ABSTRACT
Background
Right ventricular systolic dysfunction is associated with poor prognosis and increased mortality rates. Our objective was to investigate ECG changes in patients with this condition, focusing on the right‐sided precordial leads.
Methods
In this cross‐sectional study, 60 patients with right ventricular dysfunction were included from April 2020 to April 2021. Cardiac structure and function were assessed using 2D transthoracic echocardiography. Standard 12‐lead electrocardiograms and right‐sided precordial ECGs (V3R‐V4R) were obtained and analyzed for QRS complex configuration, ST‐segment elevation, and T‐wave morphology.
Results
In our study, the majority were male (70.0%) with a mean age of 58.76 years. The most common initial diagnoses were pulmonary thromboembolism (43.3%), chronic obstructive pulmonary disease (26.7%), and pulmonary hypertension (25.0%). The predominant ECG finding in the right‐sided precordial leads (V3R, V4R) was a deep negative T wave (90.0%). Patients with severe right ventricular systolic dysfunction often exhibited a qR pattern (41.2%), whereas those with nonsevere dysfunction showed rS and QS patterns (55.8%). Approximately 41.0% of severe RV dysfunction cases had ST segment depression in the right‐sided precordial leads, and 28.0% of patients displayed signs of right atrial abnormality.
Conclusion
The study found that qR, rS, and QS patterns were more prevalent in V3R and V4R leads among patients with severe and nonsevere right ventricular systolic dysfunction. The most common ECG feature observed was deep T‐wave inversion in these leads. The study recommends using right‐sided precordial leads in all patients with RV systolic dysfunction for early detection and risk stratification.
Keywords: ECG, precordial leads, right ventricle, systolic dysfunction, V3R, V4R
This study assesses the utilization of V3R and V4R right‐sided precordial ECG leads in cases of right‐sided ventricular dysfunction.
Right ventricular failure occurs when the right ventricle (RV) is unable to maintain sufficient cardiac output despite adequate preload (1). This dysfunction can be caused by increased RV afterload, decreased RV contractility, or a combination of both factors. Critically ill patients often experience RV failure, particularly because of conditions such as pulmonary embolism, pulmonary arterial hypertension (PAH), acute respiratory distress syndrome (ARDS), and sepsis (2). The presence of RV dysfunction is strongly associated with a poor prognosis and high rates of morbidity and mortality (Golpe et al. 2010).
In clinical practice, 2D transthoracic echocardiography (2D TTE) is commonly used to noninvasively evaluate RV dysfunction. However, ECG can also be a valuable tool for assessing a patient's prognosis and guiding further diagnostic and therapeutic decisions. ECG offers advantages such as simplicity, widespread availability, and low cost, making it particularly useful in emergency triage situations (Vanni et al. 2009). While right‐sided precordial ECG leads (V3R, V4R) have traditionally been used to detect right ventricular myocardial infarction (RVMI), there is currently no research on the ECG changes in these leads specifically in patients with RV dysfunction.
Therefore, the objective of this study is to investigate the ECG changes in the right‐sided precordial leads (V3R, V4R) among patients with RV dysfunction. To the best of our knowledge, this is the first study to assess these ECG changes in this specific patient population.
1. Methods
1.1. Setting and Design
This cross‐sectional study was conducted at the Khorshid Hospital, which is affiliated with the Isfahan University of Medical Sciences (IUMS). This study aimed to evaluate patients with right ventricular (RV) dysfunction over 1 year. The evaluation period for this study was from April 3, 2020 to April 4, 2021. All eligible patients who were admitted to the hospital during this period with a diagnosis of RV systolic dysfunction were included in the study (convenience sampling). RV systolic dysfunction was confirmed by using 2D TTE based on the recommendations of the American Society of Echocardiography for cardiac chamber quantification in adults (Lang et al. 2015). Echocardiography was performed using standard views, with the patient in the left lateral decubitus position, using a Philips EPIQ 7 cardiovascular ultrasound machine. A single experienced examiner, who had completed a fellowship in echocardiography, obtained conventional echocardiographic images and cine loops of all patients using an M5S transducer.
Furthermore, a total of 60 sex‐ and age‐matched controls with normal echocardiography were included for better comparison.
1.2. Inclusion and Exclusion Criteria
The inclusion criteria for this study were as follows: patients aged 18 years or older with a confirmed diagnosis of RV systolic dysfunction, and patients who provided formal consent to participate and complete the study. RV systolic dysfunction was defined using 2D TTE based on the presence of one or more of the following criteria: tricuspid annular plane systolic excursion (TAPSE) <1.6 cm, basal RV free wall velocity (S′) <10 cm/s, or RV fractional area change (FAC) <0.35 (Jaff 2011; Lang et al. 2015; Rudski et al. 2010). Patients with a body mass index (BMI) of 18 or less, skeletal anomalies, such as pectus excavatum, and those with incomplete information were excluded from the study. A total of 60 eligible patients were selected to participate.
1.3. Data Collection
Using a checklist, a general physician obtained the data. All completed questionnaires were thoroughly checked and verified for errors before the final analysis. Measurements of RV systolic function were taken, including TAPSE, RV fractional area change (FAC), and RV free wall velocity (S′). Left ventricular ejection fraction (LVEF), diastolic function, pulmonary artery pressure (PAP), pulmonary acceleration time, and right atrial (RA) size were also measured according to guidelines (Lang et al. 2015).
During the study, a standard 12‐lead ECG and two right‐sided precordial leads (V3R‐V4R) were recorded from participants in a supine position at rest, with a paper speed of 25 mm/s and calibration of 1 mV/10 mm. The standard 12‐lead ECG findings, including axis, rhythm, rate, P wave, PR interval, QRS width, and R‐wave progression in precordial leads, were analyzed. Additionally, the findings from the two right‐sided precordial leads (V3R, V4R) were examined, including P wave, QRS width, QRS pattern, QRS voltage, ST‐segment, and T wave. If a patient exhibited serial ECG changes, all ECG patterns were analyzed.
1.4. Statistical Analysis
Data were analyzed using descriptive statistics including mean ± standard deviation (SD), median, frequencies, and percentages wherever applicable. Differences between subgroups were assessed using a one‐way analysis of variance (ANOVA) for continuous and normally distributed variables and a chi‐square test (or Fisher's exact test) for categorical variables. A test was considered statistically significant if the probability value (p‐value) was <0.05. All analyses were carried out using Stata software (version 14.1; Stata Corp, College Station, TX, USA).
1.5. Ethics Statement
The study protocol (Ethics No. IR.MUI.MED.REC.1399.626) was approved by the Research Ethics Committee at Isfahan University of Medical Sciences (IUMS). Prior to participating in the study, patients were informed about the study and provided their consent by signing a consent form. The confidentiality of patient data was strictly maintained, with access limited to the researchers involved in the study.
2. Results
Table 1 presents the basic characteristics of the patients. Out of 60 patients, 18 (30.0%) were female and 42 (70.0%) were male, with an average age of 58.76 ± 2.29 years (ranging from 20 to 87). Fifteen (25.0%) patients had diabetes, 23 (38.3%) had hypertension, 10 (16.7%) were active smokers, and 14 (23.3%) had hyperlipidemia. The most common initial diagnoses were pulmonary thromboembolism (PTE), chronic obstructive pulmonary disease (COPD), and pulmonary hypertension, accounting for 43.3%, 26.7%, and 25.0% of cases, respectively.
TABLE 1.
The baseline characteristics of patients (n = 60).
| Characteristics | |
|---|---|
| Age (years) | 58.76 ± 2.29 |
| Gender (male, %) | 42 (70.0) |
| Diabetes mellitus | 15 (25.0) |
| Hypertension | 23 (38.3) |
| Hyperlipidemia | 14 (23.3) |
| Current smoker | 10 (16.7) |
| BMI (kg/m2) | 26.45 ± 4.18 |
| First diagnosis | |
| COPD | 16 (26.7) |
| PTE | 26 (43.3) |
| Bronchiectasis | 1 (1.7) |
| Pulmonary hypertension | 15 (25.0) |
| RV failure | 2 (3.3) |
Abbreviations: BMI, body mass index; COPD, chronic obstructive pulmonary disease; N, number; PTE, pulmonary thromboembolism.
Out of 60 patients, 53 (88.3%) had mild and moderate TR, and 43 (71.7%) had mild MR. The average LVEF was 47.53 ± 0.59%. The echocardiographic characteristics are detailed in Table 2.
TABLE 2.
The echocardiography characteristics of patients (n = 60).
| Characteristics | N (%) |
|---|---|
| TAPSE (mm) | 31.0 ± 12.53 |
| FAC (%) | 30.0 ± 22.48 |
| PAP (mmHg) | 52.2 ± 62.56 |
| RA area (cm2) | 0.62 ± 23.2 |
| Pulmonary acceleration time (ms) | 1.90 ± 75.1 |
| LVEF (%) | 47.53 ± 0.59 |
| RV free wall velocity (S′) (cm/s) | 0.18 ± 8.47 |
| LV diastolic dysfunction grade | |
| 1 | 57 (95.0) |
| 2 | 3 (5.0) |
| Tricuspid regurgitation | |
| Mild | 27 (45.0) |
| Moderate | 26 (43.3) |
| Severe | 7 (11.7) |
| Mitral regurgitation | |
| Mild | 43 (71.7) |
| Moderate | 14 (23.3) |
| Severe | 3 (5.0) |
Abbreviations: FAC, fractional area change; LV, left ventricle; LVEF, left ventricular ejection fraction; N, number; PAP, pulmonary artery pressure; RA, right atrial; TAPSE, tricuspid annular plane systolic excursion.
Out of the 60 patients, 21 (35.0%) exhibited a right axis deviation, while only two (3.3%) showed a left axis deviation. The majority, 52 (86.7%), were in normal sinus rhythm, and 8 (13.3%) presented with atrial fibrillation. Additionally, 17 (28.3%) patients had a right atrial abnormality, and 3 (5.0%) had a left atrial abnormality. Narrow QRS widths were observed in 52 (86.7%) cases, and wide QRS widths (RBBB pattern) were seen in 8 (13.3%). The comparison of ECG changes between patients with RV systolic dysfunction and the healthy control group showed significant differences in axis, rhythm, P wave, QRS pattern in right‐sided precordial leads, R wave progression, ST segment, and T wave (p‐value < 0.05). Two samples of ECGs of the healthy control group can be seen in Figure 1. Patients with severe RV systolic dysfunction were more likely to exhibit a qR pattern in right‐sided precordial leads (V3R, V4R; 41.2%), while those with nonsevere RV systolic dysfunction were more likely to show rS and QS patterns in V3R, V4R (55.8%; p = 0.0001). ST depression was significantly more common in patients with severe RV systolic dysfunction than in those with nonsevere RV systolic dysfunction in right‐sided precordial leads (V3R, V4R; 41.0% vs. 20.9%, p = 0.0001). Among the 60 patients with RV systolic dysfunction, deep T wave inversion was the most frequent ECG sign in right‐sided precordial leads (V3R, V4R; 90%). These findings are summarized in Table 3.
FIGURE 1.
ECG of the healthy control group. rS pattern and inverted T wave are seen in (A), and qS and positive T wave can be seen in (B).
TABLE 3.
Assessing the standard 12 ECG leads and two right‐sided precordial ECG leads based on the severity of RV dysfunction.
| Characteristic | Without RV dysfunction | With RV dysfunction | p | ||
|---|---|---|---|---|---|
| Control (N = 60) | p | Nonsevere (N = 43) | Severe (N = 17) | ||
| Axis | |||||
| Normal | 53 (88.3) | <0.001 | 19 (44.2) | 6 (35.3) | 0.814 |
| RAD | 1 (1.7) | 15 (34.9) | 6 (35.3) | ||
| LAD | 3 (5) | 1 (2.3) | 1 (5.9) | ||
| Undetermined | 3 (5) | 8 (18.6) | 4 (23.5) | ||
| Rhythm | |||||
| Atrial fibrillation | 2 (3.3) | <0.001 | 6 (14.0) | 2 (11.8) | 0.495 |
| Normal sinus rhythm | 58 (96.7) | 37 (86.0) | 15 (88.2) | ||
| P wave | |||||
| Normal | 56 (93.3) | <0.001 | 30 (69.8) | 10 (58.8) | 0.425 |
| LA abnormality | 2 (3.3) | 1 (2.3) | 2 (11.8) | ||
| RA abnormality | 2 (3.3) | 12 (27.9) | 5 (29.4) | ||
| QRS width | |||||
| Narrow | 56 (93.3) | 0.224 | 37 (86.0) | 15 (88.2) | 0.856 |
| Wide | 4 (6.7) | 6 (14.0) | 2 (11.8) | ||
| QRS pattern in right‐sided precordial leads | |||||
| QS | 2 (3.3) | <0.001 | 12 (27.9) | 1 (5.8) | 0.001 |
| R | 7 (11.7) | 6 (14.0) | 2 (11.8) | ||
| Rs | 5 (8.3) | 1 (2.3) | 2 (11.8) | ||
| qR | 4 (6.7) | 11 (25.6) | 7 (41.2) | ||
| rS | 31 (51.7) | 12 (27.9) | 5 (29.4) | ||
| rsR′ | 1 (1.7) | 1 (2.3) | 0 (0) | ||
| QRS voltage in right‐sided precordial leads | 7.13 ± 0.45 | 7.10 ± 0.31 | 0.928 | ||
| R‐wave progression | |||||
| Normal | 49 (81.7) | 0.005 | 25 (58.2) | 9 (52.9) | 0.115 |
| Late | 3 (5) | 9 (20.9) | 5 (29.5) | ||
| Early | 8 (13.3) | 9 (20.9) | 3 (17.6) | ||
| ST segment in right‐sided precordial leads | |||||
| Normal | 58 (96.7) | <0.001 | 34 (79.1) | 10 (59.0) | 0.001 |
| Depression | 2 (3.3) | 9 (20.9) | 7 (41.0) | ||
| T wave in right‐sided precordial leads | |||||
| Normal | 22 (36.7) | <0.001 | 5 (11.6) | 1 (5.9) | 0.047 |
| Negative | 38 (63.3) | 38 (88.4) | 16 (94.1) | ||
Abbreviations: LAD, left axis deviation; N, number; p, p value; RAD, right axis deviation.
Table 4 presents the right‐sided precordial ECG leads, categorized by the initial diagnosis. A significant difference was observed in the frequency of right axis deviation among patients with COPD (62.4%), PTE (30.8%), and PH (6.6%; p = 0.033). The occurrence of right atrial abnormality was 43.8% in COPD patients, 11.5% in PTE patients, and 40.0% in PH patients, respectively (p = 0.001). ST depression in the right‐sided precordial leads was notably more prevalent in COPD patients (43.8%) compared to those with PTE (19.2%) or PH (20.0%; p = 0.001).
TABLE 4.
Assessing the standard 12 ECG leads, and 2 right‐sided precordial ECG leads based on the first diagnosis.
| Characteristics | RV dysfunction | ||||||
|---|---|---|---|---|---|---|---|
| Total (N = 60) | COPD (N = 16) | PTE (N = 26) | Bronchiectasis (N = 1) | PH (N = 15) | RV failure (N = 2) | p | |
| Axis | |||||||
| Normal | 25 (41.7) | 3 (18.8) | 14 (53.8) | 0 (0) | 7 (46.7) | 1 (50.0) | 0.033 |
| RAD | 21 (35.0) | 10 (62.4) | 8 (30.8) | 1 (100.0) | 1 (6.6) | 1 (50.0) | |
| LAD | 2 (3.3) | 0 (0) | 2 (7.7) | 0 (0) | 0 (0) | 0 (0) | |
| Undetermined | 12 (20.0) | 3 (18.8) | 2 (7.7) | 0 (0) | 7 (46.7) | 0 (0) | |
| Rhythm | |||||||
| Atrial fibrillation | 8 (13.3) | 3 (18.8) | 2 (7.7) | 0 (0) | 3 (20.0) | 0 (0) | 0.562 |
| Normal sinus Rhythm | 52 (86.7) | 13 (81.2) | 24 (92.3) | 1 (100) | 12 (80.0) | 2 (100) | |
| P wave | |||||||
| Normal | 40 (66.7) | 7 (43.8) | 23 (88.5) | 0 (0) | 9 (60.0) | 1 (50.0) | 0.001 |
| LA abnormality | 3 (5.0) | 2 (12.4) | 0 (0) | 1 (100) | 0 (0) | 0 (0) | |
| RA abnormality | 17 (28.3) | 7 (43.8) | 3 (11.5) | 0 (0) | 6 (40.0) | 1 (50.0) | |
| QRS width | |||||||
| Narrow | 52 (86.7) | 13 (81.2) | 23 (88.5) | 1 (100) | 13 (86.7) | 2 (100) | 0.469 |
| Wide | 8 (13.3) | 3 (18.8) | 3 (11.5) | 0 (0) | 2 (13.3) | 0 (0) | |
| QRS pattern in right‐sided precordial leads | |||||||
| QS | 13 (21.7) | 2 (12.4) | 5 (19.2) | 0 (0) | 5 (33.4) | 1 (50.0) | 0.366 |
| R | 8 (13.3) | 3 (18.8) | 2 (7.7) | 1 (100) | 1 (6.6) | 1 (50.0) | |
| Rs | 3 (5.0) | 2 (12.4) | 0 (0) | 0 (0) | 1 (6.6) | 0 (0) | |
| qR | 18 (30.0) | 7 (43.8) | 8 (30.8) | 0 (0) | 3 (20.0) | 0 (0) | |
| rS | 17 (28.3) | 2 (12.4) | 10 (38.5) | 0 (0) | 5 (33.4) | 0 (0) | |
| rsR′ | 1 (1.7) | 0 (0) | 1 (3.8) | 0 (0) | 0 (0) | 0 (0) | |
| QRS voltage in right‐sided precordial leads | 7.11 ± 0.37 | 7.06 ± 0.25 | 7.08 ± 0.40 | — | 6.99 ± 0.51 | 7.03 ± 0.25 | 0.149 |
| R‐wave progression | |||||||
| Normal | 34 (56.7) | 5 (31.2) | 20 (77.0) | 0 (0) | 8 (53.3) | 1 (50.0) | 0.123 |
| Late | 14 (23.3) | 5 (31.2) | 5 (19.2) | 0 (0) | 4 (26.7) | 0 (0) | |
| Early | 12 (20.0) | 6 (37.6) | 1 (3.8) | 1 (100) | 3 (20.0) | 1 (50.0) | |
| ST segment | |||||||
| Normal | 44 (73.3) | 9 (56.2) | 21 (80.8) | 1 (100) | 12 (80.0) | 1 (50.0) | 0.001 |
| Depression | 16 (26.7) | 7 (43.8) | 5 (19.2) | 0 (0) | 3 (20.0) | 1 (50.0) | |
| T wave in right‐sided precordial leads | |||||||
| Normal | 6 (10.0) | 2 (12.4) | 1 (3.8) | 0 (0) | 3 (20.0) | 0 (0) | 0.524 |
| Inversion | 54 (90.0) | 14 (87.6) | 25 (96.2) | 1 (100) | 12 (80.0) | 2 (100) | |
Abbreviations: COPD, chronic obstructive pulmonary disease; LAD, left axis deviation; N, number; PH, pulmonary hypertension; PTE, pulmonary thromboembolism; RAD, right axis deviation.
3. Discussion
This study showed qR pattern in V3R, V4R was significantly most common in patients with severe RV systolic dysfunction in comparison with nonsevere RV systolic dysfunction in which rS and QS patterns in V3R, V4R (Figure 2) were significantly most common in patients with nonsevere systolic RV dysfunction (p = 0.0001). The most common ECG feature was deep negative T wave in right precordial leads (V3R, V4R; 90.0%) in both groups. Choi and Park (2012), Vanni et al. (2009), Kim et al. (2009), and Ferrari et al. (1997) demonstrated that the precordial negative T wave was the most frequent ECG feature in acute pulmonary embolism patients with RV systolic dysfunction. Moreover, Zhan and colleagues reported that the most common ECG feature was T wave changes in RV systolic dysfunction patients (Zhong‐qun et al. 2014). Kostrubiec et al. (2010) illustrated that all patients with RV systolic dysfunction showed inverted T‐wave in the precordial leads. Negative T waves were closely associated with changes in RV systolic dysfunction. In other words, improvement in RV systolic dysfunction might be predicted by the disappearance of the negative T wave on precordial leads (Choi and Park 2012).
FIGURE 2.
(A, C, and D) Show the qR pattern; and (B, E) demonstrate the rS pattern in V3R and V4R. Alternance of deep T wave inversion can be seen in B, D, and E. RBBB pattern is also notable in D.
The mechanism responsible for the appearance of the negative T waves in precordial leads in patients with RV dysfunction may be associated with the development of rapid right ventricular pressure overload and enlargement (Ferrari et al. 1997; Kosuge et al. 2006; Yoshinaga et al. 1999). Some studies have attributed the mechanism of inverted T wave to myocardial ischemia, and the release of various chemical mediators such as catecholamines and histamine (Geibel et al. 2005; Meyer, Planquette, and Sanchez 2008; Sarin, Elmi, and Nassef 2005).
Early detection of high‐risk patients with RV dysfunction by identifying inverted T waves in precordial leads on admission has significant therapeutic implications. Additionally, predicting the improvement of RV dysfunction by the disappearance of the inverted T wave is important, because persistent RV dysfunction is related to recurrent thromboembolic occurrences (Choi and Park 2012; Kim et al. 2009). Grifoni et al. (2006) found that persistent RV systolic dysfunction at hospital discharge occurred in nearly 20% of patients. Therefore, patients with persistent RV dysfunction at discharge should receive strict surveillance for recurrence.
Right axis deviation occurred in 35% of cases. The preexisting disease may also impact the axis deviation on presentation ECG. As we reported PTE was the most frequent diagnosis in patients with RV dysfunction (43.3%). Right axis deviation was described as the classic axis change associated with PTE (Nielsen et al. 1989; Panos et al. 1988; Sreeram et al. 1994).
This study showed that 28.3% of patients had right atrial abnormality and 5.0% of patients had left atrial abnormality. An increase in the P wave amplitude >2.5 mV, known as right atrial abnormality P wave, has been typically associated with RV dysfunction and PTE, consequently resulting from RV hypertrophy or enlargement and/or associated with acute obstruction from clot (Ullman et al. 2001). Previous studies indicated that right atrial abnormality has been reported in 2%–30% of PTE patients (Rodger et al. 2000; Weber and Phillips Jr 1966).
Our results illustrated that ST segment depression was a common finding on the right‐sided precordial leads in our patients (26.7%), especially patients with severe RV systolic dysfunction. Furthermore, nearly 87.0% of patients were in normal sinus Rhythm.
3.1. Limitations of the Study
Several limitations of this study can be addressed. First, the nature of the study design (cross‐sectional) did not allow for further evaluation of any apparent associations over time. Second, our experience at a single hospital may not be applicable to the broader community. Last, the interpretation of the findings is constrained by the small sample size. Longitudinal studies with larger sample sizes are necessary to investigate the ECG findings of right‐sided precordial leads in patients with RV dysfunction.
4. Conclusion
This study revealed that the qR pattern, as well as the rS and QS patterns in V3R and V4R, was significantly more common in patients with severe and nonsevere RV systolic dysfunction, respectively (p = 0.0001). The most prevalent ECG feature observed was a deep negative T wave in the right precordial leads (V3R, V4R; 90.0%) in both groups. Therefore, it is recommended that right‐sided precordial leads (V3R, V4R) be utilized in all patients with RV systolic dysfunction. This straightforward approach can aid in the early detection and risk stratification of patients presenting with RV systolic dysfunction.
Author Contributions
Reza Khosravi: conceptualization, review and editing, supervision. Hasan Shemirani: methodology, review and editing. Marziyeh Najafi: methodology, review and editing. Zahra Ghaffarinejad: writing the original draft, review and editing. Mahta Arbabi: writing the original draft, review and editing. Marzieh Tajmirriahi: conceptualization, review and editing, supervision.
Consent
Informed consent was obtained from all participants included in this study. Patient confidentiality and privacy were strictly maintained throughout the research process.
Consent for publication: The authors guarantee that the manuscript will not be published elsewhere in any language without the consent of the Annals of Noninvasive Electrocardiology journal, that the rights of third parties will not be violated, and that the publisher will not be held legally responsible should there be any compensation claims.
Conflicts of Interest
The authors declare no conflicts of interest.
Acknowledgments
We would like to express our gratitude to the Isfahan University of Medical Sciences for funding this project and extend our sincere appreciation for the excellent collaboration of Khorshid Hospital. Additionally, we would like to thank all the participants in the study.
Funding: This study was supported by the Isfahan University of Medical Sciences (IUMS).
Data Availability Statement
The data that support the findings of this study are available upon request.
References
- Choi, B.‐Y. , and Park D.‐G.. 2012. “Normalization of Negative T‐Wave on Electrocardiography and Right Ventricular Dysfunction in Patients With an Acute Pulmonary Embolism.” Korean Journal of Internal Medicine 27, no. 1: 53–59. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Ferrari, E. , Imbert A., Chevalier T., Mihoubi A., Morand P., and Baudouy M.. 1997. “The ECG in Pulmonary Embolism: Predictive Value of Negative T Waves in Precordial Leads‐80 Case Reports.” Chest 111, no. 3: 537–543. [DOI] [PubMed] [Google Scholar]
- Geibel, A. , Zehender M., Kasper W., Olschewski M., Klima C., and Konstantinides S.. 2005. “Prognostic Value of the ECG on Admission in Patients With Acute Major Pulmonary Embolism.” European Respiratory Journal 25, no. 5: 843–848. [DOI] [PubMed] [Google Scholar]
- Golpe, R. , Pérez‐de‐Llano L. A., Castro‐Añón O., et al. 2010. “Right Ventricle Dysfunction and Pulmonary Hypertension in Hemodynamically Stable Pulmonary Embolism.” Respiratory Medicine 104, no. 9: 1370–1376. [DOI] [PubMed] [Google Scholar]
- Grifoni, S. , Vanni S., Magazzini S., et al. 2006. “Association of Persistent Right Ventricular Dysfunction at Hospital Discharge After Acute Pulmonary Embolism With Recurrent Thromboembolic Events.” Archives of Internal Medicine 166, no. 19: 2151–2156. [DOI] [PubMed] [Google Scholar]
- Jaff, M. 2011. “American Heart Association Council on Cardiopulmonary CCP, Resuscitation, American Heart Association Council on Peripheral Vascular D, American Heart Association Council on Arteriosclerosis T, Vascular B. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension: A Scientific Statement From the American Heart Association.” Circulation 123: 1788–1830. [DOI] [PubMed] [Google Scholar]
- Kim, S. E. , Park D. G., Choi H. H., et al. 2009. “The Best Predictor for Right Ventricular Dysfunction in Acute Pulmonary Embolism: Comparison Between Electrocardiography and Biomarkers.” Korean Circulation Journal 39, no. 9: 378–381. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Kostrubiec, M. , Jankowski K., Pedowska‐Włoszek J., et al. 2010. “Signs of Myocardial Ischemia on Electrocardiogram Correlate With Elevated Plasma Cardiac Troponin and Right Ventricular Systolic Dysfunction in Acute Pulmonary Embolism.” Cardiology Journal 17, no. 2: 157–162. [PubMed] [Google Scholar]
- Kosuge, M. , Kimura K., Ishikawa T., et al. 2006. “Prognostic Significance of Inverted T Waves in Patients With Acute Pulmonary Embolism.” Circulation Journal 70, no. 6: 750–755. [DOI] [PubMed] [Google Scholar]
- Lang, R. M. , Badano L. P., Mor‐Avi V., et al. 2015. “Recommendations for Cardiac Chamber Quantification by Echocardiography in Adults: An Update From the American Society of Echocardiography and the European Association of Cardiovascular Imaging.” European Heart Journal‐Cardiovascular Imaging 16, no. 3: 233–271. [DOI] [PubMed] [Google Scholar]
- Meyer, G. , Planquette B., and Sanchez O.. 2008. “Long‐Term Outcome of Pulmonary Embolism.” Current Opinion in Hematology 15, no. 5: 499–503. [DOI] [PubMed] [Google Scholar]
- Nielsen, T. T. , Lund O., Rønne K., and Schifter S.. 1989. “Changing Electrocardiographic Findings in Pulmonary Embolism in Relation to Vascular Obstruction.” Cardiology 76, no. 4: 274–284. [DOI] [PubMed] [Google Scholar]
- Panos, R. J. , Barish R. A., Whye D. W. Jr., and Groleau G.. 1988. “The Electrocardiographic Manifestations of Pulmonary Embolism.” Journal of Emergency Medicine 6, no. 4: 301–307. [DOI] [PubMed] [Google Scholar]
- Rodger, M. , Makropoulos D., Turek M., et al. 2000. “Diagnostic Value of the Electrocardiogram in Suspected Pulmonary Embolism.” American Journal of Cardiology 86, no. 7: 807–809. [DOI] [PubMed] [Google Scholar]
- Rudski, L. G. , Lai W. W., Afilalo J., et al. 2010. “Guidelines for the Echocardiographic Assessment of the Right Heart in Adults: A Report From the American Society of Echocardiography: Endorsed by the European Association of Echocardiography, a Registered Branch of the European Society of Cardiology, and the Canadian Society of Echocardiography.” Journal of the American Society of Echocardiography 23, no. 7: 685–713. [DOI] [PubMed] [Google Scholar]
- Sarin, S. , Elmi F., and Nassef L.. 2005. “Inverted T Waves on Electrocardiogram: Myocardial Ischemia Versus Pulmonary Embolism.” Journal of Electrocardiology 38, no. 4: 361–363. [DOI] [PubMed] [Google Scholar]
- Sreeram, N. , Cheriex E. C., Smeets J. L., Gorgels A. P., and Wellens H. J.. 1994. “Value of the 12‐Lead Electrocardiogram at Hospital Admission in the Diagnosis of Pulmonary Embolism.” American Journal of Cardiology 73, no. 4: 298–303. [DOI] [PubMed] [Google Scholar]
- Ullman, E. , Brady W. J., Perron A. D., Chan T., and Mattu A.. 2001. “Electrocardiographic Manifestations of Pulmonary Embolism.” American Journal of Emergency Medicine 19, no. 6: 514–519. [DOI] [PubMed] [Google Scholar]
- Vanni, S. , Polidori G., Vergara R., et al. 2009. “Prognostic Value of ECG Among Patients With Acute Pulmonary Embolism and Normal Blood Pressure.” American Journal of Medicine 122, no. 3: 257–264. [DOI] [PubMed] [Google Scholar]
- Weber, D. , and Phillips J. Jr. 1966. “A Re‐Evaluation of Electrocardiographic Changes Accompanying Acute Pulmonary Embolism.” American Journal of the Medical Sciences 251, no. 4: 381–398. [DOI] [PubMed] [Google Scholar]
- Yoshinaga, T. , Ikeda S., Nishimura E., et al. 1999. “Serial Changes in Negative T Wave on Electrocardiogram in Acute D Pulmonary Thromboembolism.” International Journal of Cardiology 72, no. 1: 65–72. [DOI] [PubMed] [Google Scholar]
- Zhong‐qun, Z. , Bo Y., Nikus K. C., Pérez‐Riera A. R., Chong‐quan W., and Xian‐ming W.. 2014. “Correlation Between ST‐Segment Elevation and Negative T Waves in the Precordial Leads in Acute Pulmonary Embolism: Insights Into Serial Electrocardiogram Changes.” Annals of Noninvasive Electrocardiology 19, no. 4: 398–405. [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The data that support the findings of this study are available upon request.