During inferior acute myocardial infarction, ST-segment elevation (ST↑) often occurs in leads V 5 to V 6 , but its clinical implications remain unclear. We examined the admission electrocardiograms from 357 patients with a first inferior acute myocardial infarction who had Thrombolysis In Myocardial Infarction 3 flow of the right coronary artery or left circumflex artery within 6 hours after symptom onset. The patients were divided according to the presence (n = 76) or absence (n = 281) of ST↑ >2 mm in leads V 5 and V 6 . Patients with ST↑ in leads V 5 and V 6 were subdivided into 2 groups according to the degree of ST↑ in leads III and V 6 : ST↑ in lead III greater than in V 6 (n = 53) and ST↑ in lead III equal to or less than in V 6 (n = 23). The perfusion territory of the culprit artery was assessed using the angiographic distribution score, and a mega-artery was defined as a score of ≥0.7. ST↑ in leads V 5 and V 6 with ST↑ in lead III greater than in V 6 and ST↑ in leads V 5 and V 6 with ST↑ in lead III equal to or less than in V 6 were associated with mega-artery occlusion and impaired myocardial reperfusion, as defined by myocardial blush grade 0 to 1. Right coronary artery occlusion was most common (96%) in the former, and left circumflex artery occlusion was most common (96%) in the latter, especially proximal left circumflex occlusion (74%). Multivariate analysis showed that ST↑ in leads V 5 and V 6 with ST↑ in lead III greater than that in V 6 (odds ratio 4.81, p <0.001) and ST↑ in leads V 5 and V 6 with ST↑ in lead III equal or less than that in V 6 (odds ratio 5.96, p <0.001) were independent predictors of impaired myocardial reperfusion. In conclusion, ST↑ in leads V 5 and V 6 suggests a greater risk area and impaired myocardial reperfusion in patients with inferior acute myocardial infarction. Furthermore, comparing the degree of ST↑ in lead V 6 with that in lead III is useful for predicting the culprit artery.
In the reperfusion era, optimal reperfusion for acute myocardial infarction (AMI) is being redefined to include intact microvascular flow and restored myocardial perfusion, as well as sustained epicardial patency. Previous studies have shown that patients with impaired myocardial reperfusion have poor outcomes, even when the infarct-related arteries are patent. The present study examined the relation of ST-segment elevation (ST↑) in leads V 5 and V 6 on the admission electrocardiogram (ECG) with the angiographic findings and myocardial blush grade, an angiographic marker of myocardial reperfusion, in patients with inferior AMI who had Thrombolysis In Myocardial Infarction grade 3 of the right coronary artery or left circumflex (LC) artery. Although previous studies assessing the clinical significance of ST↑ in leads V 5 and V 6 during inferior AMI have merely focused on its presence or absence, we additionally examined the clinical implications of the pattern of ST↑ in the inferior and lateral leads.
Methods
We enrolled 357 consecutive patients with a first inferior AMI (mean age 63 ± 11 years; 283 men and 74 women). These patients fulfilled the following criteria: (1) absence of conditions precluding the evaluation of ST-segment changes on the ECG (i.e., complete left or right bundle branch block, left ventricular hypertrophy, ventricular pacing, atrial fibrillation or flutter, electrolyte abnormalities, or treatment with drugs potentially affecting the ECG); (2) fully assessable ECGs on admission; (3) achievement of Thrombolysis In Myocardial Infarction grade 3 in the right coronary or LC artery as confirmed by coronary angiography within 6 hours from symptom onset; and (4) adequate assessment of myocardial blush grade after reperfusion. The diagnosis of inferior AMI was determined by typical chest pain lasting ≥30 minutes, ST↑ of ≥1 mm in ≥2 inferior leads (II, III, or aVF), and an increase in the serum creatine kinase level to more than twice the upper limit of normal. All patients gave informed consent. The ethics committee of our institution approved the study protocol.
A 12-lead ECG was recorded on admission at a paper speed of 25 mm/s and an amplification of 10 mm/mV. ST-segment deviation was measured manually to the nearest 0.5 mm, 80 ms after the J point by a single cardiologist who was unaware of all clinical and angiographic findings. The degrees of ST-segment depression in leads V 1 to V 4 and ST↑ in leads II, III, aVF, V 5 , and V 6 were measured.
Coronary angiography was performed immediately after admission. The angiograms were evaluated by a single cardiologist who was unaware of all data apart from the coronary angiogram. The grade of collateral filling in the infarct-related artery was evaluated as described by Rentrop et al, and a good collateral channel was defined as grade 2 or 3. The allocation of reperfusion therapy was left to the discretion of the physician in charge. On angiograms obtained after reperfusion, the extent of the perfusion territory of the infarct-related artery was quantified according to the angiographic distribution score, as proposed by Wong et al. Mega-artery was defined as an angiographic distribution score of ≥0.7. In addition, myocardial blush was graded on the final angiogram. Impaired myocardial reperfusion was defined as myocardial blush grade 0 or 1.
Blood samples were obtained on admission and at 3-hour intervals during the first 24 hours, at 6-hour intervals for the next 2 days, and then daily until discharge.
Data are expressed as the mean ± SD for continuous variables and as percentages for categorical variables. Analysis of variance was used to calculate the p values for continuous variables. Chi-square analysis was used to compare the categorical variables. Differences were considered statistically significant at p <0.05. A multivariate logistic regression analysis was used to identify clinical predictors on admission of impaired myocardial reperfusion among the variables associated (p <0.05) with this finding on univariate analysis. Odds ratios and 95% confidence intervals were calculated.
Results
Patients were divided according to the presence (n = 76) or absence (n = 281) of ST↑ of >2 mm in leads V 5 and V 6 . Patients with ST↑ in leads V 5 and V 6 were subdivided into the 2 groups according to the degree of ST↑ in lead III and in lead V 6 : ST↑ in lead III greater than in V 6 (n = 53) and ST↑ in lead III equal to or less than that in V 6 (n = 23; Figure 1 ) . The baseline characteristics of the 3 groups are summarized in Table 1 . Patients with ST↑ in leads V 5 and V 6 with ST↑ in lead III greater than that in V 6 and ST↑ in leads V 5 and V 6 with ST↑ in lead III equal to or less than that in V 6 had a greater rate of Killip class ≥2 on admission and a greater peak creatine kinase level. No differences were found among the 3 groups for the other baseline characteristics.
Variable | No ST↑ in leads V 5 –V 6 (n = 281) | ST↑ in leads V 5 –V 6 | p Value | |
---|---|---|---|---|
ST↑ in lead III > V 6 (n = 53) | ST↑ in lead III ≤ V 6 (n = 23) | |||
Age (years) | 64 ± 11 | 62 ± 13 | 60 ± 12 | 0.32 |
Men | 220 (78%) | 43 (81%) | 20 (87%) | 0.58 |
Medication before acute myocardial infarction | ||||
β Blocker | 14 (5%) | 3 (6%) | 1 (4%) | 0.97 |
Calcium antagonist | 57 (20%) | 7 (13%) | 7 (30%) | 0.21 |
Angiotensin-converting enzyme inhibitor | 29 (10%) | 2 (4%) | 1 (4%) | 0.23 |
Coronary risk factors | ||||
Diabetes mellitus | 75 (27%) | 11 (21%) | 8 (35%) | 0.42 |
Hyperlipidemia | 77 (27%) | 13 (25%) | 10 (44%) | 0.22 |
Hypertension | 151 (54%) | 25 (47%) | 13 (57%) | 0.63 |
Smoking | 166 (59%) | 36 (68%) | 13 (57%) | 0.46 |
Previous angina within 24 hours before acute myocardial infarction | 91 (32%) | 15 (28%) | 6 (26%) | 0.72 |
Heart rate on admission (beats/min) | 66 ± 18 | 72 ± 23 | 74 ± 16 | 0.06 |
Systolic blood pressure on admission (mm Hg) | 133 ± 68 | 116 ± 40 | 128 ± 26 | 0.27 |
Killip class ≥2 on admission | 11 (4%) | 9 (17%) | 4 (17%) | <0.001 |
Interval from symptom onset to admission (hours) | 2.3 ± 1.9 | 2.2 ± 1.2 | 2.5 ± 1.5 | 0.73 |
Percutaneous coronary intervention | 197 (70%) | 37 (70%) | 16 (70%) | 0.99 |
Interval from symptom onset to reperfusion (hours) | 3.4 ± 1.9 | 3.5 ± 1.8 | 3.4 ± 1.5 | 0.60 |
Peak creatine kinase (IU/L) | 2,563 ± 1,660 | 4,344 ± 2,524 | 4,589 ± 2,759 | <0.001 |
The ECG findings on admission are listed in Table 2 . ST↑ in leads V 5 and V 6 with ST↑ in lead III greater than in V 6 was associated with greater ST↑ in leads II, III, and aVF, in particular, lead III. ST-segment depression in leads V 1 to V 4 was greater in both those with ST↑ in leads V 5 and V 6 with ST↑ in lead III greater than in V 6 and ST↑ in leads V 5 and V 6 with ST↑ in lead III equal to or less than that in V 6 . Among the patients with ST↑ in leads V 5 and V 6 , the degree of ST↑ in lead V 5 was similar in those with ST↑ in lead III greater than in V 6 and those with ST↑ in lead III equal to or less than that in V 6 . However, the degree of ST↑ in lead V 6 was slightly, but not significantly, greater in the latter.
Variable | No ST↑ in leads V 5 –V 6 (n = 281) | ST↑ in leads V 5 –V 6 | p Value | |
---|---|---|---|---|
ST↑ in lead III > V 6 (n = 53) | ST↑ in lead III ≤ V 6 (n = 23) | |||
ST↑ in inferior leads (mm) | ||||
Lead II | 1.9 ± 1.3 | 4.2 ± 2.1 | 2.5 ± 1.8 | <0.001 |
Lead III | 2.6 ± 1.5 | 5.4 ± 2.5 | 2.3 ± 1.5 | <0.001 |
Lead aVF | 2.2 ± 1.3 | 4.6 ± 2.1 | 2.4 ± 1.6 | <0.001 |
Sum of ST↑ in leads II, III, and aVF | 6.6 ± 3.0 | 14.2 ± 5.0 | 7.3 ± 4.0 | <0.001 |
ST↓ in precordial leads V 1 –V 4 (mm) | ||||
Lead V 1 | 0.4 ± 0.7 | 1.1 ± 1.2 | 1.9 ± 2.4 | <0.001 |
Lead V 2 | 1.3 ± 1.5 | 3.2 ± 2.7 | 3.7 ± 4.0 | <0.001 |
Lead V 3 | 1.7 ± 1.6 | 3.2 ± 3.2 | 4.2 ± 4.1 | <0.001 |
Lead V 4 | 1.7 ± 1.6 | 2.3 ± 2.4 | 2.5 ± 2.0 | 0.044 |
Sum of ST↓ leads V 1 –V 4 | 5.1 ± 3.8 | 9.6 ± 5.8 | 12.0 ± 7.7 | <0.001 |
ST↑ in precordial leads (V 5 and V 6 ) (mm) | ||||
Lead V 5 | — | 1.2 ± 1.6 | 1.3 ± 1.9 | 0.59 |
Lead V 6 | — | 2.0 ± 1.4 | 2.7 ± 1.6 | 0.05 |
Sum of ST↑ in leads V 5 and V 6 | — | 3.4 ± 1.5 | 4.0 ± 2.2 | 0.43 |
The angiographic findings are listed in Table 3 . No differences were found among the 3 groups for multivessel disease or initial Thrombolysis In Myocardial Infarction flow grade 0 or 1. Good collateral circulation was less frequently observed in patients with ST↑ in leads V 5 and V 6 with ST↑ in lead III greater than in V 6 and those with ST↑ in leads V 5 and V 6 and ST↑ in lead III equal to or less than V 6 . ST↑ in leads V 5 and V 6 with ST↑ in lead III greater than V 6 and ST↑ in leads V 5 and V 6 with ST↑ in lead III equal to or less than that in V 6 were both associated with a greater angiographic distribution score and greater rate of infarct-related mega-artery. No ST↑ in leads V 5 and V 6 and ST↑ in leads V 5 and V 6 with ST↑ in lead III greater than V 6 were associated with right coronary artery occlusion. However, ST↑ in leads V 5 and V 6 with ST↑ in lead III equal to or less than V 6 was associated with LC artery occlusion, especially proximal LC artery occlusion. ST↑ in leads V 5 and V 6 with ST↑ in lead III greater than V 6 and ST↑ in leads V 5 and V 6 with ST↑ in lead III equal to or less than that in V 6 were both associated with impaired myocardial reperfusion, as defined by myocardial blush grade 0 or 1 ( Figure 2 ) .
Variable | No ST↑ in leads V 5 –V 6 (n = 281) | ST↑ in leads V 5 –V 6 | p Value | |
---|---|---|---|---|
ST↑ in lead III > V 6 (n = 53) | ST↑ in lead III ≤ V 6 (n = 23) | |||
Multivessel disease | 73 (26%) | 11 (21%) | 4 (17%) | 0.51 |
Good collateral circulation ⁎ | 83 (31%) | 8 (15%) | 3 (13%) | 0.019 |
Infarct-related artery | ||||
Initial Thrombolysis In Myocardial Infarction flow grade 0–1 | 238 (85%) | 49 (93%) | 19 (83%) | 0.30 |
Angiographic distribution score | 0.5 ± 0.1 | 0.8 ± 0.1 | 0.8 ± 0.1 | <0.001 |
Mega-artery | 57 (20%) | 38 (72%) | 18 (78%) | <0.001 |
Right coronary artery | 254 (90%) | 51 (96%) | 1 (4%) | <0.001 |
Left circumflex artery | 27 (10%) | 2 (4%) | 22 (96%) | <0.001 |
Proximal right coronary artery (segment 1) | 118 (42%) | 28 (53%) | 0 | <0.001 |
Proximal left circumflex artery (segment 11) | 7 (2%) | 1 (2%) | 17 (74%) | <0.001 |