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Emergent coronary angiographic findings of patients with ST depression in the inferior or lateral leads, or both, during anterior wall acute myocardial infarction
In conclusion, the lateral limb leads may be the last leads to develop ST-segment depression during exercise testing, which is regarded as a specific marker for severe CAD. 1. Sketch MH, Nair CK, Esterbrooks DJ, Mohiuddin SM. Reliability of single-lead and multiple-lead electrocardiography during and after exercise. Chest 1978; 74:394-401. 2. Miller TD, Desser KB, Lawson M. How many electrocardiographic leads are required for exercise treadmill tests? J Electrocardiol 1987;20: 13 1-137. 3. Miranda CP, Liu J, Kadar A, Janosi A, Froning J, Lehmann KG, Froelicher VF. Usefulness of exercise-induced ST-segment depression in the inferior leads during exercise testing as a marker for coronary artery disease. Am J Cardiol 1992;69: 303-307. 4. Chikamori T, Yamada M, Takata .I, Furuno T, Yamasaki F, Yabe T, Doi Y. Diagnostic significance of exercise-induced ST-segment depression in the inferior leads in patients with suspected coronary artery disease. Am J Cardiol 1994,74: 1161-1164. 5. Tzivoni D, Benhorin J, Gavish A, Stem S. Halter recording during treadmill testing in assessing myocardial ischemic changes. Am .I Cardiol 1985;55:120%1203.
6. Fuchs RM, Achuff SC, Gnmwald L, Yin FCP, Griffith LSC. Electrocardiographic localization of coronary artery narrowings: studies during myocardial ischemia and infarction in patients with one-vessel disease. Circulation 198266: 1168-l 176. 7. Bruce RA, McDonough JR. Stress testing for cardiovascular disease. Bull N Y Acad Med 1969;45:1288-1294. 8. Blackbum H. The exercise electrocardiogram. Technological, procedural, and conceptual developments. In: Blackburn H, ed. Measurement in Exercise Electrocardiography. Springfield, IL: Charles C. Thomas, 1969220-258. 9. Mason RE, Likar I. A new system of multiple-lead exercise electrocardiography. Am Hearf J 1966;71:196-205. 10. Master AM, Jaffe HL. The electrocardiographic changes after exercise in angina pectoris. J Mi Sinai Hasp 1941;7:629-632. 11. AHA Committee Report. A reporting system on patients evaluated for coronary artery disease. Circulation 1975;51(suppl):5-40. 12. Hajduczki I, Berenyi I, Enghoff E, Malmberg P, Erikson U. Qualitative and quantitative evaluation of the exercise electrocardiogram in assessing the degree of coronary heat disease. J Elecfrocardiol 1985; 18:55-62. 13. Papouchado M, Walker PR, James MA, Clarke LM. Fundamental differences between the standard 1Zlead electrocardiograph and the modified (Mason-Likar) exercise lead system. Eur Heart J 1987;8:725-733. 14. Sevilla DC, Dohrtnann ML, Somelofski CA, Wawrzynski RP, Wagner NB, Wagner GS. Invalidation of the resting electrocardiogram obtained via exercise electrode sites as a standard 12-lead recording. Am J Cardiol 1989;63:35-39.
Emergent Coronary An iographie With ST Depression in t1 e inferior Both, During Anterior Fall Acute Akira
Tamura, MD, Yoshiaki Mikuriya, MD, Hajime Kataoka, Kimiaki Nagase, MD, and Masaru Nasu, MD
T depression in the inferior or lateral leads, or both, S accompanied by ST elevation in the precordial leads is often observed during anterior wall acute myocardial infarction (AMI). The presence of this electrocardiographic (ECG) finding has been shown to indicate a poorer prognosis after infarction.’ Recently, a large population study by Krone et al2 confirmed a poor long-term prognosis in patients with anterior AM1 showing this ECG finding on admission. However, there is little information about emergency coronary angiographic findings of patients with this ECG finding. Therefore, this study was conducted to clarify the coronary angiographic findings within 6 hours of the onset of infarction in patients with anterior AM1 showing ST depression in the inferior or lateral leads, or both. . . . A total of 106 patients (80 men and 26 women, aged 36 to 81 years, mean 62) with anterior AM1 who had been admitted to our hospital within 6 hours of the onset of chest pain and who met the following criteria were retrospectively selected for entry into this study: (1) typical chest pain lasting for 230 minutes; (2) ST elevation 22 mm in 22 adjacent precordial leads; (3) no history or ECG evidence of previous myocardial infarction: (4) an increase in serum creatine kinase greater than twice the upper limit of normal; (5) no ECG evidence of left ventricular hypertrophy, bundle branch block, or interventricular conduction disturbance (QRS 20.12 second); (6) no primary valvular disease or myocardial disease; (7) no thrombolytic therapy before emergent coronary angiFrom the Second Department of Internal versity, Hasama, Oita 879-55, Japan. 13, 1995; revised manuscript received
516
THE AMERICAN
Findings of Patients or Lateral Leads, or Myocardial Infarction
JOURNAL
Medicine, Oita Medical UniManuscript received March and accepted June 9, 1995.
OF CARDIOLOGY@
VOL.
76
MD,
,
ography; and (8) angiographic visualization of the entire distribution of the left anterior descending artery (LAD) after reperfusion therapy. Standard 1Zlead electrocardiograms were recorded at a paper speed of 25 mm/s and a standardization of 10 mm = 1 mV The magnitude of ST elevation or depression relative to the TP segment was measured to the nearest 0.5 mm at 80 ms after the J point. Measurements were obtained by the consensus of 2 observers who were blinded to all clinical and angiographic information. Significant ST depression was defined as deflections of 21 mm in 21 of the inferior (II, III, and aVF) and lateral (I, aVL, V,, and V,) leads. Emergent coronary arteriography was performed with the Judkins or Amplatz technique. Multiple projections were recorded to ensure optimal visualization of the coronary vessels. The grade of collateral filling in the LAD was evaluated according to the criteria of Rentrop et al3 A good collateral circulation was defined as grade 2 or 3. A wrapped LAD was defined as an LAD supplying 2% of the inferior wall of the left ventricle.4 Categorical data were analyzed by the Fisher’s exact test or chi-square test. A p value co.05 was considered significant. Admission electrocardiograms revealed that 85 patients had ST depression in the inferior or lateral leads, or both (group A), whereas 21 patients did not (group B). Group A was subdivided into the following 3 groups according to the location of leads showing ST depression: patients with ST, depression in the lateral leads alone (group A-l, n = 8), inferior leads alone (group A2, n = 52), or both (group A-3, n = 25). Emergent coronary angiographic findings are shown in Table I. On emergent coronary angiograms, groups A- 1, A-2, and ASEPTEMBER
1, 1995
TABLE I Relation
Between
Emergency
Coronary
Angiographic
Anatomy
ST Depression
(A-l; Proximal LAD occlusion Good collaterals Spontaneous recanalization Multivessel disease Wrapped LAD *p ~0.01 and inferior Values are LAD = left
lateral n = 8)
(A-2;
Inferior n = 52)
6 (75)*
36
(69)*
2 (251
7 4 9 12
(131 (8) (17) (23)
1 (13) 6 (75)tt 6 (75)*
and
Location
(+) Both n = 25)
(A-3;
18 (72)* 8 3 7 5
(321 (12) (28) (20)
versus other groups; tp ~0.01 versus those with inferior leads alone; *p co.05 leads, and those with ST depression in the inferior leads. expressed c~s number (%), anterior descending artery; + = present; - = absent.
3 had a higher incidence of LAD occlusion proximal to the lirst septal branch than group B (A-l, 75%; A-2, 69%; A-3, 72%; and B, 14%). The incidence of multivessel disease was significantly higher in group A-l than in the other 3 groups (A-l, 75%; A-2, 17%; A-3, 28%; and B, 29%). The incidence of a wrapped LAD was significantly higher in groups A-l and B than in the other groups (A-l, 75%; A-2,23%; A-3,20%; and B, 67%). There were no differences in the frequency of spontaneous recanalization and good collateral circulation between the 4 groups. . . . The present study demonstrates that there are some obvious differences in emergency coronary angiographic anatomy according to the presence or absence of ST depression and its location on an admission electrocardiogram in patients With anterior AMI. First, the patients With ST depression in the inferior or lateral leads, or both, had a higher incidence of proximal LAD occlusion than those without it. Patients with inferior ST depression have been shown to have a high prevalence of proximal LAD occlusion in anterior AMI. However, the relation between the site of LAD occlusion and ST depression in the lateral leads has not been reported. The higher incidence of proximal LAD occlusion in patients with ST depression in the inferior or lateral leads, or both, supports a poorer prognosis in such patients. Second, patients with ST depression in the lateral leads alone had a higher incidence of multivessel disease than the other groups. This finding is a clinically important observation that has not been reported. However, because the number of patients with ST depression in the lateral leads alone was small, further investigation is needed to determine whether the presence of the ECG finding can identify a group of patients with multivessel disease in anterior AMI. Third, patients without inferior ST depression had a higher incidence of a wrapped LAD than those with it. This finding can be explained by the observation of Lew et aL4 namely that occlusion of a wrapped LAD causes transmural ischemia in the
of ST Depression
ST Depression (-) (B; n = 21) 3 (14)
2
(101
6 (29) 6 (29) 14 (67)* versus group with both lateral
inferior wall, resulting in an upward shift of the ST segment in the inferior leads. The higher incidence of proximal LAD occlusion, multivessel disease, and a wrapped LAD in patients with ST depression in the lateral leads alone suggests a poor prognosis in sukh patients. To date, there have been no studies investigating angiograplhic and clinical differences between patients with inferior ST depression alone and those with lateral ST depression alone during anterior AMI. The present study showed the obvious angiographic differences in the frequency of multivessel disease and a wrapped LAD between the 2 groups. Because the subgroup size and the number of women were small, further studies with a large population are desirable to confirm our results. In conclusion, the present study indicates that there are several distinctive differences in emergent coronary angiographic linclmgs according to the presence or absence of ST depression in the inferior or lateral leads, or both, and location of the leads shalwing ST depression on admission electrocardiogralms in’ patients with anterior AMI. The coronary angiographic features of patients with this ECG ‘finding greatly support a poor prognosis. In patients with anterior AMI, analysis-of ST depression on an admission electrocardiogram should be routinely performed because it is useful in predicting coronau-y anatomy, the extent of infarction, and its prognosis.
1. Willems JL, Willems RJ, Willems GM, Arnold AER, Van de Werf F, Verstraete M. Significance of initial ST segment elevation and depression for the management of tbrombolytic therapy in acute myocardial infarction. Circulation 1990;82: 1147-l 158. 2. Krone RJ, Greenberg H, Dwyer EM Jr, Kleiger RE, Boden WE, the Multi~center Diltiazem Postinfarction Trial Research Group. Long-term prognostic significance of ST segment depression during acute myocardial infarction. JAm Coil Cardial 1993;22:361-367. 3. Rentrop KP, Cohen M, Blank H, Phillips R. Changes in collateral tilling immediately following controlled coronary artery occlusion by an angioplasty balloon in man. J Am Coil Cardiol 1985;5:587-592. 4. Lew AS, Hod H, Cercek B, Shah PH, Ganz W. Inferior ST segment chaages during acute anterior myocardial infarction: a marker of the presence or absence of concomitant inferior wall ischemia. JAm Coil Cardiol 1987;10:519-526.
BRIEF REPORTS
5117
6. Fuchs RM, Achuff SC, Gnmwald L, Yin FCP, Griffith LSC. Electrocardiographic localization of coronary artery narrowings: studies during myocardial ischemia and infarction in patients with one-vessel disease. Circulation 198266: 1168-l 176. 7. Bruce RA, McDonough JR. Stress testing for cardiovascular disease. Bull N Y Acad Med 1969;45:1288-1294. 8. Blackbum H. The exercise electrocardiogram. Technological, procedural, and conceptual developments. In: Blackburn H, ed. Measurement in Exercise Electrocardiography. Springfield, IL: Charles C. Thomas, 1969220-258. 9. Mason RE, Likar I. A new system of multiple-lead exercise electrocardiography. Am Hearf J 1966;71:196-205. 10. Master AM, Jaffe HL. The electrocardiographic changes after exercise in angina pectoris. J Mi Sinai Hasp 1941;7:629-632. 11. AHA Committee Report. A reporting system on patients evaluated for coronary artery disease. Circulation 1975;51(suppl):5-40. 12. Hajduczki I, Berenyi I, Enghoff E, Malmberg P, Erikson U. Qualitative and quantitative evaluation of the exercise electrocardiogram in assessing the degree of coronary heat disease. J Elecfrocardiol 1985; 18:55-62. 13. Papouchado M, Walker PR, James MA, Clarke LM. Fundamental differences between the standard 1Zlead electrocardiograph and the modified (Mason-Likar) exercise lead system. Eur Heart J 1987;8:725-733. 14. Sevilla DC, Dohrtnann ML, Somelofski CA, Wawrzynski RP, Wagner NB, Wagner GS. Invalidation of the resting electrocardiogram obtained via exercise electrode sites as a standard 12-lead recording. Am J Cardiol 1989;63:35-39.
Emergent Coronary An iographie With ST Depression in t1 e inferior Both, During Anterior Fall Acute Akira
Tamura, MD, Yoshiaki Mikuriya, MD, Hajime Kataoka, Kimiaki Nagase, MD, and Masaru Nasu, MD
T depression in the inferior or lateral leads, or both, S accompanied by ST elevation in the precordial leads is often observed during anterior wall acute myocardial infarction (AMI). The presence of this electrocardiographic (ECG) finding has been shown to indicate a poorer prognosis after infarction.’ Recently, a large population study by Krone et al2 confirmed a poor long-term prognosis in patients with anterior AM1 showing this ECG finding on admission. However, there is little information about emergency coronary angiographic findings of patients with this ECG finding. Therefore, this study was conducted to clarify the coronary angiographic findings within 6 hours of the onset of infarction in patients with anterior AM1 showing ST depression in the inferior or lateral leads, or both. . . . A total of 106 patients (80 men and 26 women, aged 36 to 81 years, mean 62) with anterior AM1 who had been admitted to our hospital within 6 hours of the onset of chest pain and who met the following criteria were retrospectively selected for entry into this study: (1) typical chest pain lasting for 230 minutes; (2) ST elevation 22 mm in 22 adjacent precordial leads; (3) no history or ECG evidence of previous myocardial infarction: (4) an increase in serum creatine kinase greater than twice the upper limit of normal; (5) no ECG evidence of left ventricular hypertrophy, bundle branch block, or interventricular conduction disturbance (QRS 20.12 second); (6) no primary valvular disease or myocardial disease; (7) no thrombolytic therapy before emergent coronary angiFrom the Second Department of Internal versity, Hasama, Oita 879-55, Japan. 13, 1995; revised manuscript received
516
THE AMERICAN
Findings of Patients or Lateral Leads, or Myocardial Infarction
JOURNAL
Medicine, Oita Medical UniManuscript received March and accepted June 9, 1995.
OF CARDIOLOGY@
VOL.
76
MD,
,
ography; and (8) angiographic visualization of the entire distribution of the left anterior descending artery (LAD) after reperfusion therapy. Standard 1Zlead electrocardiograms were recorded at a paper speed of 25 mm/s and a standardization of 10 mm = 1 mV The magnitude of ST elevation or depression relative to the TP segment was measured to the nearest 0.5 mm at 80 ms after the J point. Measurements were obtained by the consensus of 2 observers who were blinded to all clinical and angiographic information. Significant ST depression was defined as deflections of 21 mm in 21 of the inferior (II, III, and aVF) and lateral (I, aVL, V,, and V,) leads. Emergent coronary arteriography was performed with the Judkins or Amplatz technique. Multiple projections were recorded to ensure optimal visualization of the coronary vessels. The grade of collateral filling in the LAD was evaluated according to the criteria of Rentrop et al3 A good collateral circulation was defined as grade 2 or 3. A wrapped LAD was defined as an LAD supplying 2% of the inferior wall of the left ventricle.4 Categorical data were analyzed by the Fisher’s exact test or chi-square test. A p value co.05 was considered significant. Admission electrocardiograms revealed that 85 patients had ST depression in the inferior or lateral leads, or both (group A), whereas 21 patients did not (group B). Group A was subdivided into the following 3 groups according to the location of leads showing ST depression: patients with ST, depression in the lateral leads alone (group A-l, n = 8), inferior leads alone (group A2, n = 52), or both (group A-3, n = 25). Emergent coronary angiographic findings are shown in Table I. On emergent coronary angiograms, groups A- 1, A-2, and ASEPTEMBER
1, 1995
TABLE I Relation
Between
Emergency
Coronary
Angiographic
Anatomy
ST Depression
(A-l; Proximal LAD occlusion Good collaterals Spontaneous recanalization Multivessel disease Wrapped LAD *p ~0.01 and inferior Values are LAD = left
lateral n = 8)
(A-2;
Inferior n = 52)
6 (75)*
36
(69)*
2 (251
7 4 9 12
(131 (8) (17) (23)
1 (13) 6 (75)tt 6 (75)*
and
Location
(+) Both n = 25)
(A-3;
18 (72)* 8 3 7 5
(321 (12) (28) (20)
versus other groups; tp ~0.01 versus those with inferior leads alone; *p co.05 leads, and those with ST depression in the inferior leads. expressed c~s number (%), anterior descending artery; + = present; - = absent.
3 had a higher incidence of LAD occlusion proximal to the lirst septal branch than group B (A-l, 75%; A-2, 69%; A-3, 72%; and B, 14%). The incidence of multivessel disease was significantly higher in group A-l than in the other 3 groups (A-l, 75%; A-2, 17%; A-3, 28%; and B, 29%). The incidence of a wrapped LAD was significantly higher in groups A-l and B than in the other groups (A-l, 75%; A-2,23%; A-3,20%; and B, 67%). There were no differences in the frequency of spontaneous recanalization and good collateral circulation between the 4 groups. . . . The present study demonstrates that there are some obvious differences in emergency coronary angiographic anatomy according to the presence or absence of ST depression and its location on an admission electrocardiogram in patients With anterior AMI. First, the patients With ST depression in the inferior or lateral leads, or both, had a higher incidence of proximal LAD occlusion than those without it. Patients with inferior ST depression have been shown to have a high prevalence of proximal LAD occlusion in anterior AMI. However, the relation between the site of LAD occlusion and ST depression in the lateral leads has not been reported. The higher incidence of proximal LAD occlusion in patients with ST depression in the inferior or lateral leads, or both, supports a poorer prognosis in such patients. Second, patients with ST depression in the lateral leads alone had a higher incidence of multivessel disease than the other groups. This finding is a clinically important observation that has not been reported. However, because the number of patients with ST depression in the lateral leads alone was small, further investigation is needed to determine whether the presence of the ECG finding can identify a group of patients with multivessel disease in anterior AMI. Third, patients without inferior ST depression had a higher incidence of a wrapped LAD than those with it. This finding can be explained by the observation of Lew et aL4 namely that occlusion of a wrapped LAD causes transmural ischemia in the
of ST Depression
ST Depression (-) (B; n = 21) 3 (14)
2
(101
6 (29) 6 (29) 14 (67)* versus group with both lateral
inferior wall, resulting in an upward shift of the ST segment in the inferior leads. The higher incidence of proximal LAD occlusion, multivessel disease, and a wrapped LAD in patients with ST depression in the lateral leads alone suggests a poor prognosis in sukh patients. To date, there have been no studies investigating angiograplhic and clinical differences between patients with inferior ST depression alone and those with lateral ST depression alone during anterior AMI. The present study showed the obvious angiographic differences in the frequency of multivessel disease and a wrapped LAD between the 2 groups. Because the subgroup size and the number of women were small, further studies with a large population are desirable to confirm our results. In conclusion, the present study indicates that there are several distinctive differences in emergent coronary angiographic linclmgs according to the presence or absence of ST depression in the inferior or lateral leads, or both, and location of the leads shalwing ST depression on admission electrocardiogralms in’ patients with anterior AMI. The coronary angiographic features of patients with this ECG ‘finding greatly support a poor prognosis. In patients with anterior AMI, analysis-of ST depression on an admission electrocardiogram should be routinely performed because it is useful in predicting coronau-y anatomy, the extent of infarction, and its prognosis.
1. Willems JL, Willems RJ, Willems GM, Arnold AER, Van de Werf F, Verstraete M. Significance of initial ST segment elevation and depression for the management of tbrombolytic therapy in acute myocardial infarction. Circulation 1990;82: 1147-l 158. 2. Krone RJ, Greenberg H, Dwyer EM Jr, Kleiger RE, Boden WE, the Multi~center Diltiazem Postinfarction Trial Research Group. Long-term prognostic significance of ST segment depression during acute myocardial infarction. JAm Coil Cardial 1993;22:361-367. 3. Rentrop KP, Cohen M, Blank H, Phillips R. Changes in collateral tilling immediately following controlled coronary artery occlusion by an angioplasty balloon in man. J Am Coil Cardiol 1985;5:587-592. 4. Lew AS, Hod H, Cercek B, Shah PH, Ganz W. Inferior ST segment chaages during acute anterior myocardial infarction: a marker of the presence or absence of concomitant inferior wall ischemia. JAm Coil Cardiol 1987;10:519-526.
BRIEF REPORTS
5117