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(Circulation. 1995;91:641-644.)
© 1995 American Heart Association, Inc.
Articles |
PQ Segment Depression in Acute Q Wave Inferior Wall Myocardial Infarction
From the Second Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background PQ segment deviation is almost as characteristic as the classic ST segment deviation and is detected in most patients with pericarditis. However, as infarction-associated pericarditis remains over the infarct zone, PQ segment depression is observed much less often in patients with acute myocardial infarction.
Methods and Results We designed this study to examine the clinical significance of PQ segment depression in acute Q wave inferior myocardial infarction. We examined 171 consecutive patients with acute Q wave inferior myocardial infarction by means of auscultation, ECG, and two-dimensional echocardiography. The diagnosis of pericarditis was made on the basis of pericardial rub detected by more than two observers during the first 3 days after admission. At least 0.5 mm of PQ segment depression from the TP segment lasting more than 24 hours in both limb and precordial leads was considered diagnostic of PQ segment depression.
Conclusions PQ segment depression was present in 14 patients and absent in 157 patients. Eleven patients with and 55 patients without PQ segment depression had advanced asynergy (akinesis or dyskinesis) in the posterior segments, whereas 9 patients with and 20 patients without PQ segment depression had pericardial rub. When multivariate analysis was performed to determine the important variables related to the occurrence of PQ segment depression, pericardial rub was selected with advanced asynergy of the posterior segment as significant factors related to PQ segment depression. Major complications (ventricular fibrillation, sustained ventricular tachycardia, cardiogenic shock, need for pacing) were present in 63 patients; 9 with (64%) and 54 without (34%) PQ segment depression. PQ segment depression was one of the clinical signs of more extensive damage extending to the posterior segments and increased incidence of major complications.
Key Words: myocardial infarction • echocardiography • pericarditis
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Infarction-associated pericarditis is usually associated with transmural acute myocardial infarction,1 2 3 but it has been reported with a greatly variable frequency and its incidence with respect to the infarct site is controversial. However, in our previous report,4 we found that in the presence of ECG-evident right ventricular infarction, the incidence of pericardial rub in acute Q wave inferior myocardial infarction was nearly identical to that of Q wave anterior myocardial infarction. PQ segment deviation is detected in most patients with pericarditis and is almost as characteristic as the classic ST segment deviations.5 6 However, the incidence and clinical characteristics of PQ segment depression in acute inferior myocardial infarction are not defined. Therefore, we designed study to evaluate the clinical significance of PQ segment depression after acute Q wave inferior wall myocardial infarction.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patients
We studied 171 consecutive patients with a Q wave inferior wall acute myocardial infarction who fulfilled the following criteria: (1) admission to the coronary care unit within 24 hours from the onset of chest pain and survival in the first 3 days after admission, (2) no prior history of myocardial infarction, (3) sinus rhythm on admission, and (4) no history of chronic renal failure, collagen disease, cardiac surgery within the previous 6 months, or metastatic disease. During this period, a technically satisfactory echocardiogram could not be obtained in 14 patients, and they were not included in this study.
Clinical Evaluation
A diagnosis of Q wave inferior myocardial
infarction was made
when patients had ST segment elevation (
0.1 mV above the TP segment
measured 80 milliseconds after the J-point) with new Q wave (leads II,
III, and aVF) on serial ECGs and at least twice the normal elevation in
serum creatine kinase levels with MB isoenzyme 5%. ECGs were taken
on admission and at least every 8 hours for the first 3 days. Atrial
repolarization was assessed by studying the PQ segment with a
magnifying glass. To maximize the diagnostic accuracy in excluding
rate-dependent PQ segment depression, at least 0.5 mm of PQ segment
depression from the TP segment observed for more than 24 hours in both
limb leads (II and aVF) and precordial leads (more than two in
V3 through V6) was considered diagnostic of PQ
segment depression. PQ segment depression was considered present
only after it was independently diagnosed by at least two of three
cardiologists who had no knowledge of the clinical findings. ECG
criteria for the diagnosis of atrial infarction were PTa segment
elevation 0.5 mm in leads V5 and V6 with
reciprocal PTa segment depression in V1 and V2,
or PTa segment elevation 0.5 mm in lead I with reciprocal depression
in leads II or III.7 Abnormal P wave in the standard leads
(minor criteria of atrial infarction)7 was diagnosed when
one or more of the following findings were made: (1) P wave
configuration other than the rounded form normally seen (notched,
peaked, or other abnormal configurations), (2) amplitude in lead II
0.2 mm, and (3) duration in any one lead of >120 milliseconds. At
least 1 mm of ST segment elevation and QS or QR in the right precordial
lead (V4R) at the time of hospital admission was considered
diagnostic of right ventricular infarction.8 All patients
were examined by careful auscultation at least twice daily. These
examinations were increased in patients first seen with
pleuritic chest pain or any other recurrent chest pain. The
auscultation covered not only the left parasternal area but also the
base and xyphoid regions. Pericardial rub was considered to be a
to-and-fro scratchy, grating, or creaking noise heard in systole,
mid-diastole, presystole, or any one of these phases. Identification of
pericardial rub was based on nonconformity with the characteristic
locations, radiations, and respiratory responses of most murmurs and
thrills.9 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 at least two cardiologists who were unaware of the ECG
findings. Detection of pericardial rub during the first 72 hours after
admission was considered diagnostic of infarction-associated
pericarditis. The major hospital complications included ventricular
fibrillation, sustained ventricular tachycardia, cardiogenic shock
(systolic blood pressure <90 mm Hg with signs of impaired peripheral
circulation), and third-degree atrioventricular block or sinus arrest
requiring temporary cardiac pacing during the first 3 days after
admission.
Echocardiography
Two-dimensional echocardiography was
performed with an SSD 870
phased-array sector scanner (Aloka Co, Ltd). All classic views were
recorded on videotape for subsequent analysis by observers who were
unaware of the patients' clinical data. Analysis of the left
ventricular wall was performed in 11 segments assessed by long- and
short-axis images obtained on the third day of
hospitalization,10 and the number of segments with
advanced asynergy (akinesis or dyskinesis) was calculated by observers
blinded to the clinical data. Doppler echocardiography was performed
when pericardial rub was first detected in order to rule out mitral
regurgitation caused by papillary muscle dysfunction.
Statistical Analysis
Results are reported as mean±SD.
Statistical analysis
between the two groups was performed by Student's t test
for quantitative data and 
2 analysis for qualitative
data. Stepwise logistic regression analysis was performed using SAS
(version 6, logistic procedure) to evaluate the important variables
related to PQ segment depression and major complications. A value of
P<.05 was considered significant.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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PQ Segment Depression
Among the 171 patients with Q wave inferior wall acute myocardial infarction, PQ segment depression was detected in both limb (leads II and aVF) and precordial (more than two in V2 through V6) leads in 14 patients (group 1) and was absent in 157 patients (group 2) (Fig 1
). Five patients were excluded
from this study because atrial infarction was suspected: 2 patients
with PQ segment elevation in leads I and aVL (Fig 2) and
3 because of associated P wave abnormalities. Heart rate changes
(95±10 to 90±14 beats per minute) measured during the first 24
hours
after the detection of PQ segment depression had no apparent relation
to the appearance and disappearance of PQ segment depression. Moreover,
PQ and ST segment shifts were discordant in all cases.11
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Clinical Characteristics
There was no significant difference
in age between group 1 (68±10
years) and group 2 (65±11 years) patients. Group 1 patients had
significantly more left ventricular segments with advanced asynergy
than those in group 2, but none of the patients had advanced asynergy
in the anterior segments. Advanced asynergy in the posterior segments
was detected in 66 patients: 11 patients (79%) in group 1 and 55
patients (35%) in group 2 (Table 1). There was a
significantly higher incidence of posterior advanced asynergy in group
1 than group 2 (P<.005). Pericardial rub was present in
29 patients and absent in 142 during the first 3 days after admission.
None of the 29 patients with pericardial rub had mitral regurgitation
by Doppler echocardiography. Nine patients (64%) in group 1 had
pericardial rub and 20 (13%) in group 2 (Table 1). There was a
significantly higher incidence of pericardial rub in group 1 compared
with group 2 (P<.001). Fifty patients had ECG-evident
right ventricular infarction: 7 patients in group 1 and 43 in
group 2 (Table 1). There was no significant difference in the
incidence
of right ventricular infarction between groups 1 and 2. When stepwise
logistic regression analysis was used to determine the important
variables associated with PQ segment depression, pericardial rub
(
±SEM=2.35 ±0.63,
2=14.0,
P<.001) and advanced asynergy in the posterior segment
(±SEM=1.72±0.71,
2=6.0,
P<.05) were the important variables.
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In-Hospital Complications
Major complications (ventricular
fibrillation, sustained
ventricular tachycardia, cardiogenic shock, need for pacing) were
detected in 63 patients during the first 3 days after hospitalization:
9 patients (64%) in group 1 and 54 patients (34%) in group 2 (Table
2). There was a significantly higher incidence of major
complications in group 1 compared with group 2 (P<.05).
When stepwise logistic regression analysis was used to determine
the important variables predicting major complications, advanced
asynergy in the posterior segment
(±SEM= 1.07±0.34,
2=9.9, P<.005) and ECG-evident right
ventricular infarction
(±SEM=0.88±0.36,
2=6.1, P<.05) were the important
variables.
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Medications
Of the 171 patients, 64 received intravenous
thrombolytic therapy
(urokinase or recombinant tissue-type plasminogen activator) or
intracoronary urokinase. Six of the 14 group 1 patients and 58 of the
157 group 2 patients had thrombolytic therapy (P=NS).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Although PQ segment depression is known to be one of the typical ECG changes associated with acute pericarditis,5 6 the incidence and clinical significance of PQ segment depression in patients with acute Q wave inferior myocardial infarction have not been established. In our study, 14 of 171 patients (8%) with Q wave inferior wall acute myocardial infarction had PQ segment depression; advanced asynergy in the posterior segments and pericardial rub were found to be the important factors related to PQ segment depression. As infarction-associated pericarditis is more often observed in patients with larger myocardial infarct size, our results suggest that the patients with PQ segment depression had more extensive myocardial damage, extending to the posterior segments.
The incidence of atrial infarction in autopsy-proven cases of acute myocardial infarction is reported to be more common in the right atrium.12 13 The major ECG criteria for the diagnosis of atrial infarction are PQ segment elevation in the left chest leads with reciprocal depression in the right chest leads or elevation in lead I with reciprocal depression in leads II or III; the minor criteria are abnormal P waves.13 Among 171 patients with acute Q wave inferior myocardial infarction, 5 (3%) were diagnosed as having ECG criteria of atrial infarction. However, we excluded these 5 patients suspected of having ECG atrial infarction. Therefore, the fact that the PQ segment deviations were not localized and the absence in appropriate leads of PQ segment elevation in our patients indicate that atrial infarction was not the major factor causing PQ segment depression in group 1 patients.
Patients with an anatomically transmural infarction have some potential involvement of the epicardium, but the actual inflammatory change in infarction-associated pericarditis remains localized over the infarct zone. Pericardial rub has been reported as the most specific noninvasive sign of pericardial inflammation.1 14 In the present study, the diagnosis of pericarditis was made on the basis of pericardial rub detected by more than two observers during the first 3 days after admission. As a result, 9 patients (64%) with PQ segment depression had pericardial rub, and pericardial rub was selected with asynergy of the posterior segment as an important factor related to PQ segment depression. As anatomically transmural infarction of the posterior wall extends to the epicardial surface and is responsible for producing pericardial inflammation of the infarct zone, regardless of wall motion abnormality, higher incidences of advanced asynergy of the posterior segments and pericardial rub in group 1 indicate that the patients with PQ segment depression appear to have concomitant posterior involvement with severe wall motion abnormality, inflammation, or both. Because the atrium is closer to the posterior than the inferior wall, it is not surprising to find a relation between generalized PQ segment depression and subepicardial atrial inflammation due to a process related to extensive myocardial damage extending to the posterior segments.
Patients with PQ segment depression had a 64% risk of major complications. There is general agreement that the risk of major complication is high in acute myocardial infarction complicated by larger infarct size. When stepwise logistic regression analysis was used to define their relation to the occurrence of major in-hospital complications, advanced asynergy of the posterior segment and ECG-evident right ventricular infarction were selected as important variables related to major complications. Although PQ segment depression was not selected as a significant variable by the multivariate analysis, the patients who developed PQ segment depression had more extensive damage extending to the posterior segments. Therefore, our data are consistent with those of Zehender et al,15 indicating that not only the size but the location of the infarct zone is of clinical importance in the occurrence of major complications.
Clinical Implications
Although PQ segment depression is
observed in the minority of
patients with acute Q wave inferior myocardial infarction, early
recognition of this involvement has important clinical implications
because PQ segment depression indicates more extensive infarct
extending to the posterior segments and increased incidence of major
complications.
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Footnotes |
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Reprint requests to Yo Nagahama, MD, CCU, Kansai Medical University, 10—15 Fumizono-cho Moriguchi City, Osaka 570, Japan.
Received May 9, 1994; accepted September 23, 1994.
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References |
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TopAbstractIntroductionMethods Results Discussion References |
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1. Krainin FM, Flessas AP, Spodick DH. Infarction-associated pericarditis: rarity of diagnostic electrocardiogram. N Engl J Med. 1984;311:1211-1214. [Abstract]
2. Lichstein E, Liu HM, Gupta P. Pericarditis complicating acute myocardial infarction: incidence of complications and significance of electrocardiogram on admission. Am Heart J. 1974;87:246-252.[Medline] [Order article via Infotrieve]
3. Tofler GH, Muller JE, Stone PH, Willich SN, Davis VG, Poole K, Robertson T, Braunwald E. Pericarditis in acute myocardial infarction: characterization and clinical significance. Am Heart J. 1989;117:86-90. [Medline] [Order article via Infotrieve]
4. Sugiura T, Iwasaka T, Takahashi N, Nagahama Y, Hasegawa T, Matsutani M, Sumimoto T, Inada M. Clinical significance of pericardial rub in inferior wall Q-wave acute myocardial infarction. Am J Cardiol. 1990;66:227-228. [Medline] [Order article via Infotrieve]
5.
Spodick DH. Diagnostic electrocardiographic sequences in
acute pericarditis: significance of PR segment and PR vector changes.
Circulation. 1973;48:575-580.
6. Spodick DH. Electrocardiogram in acute pericarditis: distributions of morphologic and axial changes by stages. Am J Cardiol. 1974;33:470-474. [Medline] [Order article via Infotrieve]
7.
Liu CK, Greenspan G, Piccirillo RT. Atrial infarction of the
heart. Circulation. 1961;23:331-338.
8. Robalino BD, Whitlow PL, Underwood DA, Salcedo EE. Electrocardiographic manifestation of right ventricular infarction. Am Heart J. 1989;118:138-144. [Medline] [Order article via Infotrieve]
9. Spodick DH. Differential diagnosis of acute pericarditis. Prog Cardiovasc Dis. 1971;14:192-209. [Medline] [Order article via Infotrieve]
10. Gibson RS, Bishop HL, Stamm RB, Cramptom RS, Beller GA, Martin RP. Value of early two-dimensional echocardiography in patients with acute myocardial infarction. Am J Cardiol. 1982;49:1110-1119. [Medline] [Order article via Infotrieve]
11.
Tranchesi J, Adelardi V, Oliveira JM. Atrial repolarization:
its importance in clinical electrocardiography. Circulation. 1960;22:635-644.
12. Lowe TE, Wartman WB. Myocardial infarction. Br Heart J. 1944;6:115-128.
13. Pasternak RC, Braunwald E, Sobel BE. Pathology of acute myocardial infarction. In: Braunwald E, ed. Heart Disease. 4th ed. Philadelphia, Pa: WB Saunders; 1992;2:1201-1209.
14. Spodick DH. The normal and diseased pericardium: current concepts of pericardial physiology, diagnosis and treatment. J Am Coll Cardiol. 1983;1:240-251. [Medline] [Order article via Infotrieve]
15.
Zehender M, Kasper W, Kauder E, Schonthaler M, Geibel A,
Olschewski M, Just H. Right ventricular infarction as an independent
predictor of prognosis after acute inferior myocardial infarction.
N Engl J Med. 1993;328:981-988.
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