Summary. Introduction. Methods. Clin. Cardiol. 30, (2007)

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1 Clin. Cardiol. 30, (2007) Clinical Implications of Precordial ST-segment Elevation in Acute Inferoposterior Myocardial Infarction Caused by Proximal Right Coronary Artery Occlusion Man-Hong Jim, M.D., Annie On-On Chan, M.D., PH.D., Chun-Pong Wong, M.D., Kai-Hang Yiu, M.D., Raymond Miu, M.D., Stephen Wai-Luen Lee, M.D., Chu-Pak Lau, M.D. Cardiac Medical Unit, Grantham Hospital, Hong Kong; Department of Medicine, Queen Mary Hospital, Hong Kong Summary Background: The clinical significance of inferior wall acute myocardial infarction (MI) with combined STsegment elevation in both anterior and inferior leads, compared with inferior leads alone, is unknown. Hypothesis: Despite having more leads with precordial ST-segment elevation, these patients may have a better outcome due to less posterior involvement, which tends to drag down the precordial ST-segment. Methods: A total of 158 postinferior MI patients with documented proximal right coronary artery occlusion were retrospectively studied. They were divided into three subgroups according to the magnitude of concurrent ST-segment deviation in lead V2: Group A (n = 19) had ST-segment elevation 2.0 mm; Group B (n = 74) had ST-segment lay between +2.0 mm and 2.0 mm; and Group C (n = 65) had ST-segment depression 2.0 mm. The clinical and electrocardiographic characteristics were then compared among these threes subgroups. Results: The baseline demography, prevalence of risk factors, and treatment received were of no difference among the subgroups. However, Group A patients had significantly lower peak creatinine phosphokinase level and more preserved left ventricular function than Group B and C. Moreover, they had lower total sum of inferior Address for reprints: Man-Hong Jim, M.D. Grantham Hospital 125 Wong Chuk Hang Road Hong Kong jimmanh2002@yahoo.com Received: December 14, 2006 Accepted: January 20, 2007 Published online in Wiley InterScience ( DOI: /clc Wiley Periodicals, Inc. ST-segment magnitude, less ST-segment depression in V4-6, and more ST-segment elevation in V 4R than Group C. Group C patients had highest in-hospital and one-year mortality although it did not reach statistical significance. Conclusions: Precordial ST-segment elevation in inferior wall acute MI was associated with smaller infarct size and better left ventricular function, probably secondary to occlusion of a less dominant RCA, which did not result in a significant posterior infarction. Key words: electrocardiography, acute myocardial infarction Clin. Cardiol. 2007; 30: Wiley Periodicals, Inc. Introduction In acute myocardial infarction (MI) accompanied by combined ST-segment elevation in both anterior and inferior leads, the culprit vessel is either the left anterior descending (LAD) artery or the right coronary artery (RCA). The former scenario is usually caused by distal occlusion of a wrapped LAD 1 4 and associated with a good prognosis. 1 The latter has been reported to be associated with proximal RCA occlusion and right ventricular (RV) infarction The clinical characteristics and prognosis has yet been clearly defined. The purpose of this study was to examine the clinical implications of precordial leads ST-segment elevation in patients presented with acute inferoposterior MI caused by proximal RCA occlusion. Methods From January 1997 to November 2005, consecutive patients with documented proximal RCA occlusion by angiography, who presented with acute inferior MI to our Coronary Care Unit were retrospectively recruited. Acute

2 332 Clin. Cardiol. Vol. 30, July 2007 inferior MI was defined as typical chest pain of longer than 30 min; ST-segment elevation of 1.0 mmin two inferior leads (II, III, avf); and more than twofold increase in serum creatinine phosphokinase (CPK) levels. Patients were only included if they had first MI; symptom onset of less than 12 h; and coronary angiography performed within 6 weeks from symptom onset. Patients who had bundle branch block on electrocardiography, or more than 80% diameter stenosis in either LAD or left circumflex artery (LCx) were excluded. A total of 158 patients (114 men and 44 women, mean age of 65.8 ± 11.9 years) were analyzed. They were further divided into three subgroups according to the magnitude of concurrent ST-segment deviation in lead V2: STsegment elevation of 2.0 mm (Group A, n = 19); STsegment lay between +2.0 mm and 2.0 mm (Group B, n = 74); and ST-segment depression 2.0 mm (Group C, n = 65). The clinical and electrocardiographic features were then compared among the three subgroups. Electrocardiographic recordings A standard 12-lead and right precordial lead electrocardiograms were recorded at a speed of 25 mm/s and a voltage of 10 mm/mv at the time of admission. The electrocardiograms were magnified twofold by photocopiers and reviewed by two independent investigators who were unaware of the patients clinical and angiographic data. The ST-segment changes were measured at 40 ms from the J point using calipers. Measurements were made to the nearest 0.5 mm (0.05 mv). The preceding TP-segment was used as an isoelectric line. In cases of discrepancy, final decision was made by a third investigator. Coronary angiography Coronary angiography was performed within 6 weeks of the MI episode by experienced operators. The angiographic findings were evaluated by two independent investigators unaware of the patients clinical and electrocardiographic data. In cases of discrepancy, final decision was made by a third investigator. The infarct-related lesion was identified by either (i) total occlusion or a significant stenosis ( 70% diameter narrowing) of the LCx or RCA or their major branches, or (ii) angiographic evidence of an intraluminal thrombus. Proximal RCA was defined as the coronary segment that lay proximal to the first RV branch based on revised American College of Cardiology/American Heart Association guidelines. 11 Statistical analysis Mean value ± standard deviation was calculated for continuous variables; absolute and relative frequencies were measured for categorical variables. For continuous variables, statistical significance of differences between groups was analyzed by one-way ANOVA test. The Pearson chi-square test was used to compare differences between groups containing categorical variables. A p value of <0.05 was considered statistically significant. Results Clinical presentation The clinical characteristics, short- and long-term outcome of patients were summarized in Table 1. There was no significant difference concerning the distribution of age, sex, prevalence of cardiovascular risk factors, and time from symptom onset to hospital among the three subgroups. However, Group A patients had significantly higher left ventricular ejection fraction (LVEF) and lower CPK level than the other two subgroups. Moreover, both parameters showed a gradation of change on moving from Group A to C. The adopted treatment strategies included thrombolytic therapy, primary angioplasty, and conservative treatment followed by elective angioplasty; they demonstrated no significant difference among the three subgroups. Even after combining thrombolytic therapy and primary angioplasty into one revascularization group, the difference was still not significant. Both in-hospital death and oneyear mortality were highest for Group C, although it did not reach statistical significance. By multivariate analysis, the LVEF was the only independent risk factor for 1-year mortality. Electrocardiographic features The electrocardiographic characteristics of the three subgroups were listed in Table 2. Group A consistently had more patients with ST-segment elevations in each of the chest leads. The proportion of patients with STsegment elevation in V 4R was also the highest among the subgroups. In contrast, Group C patients had more ST-segment depression in lead V1-V6. Indeed, the frequency of STsegment depression in each precordial lead showed a gradation of change on moving across the subgroups. Moreover, the total sum of magnitude of ST-segment elevation was highest in Group C. Discussion In electrocardiography, the conventional anterior or inferior leads refer only to their positive directions. Indeed, the net amount ST-segment deviation is the sum of the positive and negative vector of injury of two opposite territories. In other words, these leads provide information regarding two opposite rather than only one myocardial region. The concept is best illustrated by studying patients of anterior wall acute MI with

3 M.-H. Jim et al.: Precordial ST elevation in inferior MI 333 TABLE 1 Comparison of clinical characteristics among the three subgroups Group A (V2 +2) n = 19 Group B (+2 > V2 > 2) n = 74 Group C (V2 2) n = 65 p value Age (years) 67.6 ± ± ± Male sex (%) 14 (73.7) 58 (78.4) 42 (64.6) 0.19 Smoking habit (%) 7 (36.8) 40 (54.1) 36 (55.4) 0.34 Diabetes mellitus (%) 7 (36.8) 23 (31.1) 21 (32.3) 0.89 Hypertension (%) 9 (47.4) 31 (41.9) 28 (43.1) 0.91 Hyperlipidemia (%) 6 (31.6) 37 (50.0) 26 (40.0) 0.23 Time from symptom 2.9 ± ± ± onset to hospital (h) LVEF (%) 51.5 ± ± ± * CPK (U/L) 1817 ± ± ± 2215 <0.0001* Treatment Thrombolysis (%) 15 (78.9) 44 (59.5) 39 (60.0) 0.26 Primary angioplasty (%) 2 (10.5) 10 (13.5) 9 (13.8) 0.9 Revascularization (%) 17 (89.5) 54 (73.0) 47 (72.3) Conservative (%) 1 (5.3) 15 (20.3) 16 (24.6) 0.12 In-hospital death (%) 3 (15.8) 6 (8.2) 12 (18.5) 0.18 One-year mortality (%) 3 (15.8) 7 (9.5) 16 (24.6) Denotes p value <0.05; Abbreviations: LVEF= left ventricular ejection fraction; CPK = creatinine phosphokinase. concomitant ST-segment elevation in inferior leads. 1 4 In these studies, the characteristic electrocardiographic change was only found in one coexisting condition. The LAD must be a wrapped LAD, which caused inferoapical ischemia and inferior ST-segment elevation; and the occlusion must be distal, otherwise it would cause anterolateral ischemia, which tended to depress the inferior leads. Conversely, the clinical significance of concomitant precordial ST-segment elevation in inferior wall acute MI is comparatively less well defined. Precordial STsegment elevation was first reported in isolated RV infarction. 5 9 In one animal model, the precordial leads were even more sensitive in picking up RV infarction than lead V 4R. 10 Multiple mechanisms are postulated to explain the clinical condition. For instance, RV infarction causes acute dilatation of RV, which is then directed TABLE 2 Comparison of electrocardiographic features among the three subgroups Group A (V2 +2) n = 19 Group B (+2 > V2 > 2) n = 74 Group C (V2 2) n = 65 p value ST elevation 1.0 mm I (%) 1 (5.3) 0 (0) 0 (0) V1 (%) 13 (68.4) 7 (9.5) 7 (10.8) <0.0001* V3 (%) 18 (94.7) 2 (2.7) 3 (4.6) <0.0001* V4 (%) 8 (42.1) 2 (2.7) 5 (7.7) <0.0001* V5 (%) 6 (31.6) 5 (6.8) 12 (18.5) 0.012* V6 (%) 5 (26.3) 5 (6.8) 15 (23.1) 0.013* V 4R (%) 19 (100) 59 (79.7) 60 (92.3) 0.006* ST depression 1.0 mm I (%) 14 (73.7) 58 (78.4) 61 (93.8) 0.012* V1 (%) 0 (0) 9 (12.2) 24 (36.9) <0.0001* V3 (%) 0 (0) 28 (37.8) 51 (78.5) <0.0001* V4 (%) 1 (5.3) 27 (36.5) 46 (70.8) <0.0001* V5 (%) 2 (10.5) 22 (29.7) 34 (52.3) 0.001* V6 (%) 2 (10.5) 22 (29.7) 26 (40.0) 0.032* Sum of ST magnitude in inferior leads (mm) 7.6 ± ± ± 4.9 <0.0001* *Denotes p value <0.05.

4 334 Clin. Cardiol. Vol. 30, July 2007 anteriorly; or the RV branch may be large and long enough to supply the RV outflow tract, of which ischemia can be detected by the adjacent precordial leads. No matter which one is true, precordial ST-segment elevation is typically present in proximal RCA occlusion, although distal RCA occlusion is also found in a small number of cases. 1 In the present study, we standardized our subjects by limiting the analysis only to those with proximal RCA occlusion so that all the subsequent clinical findings and their difference between subgroups were solely due to the dominance and size of the posterolateral branch the artery supplied. The number of leads with ST-segment elevation and the sum of ST-segment deviation in the initial electrocardiogram during acute MI correlate well with infarct size and prognosis. 12,13 In this study, Group A patients had more number of leads showing ST-segment elevation in leads V1-6. Paradoxically, they had significantly a smaller total ST-segment sum in inferior leads, lower peak CPK level, better LV function than Group C. Indeed, the peak CPK level and LVEF showed a nice gradation of change (best in Group A, worst in Group C, and intermediate in Group B). Thus, patients with precordial ST-segment elevation actually had smaller infarct size and more preserved LV function despite having more leads with ST-segment elevation. These seemingly contradictory findings are consistent with prior studies involving patients of anterior wall acute MI with inferior ST-segment elevation. 1 We could not demonstrate any significant survival advantage, although the in-hospital and 1-year mortality were both highest in Group C. This is probably due to small patient number. In inferior wall acute MI, the presence of ST-segment depression in V1-3 or V4-6 or both are associated with poor clinical outcomes Many studies, by using echocardiographic, scintigraphic or angiographic means, have already shown that the accompanying posterolateral branch ischemia in a dominant RCA depresses the precordial leads and results in larger myocardial loss This is equivalent to our Group C patients who had larger infarct size and LV dysfunction. We postulate that Group A patients probably either had nondominant RCA or with a relatively small posterolateral branch so that ischemia of the latter was not severe enough to drag down the STsegment. Another interesting observation is that Group B and C patients had significantly less ST-segment elevation in V 4R. Kosuge et al. 18 found that the absence of ST-segment elevation in V 4R in the presence of clinical evidence of RV infarction was caused by dominant proximal RCA occlusion, leading to concomitant posterior infarction which cancelled out the anterior injury vector. Thus, patients present with inferior wall acute MI and precordial ST-segment elevation are likely to have occlusion of a less dominant RCA. The absence of posterolateral injury is a prerequisite for the manifestation of precordial ST-segment elevation and associated with better prognosis, as supported by smaller infarct size and more preserved LV function in this study. Limitations This study had several limitations. First, the study population was too small for demonstration of survival advantage. Second, most of the coronary angiography was performed as elective procedures, the site of occlusion might not be identical to the one in acute setting. However, Sadanandan, et al. was able to demonstrate in his article that the acute TIMI 2 and 3 flow (after thrombolytics) were similar in all his patient groups. 1 Moreover, no data of angiographic assessment of the dominance and size or extent of the posterolateral branch supplying the posterior myocardium was available. Third, the regional wall dysfunction was not assessed in this study. The echocardiographic assessment of overall LVEF is a crude assessment of LV function, which is affected by the presence of multivessel disease. We could not completely eliminate its effect as we only excluded those patients with 80% diameter stenosis in LAD and LCx. FIG. 1 A conventional 12-lead electrocardiogram showing combined ST-segment elevation in precordial and inferior leads.

5 M.-H. Jim et al.: Precordial ST elevation in inferior MI 335 Conclusion In inferior wall acute MI caused by proximal RCA occlusion, the presence of concomitant precordial STsegment elevation is paradoxically associated with smaller infarct size and more preserved left ventricular function compared with precordial ST-segment depression as in Figure 1. This phenomenon is probably explained by the absence of posterior infarction, which tends to depress the precordial ST-segment in occlusion of a relatively less dominant RCA. References 1. Sadanandan S, Hochman JS, Kolodziej A, Criger DA, Ross A, et al.: Clinical and angiographic characteristics of patients with combined anterior and inferior ST-segment elevation on the initial electrocardiogram during acute myocardial infarction. Am Heart J 2003;146: Sasaki K, Yotsukura M, Sakata K, Yoshino H, Ishikawa K: Relation of ST-segment changes in inferior leads during anterior wall acute myocardial infarction to length and occlusion site of the left anterior descending coronary artery. Am J Cardiol 2001;87: Yip HK, Chen MC, Wu CJ, Chang HW, Yu TH, et al.: Acute myocardial infarction with simultaneous ST-segment elevation in the precordial and inferior leads. Evaluation of anatomic lesions and clinical implications. Chest 2003;123: Sapin PM, Musselman DR, Dehmer GJ, Cascio WE: Implications of inferior ST-segment elevation accompanying anterior wall acute myocardial infarction for the angiographic morphology of the left anterior descending coronary artery morphology and site of occlusion. Am J Cardiol 1992;69: Khan ZU, Chou TC: Right ventricular infarction mimicking acute anteroseptal left ventricular infarction. Am Heart J 1996;132: Geft IL, Shah PK, Rodriguez L, Hulse S, Maddahi J, et al.: ST elevations in leads V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 1984;53: Porter A, Herz I, Strasberg B: Isolated right ventricular infarction presenting as anterior wall myocardial infarction on electrocardiography. Clin Cardiol 1997;20: Celiik T, Yuksel UC, Kursaklioglu H, Iyisoy A, Kose S, et al.: Precordial ST-segment elevation in acute occlusion of the proximal right coronary artery. J Electrocardiol 2006;39: Carroll R, Sharma N, Butt A, Hussain KM: Unusual electrocardiographic presentation of an isolated right ventricular myocardial infarction secondary to thrombotic occlusion of a non-dominant right coronary artery a case report and brief review of literature. Angiology 2003;54: Fantidis P, Coma-Canella I, Peinado MJ, Padron A, Lopez-Sendon JL: A new experimental model of isolated myocardial ischemic injury. ECG findings of acute isolated right ventricular ischemic injury. J Electrocardiol 1997;30: Scanlon PJ, Faxon DP, Audet AM, Carabello B, Dehmer GJ, et al.: ACC / AHA guidelines for coronary angiography. A report of the American College of Cardiology / American Heart Association Task Force on practice guidelines (Committee on Coronary Angiography). Developed in collaboration with the Society for Cardiac Angiography and Interventions. J Am Coll Cardiol 1999;33(6): Aldrich HR, Wagner NB, Boswick J, Corsa AT, Jones MG, et al.: Use of initial ST-segment deviation for prediction of final electrocardiographic size of acute myocardial infarcts. Am J Cardiol 1988;61: Hathaway WR, Peterson ED, Wagner GS, Granger CB, Zabel KM, et al.: Prognostic significance of the initial electrocardiogram in patients with acute myocardial infarction. JAMA 1998; 279: Peterson ED, Hathaway WR, Zabel KM, Pieper KS, Granger CB, et al.: Prognostic significance of precordial ST segment depression during inferior myocardial infarction in the thrombolytic era: results in 16,521 patients. J Am Coll Cardiol 1996;28: Gibson RS, Crampton RS, Watson DD, Taylor GJ, Carabello BA, et al.: Precordial ST-segment depression during acute inferior myocardial infarction: clinical, scintigraphic and angiographic correlations. Circulation 1982;66: Lew AS, Weiss AT, Shah PK, Maddahi J, Peter T, et al.: Precordial ST segment depression during acute inferior myocardial infarction: early thallium-201 scintigraphic evidence of adjacent posterolateral or inferoapical involvement. J Am Coll Cardiol 1985;5: Nishian K, Nomoto Y, Naruse H, Kawakami K, Asakuma S, et al.: Precordial ST segment depression in acute inferior myocardial infarction: the importance of posterolateral wall infarction. J Cardiol 1989;19: Kosuge M, Kimura K, Ishikawa T, Hongo Y, Shigemasa T, et al.: Implications of the absence of ST-segment elevation in lead V4R in patients who have inferior wall acute myocardial infarction with right ventricular involvement. Clin Cardiol 2001;24: