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Significance of Negative U Waves in the Precordial Leads During Anterior Wall Acute Myocardial Infarction
Significance of Negative U Waves in the Precordial Leads During Anterior Wall Acute Myocardial Infarction Akira Tamura, MD, Toru Watanabe, MD, Kimiaki Nagase, Yoshiaki Mikuriya, MD, Masaru Nasu, MD This study was conducted to clarify the clinical significance of negative U waves in the precordial leads during anterior wall acute myocardial infarction (AMI). In all, 141 patients with first anterior wall AMI (°6 hours) were classified into 2 groups according to the presence (group A, n Å 31) or absence (group B, n Å 110) of negative U waves in the precordial leads on the admission electrocardiogram (ECG). The number of leads showing ST elevation ¢1 mm on the admission ECG was smaller in group A than in group B (5.2 { 1.3 vs 6.2 { 1.7, p õ0.01). Emergent coronary arteriography revealed that group A had a higher incidence of good collateral circulation than group B (39% vs 19%, p õ0.05). Peak creatine kinase activity was lower in group A than in group B (1,708 { 1,271 vs 2,735 { 1,865 IU/L, p
lthough the genesis of the U wave on the electrocardiogram (ECG) has not been clearly deA fined, many studies have shown that the appear1–7
ance of negative U waves during exercise8 – 12 or anginal attack13 – 15 is an important sign of myocardial ischemia. Negative U waves are frequently observed in the precordial leads during anterior wall acute myocardial infarction (AMI). However, there is little information regarding its clinical significance in the setting of such an AMI. Accordingly, the present study was conducted to clarify clinical features of patients with negative U waves in the precordial leads during anterior wall AMI.
METHODS Study patients: Between January 1989 and December 1994, 182 patients with anterior wall AMI by clinical, electrocardiographic, and enzymatic criteria underwent emergent coronary arteriography within 6 hours of the onset of AMI. Patients meeting the following criteria were retrospectively selected for this study: (1) no history of previous myocardial infarction; (2) lack of atrial fibrillation or flutter, bundle branch block or intraventricular conduction disturbance (QRS ¢0.12 second), and no electrocardiographic evidence of left ventricular hypertrophy; (3) no other heart or lung disease; (4) identification of the infarct-related lesion by emergent coronary arteriography; (5) no thrombolytic From the Second Department of Internal Medicine, Oita Medical University, Oita, Japan. Manuscript received July 8, 1996; revised manuscript received and accepted November 1, 1996. Address for reprints: Akira Tamura, MD, Second Department of Internal Medicine, Oita Medical University, Hasama, Oita 879-55, Japan.
õ0.01). The number of abnormal Q waves on the predischarge ECG was smaller in group A (2.0 { 1.5 vs 3.4 { 2.0, p õ0.01). Group A had a greater left ventricular ejection fraction and better regional wall motion in the anterobasal, anterolateral, and apical regions in the chronic phase than group B. In conclusion, patients with anterior wall AMI having negative U waves in the precordial leads on admission had a relatively smaller mass of necrotic myocardium than those without the waves. Therefore, negative U waves during anterior wall AMI may be a useful marker for identifying patients with smaller infarction partly due to better collateral circulation. Q1997 by Excerpta Medica, Inc. (Am J Cardiol 1997;79:897–900)
therapy before emergent coronary arteriography; and (6) technically adequate electrocardiographic recordings. In total, 141 patients (103 men and 38 women, mean age 63 { 10 years) met these criteria. Standard 12-lead electrocardiograms: Standard 12lead ECGs were recorded at a paper speed of 25 mm/ s (standardization of 10 mm Å 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. A negative U wave was identified if there was a discrete negative deflection of ¢0.5 mm within the TP segment. The possibility of terminal T-wave inversion was excluded by determining the QT interval in other leads where negative U waves were not present. Similarly, the inversion of the initial portion of the P wave was excluded by determining the beginning of the P wave in other leads where the longest PR interval was recorded. A typical ECG with negative U waves is shown in Figure 1. An abnormal Q wave was defined as a wave ¢0.04 second in duration. All ECGs were analyzed by the consensus of 2 observers who were blinded to all clinical and angiographic information. Emergent coronary arteriograms and reperfusion therapy: Emergent coronary arteriography was per-
formed using the Judkins or Amplatz technique. Multiple projections were recorded to ensure optimal visualization of the coronary vessels. Coronary flow in the infarct-related artery was graded according to the system used in the Thrombolysis in Myocardial Infarction (TIMI) trial.16 The infarct-related artery was considered patent if the TIMI grade was 2 or 3. The grade of collateral filling in the left anterior descending artery was determined according to the criteria of Rentrop et al.17 A collateral circulation with
Q1997 by Excerpta Medica, Inc.
0002-9149/97/$17.00 PII S0002-9149(97)00011-8
All rights reserved.
/ 2w1e 0883 Mp
897
MD,
Wednesday Mar 05 04:57 PM
EL–AJC (v. 79, no. 7 ’97)
0883
897
a grade of 2 or 3 was defined as ‘‘good.’’ After angiographic confirmation of total occlusion of the left anterior descending artery, intracoronary isosorbide dinitrate was administered followed by intracoronary urokinase or tissue plasminogen activator. If successful reperfusion was not obtained, coronary angioplasty was performed. Successful reperfusion was defined as the establishment of TIMI grade 2 or 3 flow in the infarct-related artery. Follow-up cardiac catheterization: Surviving patients underwent coronary arteriography and left ventriculography about 1 month after the onset of AMI. Left ventriculograms were recorded in the 307 right anterior oblique and 607 left anterior oblique views. End-diastolic and end-systolic endocardial contours were carefully traced by an experienced cardiologist who was unaware of the patient’s data. Global left ventricular ejection fraction was calculated by the centerline method.18 Regional wall motion in the anterobasal, anterolateral, and apical areas was expressed as SD/chord.18 Cardiac enzyme measurements: Blood samples were obtained every 3 hours during the first 24 hours and once daily from the second day until a normal value was obtained for determination of the peak serum creatine kinase activity. Statistical analysis: Data are expressed as mean { SD. Categorical data were analyzed by the Fisher’s exact test or chi-square test. Continuous variables were analyzed by the unpaired t test. A p value õ0.05 was considered statistically significant.
RESULTS Admission ECGs revealed that 31 patients had negative U waves in the precordial leads (group A), whereas 110 patients did not (group B). There were no differences between the 2 groups in age, gender, the time elapsed from the onset of AMI to electrocardiographic recordings, and the rate of successful reperfusion therapy. (Table I). Serum potassium levels at the time of admission did not differ significantly between the 2 groups (141 { 0.3 vs 140 { 0.4 mEq/L). Admission electrocardiographic findings: The number of leads showing ST elevation ¢1 mm on the admission ECG was significantly smaller in group A than in group B (5.2 { 1.3 vs 6.2 { 1.7, p õ0.01) (Figure 2). Emergent coronary arteriographic features: Emergent coronary arteriograms showed that group A had a higher incidence of good collateral circulation than group B (39% vs 19%, p õ0.05). There were no differences between the 2 groups in incidence of spontaneous recanalization, proximal left anterior descending artery occlusion, and multivessel disease (Table I). Clinical features: Peak creatine kinase activity was significantly lower in group A than in group B (1,708 { 1,271 vs 2,735 { 1,865 IU/L, p õ0.01). The number of abnormal Q waves on the predischarge ECG was significantly smaller in group A than in group B (2.0 { 1.5 vs 3.4 { 2.0, p õ0.01). In-hospital 898
THE AMERICAN JOURNAL OF CARDIOLOGYT
/ 2w1e 0883 Mp
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VOL. 79
Wednesday Mar 05 04:57 PM
FIGURE 1. A typical electrocardiogram with negative U wave obtained from a patient.
TABLE I Clinical Characteristics Group A
Group B
Age (yr) 63 { 9 63 { 11 Men (%) 25 (81%) 78 (71%) Time to ECG recordings (min) 173 { 86 162 { 80 Spontaneous recanalization 9 (29%) 22 (20%) Good collaterals 12 (39%)* 21 (19%)* Multivessel disease 8 (26%) 35 (32%) Proximal LAD occlusion 18 (58%) 65 (59%) Reperfusion therapy 22 (71%) 87 (79%) PTCR 21 (68%) 85 (77%) PTCA 10 (32%) 53 (48%) Successful reperfusion 29 (94%) 95 (86%) Peak CPK (IU/L) 1,708 { 1,271† 2,735 { 1,865† Number of abnormal 3.4 { 2.0† Q waves 2.0 { 1.5† In-hospital death (%) 0 (0%) 10 (9%) *p õ0.05; †p õ0.01. CPK Å peak creatine kinase activity; ECG Å electrocardiographic; LAD Å left anterior descending artery; PTCA Å percutaneous transluminal coronary angioplasty; PTCR Å percutaneous transluminal coronary recanalization.
mortality tended to be lower in group A, although the difference was not statistically significant (0% vs 9%, p Å NS) (Table I). Left ventricular wall motion in the chronic phase:
Global left ventricular ejection fraction in the chronic phase was significantly greater in group A than in group B (63 { 12% vs 54 { 13%, p õ0.01). Regional wall motion in the anterobasal, anterolateral, and apical regions was reduced significantly less in group A (00.4 { 1.2 vs 01.3 { 1.0, p õ0.01; 01.0 { 1.7 vs 02.6 { 1.5, p õ0.01; 00.8 { 1.5 vs 02.0 { 1.3, p õ0.01, respectively) (Table II).
DISCUSSION To date, the clinical significance of negative U waves observed during anterior wall AMI has not APRIL 1, 1997
EL–AJC (v. 79, no. 7 ’97)
0883
patients with negative U waves is thought to be partly due to the presence of collateral circulation. Relation between negative U waves and site of occlusion of the left anterior descending artery: New negative U waves during ex-
ercise have been shown to be a useful marker for predicting proximal left anterior descending lesion.8,22 However, in our study, there were no differences in the incidence of proximal left anterior descending occlusion between the 2 groups. Although the exact mechanism for this discrepancy is unknown, the difference between ischemia and infarction may have affected the results. The association of negative U waves with proximal left anterior descending lesion needs to be reevaluated. Study limitations: Our study has certain limitations. First, our study was retroFIGURE 2. Number of leads showing ST elevation on the admission electrocarspective. Second, a precise mechanism diogram. of the origin of a U wave remains elusive, although several theories have been proposed.1 – 7 Therefore, further studies are desirable TABLE II Left Ventricular Function in the Chronic Phase to clarify the electrophysiologic genesis of a negGroup A* Group B* ative U wave and determine whether the theory Number of patients 31 100 supports our results. Global LVEF (%) RWM (SD/chord) anterobasal anterolateral apical
63 { 12
00.4 { 1.2 01.0 { 1.7 00.8 { 1.5
54 { 13
01.3 { 1.0 02.6 { 1.5 02.0 { 1.3
*p õ0.01. LVEF Å left ventricular ejection fraction; RWM Å regional wall motion.
been investigated. To our knowledge, this is the first published study reporting its significance. In the present study, the sum of leads showing ST elevation ¢1 mm on admission was significantly smaller in patients with than without negative U waves in the precordial leads during anterior wall AMI. Because the number of leads showing ST elevation during the acute phase of anterior infarction has been shown to be a good indicator for predicting the infarct-size,19 – 21 it is suggested that the amount of jeopardized myocardium before reperfusion therapy was smaller in patients with than without negative U waves. The amount of necrotic myocardium estimated by peak creatine kinase activity and the number of Q waves on the predischarge ECG was significantly smaller in patients with negative U waves. Furthermore, global and regional left ventricular wall motion in the anterobasal, anterolateral, and apical regions in the chronic phase was significantly better in patients with negative U waves. These results suggest that anterior wall AMI patients with negative U waves on the admission ECG have a relatively smaller mass of necrotic myocardium. In our study, the relatively small amount of necrotic myocardium in
1. Lepeschkin E. The U wave of the electrocardiogram. Mod Concepts Car-
diovasc Dis 1969;38:39–45. 2. Watanabe Y. Purkinje repolarization as a possible cause of the U wave in
the electrocardiogram. Circulation 1975;51:1030–1037. 3. Watanabe Y, Toda H. The U wave and aberrant intraventricular conduction: further evidence for the Purkinje repolarization theory on genesis of the U wave. Am J Cardiol 1978;41:23–31. 4. Kishida H, Cole JS, Surawicz B. Negative U wave: a highly specific but poorly understood sign of heart disease. Am J Cardiol 1982;49:2030–2036. 5. Nesterenko VV, Antzelevitch C. Simulation of the electrocardiographic U wave in heterogeneous myocardium: effect of the local junctional resistance. In: Proceedings of Computers in Cardiology. Los Alamitos, CA: IEEE Computer Society Press, 1992;43–46. 6. Antzelevitch C, Sicouri S. Clinical relevance of cardiac arrhythmias generated by afterdepolarizations: the role of M cells in the generation of U waves, triggered activity and torsade de pointes. J Am Coll Cardiol 1994;23:259–277. 7. Liu DW, Antzelevitch C. Characteristics of the delayed rectifier current (Ikr and Iks) in canine ventricular epicardial, midmyocardial, and endocardial myocytes. A weaker Iks contributes to the longer action potential of the M cell. Circ Res 1995;76:351–365. 8. Gerson MC, Phillips JF, Morris SN, McHenry PL. Exercise-induced U-wave inversion as a marker of stenosis of the left anterior descending coronary artery. Circulation 1979;60:1014–1020. 9. Salmasi AM, Salmasi SN, Nicolaides AN, Vecht RJ, Hendry WG, Kidner PH, Besterman EMM. The value of exercise-induced U wave inversion on ECG chest wall mapping in the identification of individual coronary arterial lesions. Eur Heart J 1985;6:437–443. 10. Hasegawa K, Fujiwara T, Sawayama T, Nezuo S, Nakao M, Tadaoka S, Nakamura T, Kakumae S, Kawahara Y, Inoue S. Angina-induced transient positive U wave in right precordial leads. A marker of left circumflex artery/right coronary artery stenosis [in Japanese]. Heart 1988;20:1033–1039. 11. Chikamori T, Yamada M, Takata J, Furuno T, Yamasaki F, Doi YL. Exercise-induced prominent U waves as a marker of significant narrowing of the left circumflex or right coronary artery. Am J Cardiol 1994;74:495–499. 12. Chikamori T, Takata J, Furuno T, Yabe T, Matsumura Y, Kitaoka H, Doi Y. Usefulness of U-wave analysis in detecting significant narrowing limited to a single coronary artery. Am J Cardiol 1995;75:508–511. 13. Miwa K, Murakami T, Kambara H, Kawai C. U wave inversion during attacks of variant angina. Br Heart J 1983;50:378–382. 14. Matsuguchi T, Koiwaya Y, Nakagaki O, Takeshita A, Nakamura M. Transient U wave inversion during variant angina. Am Heart J 1984;108:899–904. 15. Yano H, Hiasa Y, Aihara T, Nakaya Y, Mori H. Inverted U wave in ergonovine-induced vasospastic angina. Clin Cardiol 1987;10:633–639.
CORONARY ARTERY DISEASE/NEGATIVE U WAVES
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16. The TIMI Study Group. The Thrombolysis in Myocardial Infarction (TIMI)
20. Clemmensen P, Grande P, Saunama¨ki K, Pedersen F, Svendsen JH, Wagner
trial: phase I findings. N Engl J Med 1985;312:932–936. 17. Rentrop KP, Cohen M, Blanke H, Phillips RA. Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects. J Am Coll Cardiol 1985;5:587–592. 18. Sheehan FH, Bolson EL, Dodge HT, Mathey DG, Schofer J, Woo HW. Advantages and applications of the centerline method for characterizing regional ventricular function. Circulation 1986;74:293–305. 19. Aldorich HR, Wagner NB, Boswick J, Corsa AT, Jones MG, Grande P, Lee KL, Wagner GS. Use of initial ST-segment deviation for prediction of final electrocardiographic size of acute myocardial infarcts. Am J Cardiol 1988;61:749–753.
NB, Granborg J, Madsen JK, Haedersdal C, Wagner GS. Effect of intravenous streptokinase on the relation between initial ST-predicted size and final QRSestimated size of acute myocardial infarcts. J Am Coll Cardiol 1990;16:1252– 1257. 21. Clemmensen P, Grande P, Aldrich HR, Wagner GS. Evaluation of fomulas for estimating the final size of acute myocardial infarcts from quantitative STsegment elevation on the initial standard 12-lead ECG. J Electrocardiol 1991;24:77–83. 22. Gerson MC, McHenry PL. Resting U wave inversion as a marker of stenosis of the left anterior descending coronary artery. Am J Med 1980;69: 545 – 550.
900
THE AMERICAN JOURNAL OF CARDIOLOGYT
/ 2w1e 0883 Mp
900
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Wednesday Mar 05 04:57 PM
APRIL 1, 1997
EL–AJC (v. 79, no. 7 ’97)
0883
lthough the genesis of the U wave on the electrocardiogram (ECG) has not been clearly deA fined, many studies have shown that the appear1–7
ance of negative U waves during exercise8 – 12 or anginal attack13 – 15 is an important sign of myocardial ischemia. Negative U waves are frequently observed in the precordial leads during anterior wall acute myocardial infarction (AMI). However, there is little information regarding its clinical significance in the setting of such an AMI. Accordingly, the present study was conducted to clarify clinical features of patients with negative U waves in the precordial leads during anterior wall AMI.
METHODS Study patients: Between January 1989 and December 1994, 182 patients with anterior wall AMI by clinical, electrocardiographic, and enzymatic criteria underwent emergent coronary arteriography within 6 hours of the onset of AMI. Patients meeting the following criteria were retrospectively selected for this study: (1) no history of previous myocardial infarction; (2) lack of atrial fibrillation or flutter, bundle branch block or intraventricular conduction disturbance (QRS ¢0.12 second), and no electrocardiographic evidence of left ventricular hypertrophy; (3) no other heart or lung disease; (4) identification of the infarct-related lesion by emergent coronary arteriography; (5) no thrombolytic From the Second Department of Internal Medicine, Oita Medical University, Oita, Japan. Manuscript received July 8, 1996; revised manuscript received and accepted November 1, 1996. Address for reprints: Akira Tamura, MD, Second Department of Internal Medicine, Oita Medical University, Hasama, Oita 879-55, Japan.
õ0.01). The number of abnormal Q waves on the predischarge ECG was smaller in group A (2.0 { 1.5 vs 3.4 { 2.0, p õ0.01). Group A had a greater left ventricular ejection fraction and better regional wall motion in the anterobasal, anterolateral, and apical regions in the chronic phase than group B. In conclusion, patients with anterior wall AMI having negative U waves in the precordial leads on admission had a relatively smaller mass of necrotic myocardium than those without the waves. Therefore, negative U waves during anterior wall AMI may be a useful marker for identifying patients with smaller infarction partly due to better collateral circulation. Q1997 by Excerpta Medica, Inc. (Am J Cardiol 1997;79:897–900)
therapy before emergent coronary arteriography; and (6) technically adequate electrocardiographic recordings. In total, 141 patients (103 men and 38 women, mean age 63 { 10 years) met these criteria. Standard 12-lead electrocardiograms: Standard 12lead ECGs were recorded at a paper speed of 25 mm/ s (standardization of 10 mm Å 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. A negative U wave was identified if there was a discrete negative deflection of ¢0.5 mm within the TP segment. The possibility of terminal T-wave inversion was excluded by determining the QT interval in other leads where negative U waves were not present. Similarly, the inversion of the initial portion of the P wave was excluded by determining the beginning of the P wave in other leads where the longest PR interval was recorded. A typical ECG with negative U waves is shown in Figure 1. An abnormal Q wave was defined as a wave ¢0.04 second in duration. All ECGs were analyzed by the consensus of 2 observers who were blinded to all clinical and angiographic information. Emergent coronary arteriograms and reperfusion therapy: Emergent coronary arteriography was per-
formed using the Judkins or Amplatz technique. Multiple projections were recorded to ensure optimal visualization of the coronary vessels. Coronary flow in the infarct-related artery was graded according to the system used in the Thrombolysis in Myocardial Infarction (TIMI) trial.16 The infarct-related artery was considered patent if the TIMI grade was 2 or 3. The grade of collateral filling in the left anterior descending artery was determined according to the criteria of Rentrop et al.17 A collateral circulation with
Q1997 by Excerpta Medica, Inc.
0002-9149/97/$17.00 PII S0002-9149(97)00011-8
All rights reserved.
/ 2w1e 0883 Mp
897
MD,
Wednesday Mar 05 04:57 PM
EL–AJC (v. 79, no. 7 ’97)
0883
897
a grade of 2 or 3 was defined as ‘‘good.’’ After angiographic confirmation of total occlusion of the left anterior descending artery, intracoronary isosorbide dinitrate was administered followed by intracoronary urokinase or tissue plasminogen activator. If successful reperfusion was not obtained, coronary angioplasty was performed. Successful reperfusion was defined as the establishment of TIMI grade 2 or 3 flow in the infarct-related artery. Follow-up cardiac catheterization: Surviving patients underwent coronary arteriography and left ventriculography about 1 month after the onset of AMI. Left ventriculograms were recorded in the 307 right anterior oblique and 607 left anterior oblique views. End-diastolic and end-systolic endocardial contours were carefully traced by an experienced cardiologist who was unaware of the patient’s data. Global left ventricular ejection fraction was calculated by the centerline method.18 Regional wall motion in the anterobasal, anterolateral, and apical areas was expressed as SD/chord.18 Cardiac enzyme measurements: Blood samples were obtained every 3 hours during the first 24 hours and once daily from the second day until a normal value was obtained for determination of the peak serum creatine kinase activity. Statistical analysis: Data are expressed as mean { SD. Categorical data were analyzed by the Fisher’s exact test or chi-square test. Continuous variables were analyzed by the unpaired t test. A p value õ0.05 was considered statistically significant.
RESULTS Admission ECGs revealed that 31 patients had negative U waves in the precordial leads (group A), whereas 110 patients did not (group B). There were no differences between the 2 groups in age, gender, the time elapsed from the onset of AMI to electrocardiographic recordings, and the rate of successful reperfusion therapy. (Table I). Serum potassium levels at the time of admission did not differ significantly between the 2 groups (141 { 0.3 vs 140 { 0.4 mEq/L). Admission electrocardiographic findings: The number of leads showing ST elevation ¢1 mm on the admission ECG was significantly smaller in group A than in group B (5.2 { 1.3 vs 6.2 { 1.7, p õ0.01) (Figure 2). Emergent coronary arteriographic features: Emergent coronary arteriograms showed that group A had a higher incidence of good collateral circulation than group B (39% vs 19%, p õ0.05). There were no differences between the 2 groups in incidence of spontaneous recanalization, proximal left anterior descending artery occlusion, and multivessel disease (Table I). Clinical features: Peak creatine kinase activity was significantly lower in group A than in group B (1,708 { 1,271 vs 2,735 { 1,865 IU/L, p õ0.01). The number of abnormal Q waves on the predischarge ECG was significantly smaller in group A than in group B (2.0 { 1.5 vs 3.4 { 2.0, p õ0.01). In-hospital 898
THE AMERICAN JOURNAL OF CARDIOLOGYT
/ 2w1e 0883 Mp
898
VOL. 79
Wednesday Mar 05 04:57 PM
FIGURE 1. A typical electrocardiogram with negative U wave obtained from a patient.
TABLE I Clinical Characteristics Group A
Group B
Age (yr) 63 { 9 63 { 11 Men (%) 25 (81%) 78 (71%) Time to ECG recordings (min) 173 { 86 162 { 80 Spontaneous recanalization 9 (29%) 22 (20%) Good collaterals 12 (39%)* 21 (19%)* Multivessel disease 8 (26%) 35 (32%) Proximal LAD occlusion 18 (58%) 65 (59%) Reperfusion therapy 22 (71%) 87 (79%) PTCR 21 (68%) 85 (77%) PTCA 10 (32%) 53 (48%) Successful reperfusion 29 (94%) 95 (86%) Peak CPK (IU/L) 1,708 { 1,271† 2,735 { 1,865† Number of abnormal 3.4 { 2.0† Q waves 2.0 { 1.5† In-hospital death (%) 0 (0%) 10 (9%) *p õ0.05; †p õ0.01. CPK Å peak creatine kinase activity; ECG Å electrocardiographic; LAD Å left anterior descending artery; PTCA Å percutaneous transluminal coronary angioplasty; PTCR Å percutaneous transluminal coronary recanalization.
mortality tended to be lower in group A, although the difference was not statistically significant (0% vs 9%, p Å NS) (Table I). Left ventricular wall motion in the chronic phase:
Global left ventricular ejection fraction in the chronic phase was significantly greater in group A than in group B (63 { 12% vs 54 { 13%, p õ0.01). Regional wall motion in the anterobasal, anterolateral, and apical regions was reduced significantly less in group A (00.4 { 1.2 vs 01.3 { 1.0, p õ0.01; 01.0 { 1.7 vs 02.6 { 1.5, p õ0.01; 00.8 { 1.5 vs 02.0 { 1.3, p õ0.01, respectively) (Table II).
DISCUSSION To date, the clinical significance of negative U waves observed during anterior wall AMI has not APRIL 1, 1997
EL–AJC (v. 79, no. 7 ’97)
0883
patients with negative U waves is thought to be partly due to the presence of collateral circulation. Relation between negative U waves and site of occlusion of the left anterior descending artery: New negative U waves during ex-
ercise have been shown to be a useful marker for predicting proximal left anterior descending lesion.8,22 However, in our study, there were no differences in the incidence of proximal left anterior descending occlusion between the 2 groups. Although the exact mechanism for this discrepancy is unknown, the difference between ischemia and infarction may have affected the results. The association of negative U waves with proximal left anterior descending lesion needs to be reevaluated. Study limitations: Our study has certain limitations. First, our study was retroFIGURE 2. Number of leads showing ST elevation on the admission electrocarspective. Second, a precise mechanism diogram. of the origin of a U wave remains elusive, although several theories have been proposed.1 – 7 Therefore, further studies are desirable TABLE II Left Ventricular Function in the Chronic Phase to clarify the electrophysiologic genesis of a negGroup A* Group B* ative U wave and determine whether the theory Number of patients 31 100 supports our results. Global LVEF (%) RWM (SD/chord) anterobasal anterolateral apical
63 { 12
00.4 { 1.2 01.0 { 1.7 00.8 { 1.5
54 { 13
01.3 { 1.0 02.6 { 1.5 02.0 { 1.3
*p õ0.01. LVEF Å left ventricular ejection fraction; RWM Å regional wall motion.
been investigated. To our knowledge, this is the first published study reporting its significance. In the present study, the sum of leads showing ST elevation ¢1 mm on admission was significantly smaller in patients with than without negative U waves in the precordial leads during anterior wall AMI. Because the number of leads showing ST elevation during the acute phase of anterior infarction has been shown to be a good indicator for predicting the infarct-size,19 – 21 it is suggested that the amount of jeopardized myocardium before reperfusion therapy was smaller in patients with than without negative U waves. The amount of necrotic myocardium estimated by peak creatine kinase activity and the number of Q waves on the predischarge ECG was significantly smaller in patients with negative U waves. Furthermore, global and regional left ventricular wall motion in the anterobasal, anterolateral, and apical regions in the chronic phase was significantly better in patients with negative U waves. These results suggest that anterior wall AMI patients with negative U waves on the admission ECG have a relatively smaller mass of necrotic myocardium. In our study, the relatively small amount of necrotic myocardium in
1. Lepeschkin E. The U wave of the electrocardiogram. Mod Concepts Car-
diovasc Dis 1969;38:39–45. 2. Watanabe Y. Purkinje repolarization as a possible cause of the U wave in
the electrocardiogram. Circulation 1975;51:1030–1037. 3. Watanabe Y, Toda H. The U wave and aberrant intraventricular conduction: further evidence for the Purkinje repolarization theory on genesis of the U wave. Am J Cardiol 1978;41:23–31. 4. Kishida H, Cole JS, Surawicz B. Negative U wave: a highly specific but poorly understood sign of heart disease. Am J Cardiol 1982;49:2030–2036. 5. Nesterenko VV, Antzelevitch C. Simulation of the electrocardiographic U wave in heterogeneous myocardium: effect of the local junctional resistance. In: Proceedings of Computers in Cardiology. Los Alamitos, CA: IEEE Computer Society Press, 1992;43–46. 6. Antzelevitch C, Sicouri S. Clinical relevance of cardiac arrhythmias generated by afterdepolarizations: the role of M cells in the generation of U waves, triggered activity and torsade de pointes. J Am Coll Cardiol 1994;23:259–277. 7. Liu DW, Antzelevitch C. Characteristics of the delayed rectifier current (Ikr and Iks) in canine ventricular epicardial, midmyocardial, and endocardial myocytes. A weaker Iks contributes to the longer action potential of the M cell. Circ Res 1995;76:351–365. 8. Gerson MC, Phillips JF, Morris SN, McHenry PL. Exercise-induced U-wave inversion as a marker of stenosis of the left anterior descending coronary artery. Circulation 1979;60:1014–1020. 9. Salmasi AM, Salmasi SN, Nicolaides AN, Vecht RJ, Hendry WG, Kidner PH, Besterman EMM. The value of exercise-induced U wave inversion on ECG chest wall mapping in the identification of individual coronary arterial lesions. Eur Heart J 1985;6:437–443. 10. Hasegawa K, Fujiwara T, Sawayama T, Nezuo S, Nakao M, Tadaoka S, Nakamura T, Kakumae S, Kawahara Y, Inoue S. Angina-induced transient positive U wave in right precordial leads. A marker of left circumflex artery/right coronary artery stenosis [in Japanese]. Heart 1988;20:1033–1039. 11. Chikamori T, Yamada M, Takata J, Furuno T, Yamasaki F, Doi YL. Exercise-induced prominent U waves as a marker of significant narrowing of the left circumflex or right coronary artery. Am J Cardiol 1994;74:495–499. 12. Chikamori T, Takata J, Furuno T, Yabe T, Matsumura Y, Kitaoka H, Doi Y. Usefulness of U-wave analysis in detecting significant narrowing limited to a single coronary artery. Am J Cardiol 1995;75:508–511. 13. Miwa K, Murakami T, Kambara H, Kawai C. U wave inversion during attacks of variant angina. Br Heart J 1983;50:378–382. 14. Matsuguchi T, Koiwaya Y, Nakagaki O, Takeshita A, Nakamura M. Transient U wave inversion during variant angina. Am Heart J 1984;108:899–904. 15. Yano H, Hiasa Y, Aihara T, Nakaya Y, Mori H. Inverted U wave in ergonovine-induced vasospastic angina. Clin Cardiol 1987;10:633–639.
CORONARY ARTERY DISEASE/NEGATIVE U WAVES
/ 2w1e 0883 Mp
899
Wednesday Mar 05 04:57 PM
EL–AJC (v. 79, no. 7 ’97)
0883
899
16. The TIMI Study Group. The Thrombolysis in Myocardial Infarction (TIMI)
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