Abstract
Background: Clinical picture of acute pulmonary embolism (APE), with wide range of electrocardiographic (ECG) abnormalities can mimic acute coronary syndromes.
Objectives: Assessment of standard 12‐lead ECG usefulness in differentiation at the bedside between APE and non‐ST elevation acute coronary syndrome (NSTE‐ACS).
Methods: Retrospective analysis of 143 patients: 98 consecutive patients (mean age 63.4 ± 19.4 year, 45 M) with APE and 45 consecutive patients (mean age 72.8 ± 10.8 year, 44 M) with NSTE‐ACS. Standard ECGs recorded on admission were compared in separated groups.
Results: Right bundle branch block (RBBB) and S1S2S3 or S1Q3T3 pattern were found in similar frequency in both groups (10 [11%] APE patients vs 6 [14%] NSTE‐ACS patients, 27 [28%] patients vs 7 [16%] patients, respectively, NS). Negative T waves in leads V1‐3 together with negative T waves in inferior wall leads II, III, aVF (OR 1.3 [1.14–1.68]) significantly indicated APE with a positive predictive value of 85% and specificity of 87%. However, counterclockwise axis rotation (OR 4.57 [2.74–7.61]), ventricular premature beats (OR 2.60 [1.60–4.19]), ST depression in leads V1‐3 (OR 2.25 [1.43–3.56]), and negative T waves in leads V5‐6 (OR 2.08 [1.31–3.29]) significantly predicted NSTE‐ACS.
Conclusions: RBBB, S1S2S3, or S1Q3T3 pattern described as characteristic for APE were not helpful in the differentiation between APE and NSTE‐ACS in studied group. Coexistence of negative T waves in precordial leads V1‐3 and inferior wall leads may suggest APE diagnosis.
Ann Noninvasive Electrocardiol 2010;15(2):145–150
Keywords: electrocardiogram, pulmonary embolism, NSTE‐ACS
Clinical picture of acute pulmonary embolism (APE), especially chest pain, syncope, together with electrocardiographic (ECG) abnormalities and elevated plasma troponin levels can mimic acute coronary syndromes and even may lead to an unnecessary urgent coronary angiography. 1
A wide range of ECG abnormalities have been reported in patients with APE. The most frequent ECG signs of APE include S1Q3T3 pattern, sinus tachycardia, inverted T waves in the precordial leads, ST displacement, right bundle branch block (RBBB), P pulmonale, S‐wave notch in lead V1. 2 , 3 , 4 , 5 , 6 , 7 However, none of them is unequivocally diagnostic of APE. Moreover, negative T waves in the precordial leads and ST depression can lead to diagnostic mistakes, suggesting ongoing ischemia of the left ventricular anterior wall.
Therefore, we assessed if standard 12‐lead ECG can be useful in differentiation between APE and non‐ST elevation acute coronary syndrome (NSTE‐ACS), at the bedside.
METHODS
We performed a retrospective analysis of 143 patients: 98 consecutive patients (mean age 63.4 ± 19.4 year, 45 M) with APE confirmed by spiral contrast‐enhanced computed tomography (group APE) and 45 consecutive patients (mean age 72.8 ± 10.8 year, 44 M) with NSTE‐ACS diagnosed according to European Society of Cardiology (at least two of three symptoms: chest pain, signs of myocardial ischemia on ECG, elevated troponin levels (group NSTE‐ACS). 8
Patients with chronic obstructive pulmonary disease, primary pulmonary hypertension, dilated cardiomyopathy, severe heart failure (NYHA class III or IV), significant electrolyte abnormalities on admission were not included into the study.
Left bundle branch block was found in 3 patients in APE group and in 2 patients in group NSTE‐ACS, and they were also excluded from further analysis. The analysis of ECG tracings was performed in 95 patients with APE and 43 subjects with NSTE‐ACS.
Standard 12‐lead ECGs recorded on the admission day were reviewed by three physicians blinded to the final diagnosis. Axis deviation, signs of myocardial ischemia (T‐wave inversion defined by the presence of pointed and symmetrical inverted T waves, ST depression at least 0.1 mV, at least in two continuous leads), the prevalence of supra‐ and ventricular arrhythmias, RBBB (QRS > 0.11 sec and S wave in lead I and terminal R wave in V1 with amplitude > 0.15 mV), S1S2S3 or S1Q3T3 pattern (S wave in lead I and Q wave in lead III with amplitude > 0.15 mV, associated with T‐wave inversion in lead III), P pulmonale, S‐wave notch in lead V1 were compared in both groups.
ECG tracings were also compared in patients with high, medium, and low risk of APE, defined according to European Society of Cardiology Guidelines, based on systemic systolic blood pressure on admission and the presence of right ventricular dysfunction at echocardiography and elevated plasma troponin levels.
Statistical Analysis
Data characterized by a normal distribution are expressed as mean followed by standard deviation. Parameters without such a distribution are expressed as median with range. Student's or Mann–Whitney's tests were used for comparisons between two groups, while comparisons between more than two groups were performed by ANOVA or Kruskal–Wallis tests. The chi‐square test was used to compare discrete variables. Sensitivity, specificity, negative predictive value (NPV), and positive predictive value (PPV) were calculated for the chosen parameters. Univariable logistic regression analysis was used to assess, which ECG abnormalities were significant predictors of APE or NSTE‐ACS. All tests were 2‐sided. Data were considered significant at P < 0.05. STATISTICA software (StatSoft 8.0, StatSoft Polska, Krakow, Poland) was used for statistical calculations.
RESULTS
Clinical characteristic of both groups are presented in Table 1.
Table 1.
Clinical Characteristic of Patients with APE (Group APE, n = 95) and Patients with NSTE‐ACS (Group NSTE‐ACS, n = 43)
| Parameter | Group APE n (%) | Group NSTE‐ACS n (%) | P |
|---|---|---|---|
| Age (year ± SD) | 63.4 ± 19.4 | 72.8 ± 10.8 | <000.1 |
| Sex (male) | 43 (45) | 19 (44) | NS |
| History of ischemic heart disease | 30 (32) | 32 (74) | <0.0001 |
| History of myocardial infarction | 0 | 0 | ‐ |
| History of pulmonary embolism | 0 | 0 | ‐ |
| Symptoms—Onset of Incidence | |||
| Chest pain | 40 (42) | 30 (70) | <0.01 |
| Dyspnea | 81 (85) | 19 (44) | <0.001 |
| Syncope | 24 (25) | 7 (16) | NS |
APE = acute pulmonary embolism; NSTE‐ACS = non‐ST elevation acute coronary syndrome.
The ECG abnormalities are described in Table 2.
Table 2.
Electrocardiographic Abnormalities in Patients with APE (Group APE, n = 95) and in Patients with NSTE‐ACS (Group NSTE‐ACS, n = 43)
| ECG abnormalities | Group APE n (%) | Group NSTE‐ACS N (%) | P |
|---|---|---|---|
| Clockwise axis rotation | 30 (32) | 26 (61) | <0.01 |
| ST depression* in leads II, III, aVF | 32 (34) | 12 (28) | NS |
| ST depression in leads V1‐3 | 19 (20) | 21 (49) | <0.001 |
| ST depression in leads V5‐6 | 38 (40) | 21 (49) | NS |
| Negative T waves in leads II, III, aVF | 24 (25) | 7 (16) | NS |
| Negative T waves in leads II, III, aVF with ST depression | 16 (17) | 6 (14) | NS |
| Negative T waves in leads V1‐3 | 46 (48) | 10 (23) | <0.01 |
| Negative T waves in leads V1‐3 with ST depression | 17 (18) | 11 (26) | NS |
| Negative T waves in leads V5‐6 | 4 (4) | 5 (12) | NS |
| Negative T waves in leads V5‐6 with ST depression | 13 (14) | 13 (30) | <0.05 |
| Supraventricular premature beats | 17 (18) | 9 (21) | NS |
| Ventricular premature beats | 2 (2) | 6 (14) | <0.05 |
| Right bundle branch block | 10 (11) | 6 (14) | NS |
| S1S2S3 or S1Q3T3 pattern | 27 (28) | 7 (16) | NS |
| P pulmonale | 1 (1) | 0 | NS |
| S‐wave notch in lead V1 | 9 (9) | 4 (9) | NS |
| Atrial fibrillation | 12 (13) | 7 (16) | NS |
*ST depression equal/more than 1 mm.
APE = acute pulmonary embolism; NSTE‐ACS = non‐ST elevation acute coronary syndrome.
Axis Deviation
Counterclockwise axis rotation in the horizontal axis (shift in the transition zone to V5 or beyond) was recorded in 26 (61%) patients with NSTE‐ACS and in 30 (32%) patients with APE (P < 0.01).
Signs of Myocardial Ischemia
The incidence of ST depression in leads II, III, aVF, and in leads V5–V6 were similar in both groups and the differences were not statistically significant. However, ST depression in leads V1–V3 was more frequent in patients with NSTE‐ACS than in patients with APE (21 [49%] patients vs 19 [20%] patients, P < 0.001).
There were no significant differences between both groups in the simultaneous presence of negative T waves with or without ST depression in leads II, III, aVF (16 [17%] patients in group APE vs 6 [14%] patients in group NSTE‐ACS, 24 [25%] patients vs 7 [16%] patients, respectively, NS). Moreover, negative T waves in leads V5–V6 with coexisting ST depression were significantly more frequent in group NSTE‐ACS (13 [14%] patients in group APE vs 13 [30%] patients in group NSTE‐ACS, P < 0.05).
RBBB and S1S2S3 or S1Q3T3 pattern was recorded in similar frequency in both groups (10 [11%] APE patients vs 6 [14%] NSTE‐ACS patients, 27 [28%] patients vs 7 [16%] patients, respectively, NS). Similarly, presence of S‐wave notch in lead V1 did not differentiate both groups (9 [9%] patients in group APE versus 4 [9%] patients in group NSTE‐ACS, NS).
Arrhythmias
The prevalence of supraventricular premature beats was similar in APE and NSTE‐ACS patients (17 [18%] patients vs 9 [21%] patients, NS), ventricular premature beats was recorded in 2 (2%) patients in group APE, and in 6 (14%) patients in group NSTE‐ACS (P < 0.05). There was no case of complex arrhythmias in both groups.
P pulmonale was found only in one patient in group with APE.
Sensitivity, specificity, NPV, and PPV were evaluated for the chosen parameters. The negative T waves in leads V1–V3 occurred simultaneously with negative T waves in leads II, III, aVF were high specific (87%) with a high PPV (85%) for APE. The occurrence of ventricular premature beats, ST depression in leads V1–V3, negative T waves in leads V5‐6, negative T waves in leads V5–V6 with ST depression, counterclockwise axis rotation were specific for NSTE‐ACS (specificity 69–98%) (see Table 3).
Table 3.
Sensitivity, Specificity, and Predictive Values of Chosen Electrocardiographic Parameters in Studied Groups of Patients with APE (Group APE, n = 95) and in Patients with NSTE‐ACS (Group NSTE‐ACS, n = 43)
| Predictor | Number of Patients with Positive Test | Sensitivity (%) | Specificity (%) | PPV (%) | NPV (%) | |
|---|---|---|---|---|---|---|
| APE n (%) | NSTE‐ACS n (%) | |||||
| Negative T waves in leads V1‐3 for APE | 63 (64) | 21 (47) | 64 | 53 | 75 | 41 |
| Negative T waves in leads V1‐3 and in leads II, III, aVF for APE | 33 (34) | 6 (13) | 34 | 87 | 85 | 38 |
| Counterclockwise rotation for NSTE‐ACS | 30 (31) | 26 (58) | 58 | 69 | 46 | 78 |
| Ventricular premature beats for NSTE‐ACS | 2 (2) | 6 (13) | 13 | 98 | 75 | 69 |
| ST depression in leads V1‐3 for NSTE‐ACS | 19 (19) | 21 (47) | 47 | 81 | 53 | 77 |
| Negative T waves in leads V5‐6 for NSTE‐ACS | 17 (17) | 18 (40) | 40 | 83 | 51 | 75 |
| Negative T waves in leads V5‐6 with ST depression for NSTE‐ACS | 13 (13) | 13 (29) | 29 | 87 | 50 | 73 |
PPV = positive predictive value; NPV = negative predictive value; APE = acute pulmonary embolism; NSTE‐ACS = non‐ST elevation acute coronary syndrome.
Univariate Analysis
Logistic regression analysis revealed that negative T waves in leads V1–V3 (OR 1.26 [0.99–1.61]) and negative T waves in leads V1–V3 coexisting with negative T waves in leads II, III, aVF (OR 1.3 [1.14–1.68]) are significant predictors of APE. Whereas, counterclockwise axis rotation (OR 4.57 [2.74–7.61]), ventricular premature beats (OR 2.60 [1.60–4.19]), ST depression in leads V1–V3 (OR 2.25 [1.43–3.56]), and negative T waves in leads V5–V6 (OR 2.08 [1.31–3.29]) indicate NSTE‐ACS (Table 4).
Table 4.
Odds Ratio for APE (Group APE) and NSTE‐ACS (Group NSTE‐ACS), Depending on the Presence of Selected Electrocardiographic Abnormalities
| ECG Abnormalities | OR (95% CI) | P |
|---|---|---|
| ECG abnormalities predicting APE | ||
| Negative T waves in leads V1‐3 | 1.26 (0.99–1.61) | 0.06 |
| Negative T waves in leads V1‐3, II, III, aVF | 1.3 (1.14–1.68) | <0.01 |
| ECG abnormalities predicting NSTE‐ACS | ||
| Counterclockwise axis rotation | 4.57 (2.74–7.61) | <0.01 |
| Ventricular premature beats | 2.60 (1.60–4.19) | <0.01 |
| ST depression* in leads V1‐3 | 2.25 (1.43–3.56) | <0.01 |
| negative T waves in leads V5‐6 | 2.08 (1.31–3.29) | <0.01 |
| Negative T waves in leads V5‐6 with ST depression* | 1.83 (1.13–2.97) | <0.01 |
*ST depression equal/more than 1 mm.
APE = acute pulmonary embolism; NSTE‐ACS = non‐ST elevation acute coronary syndrome.
Relationship between severity of APE and ECG changes is presented in Table 5.
Table 5.
Electrocardiographic Abnormalities in Patients with Low, Intermediate, and High Risk of APE. Risk Groups Defined According to European Society of Cardiology Guidelines
| Low‐Risk APE (n = 36) | Intermediate Risk APE (n = 57) | High‐Risk APE (n = 5) | P | |
|---|---|---|---|---|
| Clockwise axis rotation | 9 | 18 | 3 | 0.76 |
| ST depression* in leads II, III, aVF | 9 | 21 | 2 | 0.91 |
| ST depression in leads V1‐3 | 7 | 10 | 2 | 0.92 |
| ST depression in leads V5‐6 | 11 | 24 | 3 | 0.82 |
| Negative T waves in leads II, III, aVF without ST depression | 6 | 16 | 2 | 0.82 |
| Negative T waves in leads II, III, aVF with ST depression | 3 | 12 | 1 | 0.75 |
| Negative T waves in leads V1‐3 without ST depression | 13 | 31 | 2 | 0.69 |
| Negative T waves in leads V1‐3 with ST depression | 7 | 8 | 2 | 0.80 |
| Negative T waves in leads V5‐6 without ST depression | 0 | 4 | 0 | 0.93 |
| Negative T waves in leads V5‐6 with ST depression | 1 | 12 | 0 | 0.26 |
| Supra‐ and ventricular premature beats | 3 | 13 | 2 | 0.45 |
| Supraventricular premature beats | 3 | 12 | 2 | 0.45 |
| Ventricular premature beats | 0 | 1 | 1 | 0.15 |
| Right bundle branch block | 3 | 5 | 2 | 0.40 |
| S1S2S3 or S1Q3T3 pattern | 8 | 12 | 5 | 0.04 |
| S1S2S3 pattern | 2 | 3 | 2 | 0.13 |
| S1Q3T3 pattern | 6 | 9 | 5 | 0.005 |
| P pulmonale | 0 | 1 | 0 | 0.99 |
| S‐wave notch in lead V1 | 1 | 8 | 0 | 0.63 |
| Atrial fibrillation | 3 | 8 | 1 | 0.97 |
| Left bundle branch block | 1 | 2 | 0 | 0.99 |
*ST depression equal/more than 1 mm.
APE = acute pulmonary embolism.
DISCUSSION
Although pulmonary embolism is one of the most common life‐threatening cardiovascular conditions, it is often not properly diagnosed. Importantly, the prognosis in APE depends on prompt and adequate treatment. Unfortunately, the APE symptoms, such as dyspnea, chest pain, syncope, are not specific and can often mimic other acute cardiopulmonary pathologies including acute coronary syndromes. Unnecessary coronary angiographies were reported in patient with APE when initially ACS was diagnosed. 9 Because all patients hospitalized with acute chest pain or after syncope undergo standard 12‐lead electrocardiogram, it seems justified to assess differences in ECG recording between APE and NSTE‐ACS. Several studies reported that ECG abnormalities typical for APE are useful for discrimination from acute coronary syndromes. These are: clockwise axis rotation, RBBB, S1S2S3 or S1Q3T3 pattern, S‐wave notch in lead V1. 10 , 11 , 12 It was even suggested that when all above abnormalities are present in a patient with a suggestive clinical presentation and risk factors of venous thromboembolic disease, they could be regarded for diagnostic procedure. 13 Our study found that RBBB, S1S2S3 or S1Q3T3 pattern could not differentiate APE from ACS. Moreover, it was found that these abnormalities occurred rather rarely in patient with APE, and the reported frequency of S1Q3T3 pattern is 15%, while RBBB only 12%. 14 We found that counterclockwise axis rotation significantly predicted ACS (OR 4.57 [95% CI 2.74–7.61]).
Interestingly, negative T waves in precordial leads are often seen in patients with acute coronary syndrome, but may also occur in acute pulmonary embolism. Some authors regard T‐wave inversion in the precordial lead for the most common abnormality in patients with APE. Moreover, negative T waves were reported to correlate with the severity of the PE. 15 , 16 , 17 Recently, standard ECG recordings of 127 patients (40 patients with APE and 87 patients with ACS patients) with negative T waves in the precordial leads were analyzed. It was found that pulmonary negative T waves in present simultaneously in both III and V1 leads allow to differentiate APE from ACS with sensitivity, specificity, PPV, and NPV of 88%, 99%, 97%, and 95%, respectively, in studied groups. 10 Our data support these observations. Although isolated negative T wave in V1–V3 were only of borderline significance for APE (P = 0.06), their coexistence with negative T waves in inferior wall leads significantly predicted APE. Negative T waves in V5–V6 indicated ACS, especially when ST depression was present. Also premature ventricular beats instead of supraventricular beats in studied group indicated NSTE‐ACS with a very high specificity.
In conclusion, RBBB, S1S2S3 or S1Q3T3 pattern commonly reported to be characteristic for APE, in studied group of patients did not differentiate APE from NSTE‐ACS. However, coexistence of negative T waves in precordial leads and inferior wall leads should suggest APE, while negative T waves in V5–V6 especially with ST segment depression indicate ACS.
Acknowledgments
Acknowledgments: The authors have certified that the manuscript conforms to the guidelines in “Uniform Requirements for Manuscripts Submitted to Biomedical Journals,” 5th edition, published in New England Journal of Medicine 1997; 336: 309–315.
Conflict of Interest: The authors of this manuscript do not report any conflict of interest in connection with submitted article.
REFERENCES
- 1. Pruszczyk P, Szulc M, Horszczaruk G, et al Right ventricular infarction in a patient with acute pulmonary embolism and normal coronary arteries. Arch Intern Med 2003;163:1110–1111. [DOI] [PubMed] [Google Scholar]
- 2. McGinn S, White PD. Acute cor pulmonale resulting from pulmonary embolism. JAMA 1935;104:1473–1480. [Google Scholar]
- 3. Rodger M, Makropoulos D, Turek M, et al Diagnostic value of the electrocardiogram in suspected pulmonary embolism. Am J Cardiol 2000;86:807–809. [DOI] [PubMed] [Google Scholar]
- 4. Ferrari E, Imbert A, Chevalier T, et al The electrocardiogram in pulmonary embolism: Predictive value of negative T‐waves in precordial leads −80 case report. Chest 1997;11:537–543. [DOI] [PubMed] [Google Scholar]
- 5. Stein PD, Dalen JE, McIntyre KM, et al The electrocardiogram in acute pulmonary embolism. Prog Cardiovasc Dis 1975;17:247–257. [DOI] [PubMed] [Google Scholar]
- 6. Stein PD, Terrin ML, Hales CA, et al Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre‐existing cardiac or pulmonary disease. Chest 1991;100:598–603. [DOI] [PubMed] [Google Scholar]
- 7. Mirvis DM, Goldberger AL. Electrocardiography In: Zipes DP, Braunwald E. (eds.): Braunwald's Heart Disease: A Textbook of Cardivascular Medicine, 7th Edition Philadelphia : Elsevier Saunders, 2005. [Google Scholar]
- 8. Bassand JP, Hamm CW, Ardissino D, et al Task Force for diagnosis and treatment of non‐ST‐segment elevation acute coronary syndromes of European Society of Cardiology, Guidelines for the diagnosis and treatment of non‐ST‐segment elevation acute coronary syndromes. Eur Heart J 2007;28:1598–1660. [DOI] [PubMed] [Google Scholar]
- 9. Widimsky P, Stellova B, Groch L, et al PRAGUE Study Group Investigators: Prevalance of normal coronary angiography in the acute phase of suspected ST‐elevation myocardial infarction: Experience from the PRAGUE studies. Can J Cardiol 2006;22:1147–1152. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10. Kosuge M, Kimura K, Ishikawa T, et al Electrocardiographic differentiation between acute pulmonary embolism and acute coronary syndromes on the basis of negative T‐waves. Am J Cardiol 2007;99:817–821. [DOI] [PubMed] [Google Scholar]
- 11. Sreeram N, Cheriex EC, Smeets JL, et al Value of the 12‐lead electrocardiogram at hospital admission in the diagnosis of pulmonary embolism. Am J Cardiol 1994;73:298–303. [DOI] [PubMed] [Google Scholar]
- 12. Wilson GT, Schaller FA. Pulmonary embolism mimicking anteroseptal acute myocardial infarction. JAOA 2008;108:344–349. [PubMed] [Google Scholar]
- 13. Perrier A, Bounameaux H. Pulmonary thromboembolism and pulmonary vascular tumors. Diagnosis In: Peacock AJ, Rubin LJ. (eds.): Pulmonary Circulation. Diseases and Their Treatment, 2nd Edition London : Edward Arnold (Publishers) Ltd, 2004. [Google Scholar]
- 14. Golbin JM, Prakash UBS. Pulmonary embolism In: Murphy JG, Lloyd MA. (eds.): Mayo Clinic Cardiology. Concise Textbook, 3rd Edition Rochester , MN : Mayo Foundation for Medical Education and Research, 2007. [Google Scholar]
- 15. Yoshinaga T, Ikeda S, Nishimura E, et al Serial changes in negative T‐wave on electrocardiogram in acute pulmonary thromboembolism. Int J Cardiol 1999;72:65–72. [DOI] [PubMed] [Google Scholar]
- 16. Punukollu G, Gowda RM, Khan IA, et al QT interval prolongation with global T‐wave inversion: A novel ECG finding in acute pulmonary embolism. Ann Noninvasive Electrocardiol 2004;9:94–98. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17. Ciurzynski M, Kurzyna M, Ficygowski W, et al Pulmonary embolism hemodynamically significant. Electrocardiographic findings. Kardiol Pol 2000;52:458–460. [Google Scholar]