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ST-Segment Depression in Lead aVR
ST-Segment Depression in Lead aVR* A Useful Predictor of Impaired Myocardial Reperfusion in Patients With Inferior Acute Myocardial Infarction Masami Kosuge, MD; Kazuo Kimura, MD; Toshiyuki Ishikawa, MD; Toshiaki Ebina, MD; Kiyoshi Hibi, MD; Noritaka Toda, MD; and Satoshi Umemura, MD
Study objective: During inferior acute myocardial infarction (AMI), the ECG lead aVR is frequently ignored, and therefore its clinical significance remains unclear. We examined the relation between ST-segment deviation seen in lead aVR on ECGs obtained at hospital admission and myocardial reperfusion in patients who have experienced recanalized inferior AMIs. Design and setting: Retrospective study. Patients: A total of 225 patients with inferior AMIs in whom Thrombolysis in Myocardial Infarction grade 3 flow was achieved within 6 h after symptom onset. Measurements and results: Patients were classified as follows according to ST-segment deviation in lead aVR on an ECG obtained at hospital admission: group A, 103 patients with no ST-segment depression; group B, 80 patients with ST-segment depression of < 1.0 mm; and group C, 42 patients with ST-segment depression of > 1.0 mm. There were no differences in time from symptom onset to hospital admission or in the culprit lesion among the three groups. The degree of ST-segment elevation in leads II, III, aVF, V5, or V6, the degree of ST-segment depression in leads V1 to V4, and the sum of ST-segment deviation in these leads were lowest in group A and highest in group C. In groups A, B, and C, the incidence of impaired myocardial reperfusion, defined as myocardial blush grade 0/1, was 2%, 23%, and 67%, respectively (p < 0.001). The sensitivity and negative predictive values of ST-segment depression in lead aVR for impaired myocardial reperfusion were higher than those based on other ECG variables. Multivariate analysis showed that the degree of ST-segment depression in lead aVR was an independent predictor of impaired myocardial reperfusion (odds ratio 8.41; 95% confidence interval, 2.96 to 23.9; p < 0.001). Conclusions: We conclude that the degree of ST-segment depression in lead aVR is a useful predictor of impaired myocardial reperfusion in patients who have experienced inferior AMIs. (CHEST 2005; 128:780 –786) Key words: ECG; myocardial infarction; ST segment Abbreviations: AMI ⫽ acute myocardial infarction; LCX ⫽ left coronary circumflex artery; RCA ⫽ right coronary artery; TIMI ⫽ Thrombolysis in Myocardial Infarction
inferior acute myocardial infarction D uring (AMI), ECG lead aVR is frequently ignored, but some investigators have suggested that this lead can provide ECG information that is useful for the characterization of inferior AMI, which is more often *From the Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan. Manuscript received December 11, 2004; revision accepted February 8, 2005. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml). Correspondence to: Kazuo Kimura, MD, The Division of Cardiology, Yokohama City University Medical Center, 4 –57 Urafunecho, Minami-ku, Yokohama 232-0024, Japan; e-mail: c-kimura@ urahp.yokohama-cu.ac.jp 780
caused by the right coronary artery (RCA) occlusion than by the left coronary circumflex artery (LCX) occlusion. Menown and Adgey1 reported that the display of lead aVR in an inverted format as lead ⫺aVR improves the ECG classification of inferior or lateral AMI. Nair and Glancy2 reported that STsegment depression in lead aVR is useful for identifying the RCA or the LCX as the culprit artery in patients with inferior AMIs. However, the clinical significance of ST-segment depression in lead aVR remains unclear in patients with recanalized inferior AMIs. In the reperfusion era, the evaluation of myocardial reperfusion using myocardial blush grading has been reported to be useful in stratifying the prognosis of patients with recanalized AMI. 3–5 Clinical Investigations
Therefore, we examined the relation between the degree of ST-segment depression found in ECG lead aVR and myocardial reperfusion in patients with inferior AMIs. Materials and Methods Study Group We enrolled 225 consecutive patients with inferior AMI (mean [⫾ SD] age, 63 ⫾ 11 years; 172 men and 53 women) who fulfilled the following criteria for study inclusion: (1) no history of myocardial infarction or of other types of heart disease except for coronary artery disease; (2) absence of conditions precluding the evaluation of ST-segment changes on the ECG (eg, left bundle branch block, right bundle branch block, and ventricular pacing); (3) achievement of successful recanalization (Thrombolysis in Myocardial Infarction [TIMI]6 grade 3) of the RCA or the LCX as confirmed by coronary angiography within 6 h from symptom onset; and (4) adequate assessment of myocardial blush grade5 after recanalization. Patients with cardiogenic shock and those with reocclusion of the infarct-related artery during hospitalization were excluded from the study. The diagnosis of inferior AMI was based on typical chest pain lasting ⱖ 30 min, ST-segment elevation of ⱖ 1 mm in two or more inferior leads (ie, II, III, or aVF), and a typical increase in the serum creatine kinase level to more than twice the upper limit of normal. Coronary Angiography Coronary angiography was performed with informed consent immediately after hospital admission. The angiograms were evaluated by two observers who were blinded to all other data. Anterograde flow in the infarct-related artery was evaluated on a scale of 0 to 3 according to the standard TIMI flow grade, and recanalization was defined as the establishment of TIMI grade 3 flow. Collateral flow to the infarct zone was graded on a scale of 0 to 3 as described by Rentrop et al.7 A good collateral channel was defined as grade 2 or 3 flow, and a poor collateral channel as grade 0 or 1 flow. The allocation of recanalization therapy was left to the discretion of the doctor. On angiograms obtained immediately after recanalization, the extent of perfusion territory of the infarct-related artery was quantified according to the angiographic distribution score proposed by Wong et al8 All left ventricular branches of the RCA and the LCX were scored as follows: branches with a length equivalent to ⬎ 80% of that of the largest posterior descending artery were scored as 2; branches with a length between 50% and 80% of the artery were scored as 1; and small branches with a length of ⬍ 50% of the artery were scored as 0. The angiographic distribution score was defined as the ratio of the summed score of the infarct-related artery (ie, the RCA or the LCX) to the total summed score of the RCA and the LCX. In addition, myocardial blush was graded as follows: 0, no myocardial blush or contrast density; 1, minimal myocardial blush or contrast density; 2, moderate myocardial blush or contrast density, but less than that obtained during angiography of a contralateral or ipsilateral non-infarct-related coronary artery; and 3, normal myocardial blush or contrast density, comparable to that obtained during angiography of a contralateral or ipsilateral non-infarct-related coronary artery.5 When myocardial blush persisted, this finding was graded as 0. ECG Analysis A 12-lead ECG was recorded on hospital admission at a paper speed of 25 mm/s and an amplification of 10 mm/mV. The www.chestjournal.org
isoelectric line was defined as the level of the preceding TP segment. ST-segment deviation was measured manually to the nearest 0.5 mm, 20 ms after the end of the QRS complex by two independent observers who were blinded to all clinical and angiographic findings. The degree of ST-segment elevation in leads II, III, aVF, V5, or V6 and the degree of ST-segment depression in leads V1 to V4 were calculated. The right ventricular leads (ie, V3R and V4R) were recorded in 200 patients (89%) on hospital admission. ST-segment elevation of ⱖ 1.0 mm in the right ventricular lead was defined as being clinically significant.9 Cardiac Enzyme Study Blood samples were obtained on hospital admission, and at 3-h intervals during the first 24 h, at 6-h intervals for the next 2 days, and then daily until hospital discharge. Statistical Analysis The data are expressed as the mean ⫾ SD for continuous variables and as percentages for categoric variables. We made comparisons by one-way analysis of variance for continuous variables, and the statistical significance of differences was calculated by using the Scheffe´ F test. 2 analysis or Fisher exact test was used to compare categoric variables. The cutoff point of ECG variables for predicting impaired myocardial reperfusion, defined as myocardial blush grade 0 or 1, was obtained using their receiver-operating characteristic curve. Multiple logistic regression analysis was used to examine the determinants of impaired myocardial reperfusion. The variables used for analysis included age, sex, absence of previous angina within 24 h before AMI, Killip class on hospital admission, TIMI flow grade 0 at initial coronary angiography, multivessel disease, percutaneous coronary intervention, the infarct-related artery, good collateral channel, time from symptom onset to hospital admission, and the degree of ST-segment depression in lead aVR. Odds ratios and 95% confidence intervals were calculated. A two-tailed p value of ⬍ 0.05 was considered to indicate statistical significance. Analyses were performed with the use of a statistical software package (SPSS for Windows; SPSS; Chicago, IL).
Results Patient Characteristics Patients were divided into the following three groups according to ST-segment deviation in lead aVR on the ECG obtained at hospital admission: group A, 103 patients with no ST-segment depression; group B, 80 patients with ST-segment depression of ⱕ 1.0 mm; and group C, 42 patients with ST-segment depression of ⬎ 1.0 mm (Fig 1). The baseline characteristics of the three groups are summarized in Table 1. There were no differences among the three groups in age, hemodynamics or Killip class on hospital admission, percutaneous coronary intervention, time from symptom onset to hospital admission, coronary risk factors, or medication received before the occurrence of AMI. Group A patients were less likely to be men. Previous angina within 24 h before occurrence of the AMI was slightly but not significantly less frequent in group C. CHEST / 128 / 2 / AUGUST, 2005
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Figure 1. Representative ECGs of the three groups. Left, A: group A, no ST-segment depression in lead aVR (culprit lesion, segment 1; peak creatine kinase level, 1,478 mU/mL; myocardial blush grade 3). Left middle, B: group B, ST-segment depression of ⱕ 1.0 mm in lead aVR (culprit lesion, segment 3; peak creatine kinase level, 2,540 mU/mL; myocardial blush grade 2). Right middle, C: group C, ST-segment depression of ⬎ 1.0 mm in lead aVR (culprit lesion, segment 2 [dominant RCA]; peak creatine kinase level, 5,570 mU/mL; myocardial blush grade 0/1). Right, D: group C, ST-segment depression of ⬎ 1.0 mm in lead aVR (culprit lesion, segment 11; peak creatine kinase level, 7,784 mU/mL; myocardial blush grade 0/1).
The angiographic findings are shown in Table 2. There were no differences among the three groups in the incidence of multivessel disease, concomitant left anterior descending coronary artery disease, infarct-related artery, proximal lesion of the infarctrelated artery, or TIMI flow grade 0 at initial coronary angiography. A good collateral channel was less frequent in group C. The angiographic distribution score was lowest in group A and highest in group C.
more frequent in group C. The variables for predicting impaired myocardial reperfusion, defined as myocardial blush grade 0 or 1, on the basis of ST-segment deviation were calculated; the sensitivity, specificity, and positive and negative predictive values obtained with these variables were shown in Table 4. The sensitivity of the degree of ST-segment depression in lead aVR of ⱖ 1.0 mm for predicting impaired myocardial reperfusion was 92%, which was significantly higher than that based on other ECG variables.
ECG Findings
Infarct Size and Myocardial Reperfusion
The ECG findings on hospital admission are shown in Table 3. The degree of ST-segment elevation in leads II, III, aVF, V5, or V6, and the degree of ST-segment depression in leads V1 to V4 and the sum of ST-segment deviation in these leads were lowest in group A and the highest in group C. The number of leads with ST-segment elevation was lowest in group A and highest in group C. The prevalence of ST-segment elevation in the right ventricular leads was slightly but not significantly
Peak creatine kinase level was lowest in group A and highest in group C. Congestive heart failure during hospitalization was more frequent in group C. Impaired myocardial reperfusion, as defined by a myocardial blush grade of 0 or 1, was observed in 67% of group C patients, compared with only 2% of group A patients (Fig 2). On multivariate analysis, the degree of ST-segment depression in lead aVR was a powerful predictor of impaired myocardial reperfusion (Table 5).
Angiographic Findings
782
Clinical Investigations
Table 1—Baseline Clinical Characteristics* Characteristics Age, yr Men Heart rate on hospital admission, beats/min Systolic BP on hospital admission, mm Hg Killip class on hospital admission ⬎ 1 Previous angina within 24 h before AMI Percutaneous coronary intervention Time from symptom onset to hospital admission, h Medication before AMI Calcium antagonist Beta-blocker ACE inhibitor Diabetes mellitus Hypercholesterolemia Systemic hypertension Smoker Peak creatine kinase level, mU/mL Congestive heart failure during hospitalization
Group A (n ⫽ 103)
Group B (n ⫽ 80)
Group C (n ⫽ 42)
p Value
63 ⫾ 11 71 (69) 66 ⫾ 20 127 ⫾ 33 4 (4) 36 (35) 54 (52) 2.3 ⫾ 1.2
62 ⫾ 11 67 (84) 67 ⫾ 16 128 ⫾ 33 5 (6) 23 (29) 35 (44) 2.5 ⫾ 1.5
62 ⫾ 12 34 (81) 74 ⫾ 24 124 ⫾ 36 4 (10) 8 (19) 26 (62) 2.5 ⫾ 1.3
0.704 0.048 0.106 0.866 0.408 0.159 0.152 0.559
22 (21) 4 (4) 7 (7) 23 (22) 23 (23) 50 (49) 65 (63) 2,186 ⫾ 1,572 2 (2)
12 (15) 5 (6) 9 (11) 23 (29) 23 (29) 41 (51) 48 (60) 3,079 ⫾ 1,574 4 (5)
10 (24) 5 (12) 2 (5) 10 (24) 11 (26) 27 (64) 32 (76) 4,865 ⫾ 1,757 8 (19)
0.417 0.211 0.377 0.599 0.601 0.219 0.192 ⬍ 0.001 ⬍ 0.001
*Values given as the mean ⫾ SD or No. of patients (%), unless otherwise indicated. ACE ⫽ angiotensin-converting enzyme.
Discussion Several studies have suggested that even after successful recanalization of the infarct-related coronary artery, some patients do not have complete myocardial reperfusion and remain at risk for large infarcts and more frequent mortality.3–5 Therefore, the early and simple identification of such high-risk patients is required. Our study demonstrated that in patients with inferior AMIs, larger ST-segment depression in lead aVR was associated with impaired myocardial reperfusion. Two studies1,2 have investigated the clinical implications of ST-segment depression in lead aVR during an inferior AMI. Menown and Adgey1 reported that
ST-segment depression in lead aVR was associated with a large infarct size. However, their study lacked angiographic data and did not confirm the presence or absence of recanalization of the infarct-related artery. Although Nair and Glancy2 reported that ST-segment depression in lead aVR was more common in LCX-related inferior AMIs than in RCArelated inferior AMIs, their study included only five patients with LCX-related inferior AMIs. Thus, the relations of ST-segment depression in lead aVR during inferior AMI to angiographic findings and infarct size have not been clearly defined. To clarify the clinical implications of ST-segment depression in lead aVR during inferior AMI, we included only
Table 2—Angiographic Findings* Variables Multivessel disease Concomitant LAD disease Infarct-related artery RCA LCX Culprit lesion Proximal RCA (segment 1) Proximal LCX (segment 11) TIMI flow grade 0 at initial CAG Collateral grade ⬎ 2† Angiographic distribution score
Group A (n ⫽ 103)
Group B (n ⫽ 80)
Group C (n ⫽ 42)
26 (25) 18 (18)
17 (21) 13 (16)
10 (24) 7 (17)
83 (81) 20 (19)
59 (74) 21 (26)
34 (81) 8 (19)
39 (38) 5 (6) 84 (82) 30 (29) 0.5 ⫾ 0.2
37 (46) 8 (10) 66 (83) 19 (24) 0.6 ⫾ 0.1
21 (50) 5 (12) 37 (88) 4 (10) 0.7 ⫾ 0.1
p Value 0.819 0.975 0.482
0.318 0.261 0.624 0.041 ⬍ 0.001
*Values given as the mean ⫾ SD or No. of patients (%), unless otherwise indicated. LAD ⫽ left anterior descending artery; CAG ⫽ coronary angiography. †Rentrop classification. www.chestjournal.org
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Table 3—ECG Findings* ECG Variables
Group A (n ⫽ 103)
Group B (n ⫽ 80)
Group C (n ⫽ 42)
p Value
ST1in lead II, mm ST1in lead III, mm ST1in lead aVF, mm Maximal ST1in lead II, III or aVF, mm ⌺ST1in leads II,III and aVF, mm ST1in lead V5, mm ST1in lead V6, mm ⌺ST1in leads V5 and V6, mm ⌺ST1in leads II,III, aVF, V5 and V6, mm Number of leads with ST1 ST2in lead V1, mm ST2in lead V2, mm ST2in lead V3, mm ST2in lead V4, mm ⌺ST2in lead V1 to V4, mm ST1in lead V3R of ⬎ 1.0 mm† ST1in lead V4R of ⬎ 1.0 mm†
1.4 ⫾ 0.9 2.2 ⫾ 1.3 1.7 ⫾ 1.2 2.2 ⫾ 1.3 5.2 ⫾ 3.2 0.0 ⫾ 0.2 0.1 ⫾ 0.5 0.2 ⫾ 0.6 5.4 ⫾ 3.3 3.2 ⫾ 0.5 0.3 ⫾ 0.7 1.0 ⫾ 1.2 1.5 ⫾ 1.6 1.6 ⫾ 1.6 4.3 ⫾ 4.5 20 (22) 23 (26)
2.5 ⫾ 1.2 3.1 ⫾ 1.8 2.8 ⫾ 1.5 3.3 ⫾ 1.7 8.4 ⫾ 4.5 0.3 ⫾ 0.7 0.5 ⫾ 0.9 0.9 ⫾ 1.4 9.2 ⫾ 4.6 3.6 ⫾ 0.8 0.8 ⫾ 1.0 1.8 ⫾ 1.9 2.2 ⫾ 2.3 1.9 ⫾ 1.9 6.7 ⫾ 6.3 19 (26) 26 (36)
4.5 ⫾ 1.8 5.5 ⫾ 2.2 4.8 ⫾ 1.9 5.6 ⫾ 2.2 14.7 ⫾ 5.8 1.0 ⫾ 1.5 1.7 ⫾ 1.9 2.7 ⫾ 3.4 17.3 ⫾ 7.2 4.1 ⫾ 0.9 1.7 ⫾ 2.4 4.1 ⫾ 4.0 3.7 ⫾ 3.9 2.4 ⫾ 2.3 12.1 ⫾ 11.3 14 (38) 16 (43)
⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 0.002 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 0.054 ⬍ 0.001 0.192 0.120
*Values given as the mean ⫾ SD or No. of patients (%), unless otherwise indicated. ST1 ⫽ the degree of ST-segment elevation; ST2 ⫽ the degree of ST-segment depression; ⌺ST1 ⫽ the sum of ST-segment elevation; ⌺ST2 ⫽ the sum of ST-segment depression. †Available data (n ⫽ 200).
patients who had experienced a first inferior AMI with inferior ST-segment elevation in whom TIMI grade 3 flow of the RCA or LCX was achieved within 6 h from symptom onset. In this setting, ST-segment depression in lead aVR was associated with a larger infarct size and impaired myocardial reperfusion. In our study, the infarct-related artery (ie, the RCA or the LCX) and the location of the culprit lesion did not differ significantly among the three groups, but greater ST-segment depression in lead aVR was related to a larger perfusion territory of the infarct-
related artery, as assessed by the angiographic distribution score (ie, a larger ischemic area). Menown and Adgey1 reported that the display of lead aVR (⫺150°) in inverted format as lead ⫺aVR (⫹30°) bridges the gap between lead I (0°) and lead II (60°). In other words, ST-segment depression in lead aVR might be a reciprocal change resulting from STsegment elevation in the apical and inferolateral walls, which none of the standard 12 leads directly faces. Such regions of the left ventricle are usually supplied by the large posterolateral branch of the
Table 4 —Sensitivity, Specificity, Positive Predictive Value, and Negative Predictive Value of ECG Variables for Predicting Impaired Myocardial Reperfusion* ECG Variables
Sensitivity, %
Specificity, %
PPV
NPV
ST2in lead aVR ⬎ 1.0 mm ST1in lead II ⬎ 2.0 mm ST1in lead III ⬎ 3.0 mm ST1in lead aVF ⬎ 2.5 mm Maximal ST1in lead II, III, or aVF ⬎ 3.0 mm ST2in lead V1 ⬎ 1.0 mm ST2in lead V2 ⬎ 2.0 mm ST2in lead V3 ⬎ 2.5 mm ST2in lead V4 ⬎ 2.5 mm ST1in lead V5 ⬎ 0.5 mm ST1in lead V6 ⬎ 0.5 mm ⌺ST2in leads V1 to V4 ⬎ 8.0 mm ⌺ST1in leads II, III, and aVF ⬎ 8.0 mm ⌺ST1in leads V5 and V6 ⬎ 1.0 mm ⌺ST1in leads II, III, aVF, V5, and V6 ⬎ 8.5 mm
92 73† 71‡ 77† 75† 56‡ 69‡ 60‡ 44‡ 42‡ 69‡ 56‡ 77† 69‡ 75‡
67 66 72 71 71 66 66 75 75 88‡ 81† 80† 67 84† 67
43 37 41 42 37 31 33 39 31 48 50 43 38 54 42
97 90† 90† 92 91† 85‡ 89† 87‡ 83‡ 85‡ 91† 87‡ 92 91† 84‡
*PPV ⫽ positive predictive value; NPV ⫽ negative predictive value. See Table 3 for other abbreviations not used in the text. †p ⬍ 0.05 vs lead aVR. ‡p ⬍ 0.01 vs lead aVR. 784
Clinical Investigations
Figure 2. Incidence of impaired myocardial reperfusion, as indicated by myocardial blush grade 0 or 1 in the three groups.
LCX or the atrioventricular branch of the RCA. Therefore, concurrent ST-segment depression in lead aVR during inferior AMI might reflect transmural ischemia extending to the apical and inferolateral walls in addition to the inferior wall. Anterior ST-segment depression and inferior STsegment elevation have been shown to be useful for predicting evolving infarct size.10 –13 In the present study, we measured the degree of ST-segment depression in leads V1 to V4, the degree of ST-segment elevation in leads II, III, aVF, V5, or V6, and the sum of ST-segment deviation in these leads. The sensi-
tivity and negative predictive value of ST-segment depression in lead aVR for impaired myocardial reperfusion were higher than those based on other ECG variables. Multivariate analysis showed that ST-segment depression in lead aVR related to impaired myocardial reperfusion. These findings suggested that ST-segment depression in lead aVR might more closely reflect the severity and extent of myocardial injury during an inferior AMI than other ECG markers. Two studies14,15 have reported that differences in the territories perfused by the RCA and LCX may influence the direction and degree of inferior ST-segment elevation. In addition, it has been reported that patients with inferior AMI and concomitant right ventricular ischemia had smaller precordial ST-segment depression than those without concomitant right ventricular ischemia.15,16 On the basis of these observations, we can assume that ST-segment elevation in inferior leads or ST-segment depression in precordial leads might not consistently reflect the severity and extent of myocardial injury during inferior AMI. Iwakura et al17 reported that both larger ischemic area and more severe myocardial damage before recanalization are closely related to the development of the no-reflow phenomenon. In patients with ST-segment depression in lead aVR, microvascular injury might be caused by severe myocardial damage in the extensive area that is at risk. Clinical Implications
Table 5—Multivariate Analysis of Factors Associated With Impaired Myocardial Reperfusion* Variables
OR (95% CI)
p Value
Age Sex Killip class on hospital admission Absence of preinfarction angina Time from symptom onset to hospital admission Infarct-related artery TIMI flow grade 0 at initial coronary angiography Multivessel disease Percutaneous coronary intervention Good collateral channel ST1in lead II ST1in lead III ST2in lead aVR ST1in lead aVF ST2in lead V1 ST2in lead V2 ST2in lead V3 ST2in lead V4 ST1in lead V5 ST1in lead V6
0.97 (0.92–1.02) 1.76 (0.39–7.94) 3.93 (1.49–10.4) 2.01 (0.52–7.80) 1.56 (1.07–2.27)
0.276 0.465 0.006 0.280 0.020
2.77 (0.57–13.5) 7.36 (1.56–24.8)
0.206 0.040
1.55 (0.56–3.32) 1.85 (0.61–5.60) 1.82 (0.44–7.52) 1.52 (0.38–1.80) 2.71 (0.98–7.18) 8.41 (2.96–23.9) 1.20 (0.58–2.56) 0.47 (0.66–2.48) 0.27 (0.36–1.33) 0.91 (0.49–1.70) 1.53 (0.87–2.68) 0.79 (0.49–1.29) 1.33 (0.77–2.29)
0.830 0.278 0.408 0.121 0.054 ⬍ 0.001 0.384 0.468 0.272 0.767 0.137 0.349 0.301
References
*OR ⫽ odds ratio; CI ⫽ confidence interval. See Table 3 for other abbreviations not used in the text. www.chestjournal.org
Previous studies have shown that impaired myocardial reperfusion is a powerful predictor of a poor outcome, even after successful recanalization.3–5 Our findings suggest that in patients with inferior AMIs, a larger ST-segment depression in lead aVR is useful for identifying patients who are most likely to benefit from aggressive therapeutic strategies designed to improve myocardial reperfusion.
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Clinical Investigations
Study objective: During inferior acute myocardial infarction (AMI), the ECG lead aVR is frequently ignored, and therefore its clinical significance remains unclear. We examined the relation between ST-segment deviation seen in lead aVR on ECGs obtained at hospital admission and myocardial reperfusion in patients who have experienced recanalized inferior AMIs. Design and setting: Retrospective study. Patients: A total of 225 patients with inferior AMIs in whom Thrombolysis in Myocardial Infarction grade 3 flow was achieved within 6 h after symptom onset. Measurements and results: Patients were classified as follows according to ST-segment deviation in lead aVR on an ECG obtained at hospital admission: group A, 103 patients with no ST-segment depression; group B, 80 patients with ST-segment depression of < 1.0 mm; and group C, 42 patients with ST-segment depression of > 1.0 mm. There were no differences in time from symptom onset to hospital admission or in the culprit lesion among the three groups. The degree of ST-segment elevation in leads II, III, aVF, V5, or V6, the degree of ST-segment depression in leads V1 to V4, and the sum of ST-segment deviation in these leads were lowest in group A and highest in group C. In groups A, B, and C, the incidence of impaired myocardial reperfusion, defined as myocardial blush grade 0/1, was 2%, 23%, and 67%, respectively (p < 0.001). The sensitivity and negative predictive values of ST-segment depression in lead aVR for impaired myocardial reperfusion were higher than those based on other ECG variables. Multivariate analysis showed that the degree of ST-segment depression in lead aVR was an independent predictor of impaired myocardial reperfusion (odds ratio 8.41; 95% confidence interval, 2.96 to 23.9; p < 0.001). Conclusions: We conclude that the degree of ST-segment depression in lead aVR is a useful predictor of impaired myocardial reperfusion in patients who have experienced inferior AMIs. (CHEST 2005; 128:780 –786) Key words: ECG; myocardial infarction; ST segment Abbreviations: AMI ⫽ acute myocardial infarction; LCX ⫽ left coronary circumflex artery; RCA ⫽ right coronary artery; TIMI ⫽ Thrombolysis in Myocardial Infarction
inferior acute myocardial infarction D uring (AMI), ECG lead aVR is frequently ignored, but some investigators have suggested that this lead can provide ECG information that is useful for the characterization of inferior AMI, which is more often *From the Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan. Manuscript received December 11, 2004; revision accepted February 8, 2005. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml). Correspondence to: Kazuo Kimura, MD, The Division of Cardiology, Yokohama City University Medical Center, 4 –57 Urafunecho, Minami-ku, Yokohama 232-0024, Japan; e-mail: c-kimura@ urahp.yokohama-cu.ac.jp 780
caused by the right coronary artery (RCA) occlusion than by the left coronary circumflex artery (LCX) occlusion. Menown and Adgey1 reported that the display of lead aVR in an inverted format as lead ⫺aVR improves the ECG classification of inferior or lateral AMI. Nair and Glancy2 reported that STsegment depression in lead aVR is useful for identifying the RCA or the LCX as the culprit artery in patients with inferior AMIs. However, the clinical significance of ST-segment depression in lead aVR remains unclear in patients with recanalized inferior AMIs. In the reperfusion era, the evaluation of myocardial reperfusion using myocardial blush grading has been reported to be useful in stratifying the prognosis of patients with recanalized AMI. 3–5 Clinical Investigations
Therefore, we examined the relation between the degree of ST-segment depression found in ECG lead aVR and myocardial reperfusion in patients with inferior AMIs. Materials and Methods Study Group We enrolled 225 consecutive patients with inferior AMI (mean [⫾ SD] age, 63 ⫾ 11 years; 172 men and 53 women) who fulfilled the following criteria for study inclusion: (1) no history of myocardial infarction or of other types of heart disease except for coronary artery disease; (2) absence of conditions precluding the evaluation of ST-segment changes on the ECG (eg, left bundle branch block, right bundle branch block, and ventricular pacing); (3) achievement of successful recanalization (Thrombolysis in Myocardial Infarction [TIMI]6 grade 3) of the RCA or the LCX as confirmed by coronary angiography within 6 h from symptom onset; and (4) adequate assessment of myocardial blush grade5 after recanalization. Patients with cardiogenic shock and those with reocclusion of the infarct-related artery during hospitalization were excluded from the study. The diagnosis of inferior AMI was based on typical chest pain lasting ⱖ 30 min, ST-segment elevation of ⱖ 1 mm in two or more inferior leads (ie, II, III, or aVF), and a typical increase in the serum creatine kinase level to more than twice the upper limit of normal. Coronary Angiography Coronary angiography was performed with informed consent immediately after hospital admission. The angiograms were evaluated by two observers who were blinded to all other data. Anterograde flow in the infarct-related artery was evaluated on a scale of 0 to 3 according to the standard TIMI flow grade, and recanalization was defined as the establishment of TIMI grade 3 flow. Collateral flow to the infarct zone was graded on a scale of 0 to 3 as described by Rentrop et al.7 A good collateral channel was defined as grade 2 or 3 flow, and a poor collateral channel as grade 0 or 1 flow. The allocation of recanalization therapy was left to the discretion of the doctor. On angiograms obtained immediately after recanalization, the extent of perfusion territory of the infarct-related artery was quantified according to the angiographic distribution score proposed by Wong et al8 All left ventricular branches of the RCA and the LCX were scored as follows: branches with a length equivalent to ⬎ 80% of that of the largest posterior descending artery were scored as 2; branches with a length between 50% and 80% of the artery were scored as 1; and small branches with a length of ⬍ 50% of the artery were scored as 0. The angiographic distribution score was defined as the ratio of the summed score of the infarct-related artery (ie, the RCA or the LCX) to the total summed score of the RCA and the LCX. In addition, myocardial blush was graded as follows: 0, no myocardial blush or contrast density; 1, minimal myocardial blush or contrast density; 2, moderate myocardial blush or contrast density, but less than that obtained during angiography of a contralateral or ipsilateral non-infarct-related coronary artery; and 3, normal myocardial blush or contrast density, comparable to that obtained during angiography of a contralateral or ipsilateral non-infarct-related coronary artery.5 When myocardial blush persisted, this finding was graded as 0. ECG Analysis A 12-lead ECG was recorded on hospital admission at a paper speed of 25 mm/s and an amplification of 10 mm/mV. The www.chestjournal.org
isoelectric line was defined as the level of the preceding TP segment. ST-segment deviation was measured manually to the nearest 0.5 mm, 20 ms after the end of the QRS complex by two independent observers who were blinded to all clinical and angiographic findings. The degree of ST-segment elevation in leads II, III, aVF, V5, or V6 and the degree of ST-segment depression in leads V1 to V4 were calculated. The right ventricular leads (ie, V3R and V4R) were recorded in 200 patients (89%) on hospital admission. ST-segment elevation of ⱖ 1.0 mm in the right ventricular lead was defined as being clinically significant.9 Cardiac Enzyme Study Blood samples were obtained on hospital admission, and at 3-h intervals during the first 24 h, at 6-h intervals for the next 2 days, and then daily until hospital discharge. Statistical Analysis The data are expressed as the mean ⫾ SD for continuous variables and as percentages for categoric variables. We made comparisons by one-way analysis of variance for continuous variables, and the statistical significance of differences was calculated by using the Scheffe´ F test. 2 analysis or Fisher exact test was used to compare categoric variables. The cutoff point of ECG variables for predicting impaired myocardial reperfusion, defined as myocardial blush grade 0 or 1, was obtained using their receiver-operating characteristic curve. Multiple logistic regression analysis was used to examine the determinants of impaired myocardial reperfusion. The variables used for analysis included age, sex, absence of previous angina within 24 h before AMI, Killip class on hospital admission, TIMI flow grade 0 at initial coronary angiography, multivessel disease, percutaneous coronary intervention, the infarct-related artery, good collateral channel, time from symptom onset to hospital admission, and the degree of ST-segment depression in lead aVR. Odds ratios and 95% confidence intervals were calculated. A two-tailed p value of ⬍ 0.05 was considered to indicate statistical significance. Analyses were performed with the use of a statistical software package (SPSS for Windows; SPSS; Chicago, IL).
Results Patient Characteristics Patients were divided into the following three groups according to ST-segment deviation in lead aVR on the ECG obtained at hospital admission: group A, 103 patients with no ST-segment depression; group B, 80 patients with ST-segment depression of ⱕ 1.0 mm; and group C, 42 patients with ST-segment depression of ⬎ 1.0 mm (Fig 1). The baseline characteristics of the three groups are summarized in Table 1. There were no differences among the three groups in age, hemodynamics or Killip class on hospital admission, percutaneous coronary intervention, time from symptom onset to hospital admission, coronary risk factors, or medication received before the occurrence of AMI. Group A patients were less likely to be men. Previous angina within 24 h before occurrence of the AMI was slightly but not significantly less frequent in group C. CHEST / 128 / 2 / AUGUST, 2005
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Figure 1. Representative ECGs of the three groups. Left, A: group A, no ST-segment depression in lead aVR (culprit lesion, segment 1; peak creatine kinase level, 1,478 mU/mL; myocardial blush grade 3). Left middle, B: group B, ST-segment depression of ⱕ 1.0 mm in lead aVR (culprit lesion, segment 3; peak creatine kinase level, 2,540 mU/mL; myocardial blush grade 2). Right middle, C: group C, ST-segment depression of ⬎ 1.0 mm in lead aVR (culprit lesion, segment 2 [dominant RCA]; peak creatine kinase level, 5,570 mU/mL; myocardial blush grade 0/1). Right, D: group C, ST-segment depression of ⬎ 1.0 mm in lead aVR (culprit lesion, segment 11; peak creatine kinase level, 7,784 mU/mL; myocardial blush grade 0/1).
The angiographic findings are shown in Table 2. There were no differences among the three groups in the incidence of multivessel disease, concomitant left anterior descending coronary artery disease, infarct-related artery, proximal lesion of the infarctrelated artery, or TIMI flow grade 0 at initial coronary angiography. A good collateral channel was less frequent in group C. The angiographic distribution score was lowest in group A and highest in group C.
more frequent in group C. The variables for predicting impaired myocardial reperfusion, defined as myocardial blush grade 0 or 1, on the basis of ST-segment deviation were calculated; the sensitivity, specificity, and positive and negative predictive values obtained with these variables were shown in Table 4. The sensitivity of the degree of ST-segment depression in lead aVR of ⱖ 1.0 mm for predicting impaired myocardial reperfusion was 92%, which was significantly higher than that based on other ECG variables.
ECG Findings
Infarct Size and Myocardial Reperfusion
The ECG findings on hospital admission are shown in Table 3. The degree of ST-segment elevation in leads II, III, aVF, V5, or V6, and the degree of ST-segment depression in leads V1 to V4 and the sum of ST-segment deviation in these leads were lowest in group A and the highest in group C. The number of leads with ST-segment elevation was lowest in group A and highest in group C. The prevalence of ST-segment elevation in the right ventricular leads was slightly but not significantly
Peak creatine kinase level was lowest in group A and highest in group C. Congestive heart failure during hospitalization was more frequent in group C. Impaired myocardial reperfusion, as defined by a myocardial blush grade of 0 or 1, was observed in 67% of group C patients, compared with only 2% of group A patients (Fig 2). On multivariate analysis, the degree of ST-segment depression in lead aVR was a powerful predictor of impaired myocardial reperfusion (Table 5).
Angiographic Findings
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Clinical Investigations
Table 1—Baseline Clinical Characteristics* Characteristics Age, yr Men Heart rate on hospital admission, beats/min Systolic BP on hospital admission, mm Hg Killip class on hospital admission ⬎ 1 Previous angina within 24 h before AMI Percutaneous coronary intervention Time from symptom onset to hospital admission, h Medication before AMI Calcium antagonist Beta-blocker ACE inhibitor Diabetes mellitus Hypercholesterolemia Systemic hypertension Smoker Peak creatine kinase level, mU/mL Congestive heart failure during hospitalization
Group A (n ⫽ 103)
Group B (n ⫽ 80)
Group C (n ⫽ 42)
p Value
63 ⫾ 11 71 (69) 66 ⫾ 20 127 ⫾ 33 4 (4) 36 (35) 54 (52) 2.3 ⫾ 1.2
62 ⫾ 11 67 (84) 67 ⫾ 16 128 ⫾ 33 5 (6) 23 (29) 35 (44) 2.5 ⫾ 1.5
62 ⫾ 12 34 (81) 74 ⫾ 24 124 ⫾ 36 4 (10) 8 (19) 26 (62) 2.5 ⫾ 1.3
0.704 0.048 0.106 0.866 0.408 0.159 0.152 0.559
22 (21) 4 (4) 7 (7) 23 (22) 23 (23) 50 (49) 65 (63) 2,186 ⫾ 1,572 2 (2)
12 (15) 5 (6) 9 (11) 23 (29) 23 (29) 41 (51) 48 (60) 3,079 ⫾ 1,574 4 (5)
10 (24) 5 (12) 2 (5) 10 (24) 11 (26) 27 (64) 32 (76) 4,865 ⫾ 1,757 8 (19)
0.417 0.211 0.377 0.599 0.601 0.219 0.192 ⬍ 0.001 ⬍ 0.001
*Values given as the mean ⫾ SD or No. of patients (%), unless otherwise indicated. ACE ⫽ angiotensin-converting enzyme.
Discussion Several studies have suggested that even after successful recanalization of the infarct-related coronary artery, some patients do not have complete myocardial reperfusion and remain at risk for large infarcts and more frequent mortality.3–5 Therefore, the early and simple identification of such high-risk patients is required. Our study demonstrated that in patients with inferior AMIs, larger ST-segment depression in lead aVR was associated with impaired myocardial reperfusion. Two studies1,2 have investigated the clinical implications of ST-segment depression in lead aVR during an inferior AMI. Menown and Adgey1 reported that
ST-segment depression in lead aVR was associated with a large infarct size. However, their study lacked angiographic data and did not confirm the presence or absence of recanalization of the infarct-related artery. Although Nair and Glancy2 reported that ST-segment depression in lead aVR was more common in LCX-related inferior AMIs than in RCArelated inferior AMIs, their study included only five patients with LCX-related inferior AMIs. Thus, the relations of ST-segment depression in lead aVR during inferior AMI to angiographic findings and infarct size have not been clearly defined. To clarify the clinical implications of ST-segment depression in lead aVR during inferior AMI, we included only
Table 2—Angiographic Findings* Variables Multivessel disease Concomitant LAD disease Infarct-related artery RCA LCX Culprit lesion Proximal RCA (segment 1) Proximal LCX (segment 11) TIMI flow grade 0 at initial CAG Collateral grade ⬎ 2† Angiographic distribution score
Group A (n ⫽ 103)
Group B (n ⫽ 80)
Group C (n ⫽ 42)
26 (25) 18 (18)
17 (21) 13 (16)
10 (24) 7 (17)
83 (81) 20 (19)
59 (74) 21 (26)
34 (81) 8 (19)
39 (38) 5 (6) 84 (82) 30 (29) 0.5 ⫾ 0.2
37 (46) 8 (10) 66 (83) 19 (24) 0.6 ⫾ 0.1
21 (50) 5 (12) 37 (88) 4 (10) 0.7 ⫾ 0.1
p Value 0.819 0.975 0.482
0.318 0.261 0.624 0.041 ⬍ 0.001
*Values given as the mean ⫾ SD or No. of patients (%), unless otherwise indicated. LAD ⫽ left anterior descending artery; CAG ⫽ coronary angiography. †Rentrop classification. www.chestjournal.org
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Table 3—ECG Findings* ECG Variables
Group A (n ⫽ 103)
Group B (n ⫽ 80)
Group C (n ⫽ 42)
p Value
ST1in lead II, mm ST1in lead III, mm ST1in lead aVF, mm Maximal ST1in lead II, III or aVF, mm ⌺ST1in leads II,III and aVF, mm ST1in lead V5, mm ST1in lead V6, mm ⌺ST1in leads V5 and V6, mm ⌺ST1in leads II,III, aVF, V5 and V6, mm Number of leads with ST1 ST2in lead V1, mm ST2in lead V2, mm ST2in lead V3, mm ST2in lead V4, mm ⌺ST2in lead V1 to V4, mm ST1in lead V3R of ⬎ 1.0 mm† ST1in lead V4R of ⬎ 1.0 mm†
1.4 ⫾ 0.9 2.2 ⫾ 1.3 1.7 ⫾ 1.2 2.2 ⫾ 1.3 5.2 ⫾ 3.2 0.0 ⫾ 0.2 0.1 ⫾ 0.5 0.2 ⫾ 0.6 5.4 ⫾ 3.3 3.2 ⫾ 0.5 0.3 ⫾ 0.7 1.0 ⫾ 1.2 1.5 ⫾ 1.6 1.6 ⫾ 1.6 4.3 ⫾ 4.5 20 (22) 23 (26)
2.5 ⫾ 1.2 3.1 ⫾ 1.8 2.8 ⫾ 1.5 3.3 ⫾ 1.7 8.4 ⫾ 4.5 0.3 ⫾ 0.7 0.5 ⫾ 0.9 0.9 ⫾ 1.4 9.2 ⫾ 4.6 3.6 ⫾ 0.8 0.8 ⫾ 1.0 1.8 ⫾ 1.9 2.2 ⫾ 2.3 1.9 ⫾ 1.9 6.7 ⫾ 6.3 19 (26) 26 (36)
4.5 ⫾ 1.8 5.5 ⫾ 2.2 4.8 ⫾ 1.9 5.6 ⫾ 2.2 14.7 ⫾ 5.8 1.0 ⫾ 1.5 1.7 ⫾ 1.9 2.7 ⫾ 3.4 17.3 ⫾ 7.2 4.1 ⫾ 0.9 1.7 ⫾ 2.4 4.1 ⫾ 4.0 3.7 ⫾ 3.9 2.4 ⫾ 2.3 12.1 ⫾ 11.3 14 (38) 16 (43)
⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 0.002 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 0.054 ⬍ 0.001 0.192 0.120
*Values given as the mean ⫾ SD or No. of patients (%), unless otherwise indicated. ST1 ⫽ the degree of ST-segment elevation; ST2 ⫽ the degree of ST-segment depression; ⌺ST1 ⫽ the sum of ST-segment elevation; ⌺ST2 ⫽ the sum of ST-segment depression. †Available data (n ⫽ 200).
patients who had experienced a first inferior AMI with inferior ST-segment elevation in whom TIMI grade 3 flow of the RCA or LCX was achieved within 6 h from symptom onset. In this setting, ST-segment depression in lead aVR was associated with a larger infarct size and impaired myocardial reperfusion. In our study, the infarct-related artery (ie, the RCA or the LCX) and the location of the culprit lesion did not differ significantly among the three groups, but greater ST-segment depression in lead aVR was related to a larger perfusion territory of the infarct-
related artery, as assessed by the angiographic distribution score (ie, a larger ischemic area). Menown and Adgey1 reported that the display of lead aVR (⫺150°) in inverted format as lead ⫺aVR (⫹30°) bridges the gap between lead I (0°) and lead II (60°). In other words, ST-segment depression in lead aVR might be a reciprocal change resulting from STsegment elevation in the apical and inferolateral walls, which none of the standard 12 leads directly faces. Such regions of the left ventricle are usually supplied by the large posterolateral branch of the
Table 4 —Sensitivity, Specificity, Positive Predictive Value, and Negative Predictive Value of ECG Variables for Predicting Impaired Myocardial Reperfusion* ECG Variables
Sensitivity, %
Specificity, %
PPV
NPV
ST2in lead aVR ⬎ 1.0 mm ST1in lead II ⬎ 2.0 mm ST1in lead III ⬎ 3.0 mm ST1in lead aVF ⬎ 2.5 mm Maximal ST1in lead II, III, or aVF ⬎ 3.0 mm ST2in lead V1 ⬎ 1.0 mm ST2in lead V2 ⬎ 2.0 mm ST2in lead V3 ⬎ 2.5 mm ST2in lead V4 ⬎ 2.5 mm ST1in lead V5 ⬎ 0.5 mm ST1in lead V6 ⬎ 0.5 mm ⌺ST2in leads V1 to V4 ⬎ 8.0 mm ⌺ST1in leads II, III, and aVF ⬎ 8.0 mm ⌺ST1in leads V5 and V6 ⬎ 1.0 mm ⌺ST1in leads II, III, aVF, V5, and V6 ⬎ 8.5 mm
92 73† 71‡ 77† 75† 56‡ 69‡ 60‡ 44‡ 42‡ 69‡ 56‡ 77† 69‡ 75‡
67 66 72 71 71 66 66 75 75 88‡ 81† 80† 67 84† 67
43 37 41 42 37 31 33 39 31 48 50 43 38 54 42
97 90† 90† 92 91† 85‡ 89† 87‡ 83‡ 85‡ 91† 87‡ 92 91† 84‡
*PPV ⫽ positive predictive value; NPV ⫽ negative predictive value. See Table 3 for other abbreviations not used in the text. †p ⬍ 0.05 vs lead aVR. ‡p ⬍ 0.01 vs lead aVR. 784
Clinical Investigations
Figure 2. Incidence of impaired myocardial reperfusion, as indicated by myocardial blush grade 0 or 1 in the three groups.
LCX or the atrioventricular branch of the RCA. Therefore, concurrent ST-segment depression in lead aVR during inferior AMI might reflect transmural ischemia extending to the apical and inferolateral walls in addition to the inferior wall. Anterior ST-segment depression and inferior STsegment elevation have been shown to be useful for predicting evolving infarct size.10 –13 In the present study, we measured the degree of ST-segment depression in leads V1 to V4, the degree of ST-segment elevation in leads II, III, aVF, V5, or V6, and the sum of ST-segment deviation in these leads. The sensi-
tivity and negative predictive value of ST-segment depression in lead aVR for impaired myocardial reperfusion were higher than those based on other ECG variables. Multivariate analysis showed that ST-segment depression in lead aVR related to impaired myocardial reperfusion. These findings suggested that ST-segment depression in lead aVR might more closely reflect the severity and extent of myocardial injury during an inferior AMI than other ECG markers. Two studies14,15 have reported that differences in the territories perfused by the RCA and LCX may influence the direction and degree of inferior ST-segment elevation. In addition, it has been reported that patients with inferior AMI and concomitant right ventricular ischemia had smaller precordial ST-segment depression than those without concomitant right ventricular ischemia.15,16 On the basis of these observations, we can assume that ST-segment elevation in inferior leads or ST-segment depression in precordial leads might not consistently reflect the severity and extent of myocardial injury during inferior AMI. Iwakura et al17 reported that both larger ischemic area and more severe myocardial damage before recanalization are closely related to the development of the no-reflow phenomenon. In patients with ST-segment depression in lead aVR, microvascular injury might be caused by severe myocardial damage in the extensive area that is at risk. Clinical Implications
Table 5—Multivariate Analysis of Factors Associated With Impaired Myocardial Reperfusion* Variables
OR (95% CI)
p Value
Age Sex Killip class on hospital admission Absence of preinfarction angina Time from symptom onset to hospital admission Infarct-related artery TIMI flow grade 0 at initial coronary angiography Multivessel disease Percutaneous coronary intervention Good collateral channel ST1in lead II ST1in lead III ST2in lead aVR ST1in lead aVF ST2in lead V1 ST2in lead V2 ST2in lead V3 ST2in lead V4 ST1in lead V5 ST1in lead V6
0.97 (0.92–1.02) 1.76 (0.39–7.94) 3.93 (1.49–10.4) 2.01 (0.52–7.80) 1.56 (1.07–2.27)
0.276 0.465 0.006 0.280 0.020
2.77 (0.57–13.5) 7.36 (1.56–24.8)
0.206 0.040
1.55 (0.56–3.32) 1.85 (0.61–5.60) 1.82 (0.44–7.52) 1.52 (0.38–1.80) 2.71 (0.98–7.18) 8.41 (2.96–23.9) 1.20 (0.58–2.56) 0.47 (0.66–2.48) 0.27 (0.36–1.33) 0.91 (0.49–1.70) 1.53 (0.87–2.68) 0.79 (0.49–1.29) 1.33 (0.77–2.29)
0.830 0.278 0.408 0.121 0.054 ⬍ 0.001 0.384 0.468 0.272 0.767 0.137 0.349 0.301
References
*OR ⫽ odds ratio; CI ⫽ confidence interval. See Table 3 for other abbreviations not used in the text. www.chestjournal.org
Previous studies have shown that impaired myocardial reperfusion is a powerful predictor of a poor outcome, even after successful recanalization.3–5 Our findings suggest that in patients with inferior AMIs, a larger ST-segment depression in lead aVR is useful for identifying patients who are most likely to benefit from aggressive therapeutic strategies designed to improve myocardial reperfusion.
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Clinical Investigations