Download Clinical Factors Associated With Persistent

Clinical Factors Associated With Persistent
Pericardial Effusion After Successful
Primary Coronary Angioplasty*
Tetsuro Sugiura, MD, FCCP; Seishi Nakamura, MD; Yoshihiro Kudo, MD;
Toshika Okumiya, PhD; Fumiyasu Yamasaki, MD; and Toshiji Iwasaka, MD
Study objective: To evaluate the incidence and clinical factors related to the persistence of
infarct-associated pericardial effusion (PE) after primary angioplasty.
Design: Consecutive case-series analysis.
Setting: Coronary care unit in a university hospital.
Patients: Three hundred ninety-one consecutive patients with acute myocardial infarction (AMI)
who underwent successful primary percutaneous transluminal coronary angioplasty (PTCA) at
hospital admission.
Interventions: Coronary angiography and primary PTCA on hospital admission and serial
echocardiography.
Measurements and results: The status of coronary flow before and after primary PTCA was
evaluated by coronary angiography at hospital admission, while PE was studied by echocardiography within 24 h of admission and 1 month after the onset of AMI. PE was present in the acute
phase in 76 patients (19%), and patients with PE had a significantly higher incidence of in-hospital
death than those without PE (11% vs 2%, p < 0.001). Among 68 patients who had PE in the acute
phase and underwent echocardiography 1 month later, PE persisted to 1 month after the onset
of AMI (persistent PE) in 26 patients (38%). Patients with persistent PE had a significantly higher
incidence of pericardial rub (p ⴝ 0.010), Killip class > 1 (p ⴝ 0.025), no reflow after PTCA
(p ⴝ 0.026), lower incidence of collaterals (p ⴝ 0.024), and tended to have higher peak creatine
kinase (CK) [p ⴝ 0.05] levels than those with transient PE. When five variables (peak CK,
collaterals, no reflow, pericardial rub, and Killip class > 1) were used in the multivariate analysis,
pericardial rub (p ⴝ 0.023; odds ratio [OR], 5.45), absence of collaterals (p ⴝ 0.011; OR, 0.16),
and Killip class > 1 (p ⴝ 0.027; OR, 3.80) were the significant variables related to persistent PE.
Conclusions: PE remains a relatively common complication of AMI even in the era of reperfusion
therapy and is associated with increased mortality. Furthermore, the presence of a pericardial rub,
Killip class > 1, and absence of collateral flow in the early phase of the infarct are associated with
persistence of the PE to 1 month after the onset of AMI.
(CHEST 2005; 128:798 – 803)
Key words: angioplasty; myocardial infarction; pericardial effusion
Abbreviations: AMI ⫽ acute myocardial infarction; CK ⫽ creatine kinase; OR ⫽ odds ratio; PE ⫽ pericardial effusion;
PTCA ⫽ percutaneous transluminal coronary angioplasty
ericardial effusion (PE) is a relatively common
P complication
during the course of acute myocardial infarction (AMI).1–5 Prior to the introduction of
reperfusion therapy, Galve et al6 reported that reab*From the Department of Laboratory Medicine (Drs. Sugiura,
Kudo, Okumiya, and Yamasaki), Kochi Medical School, Kochi;
and Cardiovascular Center (Drs. Nakamura and Iwasaka), Kansai
Medical University, Osaka, Japan.
Manuscript received April 20, 2004; revision accepted March 16,
2005.
Reproduction of this article is prohibited without written permission
from the American College of Chest Physicians (www.chestjournal.
org/misc/reprints.shtml).
Correspondence to: Tetsuro Sugiura MD, FCCP, Department of Laboratory Medicine, Kochi Medical School, Kohasu Oko-cho Nankoku
City, Kochi, Japan 783-8505; [email protected]
sorption of PE in the acute phase of the infarct was
slow and PE could persist for weeks to months after
the infarct. Although early reperfusion therapy has
reduced the mortality rate in patients with AMI,
coronary flow to the infarct zone before, as well as
after, primary percutaneous transluminal coronary
angioplasty (PTCA) is an important determinant of
final infarct size and in-hospital complications, including PE in the acute phase.5,7–11 An echocardiogram demonstrating PE may indicate fluid retention,
but it is not diagnostic of pericarditis since pericardial fluid may also accumulate as a result of increased
hydrostatic pressure. A pericardial rub is the most
specific clinical sign of pericarditis, but the clinical
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Clinical Investigations
course of PE with and without a pericardial rub after
primary PTCA has not been determined. In this
report, we evaluated pericardial rub along with
angiographic and other clinical factors to determine
the important factors related to the course of PE
after successful primary PTCA.
Materials and Methods
Patients
We studied 391 consecutive patients admitted to the coronary
care unit with their first ST-segment elevation AMI (April 1,
1988, to March 31, 2000) who underwent successful primary
PTCA (⬍ 50% diameter stenosis of the infarct-related artery
after primary PTCA) within 12 h of the onset and adequate
echocardiographic imaging quality. All the patients who survived
to the chronic phase (377 patients) underwent follow-up coronary
angiography (1 month after the onset of AMI) with a patent
culprit lesion (⬍ 75% diameter stenosis). Patients with reinfarction or repeat PTCA were not included in this study.
The diagnosis of AMI was based on chest pain lasting ⬎ 30
min, persistent ST-segment elevation ⬎ 0.1 mV in two or more
contiguous leads, and increase in the serum creatine kinase (CK)
levels with ⬎ 5% MB fraction. Measurement of CK was carried
out every 8 h through the first 2 days after hospital admission, and
the peak value was used in this study. Each patient was monitored continuously in the coronary care unit. Major arrhythmias
included transient atrial fibrillation and third-degree atrioventricular block requiring temporary pacing during the first 3 days after
the hospital admission. Physical examinations were performed at
hospital admission, and Killip class was used to determine the
state of congestive heart failure. Careful auscultation was performed at least twice daily, and pericardial rub was considered to
be a scratchy, grating, or creaking noise heard in systole, middiastole, and presystole or in any one of these phases. Identification of pericardial rub was based on nonconformity with the
characteristic locations, radiations, respiratory responses of most
murmurs, and thrills. Auscultatory, palpatory, and respiratory
observations were performed independently within a few minutes of each other, and the diagnosis of pericardial rub was made
only after agreement by more than two cardiologists. The
detection of pericardial rub within 24 h after primary PTCA was
recorded.
A clinical history of hypertension, diabetes mellitus, hypercholesterolemia, and smoking was determined from patient interview
or medical records. Blood samples were obtained to measure
serum total protein and albumin within 2 days of the follow-up
echocardiography. Informed consent was obtained from each
patient before cardiac catheterization, and the investigational
protocol was approved by the institutional review board of the
Kansai Medical University Hospital.
Primary PTCA
All patients were administered aspirin (81 mg) and 3,000 U of
IV heparin just after the diagnosis of AMI. After written informed
consent was obtained, the patients were taken to the cardiac
catheterization laboratory as soon as possible to undergo an
emergency coronary angiogram. After arterial cannulation, all
patients received heparin (7,000 IU) and isosorbide dinitrate (2
mg), and baseline angiography was performed. PTCA was attempted whenever there was occlusion or subtotal occlusion of
the infarct-related artery with use of an exchangeable guidewire
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system. Successful PTCA was defined as a percentage diameter
stenosis of the infarct-related artery ⬍ 50% after reflow. The
culprit lesion was successfully dilated in all patients. After
catheterization, patients were admitted to the coronary care unit
for intensive monitoring. An IV infusion of heparin was maintained for 3 to 5 days, with the dose adjusted to achieve a
therapeutic level of anticoagulation. Coronary flow of the infarctrelated artery before PTCA was graded visually according to the
Thrombolysis in Myocardial Infarction study classification: grade
0 flow as total occlusion. Collateral channels were graded from
the initial angiography, and a patient was considered to have
collaterals to the infarct zone if the collateral perfusion grade was
2 or 3 described by Rentrop et al.12 Angiographic no-reflow
phenomenon following primary PTCA was defined as Thrombolysis in Myocardial Infarction grade ⬍ 3 flow in the presence of a
widely patent epicardial coronary artery, despite the absence of
dissection, thrombus, or distal vessel cut-off suggestive of macroembolization. Angiograms were analyzed by three experienced
angiographers without knowledge of the clinical data.
Echocardiography
Two-dimensional and M-mode echocardiography were performed within 24 h after hospital admission (acute phase) with an
echocardiography system (Sonos 2500, 5500; Agilent Technologies; Palo Alto, CA), and all classic views were recorded on
videotape for subsequent analysis. Analysis of the left ventricular
wall was performed in 16 segments,13 and the number of
segments with advanced asynergy (akinesis or dyskinesis) was
calculated. The presence of PE was assessed by the method
described by Horowitz et al.14 An epicardial/pericardial separation that persisted throughout the cardiac cycle (D pattern) was
considered diagnostic of PE. Left ventricular wall motion and PE
were determined by two independent observers who had no
knowledge of the clinical and angiographic data. In cases of
disagreement, consensus was established with a third observer.
Follow-up Study
In all patients who survived to the chronic phase, coronary
angiography was repeated to confirm the patency of infarctrelated artery, and echocardiography was performed to assess left
ventricular wall motion and the presence of PE (25 to 32 days
after the onset of AMI). The patients with PE in acute and
chronic phases were considered to have persistent PE. Angiograms and echocardiograms in acute and chronic phases were
analyzed by the same observers.
Statistical Analysis
Results are reported as the mean ⫾ SD. Statistical analysis
between the two groups was performed using Student t test for
continuous variables and Fisher Exact Probability Test for discrete variables. All calculated p values were two tailed. Stepwise
logistic regression analysis was performed to evaluate the important variables related to persistent PE. A p value ⬍ 0.05 was
considered significant.
Results
Clinical Characteristics
Seventy-six of 391 patients (19%) had PE in the
acute phase of AMI. Patients with PE in the acute
phase had a significantly larger number of advanced
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799
asynergic segments, higher peak CK, and higher
incidence of Killip class ⬎ 1, pericardial rub, and
angiographic no reflow than those without PE (Table
1). Fourteen patients died in the hospital. There was
a significantly higher incidence of in-hospital death
in patients with PE (six patients died of heart failure,
and two patients died of cardiac rupture) compared
to those without PE (four patients died of heart
failure, and two patients died of cardiac rupture).
Clinical Course of PE
Among 76 patients with PE in the acute phase,
echocardiography was performed at 1 month after
the onset of AMI in 68 patients (8 patients died in
the acute phase). PE was detected in 26 patients
(38%) in the chronic phase (persistent PE), while PE
was absent (transient PE) in 42 patients. None of the
68 patients had echocardiographic or clinical symptoms of cardiac tamponade, or required an alteration
of therapy. The patients with persistent PE had a
significantly higher incidence of pericardial rub and
Killip class ⬎ 1, and tended to have higher peak CK
and a larger number of advanced asynergic segments
at hospital admission than those with transient PE
(Table 2). The patients with persistent PE had a
significantly larger number of advanced asynergic
segments in the chronic phase than those with
transient PE. There were no significant differences
in total protein (7.0 ⫾ 0.8 g/dL vs 7.1 ⫾ 0.7 g/dL
[⫾ SD], p ⫽ 0.598) and albumin (3.7 ⫾ 0.8 g/dL vs
3.9 ⫾ 0.8 g/dL, p ⫽ 0.332) in the chronic phase
between the two groups.
There were no significant differences in elapsed
time from the onset of symptoms to primary PTCA,
and the incidence of total occlusion of the culprit
lesion before primary PTCA, multivessel disease,
and left anterior descending lesion between the two
groups. However, the patients with persistent PE
had a significantly lower incidence of collaterals and
a higher incidence of no reflow than those with
transient PE (Table 3). To determine the important
variables present in the acute phase of the infarct
that may be related to the subsequent development
of persistent PE, five variables (peak CK, collaterals,
no reflow, pericardial rub, and Killip class ⬎ 1) were
used in the multivariate analysis. From this analysis,
pericardial rub (regression coefficient ⫽ 1.695;
p ⫽ 0.023; odds ratio [OR], 5.45), collaterals (regression coefficient ⫽ ⫺ 1.830; p ⫽ 0.011; OR, 0.16),
and Killip class ⬎ 1 (regression coefficient ⫽ ⫺ 1.334;
p ⫽ 0.027; OR, 3.80) emerged as the significant variables related to the subsequent development of persistent PE.
Pericardial Rub Associated With PE
Among 68 patients with PE in the acute phase who
survived to the chronic phase, pericardial rub was
detected in 14 patients and was absent in 54 patients
(Table 2). Ten of 14 patients (71%) with PE and a
pericardial rub had persistent PE, while 16 of 54
patients (30%) with PE but no pericardial rub had
persistent PE; the difference was significant
(p ⫽ 0.010). The patients with PE and a pericardial
rub had a significantly higher incidence of major
arrhythmias (atrial fibrillation, six patients; thirddegree atrioventricular block, two patients) compared to those with PE but no pericardial rub (atrial
fibrillation, eight patients; third-degree atrioventricular block, five patients) [p ⫽ 0.039].
Discussion
Before the reperfusion era, the prevalence of PE
in patients with AMI was reported to be 21% at day
Table 1—Clinical Characteristics*
PE
Characterisics
Present (n ⫽ 76)
Absent (n ⫽ 315)
p Value
Male/female gender, No.
Age, yr
Asynergic segments
Peak CK, IU
Killip class ⬎ 1
Pericardial rub
Elapsed time to PTCA, h
Total occlusion before PTCA
Multivessel
Collaterals (grade ⬎ 1)
Left anterior descending lesion
No reflow
In-hospital death
49/27
62 ⫾ 11
4.1 ⫾ 1.3
4,356 ⫾ 2,243
40 (53)
17 (22)
4.6 ⫾ 2.9
56 (74)
33 (43)
25 (33)
45 (59)
13 (17)
8 (11)
233/82
60 ⫾ 11
3.1 ⫾ 1.3
2,897 ⫾ 1,961
68 (22)
9 (3)
4.6 ⫾ 1.7
228 (72)
118 (37)
123 (39)
159 (51)
19 (6)
6 (2)
0.130
0.156
⬍ 0.001
⬍ 0.001
⬍ 0.001
⬍ 0.001
1.000
0.932
0.408
0.389
0.197
0.003
0.001
*Data are presented as mean ⫾ SD or No. (%) unless otherwise indicated.
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Table 2—Clinical Characteristics of Patients With PE*
Persistent PE
Characteristics
Male/female gender, No.
Age, yr
Risk factors
Hypertension
Diabetes mellitus
Hypercholesterolemia
Current smokers
Peak CK, IU
Asynergic segments
Hospital admission
Chronic phase
Killip class ⬎ 1
Pericardial rub
Present (n ⫽ 26)
Absent (n ⫽ 42)
18/8
63 ⫾ 12
29/13
62 ⫾ 10
0.799
0.712
8 (31)
8 (31)
6 (23)
12 (46)
4,930 ⫾ 2,344
18 (43)
9 (21)
14 (33)
26 (62)
3,816 ⫾ 2,175
0.617
0.441
0.530
0.308
0.050
4.3 ⫾ 1.0
3.7 ⫾ 1.0
18 (69)
10 (38)
3.8 ⫾ 1.2
2.5 ⫾ 1.5
16 (38)
4 (10)
p Value
0.080
⬍ 0.001
0.025
0.010
*Data are presented as mean ⫾ SD or No. (%) unless otherwise indicated.
10 and 11% at 3 months after the onset of AMI.6 In
our study, despite successful primary PTCA, the
incidence of PE in the acute phase was 19%, and
patients with PE in the acute phase had a significantly larger number of advanced asynergic segments, higher peak CK, and a higher incidence of
Killip class ⬎ 1, pericardial rub, and no reflow than
those without PE. Myocardial lymph drains to the
epicardial surface of the heart, to the pericardial
space, and ultimately to the mediastinum and rightheart cavities.15 Thus, accumulation of pericardial
fluid may result from increased production of myocardial interstitial fluid and/or from slower absorption due to elevated central venous pressure. In
AMI, the occurrence of PE can be due to pericardial
irritation (infarct pericarditis) or to increased hydrostatic pressure with fluid retention (hydropericardium).1,4,16 Considering the fact that Killip class still
remains a useful indicator of left ventricular dysfunction and early mortality in patients with reperfusion
therapy,17 our data are consistent with the previous
report5 that heart failure due to larger infarct size
and pericardial irritation are the important factors
associated with the occurrence of PE in the acute
phase of AMI after successful primary PTCA.
PE in the acute phase persisted to 1 month after
the onset of AMI in 38% of our patients; pericardial
rub, along with Killip class ⬎ 1 and the absence of
collaterals, were found to be independent factors
related to the subsequent development of persistent
PE. Infarct pericarditis occurs with anatomically
transmural infarction and is localized to the infarct
zone. A pericardial rub is a most specific noninvasive
sign of pericardial inflammation, and pericardial rub
is reported to be the most frequent clinical sign
during infarct pericarditis.1,4 In our previous report,18 we found that pericardial rub was a reliable
sign of extensive myocardial damage after primary
PTCA. Therefore, a possible mechanism contributing to the close relation between pericardial rub and
persistent PE was a higher incidence of anatomically
transmural infarction in patients with a pericardial
rub.
Atrial fibrillation and third-degree atrioventricular
block in AMI occur more frequently in patients with
larger infarct size and depressed left ventricular
Table 3—Angiographic Characteristics of Patients With PE*
Persistent PE
Characteristics
Present (n ⫽ 26)
Absent (n ⫽ 42)
p Value
Elapsed time to PTCA, h
Total occlusion before PTCA
Multivessel
Collaterals (grade ⬎ 1)
Left anterior descending artery lesion
No reflow
4.9 ⫾ 2.5
18 (69)
13 (50)
4 (15)
18 (69)
8 (31)
4.2 ⫾ 3.1
33 (79)
14 (33)
19 (45)
23 (55)
3 (7)
0.335
0.564
0.267
0.024
0.944
0.026
*Data are presented as mean ⫾ SD or No. (%).
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function.19 –21 Dubois et al22 reported that the patients with a pericardial rub in the acute phase of
AMI had a higher incidence of congestive heart
failure or major arrhythmias (atrial fibrillation, second- or third-degree atrioventricular block). Consistent with these prior observations, we also found a
higher incidence of atrial fibrillation and/or thirddegree atrioventricular block when a pericardial rub
was present in patients with a PE.
Angiographic studies9,23 have indicated that approximately two thirds of patients with AMI have a
totally occluded infarct-related coronary artery before reperfusion therapy. Clements et al9 also reported that antegrade flow of the infarct-related
artery before angioplasty and collateral flow to the
infarct zone were significant determinants of final
infarct size after successful angioplasty. In our study,
we found that while there were no significant differences between the two groups in the elapsed time
from the onset of AMI to primary PTCA and the
incidence of total occlusion of the infarct-related
artery before PTCA, the patients with persistent PE
had a lower incidence of collaterals before PTCA
than those with transient PE. Moreover, a significantly larger number of left ventricular segments
with advanced asynergy was observed in the chronic
phase in patients with persistent PE compared to
those with transient PE. Thus, the absence of collateral flow to the infarct zone before primary PTCA
may have blunted the salvage of jeopardized myocardium, which lead to a larger infarct size in the
chronic phase in patients with persistent PE.
Limitation
Although conducted in consecutive patients, this
was a retrospective analysis of prospectively accumulated data in patients with successful primary PTCA.
Further studies are needed to confirm our data in a
larger group of patients with AMI. However, prompt
assessment of coronary perfusion and detection of
pericardial rub may aid in making decisions concerning the use of drugs to improve microvascular function and left ventricular function after primary
PTCA.
Conclusion
PE remains a relatively common complication of
AMI even in the era of reperfusion therapy, and the
presence of a pericardial rub, Killip class ⬎ 1, and
absence of collateral flow in the early phase of the
infarct are associated with persistence of the PE to 1
month after the onset of AMI.
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