Journal of ISSN: 2373-4396JCCR

Cardiology & Current Research
Review Article
Volume 2 Issue 6 - 2015
ST Elevation in Lead aVR and In-Hospital and Mid-Term Adverse Events in Patients with Medically Treated ST Elevation Myocardial Infarction
Mehdi Mousavi1*, Solmaz Kalhor2 and Jafar Tahmasbi3
1Interventional Cardiologist, Alborz University of Medical Sciences, Iran
2Islamic Azad University, Iran
3Cardiologist, Shahroud University of Medical Sciences, Iran
Received: April 19, 2015| Published: May 14, 2015
*Corresponding author: Mehdi Mousavi, Interventional Cardiologist, Assistant professor, Alborz University of Medical Sciences, Shahid Rajai Hospital, Karaj, Iran, Tel: +1 514 998 3284; Email: @, @
Citation: Mousavi M, Kalhor S, Tahmasbi J (2015) ST Elevation in Lead aVR and In-Hospital and Mid-Term Adverse Events in Patients with Medically Treated ST Elevation Myocardial Infarction. J Cardiol Curr Res 2(6): 00080. DOI: 10.15406/jccr.2015.02.00080

Abstract

Background: ST segment elevation and deviation in lead aVR can provide useful prognostic information in patients with ST elevation myocardial infarction (STEMI). The aim of the present study was evaluation of the effect of aVR ST elevation (aVR-STE) and aVR ST deviation (aVR-STD) the in-hospital and six-month prognosis of patients with STEMI.

Methods: The study was a cohort of medically treated patients with acute STEMI. The patients were categorized as aVR ST elevation (aVR-STE) or aVR ST deviation (aVR-STD) if there was > 0.05 mv ST elevation or ST deviation in lead aVR, respectively; otherwise, they were categorized as control groups.

Results: 334 patients [49 patients (14.67%) with aVR-STE and 159 patients (47.60%) with aVR-STD] were included. The mean age of the study group was 59.62 ± 13.03 years and 75.4% were male. In-hospital mortality was not significantly different in patients with or without aVR-STE or aVR-STD. Pulmonary edema or overt decompensated heart failure was seen more in patients with aVR-STE [Relative risk (RR): 3.393, 95% confidence interval: 1.405-8.192, P = 0.012] and it trended more in patients with aVR-STD (P = 0.06).

6-month follow up: Mortality was not significantly different among patients with or without aVR-STE or aVR-STD. Pulmonary edema or overt decompensated heart failure occurred more in patients with aVR-STE and aVR-STD (RR: 3.190, 95% confidence interval: 1.684-6.046, P < 0.0001, RR: 1.937, 95% confidence interval: 0.987-3.800, P = 0.049).

Conclusion: ST elevation or deviation in lead aVR was not an indicator of in-hospital and six-month mortality in our study. However, its effect on pulmonary edema or overt decompensated heart failure requires more study.

Keywords: ST elevation myocardial infarction; Electrocardiography; Prognosis; ST segment elevation in lead aVR

Abbreviations

CKMB: Creatine Phosphokinase type MB; RR: Relative Risks; aVR-STD: aVR ST Deviation; aVR STE: aVR ST Elevation; CAD: Coronary Artery Disease; CKMB: Creatine Phosphokinase type MB; DBP: Diastolic Blood Pressure; HDL: High Density Lipoprotein Cholesterol; LDL: Low Density Lipoprotein Cholesterol; LV: Left Ventricle; SBP: Systolic Blood Pressure; STEMI: ST Elevation Myocardial Infarction; VS: Versus; PE-HF: Pulmonary Edema or overt decompensated Heart Failure; RI-CP: Recurrent Ischemic Chest Pain

Introduction

Lead aVR is often ignored in standard 12-lead ECG [1-3], as it is oriented to the upper-right side of the heart and is not adjacent to other leads. Hence, ST-segment elevation in aVR has been associated with severe coronary artery lesions in patients with STEMI [4-7] and other acute coronary syndromes [6,8-12] and may be an indicator of more important coronary occlusion [4-7,13-19] ST segment changes in lead aVR may also be correlated with left ventricular function, mortality and prognostic findings during the hospital stay of patients with STEMI [1,4,14,15,18,20,21], and UA/NSTEMI [2,3,10]. Nonetheless, the prognostic value of ST elevation and ST deviation in lead aVR-particularly in longer follow up-requires more study. Thus, we decided to study the in-hospital and six-month prognostic value of aVR ST elevation (aVR-STE) and aVR ST deviation (aVR-STD) in STEMI.

Materials and Methods

The study was a cohort of patients with acute STEMI (started at April 2010 and finished at December 2012) in two hospitals with CCU in Shahroud, Iran, which were the only centres with CCU in the township. Patients with ST elevation (STEMI) were included if they presented within 12 hours of symptom-onset. Excluded patients were those with a left bundle branch block, left ventricular hypertrophy, ventricular paced rhythm at presentation, and those who did not sign the written informed consent. There was no facility for primary PCI in the city, and patients were treated medically according to the present guidelines, and fibrinolytic therapy with streptokinase was prescribed unless contraindicated. The initial 12-lead ECG was obtained at the emergency room at the time of admission. Heart rate, systolic and diastolic blood pressure and creatine phosphokinase type MB (CKMB) were also measured at the admition time. A single investigator blinded to clinical data examined all the ECGs. ST elevation in lead aVR was defined as > 0.05 mV of ST elevation in lead aVR, 20 ms after the J point, using the preceding TP segment as the baseline. ST deviation in lead aVR was defined as deviation of the ST segment, including ST elevation > 0.05 mv, 20 ms after the J point or ST depression > 0.05 mv 80 ms after J point.

Transthoracic 2D and Doppler echocardiography were performed for all of the patients within three days of admission and ejection fraction was detected by the eyeball method. All of the included patients were followed up during admission time and 316 patients completed six-month follow up. Our primary endpoint was a comparison of mortality during in-hospital admission among patients with and without aVR-STE. The secondary endpoint was a combination of any of the following adverse events during admission and six-month follow up:

  1. Death
  2. Recurrent STEMI
  3. Recurrent ischemic chest pain
  4. Pulmonary edema or overt decompensated heart failure (PE-HF)
A local ethical committee approved the study protocol (Registration number: 2123816) and written informed consent was obtained.
Data and analysis

For the statistical analysis, the statistical software SPSS version 16.0 for windows (SPSS Inc., Chicago, Illinois) was used. Numerical variables are presented as mean ± SD, and categorical variables are summarized by raw numbers and percentages. Continuous variables were compared using the Student's t-test or the nonparametric Mann-Whitney U test whenever the data did not appear to have a normal distribution, and categorical variables were compared using the chi-square or Fisher's exact test, as required. Relative risks (RR) and 95% confidence intervals were calculated if needed. Multivariate analysis using logistic regression or Cox regression analysis with the backward Wald method was used whenever needed and Kaplan-Meier curves were drown.

Sample size calculation: Based on the assumption that the baseline incidence of in-hospital death in patients with aVR-STE would be 19% and 5% in the those without aVR-STE, and that the incidence of aVR-STE would be about 16% [14], with an α error of 0.05, a β error of 0.2 and a power of 80%, around 47 patients in the aVR-STE group and 282 patients without aVR-STE were needed.

Results

Patient characteristics

In total, 334 patients [49 patients (14.67%) with aVR-STE] were included in the study. There were 110 patients (32.93%) with aVR ST depression, and hence 159 patients (47.60%) had aVR-STD. The mean age of the study group was 59.62 ± 13.03 years and 252 patients (75.4%) were male. The basal characteristics of the studied groups were almost uniform spatially regarding drug therapy including treatment with fibrinolythics in aVR-STE and aVR-STD groups in comparison with controls. Important basal characteristics and those with significant difference are presented in Table 1. In patients with aVR ST depression, the involvement of the inferior wall was seen in 64 patients (58.18%) and the anterior wall and the lateral wall in 24 (21.82%) and 23 (20.91%), respectively.

Variable

aVR-STE

Without aVR-STE n=285

P value

aVR-STD n=159

Without aVR-STD n=175

P value

Age(year)

59.95 ± 13.01

59.56 ± 13.05

0.845

60.6 ± 12.7

58.6 ± 13.2

0.168

Sex (male)

35 (71.4%)

217 (76.1%)

0.479

121 (76.1%)

131 (74.9%)

0.792

Hyperlipidemia

13 (26.5%)

42 (14.7%)

0.04

24 (15.1%)

31 (17.7%)

0.519

Family History of Premature CAD

14 (29.2%)

54 (19.4%)

0.125

41 (26.3%)

27 (15.9%)

0.021

Summed ST Elevation

13.64 ± 10.99

11.01 ± 9.56

0.092

13.63 ± 10.99

9.3 ± 8.09

<0.001

Summed ST Deviation

18.46 ± 11.24

14.27 ± 10.42

0.002

18.44 ± 11.72

11.66 ± 8.34

<0.001

Anterior Wall STEMI

42 (85.7%)

154 (54%)

0.0001

86 (54.1%)

110 (62.9%)

0.104

Inferior Wall STEMI

6 (12.2%)

127 (44.6%)

0.0001

70 (44%)

63 (36%)

0.135

Lateral Wall STEMI

3 (6.1%)

32 (11.2%)

0.281

26 (16.4%)

9 (5.1%)

0.001

Previous Therapy with Statins

5 (10.2%)

14 (4.9%)

0.175

7 (4.4%)

12 (6.9%)

0.321

CKMB (IU/L)

86.19 ± 113.5

112.5 ± 173.8

0.722

102.4 ± 144.6

114.5 ± 184.5

0.621

LDL (mg/dL)

93.1 ± 27.3

103.9 ± 30.2

0.023

98.1 ± 26.3

106.2 ± 32.6

0.016

HDL (mg/dL)

37.9 ± 9.5

41.8 ± 11.6

0.045

40.4 ± 10.1

42 ± 12.4

0.308

Cholesterol (mg/dL)

163.4 ± 40

179.9 ± 40.4

0.012

172.9 ± 37.2

181.7 ± 43.3

0.055

Triglyceride (mg/dL)

110.9 ± 63.3

124.8 ± 89.1

0.189

119.9 ± 71

125.4 ± 97.7

0.85

Creatinine (mg/dL)

1.18 ± 0.5

1.02 ± 0.29

0.018

1.07 ± 0.37

1.02 ± 0.30

0.23

Heart Rate

84.87 ± 15.7

77.17 ± 20.9

0.001

80.37 ± 22

76.4 ± 18.6

0.324

SBP (mmHg)

134.8 ± 38.4

129.7 ± 28.8

0.413

131.8 ± 30.9

129.3 ± 30.0

0.212

DBP (mmHg)

83.16 ± 20.5

74.49 ± 15.7

0.376

81.3 ± 16.6

78.8 ± 16.4

0.16

Ejection Fraction (%)

38.93 ± 10.1

43.32 ± 9.18

0.015

42.2 ± 9.31

43.1 ± 9.5

0.314

Table 1: Baseline characteristics of studied groups; Numerical variables are presented as mean ± SD (standard deviation), and categorical variables are summarized by raw numbers and percentages.

 aVR-STD: aVR ST Devation; aVR STE: aVR ST Elevation; CAD: Coronary Artery Disease; CKMB: Creatine phosphokinase type MB; DBP: Diastolic Blood Pressure; HDL: High Density Lipoprotein Cholesterol; LDL: Low Density Lipoprotein Cholesterol; LV: Left Ventricle; SBP: Systolic Blood Pressure; STEMI: ST Elevation Myocardial Infarction; VS: Versus

In-hospital outcome: A comparison between the in-hospital outcomes of the included patients according to aVR-STE or aVR-STD in patients is given in Table 2. The primary endpoint of the study (in-hospital death) was not significantly different in patients with or without aVR-STE [four patients (8.2%) with aVR-STE and 13 (4.6%) patients without aVR-STE, RR: 1.790, 95% confidence interval: 0.608-5.264, P = 0.290]. The in-hospital mortality was almost the same in patients with or without aVR-STD (Table 2) and the incidence of death was not significantly different among different types of STEMI (involving the anterior, inferior or lateral wall) in patients with aVR-STE or aVR-STD (Table 2).

All of the Patients

aVR-STE n=49

Without aVR-STE

P value

aVR-STD n=159

Without aVR-STD n=175

P value

Death

4 (8.2%)

13 (4.6%)

0.29

8 (5%)

9 (5.1%)

0.963

R-STEMI

0

0

0.999

0

0

0.999

RI-CP

9 (18.4%)

50(17.5%)

0.889

26 (16.4%)

33 (18.9%)

0.549

PE-HF

7 (14.3%)

12 (4.2%)

0.012

13 (8.2%)

6 (3.4%)

0.061

Composite End Point

19 (38.8%)

70 (24.6%)

0.038

43 (27%)

46 (26.3%)

0.876

Anterior wall STEMI (n=196)

aVR-STE n=42

Without aVR-STE

P value

aVR-STD n=86

Without aVR-STD n=110

P value

Death

3 (7.1%)

8 (5.2%)

0.705

5 (5.8%)

6 (5.5%)

>0.999

R-STEMI

0

0

>0.999

0

0

>0.999

RI-CP

8 (19.0%)

32(20.8%)

0.805

16 (18.6%)

24 (21.8%)

0.58

PE-HF

7 (16.7%)

6 (3.9%)

0.008

9 (10.5%)

4 (3.6%)

0.057

Composite End Point

17(40.5%)

43 (27.9%)

0.118

27 (31.4%)

33 (30.0%)

0.833

Inferior wall STEMI (n=133)

aVR-STE n=6

Without aVR-STE

P value

aVR-STD n=70

Without aVR-STD n=63

P value

Death

1 (1.7%)

5 (3.5%)

0.246

3 (4.3%)

3 (4.8%)

>0.999

R-STEMI

0

0

>0.999

0

0

>0.999

RI-CP

0 (0.0%)

18(14.2%)

>0.999

9 (12.9%)

9 (14.3%)

0.81

PE-HF

0 (0.0%)

5 (3.9%)

>0.999

4 (5.7%)

1 (1.6%)

0.369

Composite End Point

1(16.7%)

26 (20.5%)

>0.999

15 (21.4%)

12 (19.0%)

0.733

Lateral wall STEMI (n=35)

aVR-STE n=3

Without aVR-STE

P value

aVR-STD n=26

Without aVR-STD n=9

P value

Death

1 (33.3%)

0 (0.0%)

0.086

1 (3.8%)

0 (0.0%)

>0.999

R-STEMI

0

0

0.999

0

0

>0.999

RI-CP

1 (33.3%)

7 (21.9%)

0.553

8 (30.8%)

0 (0.0%)

0.081

PE-HF

0 (0.0%)

4 (12.5%)

>0.999

3 (11.5%)

1 (11.1%)

>0.999

Composite End Point

2 (66.7%)

10 (31.2%)

0.266

11 (42.3%)

1 (11.1%)

0.121

Table 2: Results of in-hospital follow up in studied groups.

aVR-STD: aVR ST Deviation; aVR-STE: aVR ST Elevation; PE-HF: Pulmonary Edema or overt decompensated Heart Failure; RI-CP: Recurrent Ischemic Chest Pain; R-STEMI: Recurrent ST-Elevation Myocardial Infarction

In total, 89 (26.65%) patients had ≥ 1 event associated with in-hospital composite endpoints. The in-hospital composite endpoint occurred more in patients with aVR-STE (Table 2, RR: 1.579, 95% confidence interval: 1.051-2.370, P = 0.038), but it was not significantly different in patients with or without aVR-STD (Table 2). Multivariate analysis showed that, among the included confounding variables in the model, ST elevation in aVR was not an independent predictor of in-hospital composite endpoint (Table 3A). Neither aVR-STE nor aVR-STD had a relationship to in-hospital recurrent STEMI and recurrent chest pain, although PE-HF was seen more in patients with aVR-STE [seven patients (14.3%) with aVR-STE, versus 12 patients (4.2%) without aVR-STE, RR: 3.393, 95% confidence interval: 1.405-8.192, P = 0.012] and it trended more in patients with aVR-STD (Table 2, RR: 2.385, 95% confidence interval: 0.929-6.124, P=0.06). Multivariate analysis showed that ST elevation in aVR was an independent predictor of in-hospital PE-HF [Ex (B): 38.46, 95% confidence interval: 1.014-1000, P = 0.04 Table 3B].

Variable

Ex (B)

95% Confidence Interval for Ex(B)

P value

A: In-hospital cumulative endpoint

Family history of premature CAD

5.556

1.587-14.286

<0.0001

Blood urea nitrogen

1.054

1.018-1.090

0.003

Summed ST elevation

1.054

1.009-1.101

0.019

Serum potassium

2.017

0.918-4.432

0.081

B: In-hospital pulmonary edema and overt decompensated heart failure

Treatment with diuretics

333.333

4.27-10000

0.009

Summed ST elevation

1.167

1.036-1.315

0.011

Treatment with beta blockers

0.008

0.0001-0.409

0.016

Aspartate transaminase

1.010

1.001-1.018

0.027

ST elevation in lead aVR

38.46

1.014-1000

0.049

Blood urea nitrogen

1.025

1.000-1.050

0.050

Serum potassium level

7.383

0.890-61.225

0.064

Ejection fraction

0.867

0.744-1.010

0.066

Table 3: Results of the final step of binary logistic regression with backward Wald method for A: independent predictors of in-hospital cumulative endpoint. B: In-hospital pulmonary edema and overt decompensated heart failure.

CAD: Coronary Artery Disease.

Six-month follow up: During six-month follow up, mortality was not significantly different among patients with or without aVR-STE or ST deviation (Table 4). Composite endpoints trended more in patients with aVR-STE (Table 4, RR: 1.262, 95% confidence interval: 0.940-1.695, P = 0.149), and it was not significantly different among patients with or without aVR-STD (Table 4). Multivariate analysis using Cox regression analysis showed that aVR-STE was not an independent predictor of a six-month composite endpoint (Table 5A).

All of the Patients

aVR-STE n=48

Without aVR-STE

P value

aVR-STD n=150

Without aVR-STD n=166

P value

Death

4 (8.3%)

25 (9.3%)

>0.999

14 (9.3%)

15 (9%)

0.927

R-STEMI

0 (0%)

2 (0.7%)

>0.999

1 (0.7%)

1 (0.6%)

>0.999

RI-CP

10 (20.8%)

67(25.0%)

0.536

34(22.7%)

43(25.9%)

0.503

PE-HF

12 (25%)

21 (7.8%)

<0.001

21 (14%)

12 (7.2%)

0.049

Composite End Point

26 (54.2%)

115 (42.9%)

0.149

70 (46.7%)

71 (42.8%)

0.487

Anterior wall STEMI

aVR-STE n=41

without aVR-STE

P value

aVR-STD n=80

Without aVR-STD n=102

P value

Death

3 (7.3%)

15 (10.6%)

0.767

8 (10%)

10 (9.8%)

0.965

R-STEMI

0

1 (0.7%)

>0.999

0

1 (1%)

>0.999

RI-CP

9 (22%)

38 (27%)

0.52

18 (22.5%)

29 (28.4%)

0.364

PE-HF

9 (22%)

12 (8.5%)

0.026

13 (16.2%)

8 (7.8%)

0.078

Composite End Point

21 (51.2%)

66 (46.8%)

0.619

39 (48.8%)

48 (47.1%)

0.821

Inferior wall STEMI

aVR-STE n=6

Without aVR-STE

P value

aVR-STD n=67

Without aVR-STD n=62

P value

Death

1 (16.7%)

10 (8.1%)

0.421

6 (9%)

5 (8.1%)

0.856

R-STEMI

0

1 (0.8%)

>0.999

1 (1.5%)

0

>0.999

RI-CP

0

28 (22.8%)

0.339

14 (20.9%)

14 (22.6%)

0.817

PE-HF

3 (50%)

8 (6.5%)

0.008

8 (11.9%)

3 (4.8%)

0.149

Composite End Point

4 (66.7%)

47 (38.2%)

0.212

29 (43.3%)

22 (35.5%)

0.365

Lateral wall STEMI

aVR-STE n=3

Without aVR-STE

P value

aVR-STD n=24

Without aVR-STD n=8

P value

Death

1 (33%)

1 (3.4%)

0.181

2 (8.3%)

0

>0.999

R-STEMI

1 (3.4%)

0

>0.999

1 (4.2%)

0

>0.999

RI-CP

1 (33.3%)

9 (31.0%)

>0.999

9 (37.5%)

1 (12.5%)

0.38

PE-HF

0

5 (17.2%)

>0.999

3 (12.5%)

2 (25%)

0.578

Composite End Point

2 (66.7%)

16 (55.2%)

>0.999

15 (62.5%)

3 (37.5%)

0.252

Table 4: Results of six-month follow up in studied groups with completed follow up.

aVR-STD: aVR ST Deviation, aVR-STE: aVR ST Elevation, PE-HF: Pulmonary Edema or overt decompensated Heart Failure, RI-CP: Recurrent Ischemic Chest pain, R-STEMI: Recurrent ST-Elevation Myocardial Infarction

Among the endpoints, PE-HF occurred more in patients with aVR-STE and aVR-STD (RR: 3.190, 95% confidence interval: 1.684-6.046, P < 0.0001 and RR: 1.937, 95% confidence interval: 0.987-3.800, P = 0.049 respectively, Table 4), but death, recurrent STEMI and recurrent chest pain were not significantly different (Table 4). Multivariate analysis showed that neither aVR-STE nor aVR-STD were independent predictors of PE-HF in six-month follow up (Table 5B).

Variable

Ex (B)

95% confidence interval for Ex (B)

P value

A: 6-month composite endpoints

Serum potassium

1.494

0.977 – 2.286

0.064

Family history of premature CAD

1.626

0.914 – 2.890

0.098

B: 6-month pulmonary edema and decompensated heart failure

Blood urea nitrogen

1.057

1.030-1.086

<0.0001

Hyperlipidemia

20.833

4.500- 10

<0.0001

Cigarette smoking

4.367

1.275-14.925

P=0.019

Table 5: Final step of Cox regression using backward Wald method for independent predictors of A: 6-month composite endpoints (death, recurrent STEMI, recurrent chest pain, pulmonary edema and decompensated heart failure), B: 6-month pulmonary edema and decompensated heart failure in the follow up.

CAD: Coronary Artery Disease.

Kaplan meier curves for death, heart failure and composite end point according to aVR-STE or aVR-STD are given in Figure 1. The mean duration of hospital stay was 6.6 ± 2.47 days in patients with aVR-STE versus 5.92 ± 2.38 days in those without aVR-STE (P = 0.01), and 6.24 ± 2.40 days in patients with aVR-STD versus 5.83 ± 2.40 days in patients without aVR-STD (P = 0.124).

Figure 1: Kaplan-meier curves for 6 month follow up.

A: 6 month occurrence of death according to aVR ST elevation,

B: 6- month occurrence of pulmonary edema and decompensated heart failure according to aVR ST elevation,

C: 6-month occurrence of composite end point according to aVR ST elevation,

D: 6 month occurrence of death according to aVR ST deviation,

E: 6- month occurrence of pulmonary edema and decompensated heart failure according to aVR ST deviation,

F: 6-month occurrence of composite end point according to aVR ST deviation.

Discussion

The incidence of aVR-STE in our study was 14.67%, which was concordant with prior work [14]. Some studies-but not all of them [22]-have shown that ST elevation in lead aVR has been an indicator of poorer prognosis and increased mortality in STEMI [1,4,12,14,20,21]. HERO-2 investigators studied 15,315 STEMI patients who received streptokinase and showed that ST elevation in aVR was associated with higher 30-day mortality regardless of the location of infarction [1,21]. However, in our study neither aVR-STE nor aVR-STD were predictors of in-hospital and six-month mortality (Tables 2 & 4). In the present study, aVR-STE was related to in-hospital composite adverse events in univariate analysis (P = 0.038, Table 2), whereas aVR-STD was not (P = 0.876, Table 2). Analysis using different types of STEMI showed that this pattern was seen mostly in anterior STEMI; however, our study was not sufficiently powerful to draw a definite comparison of the different types of STEMI. In our study, ST depression in lead aVR was seen more in inferior wall infarction. This may explain why, in our study, aVR-STD did not influence in-hospital composite adverse events (P = 0.876, Table 2). More studies are needed to confirm this.

Six-month follow up showed that neither aVR-STE nor aVR-STD were related to six-month composite endpoints (P = 0.149 and P = 0.487 respectively, Table 4). This finding was in agreement with the finding of Senaratne et al. [22], who concluded that aVR-STD was not related to the incidence of one-year adverse cardiac events [22].

Among in-hospital outcomes, neither aVR-STE nor aVR-STD was related to in-hospital recurrent ischemic chest pain and recurrent STEMI (Table 2). It seems that the major difference and relative superiority of the in-hospital composite endpoint in patients with aVR-STE is drawn from PE-HF. ST elevation in lead aVR was related to both in-hospital and six-month PE-HF (P < 0.05, Tables 2 & 4), and aVR-STD tended (P = 0.061, Table 2) to affect its in-hospital occurrence and was significantly related to six-month follow up (P = 0.049). These results were more prominent in anterior STEMI (Tables 2 & 4). There are some other studies indicating that in STEMI [14] and NSTEMI [2], aVR-STE has been associated with a worse Killip class at hospital admission and lower ejection fraction [14]. ST depression in lead aVR has been useful for predicting larger infarction and left ventricular dysfunction (lower ejection fraction) in patients with anterolateral STEMI [23]. However, this finding is not supported by some other studies [15]. The mean ejection fraction in our study was less in patients with aVR-STE (P = 0.015, Table 1), but it was not significantly different in patients with or without aVR-STD (P = 0.314, Table 1).

Patients with aVR-STE needed significantly more diuretic therapy (P = 0.018, Table 1), also those with aVR-STD tended to need more diuretic therapy, P = 0.105, Table 1) during in-hospital admission. This finding is in accordance with more in-hospital PE-HF in those with aVR-STE. A possible description of this finding in our study may be the greater involvement of the anterior wall in patients with aVR-STE and less involvement of the inferior wall (P = 0.0001, Table 1). In addition, there might be a possibility of greater extensive myocardial infarction in patients with aVR-STE or aVR-STD. More studies are needed to confirm this finding because our study was not powerful enough to determine the independent predictors of PE-HF. In the present study, the mean duration of hospital stay was more in patients with aVR-STE (P = 0.01). This finding is probably due to more in-hospital composite endpoints (P = 0.038, Table 2) and particularly heart failure in this group (P = 0.012, Table 2). The mean hospital stay also tended to be more in patients with aVR-STD; however, this was not statistically significant, which is in agreement with some other studies [22]. This finding is in concert with the finding that neither composite endpoints nor PE-HF were significantly related to aVR-STD.

In our study, patients with aVR-STE had higher heart rates (P = 0.001, Table 1). There are other studies which show that aVR-STE has been associated with a higher heart rate and lower systolic blood pressure [14]. This may be explained by a lower ejection fraction (Table 1), a higher prevalence of in-hospital heart failure (Table 2), and – possibly –a greater extent of infarction in these patients. As is shown in Table 1, the summed ST elevation and summed ST deviation were more in those patients with aVR-STE and aVR-STD. This finding is important, because the summed ST elevation and ST deviation are important predictors of the outcome and extent of myocardial infarction. To understand which one is the more powerful and the more important predictor of outcome requires more study.

Study Limitation

An ST elevation and ST deviation > 0.1 mv might have a stronger relationship with mortality [4]; however, in our study, and similar to some other previous works, we defined aVR-STE to be > 0.05 mv [14]. The incidence of an aVR-STE > 0.1 mv in our study was 4.2% and our study population was not large enough to assess its significance in mortality. Treatment with fibrinolytics and primary PCI are among the most important determinants of prognosis and the short-term and long-term outcomes in STEMI. However, treatment with streptokinase was almost uniform in those patients with aVR-STE or aVR-STD (Table 1).

Conclusion

According to the results of the present study, aVR-STE in medically treated patients with STEMI is a more powerful and useful indicator than aVR-STD for the prediction of some in-hospital and six-month outcomes, particularly PE-HF.

Acknowledgement

We would like to thank the kind assistance and cooperation of the nursing staff of Imam Hosein hospital and Islamic Azad University of Shahroud. The study was conducted as a Medical Doctorate thesis in Islamic Azad University.

References

  1. Wong CK, Gao W, Stewart RA, Benatar J, French JK, et al. (2010) aVR ST elevation: an important but neglected sign in ST elevation acute myocardial infarction. Eur Heart J 31(15): 1845-1853.
  2. Barrabes JA, Figueras J, Moure C, Cortadellas J, Soler-Soler J (2003) Prognostic value of lead aVR in patients with a first non-ST-segment elevation acute myocardial infarction. Circulation 108(7): 814-819.
  3. Szymanski FM, Grabowski M, Filipiak KJ, Karpinski G, Opolski G (2008) Admission ST-segment elevation in lead aVR as the factor improving complex risk stratification in acute coronary syndromes. Am J Emerg Med 26(4): 408-412.
  4. Alherbish A, Westerhout CM, Fu Y, White HD, Granger CB, et al. (2013) The forgotten lead: does aVR ST-deviation add insight into the outcomes of ST-elevation myocardial infarction patients? Am Heart 166(2): 333-339.
  5. Engelen DJ, Gorgels AP, Cheriex EC, De Muinck ED, Ophuis AJ, et al. (1999) Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol 34(2): 389-395.
  6. Kuhl JT, Berg RM (2009) Utility of lead aVR for identifying the culprit lesion in acute myocardial infarction. Ann Noninvasive Electrocardiol 14(3): 219-225.
  7. Ducas R, Ariyarajah V, Philipp R, Ducas J, Elliott J, et al. (2013) The presence of ST-elevation in lead aVR predicts significant left main coronary artery stenosis in cardiogenic shock resulting from myocardial infarction: the Manitoba cardiogenic shock registry. Int J Cardiol 166(2): 465-468.
  8. Rostoff P, Piwowarska W (2006) ST segment elevation in lead aVR and coronary artery lesions in patients with acute coronary syndrome. Kardiol Pol 64(1): 8-14.
  9. Hengrussamee K, Kehasukcharoen W, Tansuphaswadikul S (2005) Significance of lead aVR ST segment elevation in acute coronary syndrome. J Med Assoc Thai 2005 88(10): 1382-1387.
  10. Kosuge M, Kimura K, Ishikawa T, Ebina T, Hibi K, et al. (2006) Combined prognostic utility of ST segment in lead aVR and troponin T on admission in non-ST-segment elevation acute coronary syndromes. Am J Cardiol 97(3): 334-339.
  11. Kosuge M, Kimura K, Ishikawa T, Ebina T, Shimizu T, et al. (2005) Predictors of left main or three-vessel disease in patients who have acute coronary syndromes with non-ST-segment elevation. Am J Cardiol 95(11): 1366-1369.
  12. Gorgels AP, Vos MA, Mulleneers R, de Zwaan C, Bar FW, et al. (1993) Value of the electrocardiogram in diagnosing the number of severely narrowed coronary arteries in rest angina pectoris. Am J Cardiol 72(14): 999-1003.
  13. Kotoku M, Tamura A, Abe Y, Kadota J (2009) Determinants of ST-segment level in lead aVR in anterior wall acute myocardial infarction with ST-segment elevation. J Electrocardiol 42(2): 112-117.
  14. Aygul N, Ozdemir K, Tokac M, Aygul MU, Duzenli MA, et al. (2008) Value of lead aVR in predicting acute occlusion of proximal left anterior descending coronary artery and in-hospital outcome in ST-elevation myocardial infarction: an electrocardiographic predictor of poor prognosis. J Electrocardiol 41(4): 335-341.
  15. Goto Y, Tamura A, Kotoku M, Kadota J (2011) ST-segment deviation in lead aVR on admission is not associated with left ventricular function at predischarge in first anterior wall ST-segment elevation acute myocardial infarction. Am J Cardiol 108(5): 625-629.
  16. Sun TW, Wang LX, Zhang YZ (2007) The value of ECG lead aVR in the differential diagnosis of acute inferior wall myocardial infarction. Intern Med 46(12): 795-799.
  17. Nair R, Glancy DL (2002) ECG discrimination between right and left circumflex coronary arterial occlusion in patients with acute inferior myocardial infarction: value of old criteria and use of lead aVR. Chest 122(1): 134-139.
  18. Kanei Y, Sharma J, Diwan R, Sklash R, Vales LL, et al. (2010) ST-segment depression in aVR as a predictor of culprit artery and infarct size in acute inferior wall ST-segment elevation myocardial infarction. J Electrocardiol 43(2): 132-135.
  19. Vales L, Kanei Y, Schweitzer P (2011) Electrocardiographic predictors of culprit artery in acute inferior ST elevation myocardial infarction. J Electrocardiol 44(1): 31-35.
  20. Kukla P, Bryniarski L, Dudek D, Krolikowski T, Kawecka Jaszcz K (2012) Prognostic significance of ST segment changes in lead aVR in patients with acute inferior myocardial infarction with ST segment elevation. Kardiol Pol 70(2): 111-118.
  21. Wong CK, Gao W, Stewart RA, French JK, Aylward PE, et al. (2012) The prognostic meaning of the full spectrum of aVR ST-segment changes in acute myocardial infarction. Eur Heart J 33(3): 384-392.
  22. Senaratne MP, Weerasinghe C, Smith G, Mooney D (2003) Clinical utility of ST-segment depression in lead AVR in acute myocardial infarction. J Electrocardiol 36(1): 11-16.
  23. Kosuge M, Kimura K, Ishikawa T, Endo T, Hongo Y, et al. (2001) ST-segment depression in lead aVR predicts predischarge left ventricular dysfunction in patients with reperfused anterior acute myocardial infarction with anterolateral ST-segment elevation. Am Heart J 142(1): 51-57.
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