Significance of reciprocal S-T segment depression in anterior precordial leads in acute inferior myocardial infarction: Concomitant left anterior descending coronary artery disease?

Significance of Reciprocal S-T Segment Depression in Anterior Precordial Leads in Acute Inferior Myocardial Infarction: Concomitant Left Anterior Descending Coronary Artery Disease?

JUAN R. SALCEDO, MICHAEL G. BAIRD, FACC R. JANE (Edin), DONALD (C),

MD’ MD.

FRCP

(C),

CHAMBERS, MD, MRCP FRCP S. BEANLANDS, MD, FRCP

FACC

Ottawa, Ontario, Canada

From the University of Ottawa Cardiac Unit, Ottawa Civic Hospital, 1053 Wing Avenue, Ottawa, Ontario, Canada. This study was supported by a grant from the Ontario Heart Foundation, Toronto, Ontario, Canada. Manuscript received February 24. 1981; revised manuscript received May 12. 1981. accepted May 18. 1981. Clinical Research Fellow, Ontario Heart Foundation. Toronto, Ontario, Canada. Address for reprints: Michael G. Baird. MD, FACC. University of Ottawa Cardiac Unit, Ottawa Civic Hospital. 1053 Cariing Avenue, Ottawa, Ontario KlY 4E9. Canada. l

The reciprocal changes of S-T segment depression in the anterior precordial leads of the electrocardiogram in acute inferior myocardial infarction may be due to left anterior descending coronary artery disease and anterior wall &hernia. The electrocardiograms of 45 patients with acute inferior infarction who had subsequent cardiac catheterization (41 patients) or necropsy (4 patients) were examined to test this hypothesis. Significant left anterior descending coronary artery disease (greater than 70 percent stenosis of luminal diameter) was observed in 31 (69 percent) of the 45 patients. The sensitivity, specificity and predictive value of S-T depression (1 mm or greater) in various anterior precordial leads singly or In combination was determined for this lesion. Left anterior descending coronary artery disease was present in 23 of 24 patients with S-T depression in one or more leads from VI to V4 (predictive value 95 percent), and this index had the best combination of sensitivity (74 percent), specificity (93 percent) and predictive value in this group. Seven of 13 patients with lefl anterior descending coronary artery disease had S-T depression only in lead I or aVL, or both (sensitivity 100 percent, specifictty 53 percent and predictive value 54 percent). S-T depression in any of leads I, aVL and VI to Vs occurred in 37 patients, and 31 of these had lefl anterior descending coronary artery disease (sensitivity 100 percent, specifkfty 57 percent and predictive value 64 percent). The eight patients without anterior precordial lead S-T depression did not have left anterior descending coronary artery disease. Complications of infarction developed In 13 patients; S-T depression in at least one of leads VI to V4 occurred In 12 (92 percent) of these 13 but in only 12 (36 percent) of 32 patients without complications. Thus the predictive value of S-T depression in leads VI to V,, (95 percent) for left anterior descending coronary artery disease is greater than the occurrence of the latter (69 percent) in ail cases of acute inferior myocardial infarction (p
S-T segment elevation in electrocardiographic leads II, III and aVF is characteristically seen during the early phase of acute inferior wall myocardial infarction. If an electrocardiogram is obtained early enough it will often show S-T segment depression in leads facing noninfarcting areas of myocardium. Such S-T depression has been called reciprocal1-8 and occurs in any or all of leads I, aVL and Vi to Vs. This reciprocal S-T depression is often explained as a purely electrical phenomenon; that is, acute inferior wall injury causes S-T elevation in inferior leads but

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depression in leads recorded from the opposite side of the heart. However, the exact mechanism underlying these S-T segment shifts is still controversial.gJO Recent investigations’l-l3 have suggested that precordial lead S-T depression in acute inferior infarction may indicate concomitant anterior ischemia or non-

transmural myocardial infarction rather than simply a “reciprocal” electrical phenomenon. To test this hypothesis we studied 45 patients with an acute inferior wall infarction who subsequently underwent cardiac catheterization or necropsy.

Methods Patients: Forty-five patients with acute inferior wall myocardial infarction were studied. Thirty-five were selected from 216 consecutive patients admitted to our coronary care

TABLE I

unit with the diagnosis of acute inferior infarction between January 1,197s and July 1,198O. Acute infarction was diagnosed from a history of typical prolonged chest pain, electrocardiographic changes and characteristic serial elevation of serum enzymes (creatinine kinase [CK], glutamic oxaloacetic transaminase [GOT] and lactic dehydrogenase [LDH]). Patients were excluded for any of the following reasons: myocardial infarction related to recent coronary arterial surgery; an interval between the onset of symptoms and the first electrocardiogram of more than 24 hours; evidence of an old or new anterior wall infarct in the electrocardiogram; electrocardiographic evidence of left ventricular hypertrophy or an interval of more than 6 months between the acute infarction and cardiac catheterization or necropsy. Ten additional patients meeting the same criteria were referred for angiography from other centers. The total group comprised 40 men and 5 women whose ages ranged from 26 to 68 years (mean 48). Patients underwent cardiac catheterization for various reasons including (1) complications within 2 weeks of the acute inferior infarction (13 patients), (2) age less than 40 years (12 patients), and (3) angina occurring more than 2 weeks after infarction (20 patients).

Distribution of Significant Coronary Artery Disease* in 45 Patients With Acute Inferior Infarction

Patients

Vessels Affected

n

%

Single Vessel Disease RCA LCX Total

11 2 13

24 4 29

Double Vessel Disease RCA + LCx RCA + LAD LCx + LAD Total

1 13 3 17

2 29 7 38

Triple Vessel Disease 33

15

Total

All LAD Disease Total

69

31

Seventy percent or greater luminal narrowing of diameter. LAD = left anterior descending coronary artery; LCx = left circumflex coronary artery; RCA = right coronary artery.

Electrocardiography: Acute inferior wall myocardial infarction was diagnosed according to the following criteria:

l

TABLE II Efficacy of S-T Depression in Different Leads for Predicting Left Anterior Descending Coronary Artery Disease in 45 Patients With Acute Inferior Infarction Patients (n)

Leads With S-T1

Total

S-T Depression

With LAD Stenosis

11 22 20 16 13

Vi

Predictive Value (%)

Sensitivity (%)

Specificity (%)

:z

91 95 100 100

100 100

V6

::

E

aVL

::

70 57

v2 V3 v4 V5

VI and V2 Vs and V4 V5 and V6 I and aVL V1,V2 V2.V3 V3.V4 V4.V5

and and and and

91 100

V3 V4 V5 Vs

Vl,V2,V3 and V4 Any of I. aVL. VI to V6 ::

2;

LAD = left anterior descending coronary artery; S-T1 = S-T segment depression.

December 1961

::

85 70

100 100 100 100 100

100 100 100 100 100

.b.S 19

57

a4

I and/or aVL only (none in VI-V4) Any of VI to V4

1004

1::

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::

100 74

;:

RECIPROCAL S-T SEGMENT DEPRESSION-SALCEDO ET AL.

FIGURE 1. Twelve lead electrocardiogram in a patient with pronounced S-T depression in leads aVL and VI to Vs (arrow). This patient had several complications after infarction including ventricular tachycardia, ventricular fibrillation, third degree heart block, stroke and, ultimately, death. Autopsy revealed severe triple vessel coronary artery disease.

typical S-T segment elevation in two of three electrocardiographic leads (II, III, aVF) with the development of abnormal Q waves (greater than 40 ms in duration) in the same leads. “Reciprocal” S-T depression in this group was defined as horizontal or downsloping S-T segment depression of 1 mm or greater in any of the leads I, aVL, Vi to Vs. Angiography: After giving written informed consent, the patients underwent selective coronary arteriography by the Judkins technique14 a mean of 72 days (range 3 to 180) after the index infarction. A significant coronary stenosis was defined as an obstruction of 70 percent or more of the luminal diameter in one or more projections. The coronary anatomy was reviewed independently by two observers who had no prior knowledge of the patient’s electrocardiogram; if a discrepancy occurred in the interpretation of these two observers, the opinion of a third experienced angiographer was sought. Although left ventriculograms were performed, no attempt was made to quantify ventricular function. Postmortem examination: At the time of postmortem examination the coronary vessels were serially sectioned at 0.5 cm intervals. Critical coronary arterial stenosis was assessed as a 70 percent or greater reduction in intraluminal dimension. Complications of infarction: The clinical course of the patients was classified as complicated or uncomplicated depending on whether or not one or more of the following complications occurred within 2 weeks of the onset of infarction:

(1) pulmonary edema, (2) heart block requiring an artificial pacemaker, (3) persistent hypotension with shock syndrome, (4) life-threatening arrhythmias (ventricular tachycardia, ventricular fibrillation), (5) persistent chest pain after the first 24 hours of the onset of infarction, (6) acute mitral regurgitation requiring surgery, or (7) death. Statistical analysis: S-T segment depression was measured in each lead independently and in groups; the presence or absence of left anterior descending coronary artery disease was determined to calculate sensitivity, specificity and predictive value. Fisher’s exact test was used to determine if there were significant differences between the various lead groups.

Results Of the 45 patients, 41 underwent cardiac catheterization and 4 had necropsy. Triple vessel coronary artery disease was observed in 15 patients (33 percent) (Table I). Thirty-one patients (69 percent) had significant narrowing of the left anterior descending coronary artery. Anterior precordial lead S-T depression and left anterior descending coronary artery disease: Table II describes our results and the correlation between S-T segment depression in different lead groups and left anterior descending coronary artery disease.

FIGURE 2. Twelve lead electrocardiogram in a patient with 1 to 2 mm S-T elevation in leads II, Ill and aVF but no evidence of S-T depression in the precordial leads. Cardiac catheterization revealed isolated right coronary artery disease.

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TABLE

III

Complications

in 13 Patients

Within 2 Weeks

of the Onset of Acute

30M 50F 52M 39M 65M

vi-v4

Comolications

(mm)

Ventricular tachycardia, ventricular fibrillation, third degree heart block, stroke, death Ventricular fibrillation Pulmonary edema, acute mitral regurgitation (rupture of posterior papillary muscle) Postmyocardial infarction angina Pulmonary edema, ventricular tachycardia, cardiogenic shock, death Third degree heart block, death Postmyocardial infarction angina, ventricular fibrillation Pulmonary edema, ventricular tachycardia, acute mitral regurgitation (rupture of posterior chordae and posterior papillary muscle) Ventricular tachycardia Postmyocardial infarction angina, shock syndrome, ventricular fibrillation Third degree heart block Ventricular fibrillation Ventricular fibrillation, postmyocardial infarction angina

17.0 5.0 4.0 2.0 1.5

Twenty-three (96 percent) of 24 patients with S-T segment depression in any of leads Vr to V4 had significant disease of the left anterior descending coronary artery (Fig. 1). The remaining patient had 50 percent narrowing of this artery, which did not fulfill our criterion for significant disease. Eight patients did not have “reciprocal” S-T depression and all had isolated right coronary artery disease (Fig. 2). Reciprocal S-T depression in any of leads I, aVL and Vr to Vs is a sensitive test for left anterior descending coronary artery disease but has poor specificity. The predictive value is 84 percent. In contrast, S-T depression in any of leads Vr to V4 is sensitive, specific and very predictive (96 percent) of significant stenosis of the left anterior descending coronary artery. Patients with and without complications: During the course of the acute inferior wall infarction complications developed in 13 patients (Table III). Twelve (92

11

cl q

10 9

NO

COMPLICATIONS (n = 32)

CO;P~G$ONS

8 ? t

7 6

2 CL 5 4 3 2 1

.

SL

o-1 9 MAXIMUM

!9

3 o-3 9

140

ST SEGMENT DEPRESSION (MM

)

FIGURE 3. Relation of S-T segment depression to presence or absence of complications in patients after acute inferior myocardial infarction.

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Infarction Maximal S-T Depression in Leads

Age (yr) 8 Sex 68M 53M 66F 60M 63M 61F 46M 65M

Inferior

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percent) of these had S-T depression in leads Vr to V4 and one patient had such depression in leads I and aVL. S-T segment depression occurred in only 12 (38 percent) of the 32 patients without complications. Figure 3 depicts the relation between S-T depression and the presence or absence of complications after acute inferior infarction. Patients with a complicated course tended to have greater degrees of S-T segment depression than did patients without complications. Discussion Electrophysiology of S-T segment depression in acute infarction: The genesis of S-T segment shifts in acute myocardial infarction has been a subject for disagreement. Classic electrocardiographic theory explains S-T segment elevation on the basis of decreased ability of the cell membrane to depolarize and repolarize and is regarded as an expression of injury currents.lO S-T segment depression by contrast has been explained by “reciprocal” effects.1J,4 Prinzmetal et algJo emphasized that S-T depression is not a “reciprocal” change but a primary response, and that the ischemic shifts were probably due to changes in the sodium-potassium gradient across the cell membrane. In other experiments, leads recorded over uninjured portions of the ventricle either near or opposite injured regions showed isoelectric S-T segments in some instance&l5 and depressed S-T segments in others.3,6 Alternative descriptions of electrophysiologic changes for S-T segment depression include partial diminution of blood flow,16J7 changes in the pH level,rs partial diastolic depolarization,g alteration in ion transportgJ0J8Jg and subendocardial ischemia.7 It is evident that the reported data on S-T segment shifts are controversial and at times contradictory. Recently, Shah et al.ll suggested that such S-T depressions in the precordial leads in acute inferior myocardial infarction may indicate concomitant anterior ischemia or nontransmural infarction rather than a benign “reciprocal” electrical phenomenon. Our study provides anatomic proof of significant stenosis of the

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left anterior descending coronary artery in inferior myocardial infarction with associated S-T depression in precordial leads VI to Vq, Predictive value of S-T segment depression in leads VI to VJ for left anterior descending coronary artery disease: Miller et a1.20studied 84 patients with

previous uncomplicated inferior myocardial infarction and found that 63 percent had significant involvement of the left anterior descending coronary artery. Turner et a1.21 evaluated 117 consecutive survivors of acute myocardial infarction and found that 66 percent of those with inferior myocardial infarction had left anterior descending or left main coronary artery disease. In our study we found a similar incidence rate (69 percent) of left anterior descending coronary artery disease. Because the 95 percent predictive value of S-T segment depression in any of leads VI to VJ is significantly higher than this 69 percent value, this index adds to our ability to predict left anterior descending coronary artery disease. Effect on prognosis: In previous studies22,23 inferior wall myocardial infarction was associated with a better prognosis and less impairment of left ventricular function than was anterior infarction. Shah et a1.,12 measuring left ventricular ejection fraction with multiple gated equilibrium cardiac blood pool scintigraphy within 24 hours of the onset of symptoms of a first acute transmural myocardial infarction, found a more depressed ejection fraction in patients with anterior than with inferior infarction. However, patients with inferior infarction and S-T depression in the precordial leads had similar degrees of depression of left ventricular function as did the patients with anterior infarction. Recently, Shah et a1.13evaluated 44 patients within 48 hours of onset of acute inferior infarction, studying left ventricular ejection fraction and regional wall motion patterns with multiple gated equilibrium cardiac blood pool scintigraphy. Patients with greater than 1 mm S-T

ET AL.

depression in the precordial leads had more severe wall motion abnormalities, more depressed ejection fraction and more complications than did the group with less than 1 mm S-T depression. The results of our study are similar, in that patients with S-T depression in leads Vi to V4 were more likely to have complications whereas patients with no S-T segment depression had an uncomplicated course. Limitations of study: Our study group was not unselected because 10 patients were referred from other centers, although the majority (35 patients) came from a consecutive series of patients. We do not believe this is a major drawback because similar populations have been found in both unselected20,21 and prospective studies.13 Implicatiqns: S-T segment depression in leads Vr to Vq in patients with acute inferior wall myocardial infarction is presumably related to anterior wall ischemia due to significant stenosis of the left anterior descending coronary artery. S-T depression in these leads should not be called “reciprocal.” S-T depression in leads I and aVL is not specific for or predictive of left anterior descending disease and may be a true reciprocal electrocardiographic phenomenon. In the first 24 hours of an acute inferior wall myocardial infarction, the physician is confronted with two different subsets of patients: one group without S-T depression in leads Vi to Vq who might have isolated right coronary or left circumflex coronary artery disease and another group of patients with S-T depression in leads VI to Vq who are likely to have concomitant left anterior descending coronary artery disease. Acknowledgment We thank Kathleen Allan, Ellen Kubisewsky, Cheryl Langlois and Holly Theiss for technical assistance and Claire Flowers for secretarial assistance.

References 1.

2. 3.

4.

5. 6. 7.

8.

RakltaL, Borduas J, Rothman S, Prinzmetal M. Studies on the mechanisms of ventricular activity. XII. Early changes in the RS-T segment and QRS complex following acute coronary artery occlusion: experimental study and clinical applications. Am Heart J 1954;48:351-72. Samson W, Scher A. Mechanism of S-T segment alteration during acute myocardial injury. Circ Res 1960;8:780-7. Wolferth C, Bellet S, Llvezey M, Murphy F. Negative displacement of the RS-T segment in the electrocardiogram and its relationships to positive displacement. An experimental study. Am Heart J 1945;29:220-45. Myers GB, Klein HA, Hlratzka T. Correlations of electrocardiographic and pathologic findings in anteroposterior infarction. Am Heart J 1949;37:205-36. Goldberger AL. Myocardial Infarction. Electrocardiographic Differential Diagnosis. St Louis: CV Mosby, 1975: 111. Hellersteln HK, Katz LN. The electrical effects of injury at various myocardial locations. Am Heart J 1948;36:184-220. Llpman BS, Massle E, Klelger RE. Myocardial Infarction. Injury. and Ischemia. 6th ed. Chicago: Year Book Medical Publishers, 1972:204. Kwoceynskl JK, Ekmekcl A, Toyoshlma H, Prlnzmetal M. Electrocardiographic ischemic patterns without coronary artery disease. Dis Chest 1961;39:305-16.

9. Prlnzmetal M, Toyoshlma H, Ekmekcl A, Mlzuno Y, Nagaya T. Myocardial ischemia: Nature of ischemic electrocardiographic patterns in the mammalian ventricles as determined by intracellular electrocardiographic and metabolic changes. Am J Cardiol 1961;8:493-503. 10. Prlnzmetal M, Ekmekcl A, Toyoshlma H, Kwoczynskl JK. Angina pectoris. Ill. Demonstration of a chemical origin of ST deviation in classic angina pectoris, its variant form, early myocardial infarction and some non-cardiac conditions. Am J Cardiol 1959;3: 276-93. 11. Shah PK, Maddahi J, Berman D, et al. Scintigraphic correlates of precordial ST depression in acute inferior myocardial infarction: identification of a high risk subset (abstr). Clin Res 1978;26: 271. 12. Shah PK, Plchler M, Berman DS, Singh BN, Swan HJC. Left ventricular ejection fraction determined by radionuclide ventriculography in early stages of first transmural myocardial infarction: relation to short-term prognosis. Am J Cardiol 1980;45:542-6. 13. Shah PK, Plchler M, Berman DS, et al. Noninvasive identification of a high risk subset of patients with acute inferior myocardial infarction. Am J Cardiol 1980;46:915-21. 14. Judklns MP. Percutaneous transfemoral selective coronary angiography. Radio1 Clin North Am 1968;6:467-92. 15. Bellet S, Johnston C. The effect of coronary occlusion upon the

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17.

18.

19.

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initial phase of the ventricular complex in precordial leads. J Clin Invest 1934; 13:725-41. Timogiannakis G, Amenda I, Martine E, Thomas M. ST deviation and regional myocardial blood flow during experimental partial coronary artery occlusion. Cardiovasc Res 1974;8:469-77. Wegria R, Segers M, Keating RP, Ward BS. Relationship between the reduction in coronary flow and the appearance of electrocardiographic changes Am Heart J 1949;39:90-6. Case RB, Rosella HA, Crampton RS. Relation of S-T depression to metabolic and hemodynamic events. Cardiologia 1966;48: 32-41. Lie JT, Pairolero PC, Halley KE, McCall JT, Thompson HK, Titus JL. Time course and zonal variations of ischemia-induced myocardial cationic electrolyte derangements. Circulation 1975;51: 860-6.

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20. Miller RR, DeMaria AN, Vismara LA, et al. Chronic stable inferior myocardial infarction: unsuspected harbinger of high-risk proximal left coronary arterial obstruction amenable to surgical revascularization Am J Cardiol 1977;39:954-60. 21. Turner JD, Rogers WJ, Mantle JA, Rackley CE, Russell RO. Coronary angiography soon after myocardial infarction. Chest 1980;77:58-64. 22. Russell RO, Hunt D, Rackley CE. Left ventricular hemodynamics in anterior and inferior myocardial infarction Am J Cardiol 1973;32:8-16. 23. Reduto LA, Berger HJ, Cohen LS, Got&chalk A, Zaret BL. Sequential radionuclide assessment of left and right ventricular performance after acute transmural myocardial infarction. Ann Intern Med 1978:89:441-7.

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