Article, Cardiology

ST elevation measurements differ in patients with inferior myocardial infarction and right ventricular infarction

Unlabelled imageAmerican Journal of Emergency Medicine (2011) 29, 1067-1073

Original Contribution

ST elevation measurements differ in patients with Inferior myocardial infarction and Right ventricular infarction

Dong-Woo Seo MD a, Chang Hwan Sohn MD a, Jeong Min Ryu MD a,

Jae Chol Yoon MD b, Shin Ahn MD a, Won Kim MD, PhD a,?

aDepartment of Emergency Medicine, University of Ulsan, College of Medicine, Asan Medical Center,

Seoul 138-736, South Korea

bDepartment of Emergency Medicine, Chonbuk National University, College of Medicine, Chonbuk National University Hospital, Chon-Ju, 561-712, South Korea

Received 1 January 2010; revised 19 June 2010; accepted 22 June 2010

Abstract

Purpose: Few studies specify the methods used to measure ST-segment elevation . We therefore assessed differences in electrocardiography results depending on STE measurement methods for patients with inferior acute myocardial infarction (MI) and right ventricular infarction.

Methods: This study was a retrospective analysis. The STE group consisted of 88 patients consecutively admitted to the emergency department with inferior ST elevation MI associated with occlusion of right coronary artery or left circumflex coronary artery who underwent primary percutaneous coronary intervention. The control group consisted of 109 patients with non-ST elevation MI who had occlusion of right coronary artery or left circumflex coronary artery and underwent percutaneous coronary intervention. Measurements were performed at the J point and 60 milliseconds later for limb lead and right precordial V4 lead (V4R). The criterion of at least 1-mm STE in 2 consecutive leads was applied, and the diagnostic accuracy of V4R was calculated.

Results: In the STE group, the measurements 60 milliseconds after the J point were significantly higher than measurements at the J point at the II, III, aVF, and V4R leads. In the control group, only the measurements at lead I differed significantly. There was a 5% difference in diagnostic sensitivity depending on the measuring points in the STE group, a 1% to 3% difference in the control group, and a 10% to 11% difference at the V4R lead.

Conclusion: In patients with inferior MI, STE depends on the method of measurement, indicating a need for the standardization of measurements.

(C) 2011

Introduction

Electrocardiography is an important tool in diagnosing acute myocardial infarction (AMI) and in determining the eligibility of patients presenting with ST-

* Corresponding author. Tel.: +82 2 3010 3350; fax: +82 2 3010 3360.

E-mail address: [email protected] (W. Kim).

segment elevation (STE) AMI for reperfusion therapy [1]. Although many clinical studies have suggested ECG criteria for the diagnosis of ST-segment elevation myocardial infarction , many of the criteria are incomplete and confusing. Among the causes of confusion are variations in measuring point and timing, including the J point [2,3] and 80 milliseconds after the J point [4], with some studies not mentioning the J point [5]. Another cause of confusion in

0735-6757/$ – see front matter (C) 2011 doi:10.1016/j.ajem.2010.06.033

ECG criteria is the discrepancies in voltage criteria for the ST segment. In the 2005 standardized guidelines of the American Heart Association (AHA), STE or presumed new Left bundle-branch block (BBB) was characterized by STE of 1 mm in 2 consecutive precordial or limb leads, and was classified as STEMI [5]. However, in the 2000 standardized guidelines of the American College of Cardiology (ACC) and the European Society of Cardiology (ESC), a new or presumed new STE at the J point in 2 consecutive leads, with cutoff points of 2 mm in leads V1, V2, or V3 and 1 mm in other leads contiguous in the frontal plane, was defined by the lead sequence aVL, I, inverted aVR, II, aVF, and III [2]. More recently, consensus ECG guidelines of the AHA, ACC, and ESC have defined the voltage criteria for STEMI as STE at the J point in 2 consecutive leads, with cutoff points of least 2 mm in men and at least 1.5 mm in women at leads V2 and V3, and/or at least 1 mm at the other leads [3]. A third cause of confusion in ECG criteria is whether the baseline reference is based on the PR or TP segment. When the PR segment is the baseline reference, STE based on this segment is lower than STE based on the TP segment because of an impact of the atrial repolarization wave. To determine how these differ- ences in ECG criteria affected determination of which STEMI patients needed reperfusion therapy, STEs at the J point and 60 milliseconds later were evaluated to assess whether they met the 1- and 2-mm criteria [6]. The ability to satisfy ECG criteria was found to depend on the measuring points of the precordial leads. However, there have been few studies assessing limb leads and right precordial V4 lead (V4R). If STEs at these leads depend on the points of measurement, this could affect the initial treatment direction in an emergency department (ED) because of the hemody- namic consequence of right ventricular infarction. We therefore compared differences between STE at the J point and 60 milliseconds later in the limb lead and V4R. We also assessed the diagnostic sensitivity of each result based on the consensus standard of Thygesen et al [3].

Methods

We retrospectively analyzed electrocardiographic and angiographic findings of consecutive patients admitted to the ED between November 2005 and October 2007 in a case- control manner. Among the 151,143 patients admitted to the ED during this period, those suspected of having STE and diagnosed with inferior STEMI by direct percutaneous coronary intervention (PCI) were designated the STE group. The control group consisted of patients admitted to the ED with similar symptoms as those of patients in the STE group, but who were suspected of having non-ST elevation myocardial infarction (NSTEMI) and identified with inferior MI based on PCI results. For both groups, PCI results included only right coronary artery or left circumflex

coronary artery (LCX) occlusion supplying the inferior wall. This study was approved by our Institutional Review Board. Our ED has an Annual patient volume of 75,000 and serves a primarily urban area. Our hospital performs more coronary angiography procedures than any other hospital in the country and has a medical team exclusively devoted to round-the-clock coronary angiography throughout the year. During the study period, PCI was performed on all participating patients diagnosed with STEMI and recom- mended for reperfusion therapy. Each patient presenting with chest pain or related symptoms was evaluated by Attending emergency physicians, and an ECG was performed within

10 minutes of admission. Patients suspected of having STEMI, based on ECG interpretation, were referred immediately to interventional cardiologists and members of the coronary angiography team. In general, AHA guidelines were followed in the interpretation of ECG for diagnosis of STEMI, although there are no Consensus guidelines [1,7]. Cardiac biomarkers were assessed in patients who did not present with STE based on ECG results, and those positive for such biomarkers were admitted to hospital. Patients who had Persistent symptoms or who were in high-risk groups were admitted to hospital or underwent cardiac biomarker tests. Percutaneous coronary intervention was performed selectively for certain patients admitted to hospital.

This study was a retrospective analysis of patients suspected of presenting with acute coronary syndrome (ACS) symptoms. When initial ECG interpretation identified STE, direct PCI was performed (STE group). Patients who did not have STE on initial ECG, but who were later positive for cardiac biomarkers, were included in the control group. Both groups consisted of patients who presented with RCA or LCX occlusion supplying the inferior wall based on PCI results. Critical stenosis was defined as a 70 % or more narrowing of the luminal diameter of the coronary artery. A culprit artery was defined as the most stenosed or occluded artery of the coronary arteries, with critical stenosis, as determined by the interventional cardiologist performing PCI. Patients were excluded if the left anterior descending coronary artery was the culprit artery, if they did not undergo right precordial ECG (STE group only), if they presented with BBB, if they were diagnosed with pericar- ditis, and if they did not have any medical records. Electrocardiograms were reviewed by 2 independent inves- tigators blinded to patient clinical and angiographic data.

All measurements were performed by 2 investigators blinded to the aims of the study. ST-segment elevation was measured at the J point and 60 milliseconds later in 6 leads: I, II, III, aVR, aVL, and aVF, based on the PR segment. Subsequently, the investigators determined if each elevation met the criterion of at least 1 mm in 2 consecutive leads, defined as meeting the Cabrera display (ie, aVL, I, aVR, II, aVF, and III, in that order) [3,8]. For the right precordial ECG in the STE group, STE was measured at the J point and 60 milliseconds later in V4R based on the PR segment for diagnosing right ventricular infarction. We also determined if

each elevation met the criterion of least 1 mm. Measurements at V4R were not performed in the control group because right precordial ECG was not performed on most of these patients. The PCI results were noted, and the diagnostic accuracy of V4R was assessed in comparison with the PCI data. All ECG data were scanned, presented, and interpreted using a computer system. Measurements were performed using Cardio Caliper 3.3 (Version 3.3; ICONICO, Inc, New York, NY) at 0.1-mm intervals, with results entered to the nearest 0.5 mm. Data were inputted using Excel (Version 2003; Microsoft Corp, Redmond, CA).

To determine interrater reliability for each group, the arithmetic mean for each investigator was summarized by calculating the intraclass correlation coefficient for each lead, taking subjects and leads into account. To compare STE at each lead measured at the J point and 60 milliseconds later, the measurements of the 2 raters were combined; and the mean and 95% confidence interval (CI) at each lead were determined and analyzed by descriptive statistics. Differ- ences at each lead were compared using a 2-tailed paired t test. Eligibility for reperfusion therapy was determined using the 1-mm STE criterion at the J point and 60 milli- seconds later in the limb lead and V4R, and the results for each rater were evaluated using 1-tailed ?2 test or Fisher exact test. In the STE group, the 1-tailed test was appropriate because measurements 60 milliseconds after the J point were higher than those at the J point. In the control group, the 2-tailed ?2 test or Fisher exact text was used. Statistical

Table 1 Clinical characteristics of patients

analyses were performed using SPSS for Windows (Version 12.0K; SPSS Inc, Chicago, IL).

Results

Of the 151,143 patients admitted to the ED during the study period, 919 were suspected of having AMI; and 269 were diagnosed with STEMI. Based on PCI results, 112 of 216 patients were identified with acute inferior STEMI; 24 of these patients were excluded from this study for the following reasons: PCI was not performed because of old age or refusal of therapy (n = 8); no V4R ECG data were available in medical records (n = 6); acute inferior STEMI was associated with BBB (n = 3) or pericarditis (n = 2); patients died before PCI (n = 2); LAD areas were jointly elevated (n = 2); and a pulmonary embolism was present (n = 1). A total of 88 patients (80 men and 8 women; mean age, 61 +- 12 years) constituted the STE group. The median of time from symptom onset to recording of the initial ECG was 125 minutes.

Of the 650 patients suspected of having NSTEMI, 143 were admitted to hospital, underwent PCI, and were identified as having inferior MI; 44 of these patients were excluded from this study for the following reasons: PCI indicated 3-vessel disease with multiple culprit arteries including the LAD (n = 24); repeat admissions (n = 6);

All patients (N = 197)

STE group (n = 88)

Control group (n = 109)

P value

Age, y (+-SD)

63 +- 12

61 +- 12

65 +- 13

.013

Men/women, n

167/30

80/8

87/22

.031

Time from symptom development onset

240

125

360

b.001

to first ECG, min, median

Medical history, n (%)

Active smoker

86 (43.7)

46 (52.3)

40 (36.7)

.028

Diabetic

63 (32.0)

23 (26.1)

40 (36.7)

N.05

Hypertension

117 (59.4)

48 (54.5)

69 (63.3)

N.05

Dyslipidemia

134 (68.0)

68 (77.3)

66 (60.6)

.012

Previous coronary artery disease

55 (27.9)

18 (20.5)

37 (33.9)

.036

Familial history

12 (6.1)

6 (6.8)

6 (5.5)

N.05

Stroke

28 (14.2)

11 (12.5)

17 (15.6)

N.05

Left ventricular ejection fraction, % (+-SD)

53 +- 10

55 +- 8

51 +- 11

.014

Enzyme peaks

CPK, IU/L (+-SD)

1673 +- 1797

2504 +- 1731

1003 +- 1559

b.001

CK-MB, ng/mL (+-SD)

124 +- 120

195 +- 126

67 +- 77

b.001

Troponin I, ng/mL (+-SD)

32.8 +- 59

49 +- 79

19.5 +- 31.2

.001

Hemodynamic complication, n (%)

56 (28.4)

32 (36.4)

24 (22.0)

.026

Death in acute phase, n (%)

8 (4.1)

4 (4.5)

4 (3.7)

N.05

Culprit artery, n (%)

RCA

153 (77.7)

76 (86.4)

77 (70.6)

.008

LCX

37 (18.8)

11 (12.5)

26 (23.9)

.043

Right and left circumflex coronary artery

7 (3.6)

1 (1.1)

6 (5.5)

N.05

CPK indicates Creatine phosphokinase; CK, creatine kinase.

Lead

STE at J point, mm (95% CI)

STE at 60 ms after J point, mm (95% CI)

P value

STE range at J point, mm

STE range at 60 ms after J point, mm

STE group

I

-0.72 (-0.84 to -0.60)

-0.71 (-0.84 to -0.57)

.777

-3.5 to

1.0

-3.5 to 1.5

II

1.50 (1.36 to 1.67)

1.94 (1.73 to 2.14)

.000

-2.5 to

6.5

-1.0 to 8.0

III

2.29 (2.09 to 2.48)

2.65 (2.42 to 2.87)

.000

0.0 to

7.0

0.5 to 7.5

aVR

-0.44 (-0.56 to -0.31)

-0.46 (-0.59 to -0.32)

.705

-4.0 to

1.0

-5.0 to 1.5

aVL

-1.52 (-1.66 to -1.39)

-1.59 (-1.74 to -1.45)

.057

-4.5 to

0.0

-5.0 to 0.0

aVF

1.82 (1.64 to 2.00)

2.23 (2.03 to 2.44)

.000

0.0 to

7.0

0.5 to 7.5

V4R

0.27 (0.18 to 0.37)

0.43 (0.31 to 0.54)

.000

-1.0 to

3.0

-1.0 to 3.5

Control group

I

-0.33 (-0.44 to -0.22)

-0.30 (-0.41 to -0.19)

.039

-5.0 to

0.5

-4.0 to 1.0

II

-0.13 (-0.26 to 0.00)

-0.10 (-0.22 to 0.02)

.221

-4.0 to

1.5

-4.0 to 1.5

III

0.21 (0.11 to 0.31)

0.17 (0.07 to 0.26)

.087

-1.0 to

1.5

-1.0 to 2.0

aVR

0.24 (0.12 to 0.35)

0.24 (0.13 to 0.34)

.975

-1.0 to

4.0

-1.0 to 4.0

aVL

-0.22 (-0.33 to -0.14)

-0.24 (-0.36 to -0.12)

.919

-3.0 to

1.0

-4.0 to 1.5

aVF

0.02 (-0.10 to 0.13)

0.02 (-0.09 to 0.13)

.972

-3.0 to

1.5

-3.0 to 1.5

Data from the 2 raters were combined.

incomplete or missing ECG data (n = 3); and association with BBB (n = 1). A total of 109 patients (87 men and 22 women; mean age, 65 +- 13 years) thus constituted the control group. The median time from symptom onset to recording of the initial ECG was 360 minutes. Table 1 shows the clinical characteristics of the STE and control groups.

Table 2 Comparison of mean STE values

The STE group patients were younger and contained more men. Active smoking and dyslipidemia were more common in the STE group patients, but patients who had previous coronary artery disease were more frequent in the control group. Left ventricular ejection fraction was higher in the STE group, and cardiac biomarkers and hemodynamic complications were lower in the control group. The RCA was the more common culprit artery in both group, and the proportion of the LCX was higher in the control group than the STE group. These findings are shown in Table 1 and were statistically significant. P values were obtained from

Table 3 Numbers of patients who met the criteria below, as measured by raters 1 and 2

2-tailed t tests comparing numerical variables and either the 2-tailed ?2 test or Fischer exact test for comparison of nominal variables.

To determine interrater reliability, the intraclass correlation coefficient was calculated for each lead, taking subjects and leads into account. The mean calculated intraclass correlation coefficient was 0.92. To determine the intrarater coefficient, Pearson Correlation coefficients were calculated for each lead. The mean Pearson correlation coefficient was 0.90.

When the results at each lead were compared in the STE group, STE measured 60 milliseconds after the J point was statistically significantly higher than STE measured at the J point at leads II, III, aVF, and V4R (P b .05), but not at the aVL, I, or aVR leads (Table 2). In the control group, only STE measured at the 2 points of lead I differed significantly (P b .05); there were no differences in measurements at other leads (Table 2).

Criteria

Met criteria when measured at the J point, n (%)

Met criteria

0.06 s after

when the J

measured point, n (%)

P value

Rater 1

STE group ?

1-mm STE in 2 consecutive leads (limb leads) 1-mm STE in V4R

Control group

1-mm STE in 2 consecutive leads (limb leads) Rater 2

STE group ?

1-mm STE in 2 consecutive leads (limb leads) 1-mm STE in V4R

Control group

1-mm STE in 2 consecutive leads (limb leads)

81 (92.0)

85 (97)

.165

17 (19)

26 (30)

.080

8 (7)

11 (10)

.316

78 (89)

83 (94)

.14

14 (16)

23 (26)

.069

6 (6)

8 (7)

.392

* One-tailed ?2 test or Fisher exact test.

Table 4 Culprit artery of V4R in ST elevation patients

Culprit artery Met criteria when Met criteria when

measured at the J point in

V4R, n (%)

measured 0.06 s after the J point in V4R, n (%)

P

value

Rater 1 RCA as a

culprit artery Rater 2

RCA as a culprit artery

16 (94)

25 (96)

1.000

12 (86)

22 (96)

.544

In the STE group, rater 1 found that 81 patients (92%) met at least the 1-mm STE criterion in the limb lead measured at the J point, whereas 85 patients (97%) met this criterion at 60 milliseconds after the J point (Table 3). The difference in diagnostic sensitivity was 5%, but this was not statistically significant (P = .165). At V4R, 17 patients (19%) met this criterion at the J point, whereas 26 (30%) met the criterion at 60 milliseconds after the J point; this difference of 11% was statistically significant (P = .080). In the control group, rater 1 found that 8 patients (8%) met the criterion at the J point, whereas 11 (10%) met the criterion at 60 milliseconds; this difference of 2% was not statistically significant (P = .315). In the STE group, rater 2, who used the same method as rater 1, found that 78 patients (89%) met the criterion at the J point in the limb lead, whereas 83 (94%) met the criterion at 60 milliseconds after the J point; this difference of 5% was not statistically significant (P = .140, Table 3). At V4R, 14 patients (16%) met the criterion at the J point, whereas 23 (26%) met the criterion at 60 milliseconds after the J point; this difference in diagnostic sensitivity of 10% was statistically significant (P = .069). In the control group, rater 2 found that 6 patients (6%) met the criterion at the J point in the limb lead, whereas 8 (7%) met this criterion at 60 milliseconds after the J point; this difference of 1% was

not statistically significant (P = .392) (Table 3).

In the patients having V4R STE, the number of RCA as a culprit artery was described in Table 4. In the STE group, rater 1 found that 16 patients (94%) met the criterion at the J point of the V4R, whereas 25 (96%) met the criterion

Table 5 Diagnostic accuracy of V4R for RCA as a culprit artery

Diagnostic accuracy of V4R

Met criteria when measured at the

J point in V4R, %

Met criteria when measured 0.06 s after the J point in V4R, %

Rater 1

Sensitivity

20.8

32.5

Specificity

90.9

90.9

Rater 2

Sensitivity

15.6

28.6

Specificity

81.8

90.9

60 milliseconds after the J point; this difference of 2% was not statistically significant (P = .000) (Table 4). Rater 2 found that 12 patients (86%) had STE in the V4R at the J point, whereas 22 patients (96%) met the criterion 60 milli- seconds after the J point; this difference of 10% was again not statistically significant (P = .544) (Table 4).

The diagnostic accuracy of V4R was measured. The sensitivity and specificity of V4R in detection of the RCA as a culprit artery were calculated for each rater (Table 5). For rater 1, the sensitivity of V4R STE was 20.8% at the J point and 32.5% 60 milliseconds after the J point. Specificity was

90.9 % at both points. For rater 2, the sensitivity of V4R STE was 15.6% at the J point and 28.6% 60 milliseconds after the J point. Specificity was 81.8% at the J point and 90.9% 60 milliseconds after the J point (Table 5).

Discussion

The results of this study clearly show that STE measured 60 milliseconds after the J point was consistently higher than STE measured at the J point in leads II, III, aVF, and V4R (Tables 2 and 3). The sensitivity of V4R STE at 60 milli- seconds after the J point was higher than the STE measured at the J point (Table 5). The correct diagnosis and treatment of STEMI affect patient prognosis [1]. Electrocardiography is the primary diagnostic method used to determine therapy. Specifically, the presence of STE is a critical factor in deciding the direction of therapy [1,8]. However, although there have been many studies on MI, the inclusion criteria for ECG have been uncertain. These uncertainties include the point at which STE is measured, the voltage criterion for STE, and the baseline for STE measurements. Most previous studies have used the J point or 60 to 80 milliseconds after the J point as the point of STE measurement [2,3,9-15], whereas other studies do not mention the measuring points at all [5]. We found, however, that differences in measuring points can affect ECG interpretation, thereby affecting further therapy. In the absence of a clear measuring point, the rate of misdiagnosis can be as high as 12% [16], with the precordial lead having a possible impact [6]. Indeed, we found that the difference in diagnostic sensitivity was 5%.

Several studies have reported that the voltage criteria for STE in the precordial lead are 1 or 2 mm, or 2 mm in men and

1.5 mm in women, whereas the criteria for STE in the inferior lead are 1 mm [1,3,5,17-21]. As our measurements were performed only in the limb leads and V4R, we did not have a voltage criterion problem. Diagnosis of STEMI is defined at 2 consecutive leads, with criteria for STEMI diagnosis with or without the Cabrera display in limb leads [1-3]. It is currently unclear whether the PR or TP segment should be the baseline for STE measurements [3].

According to the 2007 ACC/AHA/ESC consensus univer- sal definition of myocardial infarction, the diagnostic standard for STEMI is defined as new ST elevation at the J point in 2

contiguous leads with the cutoff points of at least 0.2 mV in men and at least 0.15 mV in women in leads V2 through V3 and/or cutoff point of at least 0.1 mV in other leads [3]. We found that, in the STE group, the difference in diagnostic sensitivity at the inferior lead was 5%, depending on whether STE was measured at the J point or 60 milliseconds after the J point. Although this difference was not statistically significant, it should not be disregarded. In misdiagnosis of AMI in EDs, a difference of 2% was found to be important, although not statistically significant [22]. Thus, our finding of a 5% difference in diagnostic sensitivity may also be biologically important, regardless of statistical significance.

Our control group consisted of patients diagnosed as not having STE based on initial ECG data when admitted to the ED. Although there was some discrepancy between raters, STE was present in 6% to 7% of patients at the J point and in 7% to 10% 60 milliseconds after the J point. This is an area where standardization is needed.

The median time from symptom development to ECG was different in the STE and control groups. Several possible explanations may be advanced. Patients in the STE group were more severely ill and had clear symptoms attributable to ACS. Therefore, such patients came to hospital in a timely manner. The symptoms of NSTEMI are more vague and indistinguishable from those of other diseases. Thus, NSTEMI patients came to hospital later; and more time was required to diagnose ACS.

Recognition of right ventricular infarction is very important because it is an independent predictor of major complications and in-hospital mortality [23]. Physicians should also consider intravascular Volume expansion and the occasional need for an infusion of dobutamine [24]. Right precordial V4 lead is very useful for assessment of right ventricular involvement [24]. In the present study, specificity was high but sensitivity was low. The sensitivity of V4R for detection of right ventricular infarction was greater 60 milli- seconds after the J point than at the J point.

Although V4R is not mentioned in the criteria of Thygesen et al [3], we observed differences in STE measurements, with the diagnostic sensitivity being signif- icantly dependent on the points of measurement in the STE group. The median duration from symptom development to ECG differed between the STE and control groups. However, V4R was measured only in STE group patients and may have no effect on diagnostic sensitivity.

This study had several limitations, including a retrospec- tive design. As we assessed patients diagnosed with MI, these results are not applicable to Clinical cases. Because measurements were performed in the inferior lead and V4R, not in the precordial lead, we could not predict results involving the precordial lead. Results may also differ depending on measuring points, voltage criteria, and chosen baseline. Clinically, the shape of the ST elevation and the appearance of the patient are very important for the ultimate diagnosis. The fact that the duration from symptom development to ECG time differed in the 2 groups may

affect accuracy slightly. In addition, our study design made it impossible to describe the exact lesion within the RCA. Lastly, we did not obtain any data at V4R for the control group. Future studies should specify criteria and baselines prospectively, as well as involving multiple institutions.

In conclusion, STE measurements in limb leads and V4R may differ, depending on STE measuring points. ST-segment elevation criteria and measurement methods need to be specified to avoid confusion and to standardize diagnosis.

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