Abstract
Background
The predictive significance of ST‐segment elevation (STE) in lead V4R in patients with anterior ST‐segment elevation myocardial infarction (STEMI) has not been well‐understood. In this study, we evaluated the prognostic value of early and late STE in lead V4R in patients with anterior STEMI.
Methods
A total 451 patients with anterior STEMI who treated with primary percutaneous coronary intervention (PPCI) were prospectively enrolled in this study. All patients were classified according to presence of STE (>1 mm) in lead V4R at admission and/or 60 min after PPCI. Based on this classification, all patients were divided into three subgroups as no V4R STE (Group 1), early but not late V4R STE (Group 2) and late V4R STE (Group 3).
Results
In‐hospital mortality had higher rates at group 2 and 3 and that had 2.1 and 4.1‐times higher mortality than group 1. Late V4R STE remained as an independent risk factor for cardiogenic shock (odds ratio [OR] 2.6; 95% confidence interval [CI] 1.9–4.3; p < .001) and in‐hospital mortality (OR 2.3; 95% CI 1.8–4.1; p < .001). The 12‐month overall survival for group 1, 2, and 3 were 91.1%, 82.4%, and 71.4% respectively. However, the long‐term mortality also had the higher rate at group 3; late V4R STE did not remain as an independent risk factor for long‐term mortality (OR 1.5; 95% CI 0.8–4.1; p: .159).
Conclusion
Late V4R STE in patients with anterior STEMI is strongly associated with poor prognosis. The record of late V4R in patients with anterior STEMI has an important prognostic value.
Keywords: basic noninvasive techniques─electrocardiography, basic ventricular tachycardia/fibrillation, cardiac fibrillation/defibrillation, clinical
1. INTRODUCTION
It is commonly established that right ventricular (RV) infarction frequently occurs in patients with inferior ST‐segment elevation myocardial infarction (STEMI) (Zehender et al., 1993). Numerous studies recommend recording right precordial leads (especially V4R) in these patients at admission. ST elevation (STE) in lead V4R has been associated with severe conduction disorders, ventricular arrhythmia and death (Braat, Brugada, de Zwaan, Coenegracht, & Wellens, 1983; Braat, de Zwaan, Brugada, Coenegracht, & Wellens, 1984; Braat, Gorgels, Bar, & Wellens, 1988; Zehender et al., 1993). Along with that, interventricular septum and anterior wall of the RV is partially supplied by the left anterior descending artery (LAD) (Charlap et al., 1989; Erhardt, 1974; Ratliff & Hackel, 1980). Some recent studies demonstrated a relatively high incidence of concurrent RV infarction in patients with anterior STEMI (Barsheshet et al., 2011; Bodi et al., 2010; Pourafkari et al., 2016; Tusun et al., 2015). However, less data have been reported about the prognostic importance of STE in lead V4R in patients with anterior STEMI and authors are in conflict on how this STE has an impact on the prognosis (Barsheshet et al., 2011; Bodi et al., 2010; Ghaffari, Taban Sadeghi, & Sayyadi, 2017; Tusun et al., 2015). Additionally, RV infarction is considered as temporary and final infarct size is considered as small due to its thinner wall and subendocardial oxygenization (Bodi et al., 2010). The studies evaluating STE in lead V4R in patients with anterior STEMI only recorded admission electrocardiogram (ECG) but not postrevascularization control ECG and did not reveal long‐term outcomes (Barsheshet et al., 2011; Pourafkari et al., 2016; Tusun et al., 2015). In this study, we investigated the effect of early and late STE in lead V4R on in‐hospital and 12‐month long‐term outcomes in patients with first anterior STEMI.
2. METHODS
This prospective study was performed in a tertiary heart center and evaluated 455 consecutive patients with confirmed first anterior STEMI who were admitted to the emergency department of a tertiary heart center within 12 hr after the onset of symptoms. All patients underwent immediate coronary angiography with primary percutaneous coronary intervention (PPCI) to the LAD. A complete 15‐lead electrocardiogram (including 12 conventional leads and V3R to V5R) was recorded on admission. The STE was measured manually. All patients were classified according to presence or absence STE (≥1 mm) in V4R lead at admission and/or 60 min after PPCI. Based on this classification, all patients were divided into three subgroups as no V4R STE (Group 1), early but not late V4R STE (Group 2) and late V4R STE (Group 3). Patients with bundle branch (left and right) block and that have a marked left ventricular hypertrophy were not enrolled. Marked left ventricular hypertrophy was defined as left ventricular septal thickness ≥1.6 cm for women and left ventricular septal thickness ≥1.7 cm for men (Lang et al., 2005). A Q wave >0.03 s and 1/4 of the R‐wave amplitude in lead V1–6 defined as significant Q wave (Thygesen et al., 2007). The duration of study was 12 months, from March 2015 to February 2016. A total of two patients were excluded from the study because of lost of data after hospitalization and two patients were excluded because refused to participate to the study. Therefore 451 patients without known coronary artery disease (CAD) who admitted to emergency department with anterior STEMI and treated with PPCI were enrolled in the study. In‐hospital and long‐term outcomes were compared between these three groups (Figure 1). The primary end points were the incidence of in‐hospital and long‐term all‐cause of mortality. Acute kidney injury (AKI) is defined as an increase in serum creatinine level of ≥0.3 mg/dl or a relative increase in serum creatinine level of ≥50% (Hsu & Hsu, 2012; Mehta et al., 2007). Baseline demographic characteristics and related clinical information were obtained from each patient at the time of emergency department admission. Before the PPCI, transthoracic echocardiography was performed using a Vivid 7 system (GE Vingmed Ultrasound AS, Horten, Norway) to study patients by an expert on cardiovascular imaging. Coronary artery stenosis of >70% in the luminal diameter was considered as significant. The location of the culprit lesion in the LAD was determined to be osteal, proximal or mid‐distal according to the origin of the first major septal branch. ECG was performed in 100% patients at admission, PPCI was performed by a trained interventional cardiologist in 100% patients and echocardiogram was performed in 98% patients before the PPCI. This study was conducted in a tertiary heart center where an expert on cardiovascular imaging and trained interventional cardiologists were consistently available. The drugs were administered during and after the hospitalization according to the European Society of Cardiology Guidelines (Windecker et al., 2014).
Figure 1.
Kaplan–Meier survival curve for overall survival in patients with first anterior ST segment elevation myocardial infarction (n = 451) stratified by presence or absence of early and late ST‐segment elevation in lead V4R
Ethical clearance was obtained from the Ethics and Research Committee of our hospital. All participants gave written informed consent prior to enrollment in the study. The research was conducted in accordance with the principles of the Declaration of Helsinki.
2.1. Statistical analysis
Kolmogorov–Smirnov test was used for testing of normality. Continuous variables with normal distributions were expressed as mean ± SD and compared using one‐way analysis of variance. The control of the homogeneity of variances for variance analysis was done with Levene test. One‐way ANOVA was used for the homogeneity of variance ensured parameters; Welch robust test was used when the homogeneity of variance was not ensured. Continuous variables with skewed distributions were expressed as mean ± SD and compared using the Kruskal–Wallis test. Categorical variables were expressed as number and percentages and Pearson's chi‐square or Fisher's exact tests were used to evaluate the differences. Hierarchical logistic regression analysis was used for multivariable analysis to evaluate the prognostic confounders for in‐hospital outcomes. The odds ratio (OR) indicates the relative risk of in‐hospital outcomes of group 2 and 3 compared with group 1. After follow‐up periods of 11 ± 3 months, the survival of three groups was compared using the Kaplan–Meier survival method. Overall survival was calculated from the day of diagnosis to the day of death. Differences between the groups were analyzed by the log‐rank test. A Forward Cox proportional regression analysis was performed to assess the in‐hospital outcomes of the patients compared with the no V4R STE group. The hazard ratio (HR) indicates the relative risk of long‐term outcomes of patients compared with no V4R STE subgroup. To analyze the prediction for in‐hospital and long‐term outcomes, data from the admission parameters were employed as independent variables. In multivariable models, confounders in multivariate analysis as predictors of in‐hospital and long‐term outcomes were considered. Four models were generated to obtain the impact of potential confounders on the association between early and late V4R STE and outcomes. These four models include: (1) unadjusted; (2) adjusted for age, gender, body mass index and left ventricular ejection fraction (LVEF); (3) adjusted for comorbidities; (4) adjusted for all covariates which includes demographics (age, gender, body mass index); first measurement of systolic blood pressure and heart rate; first measurement during hospitalization of the following laboratory values (creatinine, admission glomerular filtration rate calculated by CKD‐EPI, hematocrit); comorbidities (diabetes, chronic kidney disease, hypertension, hyperlipidemia); electrocardiographic confounders (maximal and total STE in leads V1–6, the number of leads with STE, ST‐segment resolution >50% and prolonged corrected QT >440 ms); left ventricular ejection fraction and in‐hospital medication. A two‐tailed p value of <.05 was considered as statistically significant, and 95% CIs were presented for all odds ratios and hazard ratios. Analyses were performed using Statistical Package for Social Sciences software, version 20.0 (SPSS; IBM, Armonk, NY, USA).
3. RESULTS
The patients’ baseline characteristics, echocardiographic and angiographic analyses, and in‐hospital medication were listed in Table 1. A total of 451 patients (mean age 59 ± 13 years; men 81%) with STEMI were included. Group 1, 2, and 3 were consisted of total number of 304, 91 and 56 patients respectively. There was no difference in age, male gender, history of hypertension, diabetes mellitus, hyperlipidemia, current smoking status, and chronic kidney disease between the groups. At admission, the patients had similar pre‐infarction angina pectoris, chest pain and door‐to‐balloon time, creatinine, estimated glomerular filtration rate, and hematocrit. Whereas, group 2 had lower systolic blood pressure, higher Killip class III–IV, GRACE and TIMI score compared to group 1, and group 3 patients had lower systolic blood pressure, higher Killip class and higher GRACE and TIMI score compared to the other two groups. Group 2 and 3 had lower LVEF, tricuspid annular plane systolic excursion (TAPSE), and tricuspid valve S velocity compared to group 1. Along with that group 3 had the poorest biventricular systolic function. Laboratory variables were similar between the groups. The patients had similar in‐hospital medication. Angiographic analysis demonstrated no significant differences between the groups regarding osteal or proximal LAD involvement, and the number of significantly narrowed coronary arteries. Whereas group 3 had higher left main coronary artery stenosis compared to the other two groups. Additionally, group 3 had higher SYNTAX score and diuretic use compared to other two groups. The patients’ electrocardiographic analysis was listed in Table 2. Patients had similar maximal and total STE in leads V1–6, STE in lead V3R and V5R, the number of leads with STE, ST‐segment resolution >50%, ST‐segment depression in lead V5–6 and the number of leads with significant Q wave.
Table 1.
Baseline characteristics of patients stratified by early and late V4R ST‐segment elevation
| Parameters | Early V4R ST <1 mm (n = 304) | Early V4R ST ≥1 mm but Late V4R ST<1 mm (n = 91) | Early and late V4R ST ≥1 mm(n = 56) | p |
|---|---|---|---|---|
| Age, y | 58 ± 13 | 56 ± 11 | 61 ± 14 | .101 |
| Male gender | 248 (81.6) | 76 (83.5) | 43 (76.8) | .588 |
| Body mass index | 28.0 ± 4.3 | 27.3 ± 4.3 | 27.7 ± 5.2 | .917 |
| History | ||||
| Hypertension | 114 (37.5) | 35 (38.5) | 19 (33.9) | .848 |
| Diabetes mellitus | 69 (22.7) | 21 (23.1) | 21 (37.5) | .057 |
| Hyperlipidemia | 58 (19.1) | 22 (24.2) | 13 (23.2) | .503 |
| Current smoking status | 170 (55.9) | 54 (59.3) | 29 (51.8) | .665 |
| Chronic kidney disease | 16 (5.3) | 4 (4.4) | 4 (7.1) | .772 |
| Family history of coronary artery disease | 107 (35.2) | 25 (27.5) | 18 (32.1) | .383 |
| At admission | ||||
| Systolic blood pressure, mmHg | 136 ± 27 | 124 ± 23 | 118 ± 21 | <.001 |
| Pre‐infarction angina pectoris | 117 (38.5) | 35 (38.5) | 21 (37.5) | .990 |
| Killip class ≥3 | 20 (6.6) | 11 (12.1) | 14 (25.0) | <.001 |
| Chest pain period, hr | 3.6 ± 3.2 | 3.4 ± 3.6 | 3.2 ± 3.2 | .278 |
| Door‐to‐balloon time, min | 30 ± 17 | 28 ± 14 | 34 ± 19 | .162 |
| Creatinine, mg/dl | 0.82 ± 0.20 | 0.81 ± 0.24 | 0.83 ± 0.23 | .641 |
| Glomerular filtration rate, ml/min | 114 ± 42 | 116 ± 28 | 100 ± 48 | .060 |
| Hematocrit, % | 39.9 ± 5.2 | 40.4 ± 4.7 | 41.1 ± 6.3 | .462 |
| Troponin I, ng/ml | 22.0 ± 20.8 | 18.4 ± 18.7 | 24.9 ± 21.1 | .106 |
| GRACE score | 103 ± 32 | 110 ± 39 | 116 ± 33 | .003 |
| TIMI score | 3.2 ± 2.1 | 3.8 ± 2.3 | 4.3 ± 2.3 | .002 |
| Echocardiographic parameters | ||||
| Left ventricle ejection fraction, % | 42 ± 7 | 39 ± 7 | 37 ± 6 | .012 |
| Left ventricle end‐diastolic diameter, cm | 4.4 ± 0.5 | 4.6 ± 0.6 | 4.9 ± 0.6 | .005 |
| TAPSE, cm/s | 2.3 ± 1.4 | 1.8 ± 0.3 | 1.7 ± 0.2 | <.001 |
| Right ventricle S’ velocity, cm/s | 14.7 ± 2.9 | 10.7 ± 3.8 | 9.3 ± 2.3 | <.001 |
| Culprit segment of the left anterior descending artery | ||||
| Osteal | 36 (11.8) | 16 (17.6) | 11 (19.6) | .163 |
| Proximal | 148 (48.7) | 39 (42.9) | 27 (48.2) | .616 |
| Mid‐distal | 110 (36.2) | 32 (35.2) | 18 (32.1) | .843 |
| Vessel stenosis >70% | ||||
| Left main coronary artery | 3 (1.0) | 4 (4.4) | 4 (7.1) | .009 |
| Right coronary artery | 60 (19.7) | 20 (22.0) | 13 (23.2) | .788 |
| Left circumflex artery | 52 (17.1) | 22 (24.2) | 13 (23.2) | .237 |
| SYNTAX score | 17.6 ± 6.2 | 20.9 ± 7.4 | 23.3 ± 7.6 | .013 |
| In‐hospital medication | ||||
| Aspirin | 298 (98.0) | 90 (98.9) | 56 (100.0) | .507 |
| PY212 receptor inhibitors | 302 (99.3) | 91 (100.0) | 56 (100.0) | .615 |
| Βeta blockers | 277 (91.1) | 88 (96.7) | 50 (89.3) | .163 |
| Statins | 257 (84.5) | 82 (90.1) | 52 (92.9) | .136 |
| Diuretics | 26 (8.6) | 14 (15.4) | 16 (28.6) | <.001 |
| Angiotensin converting enzyme inhibitor or angiotensin receptor blocker | 246 (80.9) | 82 (90.1) | 45 (80.4) | .112 |
Continuous variables are presented as mean ± SD; nominal variables presented as frequency (%).
Table 2.
Electrocardiographic analysis of patients stratified by early and late V4R ST‐segment elevation
| Parameters | Early V4R ST <1 mm (n = 304) | Early V4R ST ≥1 mm but Late V4R ST<1 mm (n = 91) | Early and late V4R ST ≥1 mm(n = 56) | p |
|---|---|---|---|---|
| Normal sinus rhythm | 298 (98.0) | 87 (95.6) | 54 (96.4) | .408 |
| Resting heart rate >100 beats/min | 59 (19.4) | 21 (23.1) | 12 (21.4) | .733 |
| Maximal ST‐segment elevation in leads V1–6, cm | 0.39 ± 0.22 | 0.36 ± 0.14 | 0.43 ± 0.14 | .789 |
| Total ST‐segment elevation in leads V1–6, cm | 1.17 ± 0.71 | 1.15 ± 0.48 | 1.36 ± 0.49 | .111 |
| ST‐segment elevation in lead V3R | 10 (3.3) | 91 (100.0) | 56 (100.0) | <.001 |
| ST‐segment elevation in lead V5R | 8 (2.6) | 39 (42.9) | 42 (75.0) | <.001 |
| No. of leads with ST‐segment elevation | 4.8 ± 1.1 | 4.7 ± 1.0 | 4.7 ± 1.1 | .100 |
| ST‐segment resolution >50% | 230 (75.7) | 64 (70.3) | 43 (76.8) | .550 |
| ST‐segment depression in lead V5 | 11 (3.6) | 5 (5.5) | 2 (3.6) | .714 |
| ST‐segment depression in lead V6 | 26 (8.6) | 9 (9.9) | 2 (3.6) | .370 |
| Significant Q waves | 12 (3.9) | 7 (7.7) | 5 (8.9) | .165 |
| Prolonged corrected QT >440 ms | 72 (23.7) | 17 (18.7) | 12 (21.4) | .594 |
Continuous variables are presented as mean ± SD; nominal variables presented as frequency (%).
Table 3 presents in‐hospital and 1‐year outcomes of the study population. Group 1 had lower cardiogenic shock, ventricular fibrillation (VF), AKI, and mortality compared to other two groups. Along with this, group 3 had higher cardiogenic shock, VF, AKI and mortality compared to other two groups. Although group 3 had higher long‐term mortality compared to other two groups; the difference did not reach to statistical significance (p: .358). Table 4 lists unadjusted and adjusted hierarchical logistic regression for in‐hospital events (cardiogenic shock and mortality) and Cox proportional regression analysis for long‐term mortality. Cardiogenic shock had higher rates at group 2 and 3 and that had 2.1 (95% Confidence interval [CI] 1.1–4.1) and 5.6 times (95% CI 2.9–10.9) higher cardiogenic shock than group 1, which had the lower rates and which was used as the reference. In‐hospital mortality had higher rates at group 2 and 3 and that had 2.1 (CI 1.1–4.2) and 4.1 times (2.0–8.2) higher mortality than group 1, which had the lower rates and was used as the reference. After adjustment for all confounders, late V4R STE remained as an independent risk factor for cardiogenic shock (OR 2.6; 95% CI 1.9–4.3) and in‐hospital mortality (OR 2.3; 95% CI 1.8–4.1). The 12‐month overall survival for group 1, 2, and 3 were 91.1%, 82.4%, and 71.4% respectively. The Kaplan–Meier cumulative survival curve was shown in Figure 1. However, the long‐term mortality also had the higher rates at group 3, late V4R STE did not remain as an independent risk factor for long‐term mortality (HR 1.5; 95% CI 0.8–4.1). Similarly, group 2 had higher cardiogenic shock and in‐hospital and long‐term mortality compared to group 1, however, early V4R STE did not remain as an independent risk factor for cardiogenic shock (OR 1.6; 95% CI 0.9–4.1), in‐hospital mortality (OR 1.5; 95% CI 1.1–3.9) and long‐term mortality (HR 1.2; 95% CI 0.6–3.6) after adjustment for all confounders.
Table 3.
Outcomes of patients stratified by early and late V4R ST‐segment elevation
| Early V4R ST <1 mm (n = 304) | Early V4R ST ≥1 mm but late V4R ST <1 mm (n = 91) | Early and late V4R ST ≥1 mm (n = 56) | p | |
|---|---|---|---|---|
| In‐hospital course | ||||
| Cardiogenic shock | 31 (10.2) | 18 (19.8) | 22 (39.3) | <.001 |
| Ventricular arrhythmia | 14 (4.6) | 11 (12.1) | 9 (16.1) | .002 |
| Acute kidney injury | 10 (3.3) | 8 (8.8) | 10 (17.9) | <.001 |
| Mortality | 27 (8.9) | 16 (17.6) | 16 (28.6) | <.001 |
| Out‐hospital course | ||||
| All‐cause mortality | 13 (4.7) | 5 (6.7) | 4 (10.0) | .358 |
Table 4.
In‐hospital event rates and logistic regression models for cardiogenic shock and mortality by early and late V4R ST‐segment elevation and Cox proportional analysis and long‐term mortality by early and late V4R ST‐segment elevation
| Early V4R ST<1 mm(n = 304) | Early V4R ST ≥1 mm but Late V4R ST <1 mm(n = 91) | Early and late V4R ST ≥1 mm(n = 56) | |
|---|---|---|---|
| Cardiogenic shock | |||
| Number of events | 31 | 18 | 22 |
| Event rate % | 10.2 | 19.8 | 39.3 |
| Cardiogenic shock, OR (%95 CI) | |||
| Model 1: unadjusted | 1[Reference] | 2.1 (1.1–4.1) | 5.6 (2.9–10.9) |
| Model 2: adjusted for age, gender, body mass index and left ventricular ejection fraction | 1[Reference] | 2.0 (1.0–3.4) | 3.8 (2.4–7.8) |
| Model 3: adjusted for comorbities | 1[Reference] | 2.0 (1.2–3.7) | 3.5 (2.3–6.6) |
| Model 4: adjusted for all covariatesa | 1[Reference] | 1.6 (0.9–4.1) | 2.6 (1.9–4.3) |
| In‐hospital mortality | |||
| Number of deaths | 27 | 16 | 16 |
| Mortality,% | 8.9 | 17.6 | 28.6 |
| Mortality, OR (%95 CI) | |||
| Model 1: unadjusted | 1[Reference] | 2.1 (1.1–4.2) | 4.1 (2.0–8.2) |
| Model 2: adjusted for age, gender, body mass index and left ventricular ejection fraction | 1[Reference] | 1.8 (1.3–3.8) | 3.2 (2.2–6.4) |
| Model 3: adjusted for comorbities | 1[Reference] | 1.8 (1.2–4.5) | 3.1 (2.3–5.7) |
| Model 4: adjusted for all covariatesa | 1[Reference] | 1.5 (1.1–3.9) | 2.3 (1.8–4.1) |
| Long‐term mortality | |||
| Number of deaths | 13 | 5 | 4 |
| Mortality,% | 4.7 | 6.7 | 10.0 |
| Mortality, HR (%95 CI) | |||
| Model 1: unadjusted | 1[Reference] | 1.4 (0.5–4.2) | 2.2 (0.6–7.2) |
| Model 2: adjusted for age, gender, body mass index and left ventricular ejection fraction | 1[Reference] | 1.6 (0.5–7.2) | 2.0 (0.6–9.5) |
| Model 3: adjusted for comorbities | 1[Reference] | 1.4 (0.6–4.6) | 2.1 (0.7–6.8) |
| Model 4: adjusted for all covariatesa | 1[Reference] | 1.2 (0.6–3.6) | 1.5 (0.8–4.1) |
OR, odds ratio; HR, hazard ratio.
Includes demographics (age, gender, body mass index); first measurement of systolic blood pressure and heart rate; first measurement during hospitalization of the following laboratory values (creatinine, admission glomerular filtration rate calculated by CKD‐EPI, hematocrit and troponin I); comorbidities (diabetes, chronic kidney disease, hypertension, hyperlipidemia), electrocardiographic confounders (maximal ST‐segment elevation in leads V1–6, total ST‐segment elevation in lead V1–6, the number of leads with ST‐segment elevation, ST‐segment resolution >50% and prolonged corrected QT >440 ms), left ventricular ejection fraction and in‐hospital medication.
4. DISCUSSION
It was observed that late STE in lead V4R can significantly change prognosis. The patients with early STE in lead V4R had lower in‐hospital and long‐term survival compared to the patients with no‐STE in lead V4R, although it did not remain as an independent risk factor after adjustment for all confounders. The patients with late STE in lead V4R had lower in‐hospital and long‐term survival compared to the other two groups. Additionally, it remained as an independent risk factor for in‐hospital but not for long‐term mortality after adjustment for all confounders.
Right precordial leads are commonly recorded in patients with inferior STEMI due to its prognostic value. STE in lead V4R has been associated with poor outcomes in these patients (Braat et al., 1983, 1984, 1988; Mehta et al., 2001; Zehender et al., 1993). However, the clinical significance of RV has been thoroughly understood; in STEMI, interest has been mainly given to the left ventricle (Mehta et al., 2001). Previous studies evaluating RV infarction after STEMI mainly examined the patients with acute RCA occlusion; although blood flow of the septum and anterior wall of the RV is provided by LAD. Thus, acute LAD occlusion may cause RV ischemia in different severity (Foppa et al., 2016; Haddad, Hunt, Rosenthal, & Murphy, 2008; Pfisterer, 2003). Thus, the current study was designed to evaluate the prognostic effect of early and late RV ischemia on clinical outcomes in patients with first anterior STEMI.
There are several studies reported a relatively high incidence of concurrent right precordial STE in patients with anterior STEMI (Barsheshet et al., 2011; Pourafkari et al., 2016; Tusun et al., 2015). Similar to results, Barsheshet et al. reported that one‐third of patients with anterior STEMI had STE in lead V4R, which was associated with increased incidence of VF, heart failure, and death (Barsheshet et al., 2011). They demonstrated the first relationship of RV infarction with in‐hospital outcomes in patients with anterior STEMI. However, they did not exclude the patients with previous myocardial ischemia and could not show long‐term outcomes. They proposed that, infarction or ischemia of a specific segment of myocardium could be more related to acute heart failure risk and VF initiation rather than infarct size and elevation of cardiac enzymes. They found an independent relationship between the involvement of middle anteroseptal wall motion impairment and VF (Barsheshet et al., 2011). Besides, James reported that blood flow of right paraseptal region might be supplied by either first big septal branches of LAD or conal branch of the right coronary artery (RCA) (James, 1975). Ben‐Gal et al. noted that STE in right precordial leads was associated with a small conus branch not big enough to reach right paraseptal region. They concluded that the presence of small conus branch of the RCA is related to ischemic changes and higher incidence of ventricular arrhythmia (Ben‐Gal et al., 1997). In another study, Sicouri et al. has shown the importance of the interventricular septum at the initiation of the torsades de pointes in canine wedge preparations (Sicouri, Glass, Ferreiro, & Antzelevitch, 2010). Anatomic variations of this branch can be an important limiting factor leading to different conclusions about the frequency of arrhythmias and death. However, the middle anteroseptal wall motion was not evaluated in the current study, the presence of RCA and proximal LAD lesions were similar between the groups, similar to Barsheshet et al. (Barsheshet et al., 2011). Both in this study and the Barsheshet et al. study, the presence of a large conal branch of right coronary artery was not recorded. Tusun et al. reported that admission STE in lead V4R is associated with multivessel disease in anterior STEMI and could predict increased in‐hospital major adverse cardiac events mostly derived by mortality (Tusun et al., 2015). Nevertheless, they did not reveal long‐term analysis. Our results were in line with this study. Furthermore, we observed that the patients with late STE in V4R had higher SYNTAX score compared to other two groups. On the contrary, Pourafkari et al. investigated the prognostic value of STE in lead V4R in patients with anterior STEMI and they concluded that it does not seem to predict the prognosis (Pourafkari et al., 2016). However, they found that patients with STE in lead V4R had lower LVEF, their study population is relatively small to reach to statistical significance.
4.1. Limitations
Our study has some limitations. It is a single center study. Global LVEF was evaluated, rather than regional wall motion impairment. That is why the relation between specific wall region and coronary artery could not be assessed. In this study, the conal branch of RCS was not recorded and evaluated. Also the LAD branches that supply the R wall was not recorded. Finally, however RV ischemia at the time of patient enrollment was an important predictor of outcomes in these patients; we cannot exactly show the predictive role of RV ischemia at different periods after STEMI.
5. CONCLUSION
The current study indicates that significant STE in lead V4R during anterior STEMI is associated with more severe coronary artery disease and higher incidence of VF, cardiogenic shock and death in patients with anterior STEMI. We observed that late but not admission STE in lead V4R is strongly related to poor outcomes in these patients. The record of a combination of standard admission and post‐PPCI V4R in patients with anterior STEMI has a big prognostic value. Further prospective studies are warranted before implementation in routine clinical practice.
Keskin M, Uzun AO, Börklü EB, et al. The prognostic significance of early and late right precordial lead (V4R) ST‐segment elevation in patients with acute anterior myocardial infarction. Ann Noninvasive Electrocardiol. 2018;23:e12513 10.1111/anec.12513
REFERENCES
- Barsheshet, A. , Hod, H. , Oieru, D. , Goldenberg, I. , Sandach, A. , Beigel, R. , … Matetzky, S. (2011). Right precordial lead (V4R) ST‐segment elevation is associated with worse prognosis in patients with acute anterior myocardial infarction. Journal of the American College of Cardiology, 58, 548–549. [DOI] [PubMed] [Google Scholar]
- Ben‐Gal, T. , Sclarovsky, S. , Herz, I. , Strasberg, B. , Zlotikamien, B. , Sulkes, J. , … Sagie, A. (1997). Importance of the conal branch of the right coronary artery in patients with acute anterior wall myocardial infarction: Electrocardiographic and angiographic correlation. Journal of the American College of Cardiology, 29, 506–511. [DOI] [PubMed] [Google Scholar]
- Bodi, V. , Sanchis, J. , Mainar, L. , Chorro, F. J. , Nunez, J. , Monmeneu, J. V. , … Llacer, A. (2010). Right ventricular involvement in anterior myocardial infarction: A translational approach. Cardiovascular Research, 87, 601–608. [DOI] [PubMed] [Google Scholar]
- Braat, S. H. , Brugada, P. , de Zwaan, C. , Coenegracht, J. M. , & Wellens, H. J. (1983). Value of electrocardiogram in diagnosing right ventricular involvement in patients with an acute inferior wall myocardial infarction. British Heart Journal, 49, 368–372. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Braat, S. H. , de Zwaan, C. , Brugada, P. , Coenegracht, J. M. , & Wellens, H. J. (1984). Right ventricular involvement with acute inferior wall myocardial infarction identifies high risk of developing atrioventricular nodal conduction disturbances. American Heart Journal, 107, 1183–1187. [DOI] [PubMed] [Google Scholar]
- Braat, S. H. , Gorgels, A. P. , Bar, F. W. , & Wellens, H. J. (1988). Value of the ST‐T segment in lead V4R in inferior wall acute myocardial infarction to predict the site of coronary arterial occlusion. American Journal of Cardiology, 62, 140–142. [DOI] [PubMed] [Google Scholar]
- Charlap, S. , Schulhoff, N. , Mylavarapu, S. , Greengart, A. , Gelbfish, J. , Budzilowicz, L. , … Shani, J. (1989). Effects of occlusion of the left anterior descending coronary artery during angioplasty on right‐sided cardiac pressures and electrocardiographic changes. American Journal of Cardiology, 64, 577–580. [DOI] [PubMed] [Google Scholar]
- Erhardt, L. R. (1974). Clinical and pathological observations in different types of acute myocardial infarction. Acta Medica Scandinavica Supplemenum, 560, 1–78. [PubMed] [Google Scholar]
- Foppa, M. , Arora, G. , Gona, P. , Ashrafi, A. , Salton, C. J. , Yeon, S. B. , … Chuang, M. L. (2016). Right ventricular volumes and systolic function by cardiac magnetic resonance and the impact of sex, age, and obesity in a longitudinally followed cohort free of pulmonary and cardiovascular disease: the Framingham heart study. Circulation: Cardiovascular Imaging, 9, e003810. [DOI] [PubMed] [Google Scholar]
- Ghaffari, S. , Taban Sadeghi, M. , & Sayyadi, M. H. (2017). The association of right coronary artery conus branch size and course with ST segment elevation of right precordial leads and clinical outcome of acute anterior myocardial infarction. Journal of Cardiovascular and Thoracic Research, 9, 49–53. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Haddad, F. , Hunt, S. A. , Rosenthal, D. N. , & Murphy, D. J. (2008). Right ventricular function in cardiovascular disease, part I: Anatomy, physiology, aging, and functional assessment of the right ventricle. Circulation, 117, 1436–1448. [DOI] [PubMed] [Google Scholar]
- Hsu, R. K. , & Hsu, C. Y. (2012). Acute kidney injury: Comment on “trends in the incidence of acute kidney injury in patients hospitalized with acute myocardial infarction”. Archives of Internal Medicine, 172, 253–254. [DOI] [PMC free article] [PubMed] [Google Scholar]
- James, T. N. (1975). Coronary anatomy and cardiac arrhythmias. Verhandlungen der Deutschen Gesellschaft fur Herz‐ und Kreislaufforschung, 41, 47–53. [PubMed] [Google Scholar]
- Lang, R. M. , Bierig, M. , Devereux, R. B. , Flachskampf, F. A. , Foster, E. , Pellikka, P. A. , … Stewart, W. J. (2005). Recommendations for chamber quantification: A report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. Journal of the American Society of Echocardiography, 18, 1440–1463. [DOI] [PubMed] [Google Scholar]
- Mehta, S. R. , Eikelboom, J. W. , Natarajan, M. K. , Diaz, R. , Yi, C. , Gibbons, R. J. , & Yusuf, S. (2001). Impact of right ventricular involvement on mortality and morbidity in patients with inferior myocardial infarction. Journal of the American College of Cardiology, 37, 37–43. [DOI] [PubMed] [Google Scholar]
- Mehta, R. L. , Kellum, J. A. , Shah, S. V. , Molitoris, B. A. , Ronco, C. , Warnock, D. G. , & Levin, A. (2007). Acute Kidney Injury Network: Report of an initiative to improve outcomes in acute kidney injury. Critical Care, 11, R31. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Pfisterer, M. (2003). Right ventricular involvement in myocardial infarction and cardiogenic shock. Lancet, 362, 392–394. [DOI] [PubMed] [Google Scholar]
- Pourafkari, L. , Joudi, S. , Ghaffari, S. , Tajlil, A. , Kazemi, B. , & Nader, N. D. (2016). ST‐segment elevation in the right precordial leads in patients with acute anterior myocardial infarction. Balkan Medical Journal, 33, 58–63. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Ratliff, N. B. , & Hackel, D. B. (1980). Combined right and left ventricular infarction: Pathogenesis and clinicopathologic correlations. American Journal of Cardiology, 45, 217–221. [DOI] [PubMed] [Google Scholar]
- Sicouri, S. , Glass, A. , Ferreiro, M. , & Antzelevitch, C. (2010). Transseptal dispersion of repolarization and its role in the development of Torsade de Pointes arrhythmias. Journal of Cardiovascular Electrophysiology, 21, 441–447. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Thygesen, K. , Alpert, J. S. , White, H. D. , Jaffe, A. S. , Apple, F. S. , Galvani, M. , … Al‐Attar, N. (2007). Universal definition of myocardial infarction. Circulation, 116, 2634–2653. [DOI] [PubMed] [Google Scholar]
- Tusun, E. , Uluganyan, M. , Ugur, M. , Karaca, G. , Osman, F. , Koroglu, B. , … Bolca, O. (2015). ST‐segment elevation of right precordial lead (V4 R) is associated with multivessel disease and increased in‐hospital mortality in acute anterior myocardial infarction patients. Annals of Noninvasive Electrocardiology, 20, 362–367. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Windecker, S. , Kolh, P. , Alfonso, F. , Collet, J. P. , Cremer, J. , Falk, V. , … Witkowski, A. (2014). 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio‐Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). European Heart Journal, 35, 2541–2619. [DOI] [PubMed] [Google Scholar]
- Zehender, M. , Kasper, W. , Kauder, E. , Schonthaler, M. , Geibel, A. , Olschewski, M. , & Just, H. (1993). Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. New England Journal of Medicine, 328, 981–988. [DOI] [PubMed] [Google Scholar]