Significance of precordial ST-segment depression in inferior acute myocardial infarction as determined by echocardiography

Significanceof PrecordialST-SegmentDepression in Inferior Acute MyocardialInfarction as Determinedby Echocardiography LUC A. PIERARD, MD, MURIEL SPRYNGER, MD, FREDliRlC GILIS, MD, and JEAN CARLIER, MD

Despite numerous studies, the significance of precordial ST-segment depression in inferior wall acute myocardial infarction (AMI) remains unclear. No clinical studies have used P-dimensional (2-D) echocardiography to compare AMI location in patients with or without so-called reciprocal ST changes. Therefore, the clinical, electrocardlographic, echocardiographic and angiographic features of 22 patients with their first transmural inferior AMI were prospecthrely examined. During the first day of AMI an echocardiographic mapping of the area of necrosis was obtained using all conventional views and a ventrZcular segmentation related to anatomic landmarks. Patients were categorized according to the presence (group I, n = 13) or absence (group

II, n = 9) of precordial ST-segment depression, defined as more than 1 mm, measured 80 ms after the J point in at least 2 of the leads VI to V,,. Basal posterolateral akinesia was observed in 11 of the 13 patients in group I and in no patient in group II (p X0.001). Posterior right ventricular free wall akinesia was more frequent In group II (p CO.02). There was no difference in the prevalence of sign&ant left anterior descending artery (LAD) narrowing (group I, 4 patients, group II, 3 patients). Posterolatera1 involvement should be strongly considered In the presence of precordial ST-segment depression In association with transmural inferior AMI. (Am J Cardiol 1988;57:82-85)

N

Methods

From the Department of Cardiology, Institute of Medicine, University Hospital, Li&ge, Belgium. Manuscript received April 15, 1985; revised manuscript received July 3,1985, accepted July 5, 1985. Address for reprints: Luc A. Pidrard, MD, Service de Cardiologie, Boulevard de la Constitution, 59, B-4020 Li&ge, Belgium.

Patients: From October 1983 to February 1984, all consecutive patients admitted to our coronary care unit with a first transmural inferior AM1 were prospectively included if they satisfied the following criteria: (1) history of typical prolonged ischemic chest pain, serial electrocardiographic (ECG) changes (STsegment elevation followed by ST-T changes and new Q waves at least 30 ms wide in at least 2 of the leads: II, III or aVF) and characteristic rise of serum levels of total creatine kinase (CK] and the CK-MB isoenzyme; (2) no history or ECG evidence of prior AMI; (3) absence of left bundle branch block and right or left ventricular hypertrophy by ECG criteria: (4) no digitalis therapy; (5) absence of artificial pacemaker and valvular or noncoronary heart disease; and (6) coronary angiography performed within 4 weeks. The 22 patients who met these selection criteria underwent 2-D echocardiography during the first day after onset of chest pain. All had good-quality echocardiographic studies and constituted the study population. There were 19 men and 3 women, mean age 57 years (range 32 to 73). Electrocardiography: In all patients, the first standard 12-lead electrocardiogram was recorded between 15 minutes and 8 hours after the onset of chest pain. ECGs were also recorded 4 hours after the first

umerous studies have assessed the significance of precordial ST-segment depression in inferior wall acute myocardial infarction (AMI). Such ST-segment changes have variously been interpreted as a benign electrical phenomenonl-6 or as an indicator of extensive AMI,‘-ll or of concomitant remote ischemia owing to significant stenosis of the left anterior descending artery (LAD).11-15 Persistence of anterior precordial ST changes better correlates with LAD disease.lsJ7 However, for clinical implications, correct interpretation of early ST changes is more important as therapeutic interventions aimed at salvaging ischemic myocardium must be attempted early in the clinical course. Two-dimensional (2-D) echocardiography is a widely available technique providing reproducible description of AM1 topographies.l* This prospective study relates precordial ST depression in the acute phase of a first inferior AM1 to a precise myocardial mapping of the area of necrosis obtained by 2-D echocardiography.

January

recording, daily during the first 4 days and at least once before dischdrge. All ECGs were recorded at a paper speed of 25 mm/s and at 1 cm = 1 mV. Precordial ST-segment depression was defined as more than 1 mm. measured 80 ms after the J point in ar least 2 of leads V1 to V4. Posterior involvement was defined by the occurrence of an R wave of at least 40 ms and R/S ratio of 1 or more in leads VI or V2 and lateral involvement by serial ECG changes in leads I, aVL, V5 or V6. Echocardiography: All patients underwent bedside 2-D echocardiography during the first day of infarction, using a phased-array (Diasonics V3400R) sector scanner. All conventional views were obtained and recorded on videotape. A segmentation of the ventricles was used to determine anatomic location of infarction. The left ventricle was considered as a cone and divisions were defined on the length and on the circle of the cone.lg The length was divided into 3 thirds (basal, middle and apical). The circle was separated into 6 parts, roughly identical in size (Fig. 1). Nomenclature of the segments was as follows: the ventricular septum was divided in an anterior (anterosep tal) and a posterior half (posteroseptal). The free wall was separated into an anterior segment (from the anterior interventricular groove to the anterior edge of the anterolateral papillary muscle), a posteromedial segment (from the posterior interventricular groove to the lateral edge of the posterior papillary muscle), and a lateral wall (from the anterior edge of the anterolateral papillary muscle to the lateral edge of the posterome-

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dial papillary muscle). This lateral wall was separated into anterolateral and posterolateral segments. At the apical level, 4 segments were identified: septal, anterior, lateral and posteromedial. Each segment was visualized on 2 orthogonal views: short-axis and longitudinal [Fig. 1). The right ventricular free wall was separated into 5 segments: an anterolateral and a posterior segment at both basal and middle levels and an apical segment. Topography of infarction was assessed by 2 independent experienced observers without prior knowledge of clinical, electrocardiographic or angiographic data. Transmural infarction was considered involving a segment when no systolic thickening was present in this area. Each of the segments was assigned a number that corresponded to the wall motion analysis (0 = hyperkinetic, 1 = normal, 2 = hypokinetic, 3 = akinetic, 4 = dyskinetic and 5 = aneurysmal). A wall motion score index was calculated by dividing the sum of the assigned numbers by the number of segments visualized. Angiography: Coronary arteriography was performed in all 22 patients within 4 weeks of infarction. Significant stenosis was defined as at least 70% luminal diameter narrowing as judged by an experienced radiologist, unaware of electrocardiographic and echocardiographic data. Statistical analysis: Data are expressed as mean f standard deviation. Unpaired Student t tests were performed for differences within and between groups. The chi-square test was used for differences in event

PSSAX s\

PSSAX \

basal

mid 113

2c

Volume

113 \

;LAX

,,.. -5c

!:

:LAX

FIGURE 1. Echocardiographic views and the ventricular segmentation used in the analysis of infarction topography. The length of the left ventricle is separated into 3 thirds: basal (b), middle (m) and apical (a). The &c/e Is separated into 0 parts: posteroseptal (PS), anteroseptal (AS), anterior (A), anterolateral (AL), posterolateral (PL). posteromedlal (PM). On the dlagrams of the short-ax18 vlews, the lntersectlon of the 3 longltudlnal vlews are indicated. AP4C = apical 4-chamber; APLAX = aplcal long-axis; APPC = aplcal2-chamber; L = lateral; P = posterior; PSLAX = parasternal long-axis; PSSAX = parasternal short-axls; S = septal.

84

INFERIOR

INFARCTION:

TABLE

I

PRECORDIAL

ST DEPRESSION

Characteristics

of the Two

Groups (jloup

Age (YV Male/female Interval between onset of symptoms and first ECG (hours)‘ Killip class Peak creatine kinase (IUlliter)’ LV ejection fraction (%)’ Infarct-related vessel Patent at angiography Right coronary Left circumflex (LC) Right + LC Significant LAD narrowing Echocardiography No. of segments involved* Wall motion score index’ First ECG Posterior involvement Lateral involvement Predischarge ECG Posterior involvement Lateral involvement

Segments Basal posteromedial Mid-posteromedial Apical posteromedial Basal posterolateral Mid-posterolateral Apical posterolateral Basal anterolateral Mid-posterolateral Basal posteroseptal Mid-posteroseptal Right ventricular free wall Basal posterior Basal anterolateral

Group

50 f 6.7 1112 4.6 f 3.2

1.11 f 953 f 51 f

6 9 3 1 4 5.15 f 1.42 1.58 i 0.12

12 11 2 11 6 1 3 2 6 2

8 6 1 0 0 0 0 0 4 0

NS NS NS
5 4

6 6

<0.02 NS

NS

NS <0.02 NS

5 9 0

NS

3

NS

4.89 f 1.50 i

1.26 0.17

NS NS NS NS

6 4

2 2

NS NS

p Value

NS = not significant.

frequency between groups. Statistical significance defined as a p value of
NS

0 3

Assessed by Two-Dlmensional Inferfor Acute Myocardial

Group II (n = 9)

0.2 230 8

p Value

2 3

descending

Group I (n = 13)

II (n = 9)

59 f 5 811 5.1 f 4.7

1.23 f 0.46 1,649 f 361 47 f 6.2

l Values are mean f standard deviation. ECG = electrocardiogram: LAD = left anterior

TABLE II Topography of Necrosis Echocardiography in Patients with Infarction

I (n = 13)

was

Results ST-segment subgroups: Of 22 patients, 13 had significant precordial ST-segment depression on admission (group I) and 9 did not (group II). The characteristics of these 2 groups are presented in Table 1. Peak CK level was higher in group I, 1,649 f 361 vs 953 f 230 III/liter (p <0.02). Echocardiographic studies (TBble II): Most patients had involvement of the posteromedial segments, more often at the basal level (92% in group I and 89% in group II) than at the middle level (85% in group I and 67% in group II). The frequency of basal posteroseptal involvement was not significantly different in

artery;

LV = left ventricular;

NS = not significant.

the 2 groups (46% in group I, 44% in group II). Involvement of the posterior segment of the right ventricular free wall was more frequently seen in group II (89%) than in group I (38%) (p <0.02). Posterolateral involvement was observed only in patients with “reciprocal” ST changes. At the basal level, 11 patients in group I (15%) and no patient in group II showed akinesia of the posterolateral segment (p
+a~fuary

Discussion Controversy persists about the significance of precordial ST depression in transmural inferior AMI; therefore, its clinical implications remain unclear. Previous studies have considered precordial ST depression as a benign electrical phenomenon3T5p6 or a marker for more extensive necrosis’-lo or for LAD disease with anterior wall ischemia.llJ3-15 If either of the last 2 explanations is correct, it implies that precordial ST depression may identify a high-risk subset among patients with inferior AMI. Our data indicate that precordial ST depression during the early phase of inferior AM1 is largely dependent on infarct topography and is a sensitive and specific marker of posterolateral involvement. Basal posterolateral akinesia demonstrated by 2-D echocardiography best separated patients with and without “reciprocal” ST depression. None of our 9 patients without precordial ST depression had posterolateral akinesia. Eleven of our 13 patients with such ST change had basal posterolateral akinesia. Our findings are in agreement with those of Goldberg et al,7 who correlated electrocardiographic findings and results of radionuclide cineangiography. The incidence of posteroseptal involvement was similar in the 2 groups, a finding that does not support the contention of Boden et a1,21who suggested inferoseptal infarction as an explanation for the precordial ST-segment depression. The significance of septal asynergy in their patients with inferior AMI is unclear because coronary anatomy was not assessed in their study. We observed a higher incidence of right ventricular posterior free wall infarction in patients without reciprocal ST changes. Although peak CK level was higher in group I, no significant difference between the 2 groups was found in the number of akinetic segments bnd in the echocardiographic wall motion score index. This discordance between markers of infarct size may be explained by the different topographic characteristics in the groups. Patients of group I had larger involvement of the left ventricular free wall and those of grotlp II had larger involvement of the right ventricular free wall. Because of differences in the thickness between the 2 ventricular walls, similar surface extent of infarcted myocardium may lead to greater infarct mass and higher CK levels with involvement of the left ventricle. We observed no significant difference between the 2 groups in the prevalence of LAD disease. We did not observe remote akinesia with echocardiography, but myocardial thickening may persist in an ischemic noninfarcted area. Conflicting results in different reports may be due to differences in the methods used for correlation with electrocardiographic changes. Although left ventriculography is generally considered the standard for the assessment of segmental wall motion abnormalities, it must be recognized that the right ventricular free wall is not viewed and that the posterolateral segment as defined in our study is not specifically identified from the left or right anterior oblique ventriculograms. Clinical implications: Our findings are in agreement with those in the earlier studies of Myers et al.22

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early precordial ST changes in infethe involvement of the posterolatercontrary, the absence of such ST predudu, 0~ posterolateral extension.

Acknowledgment: We gratefully acknowledge H. E. Kulbertus, MD, for critical review of the manuscript and M. Leroi for secretarial assistance.

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