hours after admission, ST elevations were seen in the precordial leads V1, V2 and V3, followed by rounded T changes in leads V4, V5 and V6, changing to negative T waves from two to eight days after admission, compatible with pericarditis (figure 1). On the day after admission a loud precordial friction rub was heard at the level of the fourth intercostal space, which in the following days decreased to a soft friction rub that was sometimes audible. Five days after admission the first signs of pericardial effusion were observed on the chest X-ray, which was repeated three days later (figure 2). Echocardiography confirmed the eff-usion. A small pleural effusion developed on the right side. Fever existed from the first day with peaks to 38.5 OC. Treatment with 50 mg indomethacine suppositories, twice daily, was started on the tenth day and continued for ten days with good results. Both the fever level and the pericardial effusion decreased. Three weeks later the pericardial effusion had disappeared. From the first day of admission the patient was anticoagulated with acenocoumarol. The ESR on admission was 41 mm/h. There were 8600 leukocytes per mm3 with normal differentiation on day 7. Antibodies against myocardial tissue could not be detected. The antistreptolysin titre was 160 E (normal(200); coarsegrained antinuclear antibodies were found in a titre of 1:40. Cold agglutinins and cryoglobulins were not found. No increases were found in the complement fixing antibody titres against influenza A and B, herpes simplex and cytomegalovirus. Neutralising antibody titres against the Coxsackie B viruses were 1:4 for Coxsackie BI, B2 and B6 on day 2, day 6 and five months later; levels of 1:6 for B4, 1:16 for B5 and 1:501 for B3 were found on all three occasions. The pleural fluid had the following composition: total Netherlands Heart Journal, Volume 9, Number 6, Septenber 2001
A case of early postmyocardial infarction syndrome
Figure IA. ECG taken on admizson. There are ST elevations in leads II, II, AVF with a &&
I
------------I
pathological Q wave in lead III and a smaller Q wave in AVF.
Leads V4, V5 and V6 were
notavailable. A total A V block is evi-
dent.
protein 27g/l, 500 x 106/1 leukocytes (differentiation: 16 segmented neutrophils, 82 lymphocytes and 2 monocytes). Discussion In 1956 Dressler described a pericarditis that differed from the pericarditis epistenocardica occurring after
acute myocardial infarction. It was characterised by inflammation of the pericardium, pleura and lung parenchym, usually beginning in the second week or later after the infarction.3 For manyyears it was believed that postmyocardial infarction syndrome was an autoimmune phenomenon, but this theory has now been abandoned.4'5 Recently, several cases of post-
T1
1
1
............
X
ig re lB six hours later ST eleA....
......
[
....................
| ........
1
I1.11
11111
vations were _seen in the .
...
cordial leads -"': 8
[anterior ,IT.1i' l,V2N and z V3,
pre-
,
suggestive of
pericarditis.
Netherlands Heart Journal, Voluim 9, Number 6, September 2001
241
A case of early postmyocardial infarction syndrome
Figure 1G. Twelve hours after admission the ECG showed rapid changes in the ST segments in anterior s Pslww-sewa@t etsBslar wall leads.
**. .e,. ~~~...
pericardiotomy syndrome and postmyocardial infarction syndrome due to a viral reactivation or infection have been reported. Decreased resistance of proliferating mesothelial tissue to viral infection is thought to be responsible.5 From the first day the subject patient, with an early postmyocardial infarction syndrome, showed ECG changes characteristic of pericarditis with development
est]r tm_
of a pericardial effusion and a small pleural effusion on the right side. In this patient, true pericarditis originated so rapidly after acute myocardial infarction that the most plausible explanation is that this was due to an exacerbation of a latent inflammation, whether or not triggered by the acute infarction. The origin of this inflammation is speculative. Connection with a viral infection is possible considering the pharyngitis with .......
.....l..
......
ig
.I
MTI .T
.......
Two
..
days af-
...
. . . .crosis as evi-
ter admission,
infrrior
ne-
dent in the inferior leads. ST seg-
The
.XD.l. 1..... .M ....... ..... ..... ... ... ments in the re rd ia
......
.........
...
n mlm_ _ M
Mg . .
leads showed the rather
I1typipicture of a pericarditiswithfurtherchanging rounded
T
waves in leads
V,4, Vs and V,.
242
Netherlands Heart Journal, Volume 9, Number 6, September 2001
A case of early postmyocardial infarction syndrome
UI mr W X JW rm m gr if g Tz FE'T=;
m mn
Tm 1
"
.
Uq
U
4.AU Fi,gure 1E
Six~days after
..i ....U
~~~~admissionQ
f
1~~~~~~~'I'' the in ~~waves h.: LI fj~~~~~~~~~~~~~ Ijjj iJi III IL IL
WGWG' S 1 0 1 ! lil l ^ 1 1 l l! l! 1 tand negative ----.
Ililillililimlminmx ~l l lil liP lblHlm.-terior and
ImomImo1Dmmm milumEIImm11 hU'l 'fl Elil[11111111 ilil Ult!linI' l WlE"lifII'ElilE lDM lilid'l.llzil lul,'1!lllelilu0SIlER Inl
l l
:milm
II1i' Ip~I
1 l111 Il1XI
1 I
~
ST
segments
an the
III
Htflf
111iO~~It 1E E :IMM m 11 H1mn111nT nZ11 T n IIm
a inD
lateral wall
k
lads
Conclusion After the first publication in 1973 that mentioned early postmyocardial infarction syndrome, the existence of
gX 1111 111.......11411011110
this diagnosis was later denied.6 The subject patient with ECG changes of true pericarditis shortly after acute myocardial infarction and the development of pericardial effusion proves that this diagnosis exists, but is very uncommon. It is not obvious whether the pericarditis had developed spontaneously without acute myocardial infarction or that the trigger for an exacerbation ofa latent inflammation was caused by the acute infarction, for example by a change in cellular immunity after tissue damage.7 It is possible that this inflammation was related to the persistent pharyngitis six weeks before admission. N References 1 2
3 4
5
Figure2. Chest X-ray, taken in anteroposteriorposition, eightdayw after admission. The cardiac silhouette is markedly enlarged by effusion. The rtghtand lefthilum are obscured by thesshadow ofthe heart. The rtht diaphragm ispardy elvated with asmall infiltrate on the upper side.
Netherlainds Heart Journal, Volume 9, Number 6, September 2001
6 7
were
evident.i
i.I cervical lymphadenopathy six weeks before admission, the small lung infiltrate and the high Coxsackie B3 antibody titre.
-
Kossowsky WA, Epstein PJ, Levine RS. Postmyocardial infarction syndrome: an early complication of myocardial infarction. Chest 1973;63:35-40. Galve E, Garcia-Del Castillo H, Evangelista A, Battle J, Pemanyer-Miralda G, Soler-Soler J. Pericardial effusion in the course of myocardial infarction: Incidence, natural history and clinical relevance. Circulation 1986;73:294-9. Dressler W. A postmyocardial infarction syndrome. Preliminary report of a complication resembling idiopathic, recurrent, benign pericarditis. JAMA 1956;160:1379-83. Kossowsky WA, Lyon AF. The postmyocardial infarction syndrome - Vanished or vanquished? A twenty-five-year follow-up. A Case Report. Angiology 1996;47:83-5. Beekhuis JW. Is er een rol voor virusinfectie als oorzaak van het postmyocardinfarctsyndroom en postpericardiotomiesyndroom? Cardiologie 2000;7:196-9. Lichstein E, Arsura E, Hollander G, Greengart A, Sanders M. Current incidence ofpostmyocardial infarction (Dressler's) syndrome. AmjCardiol 1982;50:1269-71. Berenbaum MCM, Fluck PA, Hurst NP. Depression of lymphocyte response after surgical trauma. BrJExp Pathol 1973;54:597607.
243
Acase of earl postmycardial 'infarct'ion syndrome
J.W. Beekhuis
A 65-year old woman was admitted with an inferior infarction. Six hours later she developed a pericarditis with specific ECG alterations in the anterior wall accompanied with pericardial and pleural effuision. This early form of true pericarditis after acute myocardial infarction can be explained as an exacerbation of a latent inflammation, whether or not triggered by the acute infarction. (Neth HeartJ2001;9:240-3.) Key words: pericardial effusion, postmyocardial infarction syndrome, virus infection n 1973, Kossowsky et al. reported on patients with * early postmyocardial infarction syndrome within one week after acute myocardial infarction. They based their diagnosis on the finding ofpencardial effiusion on chest X-ray, which they believed does not occur with pericarditis epistenocardica. None of these patients showed ECG changes characteristic of pericarditis.' Later on in 1986, when echocardiography became available, pericardial effusion was diagnosed in 28 of 138 patients (20.3%) with acute myocardial infarction.2 Consequently, the diagnosis of early postmyocardial infarction syndrome can only be made if, as well as pericardial effusion, changes in the ECG characteristic of pericarditis are also present.
Case report A 65-year-old woman was admitted in 1985 with an inferior infarction with a maximal aspartate aminotransferase (ASAT) of 134 u/l (normal (20) and a lactate dehydrogenase (LDH) of 933 u/l (normal (370). The creatinine phosphokinase (CPK) was not measured. Six weeks earlier, the patient had had a persistent pharyngitis with enlarged cervical lymph J.W. Beekhuls. Wilhelmina Hospital, Wilhelminastraat 27, 9401 NN Assen. Address for correspondence: J.W. Beekhuis.
E-mail:[email protected]
240
nodes and fever for ten days; there was no response to antibiotics. The patient remained tired until the infarction occurred. On admission, the ECG showed a total AV block, and she was hypotensive with a systolic pressure of 60 mmHg. When treated with dobutamine and isoprenaline, her heart rhythm soon became normal and there was an increase in systolic blood pressure to 100 mmHg. Central venous pressure remained slightly elevated for a long time. Six hours after admission, ST elevations were seen in the precordial leads V1, V2 and V3, followed by rounded T changes in leads V4, V5 and V6, changing to negative T waves from two to eight days after admission, compatible with pericarditis (figure 1). On the day after admission a loud precordial friction rub was heard at the level of the fourth intercostal space, which in the following days decreased to a soft friction rub that was sometimes audible. Five days after admission the first signs of pericardial effusion were observed on the chest X-ray, which was repeated three days later (figure 2). Echocardiography confirmed the eff-usion. A small pleural effusion developed on the right side. Fever existed from the first day with peaks to 38.5 OC. Treatment with 50 mg indomethacine suppositories, twice daily, was started on the tenth day and continued for ten days with good results. Both the fever level and the pericardial effusion decreased. Three weeks later the pericardial effusion had disappeared. From the first day of admission the patient was anticoagulated with acenocoumarol. The ESR on admission was 41 mm/h. There were 8600 leukocytes per mm3 with normal differentiation on day 7. Antibodies against myocardial tissue could not be detected. The antistreptolysin titre was 160 E (normal(200); coarsegrained antinuclear antibodies were found in a titre of 1:40. Cold agglutinins and cryoglobulins were not found. No increases were found in the complement fixing antibody titres against influenza A and B, herpes simplex and cytomegalovirus. Neutralising antibody titres against the Coxsackie B viruses were 1:4 for Coxsackie BI, B2 and B6 on day 2, day 6 and five months later; levels of 1:6 for B4, 1:16 for B5 and 1:501 for B3 were found on all three occasions. The pleural fluid had the following composition: total Netherlands Heart Journal, Volume 9, Number 6, Septenber 2001
A case of early postmyocardial infarction syndrome
Figure IA. ECG taken on admizson. There are ST elevations in leads II, II, AVF with a &&
I
------------I
pathological Q wave in lead III and a smaller Q wave in AVF.
Leads V4, V5 and V6 were
notavailable. A total A V block is evi-
dent.
protein 27g/l, 500 x 106/1 leukocytes (differentiation: 16 segmented neutrophils, 82 lymphocytes and 2 monocytes). Discussion In 1956 Dressler described a pericarditis that differed from the pericarditis epistenocardica occurring after
acute myocardial infarction. It was characterised by inflammation of the pericardium, pleura and lung parenchym, usually beginning in the second week or later after the infarction.3 For manyyears it was believed that postmyocardial infarction syndrome was an autoimmune phenomenon, but this theory has now been abandoned.4'5 Recently, several cases of post-
T1
1
1
............
X
ig re lB six hours later ST eleA....
......
[
....................
| ........
1
I1.11
11111
vations were _seen in the .
...
cordial leads -"': 8
[anterior ,IT.1i' l,V2N and z V3,
pre-
,
suggestive of
pericarditis.
Netherlands Heart Journal, Voluim 9, Number 6, September 2001
241
A case of early postmyocardial infarction syndrome
Figure 1G. Twelve hours after admission the ECG showed rapid changes in the ST segments in anterior s Pslww-sewa@t etsBslar wall leads.
**. .e,. ~~~...
pericardiotomy syndrome and postmyocardial infarction syndrome due to a viral reactivation or infection have been reported. Decreased resistance of proliferating mesothelial tissue to viral infection is thought to be responsible.5 From the first day the subject patient, with an early postmyocardial infarction syndrome, showed ECG changes characteristic of pericarditis with development
est]r tm_
of a pericardial effusion and a small pleural effusion on the right side. In this patient, true pericarditis originated so rapidly after acute myocardial infarction that the most plausible explanation is that this was due to an exacerbation of a latent inflammation, whether or not triggered by the acute infarction. The origin of this inflammation is speculative. Connection with a viral infection is possible considering the pharyngitis with .......
.....l..
......
ig
.I
MTI .T
.......
Two
..
days af-
...
. . . .crosis as evi-
ter admission,
infrrior
ne-
dent in the inferior leads. ST seg-
The
.XD.l. 1..... .M ....... ..... ..... ... ... ments in the re rd ia
......
.........
...
n mlm_ _ M
Mg . .
leads showed the rather
I1typipicture of a pericarditiswithfurtherchanging rounded
T
waves in leads
V,4, Vs and V,.
242
Netherlands Heart Journal, Volume 9, Number 6, September 2001
A case of early postmyocardial infarction syndrome
UI mr W X JW rm m gr if g Tz FE'T=;
m mn
Tm 1
"
.
Uq
U
4.AU Fi,gure 1E
Six~days after
..i ....U
~~~~admissionQ
f
1~~~~~~~'I'' the in ~~waves h.: LI fj~~~~~~~~~~~~~ Ijjj iJi III IL IL
WGWG' S 1 0 1 ! lil l ^ 1 1 l l! l! 1 tand negative ----.
Ililillililimlminmx ~l l lil liP lblHlm.-terior and
ImomImo1Dmmm milumEIImm11 hU'l 'fl Elil[11111111 ilil Ult!linI' l WlE"lifII'ElilE lDM lilid'l.llzil lul,'1!lllelilu0SIlER Inl
l l
:milm
II1i' Ip~I
1 l111 Il1XI
1 I
~
ST
segments
an the
III
Htflf
111iO~~It 1E E :IMM m 11 H1mn111nT nZ11 T n IIm
a inD
lateral wall
k
lads
Conclusion After the first publication in 1973 that mentioned early postmyocardial infarction syndrome, the existence of
gX 1111 111.......11411011110
this diagnosis was later denied.6 The subject patient with ECG changes of true pericarditis shortly after acute myocardial infarction and the development of pericardial effusion proves that this diagnosis exists, but is very uncommon. It is not obvious whether the pericarditis had developed spontaneously without acute myocardial infarction or that the trigger for an exacerbation ofa latent inflammation was caused by the acute infarction, for example by a change in cellular immunity after tissue damage.7 It is possible that this inflammation was related to the persistent pharyngitis six weeks before admission. N References 1 2
3 4
5
Figure2. Chest X-ray, taken in anteroposteriorposition, eightdayw after admission. The cardiac silhouette is markedly enlarged by effusion. The rtghtand lefthilum are obscured by thesshadow ofthe heart. The rtht diaphragm ispardy elvated with asmall infiltrate on the upper side.
Netherlainds Heart Journal, Volume 9, Number 6, September 2001
6 7
were
evident.i
i.I cervical lymphadenopathy six weeks before admission, the small lung infiltrate and the high Coxsackie B3 antibody titre.
-
Kossowsky WA, Epstein PJ, Levine RS. Postmyocardial infarction syndrome: an early complication of myocardial infarction. Chest 1973;63:35-40. Galve E, Garcia-Del Castillo H, Evangelista A, Battle J, Pemanyer-Miralda G, Soler-Soler J. Pericardial effusion in the course of myocardial infarction: Incidence, natural history and clinical relevance. Circulation 1986;73:294-9. Dressler W. A postmyocardial infarction syndrome. Preliminary report of a complication resembling idiopathic, recurrent, benign pericarditis. JAMA 1956;160:1379-83. Kossowsky WA, Lyon AF. The postmyocardial infarction syndrome - Vanished or vanquished? A twenty-five-year follow-up. A Case Report. Angiology 1996;47:83-5. Beekhuis JW. Is er een rol voor virusinfectie als oorzaak van het postmyocardinfarctsyndroom en postpericardiotomiesyndroom? Cardiologie 2000;7:196-9. Lichstein E, Arsura E, Hollander G, Greengart A, Sanders M. Current incidence ofpostmyocardial infarction (Dressler's) syndrome. AmjCardiol 1982;50:1269-71. Berenbaum MCM, Fluck PA, Hurst NP. Depression of lymphocyte response after surgical trauma. BrJExp Pathol 1973;54:597607.
243
