Electrocardiographic abnormalities in patients with acute pulmonary ...

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b Department of Internal Medicine, Section of Cardiology, University of Manitoba, ... Interventional Electrocardiology and Hypertension, Jagiellonian University, ...
American Journal of Emergency Medicine 32 (2014) 507–510

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Original Contribution

Electrocardiographic abnormalities in patients with acute pulmonary embolism complicated by cardiogenic shock☆ Piotr Kukla, MD, PhD a,⁎, William F. McIntyre, MD b, Kamil Fijorek, MSc c, Ewa Mirek-Bryniarska, MD, PhD d, Leszek Bryniarski, MD, PhD e, Ewa Krupa, MD f, Marek Jastrzębski, MD, PhD e, Krzysztof L. Bryniarski, MD g, Zhan Zhong-qun, MD h, Adrian Baranchuk, MD, PhD i a

Department of Cardiology, Specialistic Hospital, Gorlice, Poland Department of Internal Medicine, Section of Cardiology, University of Manitoba, Winnipeg, Manitoba, Canada c Department of Statistics, Cracow University of Economics, Cracow, Poland d Department of Cardiology, Dietl’s Hospital, Cracow, Poland e First Department of Cardiology, Interventional Electrocardiology and Hypertension, Jagiellonian University, Cracow, Poland f Department of Cardiology, Szczeklik Hospital, Tarnow, Poland g First Department of Internal Medicine, Dietl’s Hospital, Cracow, Poland h Department Of Cardiology, Shiyan Taihe Hospital, Hubei University of Medicine, Hubei Province, China i Division of Cardiology, Kingston General Hospital, Queen’s University, Kingston, Ontario, Canada b

a r t i c l e

i n f o

Article history: Received 20 January 2014 Accepted 24 January 2014

a b s t r a c t Background: Cardiogenic shock (CS) is a predictor of poor prognosis in patients with acute pulmonary embolism (APE). Objectives: The aim of this study was to compare electrocardiography (ECG) parameters in patients with APE presenting with or without CS. Methods: A 12-lead ECG was recorded on admission at a paper speed of 25 mm/s and 10 mm/mV amplification. All ECGs were examined by a single cardiologist who was blinded to all other clinical data. All ECG measurements were made manually. Results: Electrocardiographic data from 500 patients with APE were analyzed, including 92 patients with CS. The following ECG parameters were associated with CS: S1Q3T3 sign, (odds ratio [OR]: 2.85, P b .001), qR or QR morphology of QRS in lead V1, (OR: 3.63, P b .001), right bundle branch block (RBBB) (OR: 2.46, P = .004), QRS fragmentation in lead V1 (OR: 2.94, P = .002), low QRS voltage (OR: 3.21, P b .001), negative T waves in leads V2 to V4 (OR: 1.81, P = .011), ST-segment depression in leads V4 to V6 (OR: 3.28, P b .001), ST-segment elevation in lead III (OR: 4.2, P b .001), ST-segment elevation in lead V1 (OR: 6.78, P b .01), and ST-segment elevation in lead aVR (OR: 4.35, P b .01). The multivariate analysis showed that low QRS voltage, RBBB, and ST-segment elevation in lead V1 remained statistically significant predictors of CS. Conclusions: In patients with APE, low QRS voltage, RBBB, and ST-segment elevation in lead V1 were associated with CS. © 2014 Elsevier Inc. All rights reserved.

1. Introduction Acute pulmonary embolism (APE) is one of the most frequent cardiovascular causes of death. Reducing mortality by rapid diagnosis and treatment remains a challenge. Total mortality is as high as 15% in the subgroup of patients who present with severe hypotension or cardiogenic shock (CS) [1]. Electrocardiography (ECG) has poor sensitivity and specificity for diagnosing APE, but it is still one of the first procedures performed at admission, mostly in patients who present with chest pain or dyspnea [2]. The ECG in patients with APE and CS can lead to the misdiagnosis of an acute coronary syndrome. ☆ Kamil Fijorek has received financial support from “The Foundation for Polish Science.” ⁎ Corresponding author. Department of Cardiology and Internal Medicine, Specialistic Hospital, Gorlice 38-300, Poland. Tel.: +48 18 35 53 422; fax: +48 18 35 53 446. E-mail address: [email protected] (P. Kukla). http://dx.doi.org/10.1016/j.ajem.2014.01.043 0735-6757/© 2014 Elsevier Inc. All rights reserved.

Recognizing the APE ECG pattern may help in establishing the right diagnosis and lead to the rapid initiation of proper treatment. The aims of this study were as follows: (i) To compare the prevalence of different ECG patterns in patients diagnosed with APE with or without CS on presentation to hospital; and (ii) To evaluate the impact of these ECG patterns on prognosis and complications during the hospitalization due to APE.

2. Methods Retrospective chart review analysis of patients who experienced APE and were hospitalized in 7 cardiology departments in Poland between 2005 and 2012. The study was performed as part of the regional

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pressure more than 40 mm Hg lasting at least 15 minutes and requiring treatment with inotropic drugs.

Table 1 Demographic and clinical characteristics of enrolled patients Characteristic

Value

Age (y) Female:male Stenocardia Syncope Obesity Immobilization Thrombophlebitis Hemoptysis Neoplastic disease Oral contraception CHF class NYHA II-IV COPD Prefebrile status under diagnosis

65.4 ± 15.5 290:210 (62.7%:37.3%) 206 (41.2%) 131 (26.2%) 123 (24.6%) 124 (24.8%) 210 (42.0%) 21 (4.2%) 52 (10.4%) 12 (2.4%) 73 (14.6%) 42 (8.4%) 86 (17.2%)

Abbreviations: CHF, congestive heart failure; NYHA, New York Heart Association; COPD, chronic obstructive pulmonary disease.

“Malopolska Acute Pulmonary Registry [3].” The study group consisted of 500 consecutive patients (290 females and 210 males), with a mean age of 66.3 ± 15.2 years (range, 17-91 years). The length of stay was 15 ± 10 days (range, 1-46 days). Table 1 shows baseline clinical and demographic characteristics of all patients. Acute pulmonary embolism was diagnosed based on spiral computed tomography in 469 (93.8%) patients. The diagnosis was made by echocardiography in 24 patients (4.8%). This included 16 patients with CS and right ventricular overload and 8 patients with thrombus in the right atrium or right ventricle. Five (1%) patients were diagnosed by scintigraphy, and 2 (0.4%) patients were diagnosed by autopsy. 2.1. ECG analysis Standard 12-lead ECG was recorded on admission with a paper speed of 25 mm/s. The first available ECG was used for analysis. The following ECG parameters were analyzed: heart rate; supraventricular or ventricular arrhythmia; QRS axis deviation; P pulmonale; amplitude of the P wave greater than 0.25 mV in at least 1 limb lead (II, III, and aVF); right bundle branch block (RBBB); McGinn-White sign (S1Q3T3 complex); negative T waves in leads III and aVF; negative T waves in leads V2 to V4; ST-segment depression in leads V4 to V6; ST-segment elevation in leads aVR, III, and V1; “new ST index” (STsegment elevation in lead aVR with ST-segment depression in the lateral leads), fragmented QRS (R-wave notch or S-wave notch) in leads V1; QR pattern in lead V1; clockwise rotation; ratio of amplitude of R wave to S wave at least 1 in lead V5; low QRS voltage (b 5 mm) in the limb leads; and number of leads with negative T waves. The following clinical events were recorded: CS/hypotension on admission or during the hospitalization and death from all causes. Cardiogenic shock was defined as a blood pressure less than 90/60 mm Hg requiring treatment with inotropic drugs or a drop in blood

2.2. Statistical analysis Categorical variables were expressed as numbers and percentages and continuous variables as means and standard deviations. Differences between the groups were assessed by univariate logistic regression model. The univariate analyses were performed on all available data for a given comparison. Mortality in the CS group showed no significant significance and was not carried out to a multivariate analysis. The statistically optimal multivariate logistic regression model was identified by stepwise selection of predictors resulting in the lowest value of Bayesian Information Criterion. The predictive abilities of the models were summarized by the area under receiver operating characteristic curve (AUC). The direction and strength of association between dependent variable and predictors were summarized by odds ratios (ORs) with 95% confidence intervals. A 2-tailed P b .05 was considered statistically significant. All statistical analyses were performed using R 3.0 (http://R-project.org), a language and environment for statistical computing [4]. 3. Results 3.1. Clinical characteristics Among 500 patients with APE, there were 51 deaths, corresponding to a mortality rate of 10.2%. Cardiogenic shock was observed in 92 patients (18.4%). The population of patients with and without CS did not differ in age (66.2 ± 15.1 vs 67.1 ± 15.6 years) or sex (58.6% males vs 55.4% females). The CS group included significantly more patients with syncope (48.9% vs 21.1%, P b .001) and heart failure symptoms or a history of heart failure (21.7% vs 13.0%, P = .04). In the group without CS, stenocardia on admission (43.4% vs 31.5%, P = .036) and a history of previous myocardial infarction (8.09% vs 1.09%, P = .008) were more common. Patients with CS presented with faster heart rate than those without CS (112 ± 28 vs 97 ± 24 beats per minute; OR: 1.25 for each 10 beats per minute, P b .001). 3.2. ECG changes Electrocardiographic patterns among the entire study group are shown in Table 2. 3.2.1. Depolarization abnormalities In patients with CS, the following “depolarization abnormalities” were seen more frequently: McGinn-White sign (S1Q3T3 sign, OR: 2.85, P b .001); Kocher sign (qR, QR pattern in lead V1) (OR: 3.63, P b .001); complete RBBB (OR: 2.46, P = .004); fragmented QRS in lead V1 (OR: 2.94, P = .002), and low QRS voltage (OR: 3.21, P b .001) (Table 2).

Table 2 Electrocardiographic changes in patients with or without CS ECG parameters

All patients, N = 500

Without CS, n = 408

With CS, n = 92

OR

P

No. of leads with negative T wave Atrial fibrillation Premature ventricular contraction S1Q3T3 sign Negative T wave V2-V4 ST-segment elevation in lead III RBBB qR sign in lead V1 ST-segment elevation in lead V1 ST-segment elevation in lead aVR ST-segment depression in V4-V6 New ST index Fragmented QRS in lead V1

2.91 (2.6) 101 (20.2%) 26 (5.2%) 16 (32.6%) 199 (40.3%) 61 (12.5%) 61 (12.6%) 55 (11.3%) 115 (23.6%) 178 (36.2%) 145 (29.5%) 99 (19.8%) 49 (9.8%)

2.76 (2.6) 76 (18.6%) 20 (4.9%) 114 (28.1%) 151 (37.6%) 35 (8.8%) 41 (10.4%) 33 (8.27%) 64 (16.1%) 119 (29.7%) 98 (24.5%) 62 (15.2%) 31 (7.6%)

3.56 (2.7) 25 (27.2%) 6 (6.5%) 48(52.7%) 48 (52.2%) 26 (28.9%) 20 (22.2%) 22 (24.7%) 51 (56.7%) 59 (64.8%) 47 (51.6%) 37 (40.2%) 18 (19.6%)

1.11 [1.02;1.21] 1.63 [0.95;2.73] 1.38 [0.48;3.37] 2.85 [1.79;4.56] 1.81 [1.15;2.87] 4.20 [2.35;7.46] 2.46 [1.34;4.42] 3.63 [1.97;6.61] 6.78 [4.14;11.2] 4.35 [2.70;7.10] 3.28 [2.05;5.27] 3.73 [2.26;6.14] 2.94 [1.53;5.50]

.012 .073 .522 b .001 .011 b .001 .004 b .001 b .001 b .001 b .001 b .001 .002

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Table 3 Frequency of ECG changes in patients with APE complicated by CS, classified according to survival ECG parameters

All CS, N = 92

CS survivor, n = 52

CS death, n = 39

OR

No. of leads with negative T waves Atrial fibrillation Premature ventricular contraction S1Q3T3 sign Negative T waves in leads V2-V4 ST-segment elevation in lead III RBBB qR sign in lead V1 ST-segment elevation in lead V1 ST-segment elevation in lead aVR ST-segment depression in leads V4-V6 New ST index Fragmented QRS in lead V1

3.56 (2.74) 25 (27.2%) 6 (6.52%) 48 (52.7%) 48 (52.2%) 26 (28.9%) 20 (22.2%) 22 (24.7%) 51 (56.7%) 59 (64.8%) 47 (51.6%) 37 (40.2%) 18 (19.6%)

3.51 14 4 28 27 13 9 11 29 35 26 21 8

3.62 11 2 20 21 13 11 11 22 24 21 16 10

1.01 1.10 0.69 0.99 1.12 1.55 2.05 1.47 1.09 0.88 1.28 1.06 1.92

(2.68) (26.4%) (7.55%) (52.8%) (50.9%) (25.0%) (17.0%) (21.6%) (55.8%) (66.0%) (49.1%) (39.6%) (15.1%)

3.2.2. Repolarization abnormalities In patients with CS, the following “repolarization abnormalities” were seen more frequently: negative T waves in leads V2 to V4 (OR: 1.81, P = .011); ST-segment depression in leads V4 to V6 (OR: 3.28, P b .001); ST-segment elevation in leads III (OR: 4.2, P b .001); STsegment elevation in lead V1 (OR: 6.78, P b .01); ST-segment elevation in lead aVR (OR: 4.35, P b .01); “new ST-segment index” (OR: 3.73, P b .001); and more leads with negative T waves (OR: 1.11, P = .012) (Table 2). 3.2.3. Other ECG changes P pulmonale (OR: 0.81, P = .61) and right axis deviation (OR: 1.82, P = .072) were observed with similar frequency in patients with or without CS, and these parameters did not predict mortality (Table 2, 3). 3.2.4. Arrhythmia The presence of arrhythmias, including atrial fibrillation (OR: 1.63, P = .073) and premature ventricular contractions (OR: 1.38, P = .522) was not uncommon in CS patients with APE but did not predict mortality (Tables 2 and 3). 3.3. High-risk patients and mortality Among 92 patients in the CS group, 39 patients (42%) died during hospitalization. There were no significant differences in ECG parameters between patients with CS who survived and those who did not (Table 3).

(2.84) (28.2%) (5.13%) (52.6%) (53.8%) (34.2%) (29.7%) (28.9%) (57.9%) (63.2%) (55.3%) (41.0%) (25.6%)

P [0.87;1.18] [0.42;2.79] [0.08;3.95] [0.43;2.31] [0.49;2.60] [0.61;3.96] [0.74;5.80] [0.55;3.97] [0.46;2.57] [0.37;2.14] [0.55;2.99] [0.45;2.48] [0.67;5.67]

.855 .849 .683 .985 .788 .354 .167 .438 .846 .780 .568 .893 .224

4. Discussion The surface ECG is the one of the first diagnostic tools used for patients who present to the emergency department with symptoms suggesting APE. Electrocardiographic results, however, are not always specific to APE. In general, ECG is regarded as a helpful tool in the differential diagnosis of acute cardiac diseases. According to current European Society of Cardiology (ESC) guidelines, patients with APE and CS are considered at high risk of death [1]. Electrocardiographic measurements, however, are not considered in the ESC risk stratification. On the other hand, several previous studies have suggested that ECG may be useful for APE risk stratification, mainly in predicting right ventricular dysfunction [5-9]. Recently, our group’s pilot study and Janata et al [10,11] have reported on the ability of the surface ECG to recognize a group of patients with APE and worse outcomes. In our study, we analyzed the frequency of ECG patterns in patients who belong to the high-risk population in the risk stratification model of the ESC guideline recommendations. We hypothesized that CS in patients with APE leads to profound right and left ventricular ischemia leading to misdiagnosis of APE as primarily ischemic disease. For this reason, we decided to analyze ECG patterns for both depolarization abnormalities and repolarization abnormalities to increase the ability to make the proper diagnosis. The present study confirmed our hypothesis that, in the high-risk APE patients (patients evolving into CS), both depolarization and repolarization abnormalities are observed significantly more frequently.

3.4. ECG predictors of CS We calculated 2 models of ECG parameters to predict CS. In “model 1,” we assessed all analyzed ECG parameters shown in Table 2. Independent ECG parameters predicting CS by multivariate regression analysis in “model 1” included low QRS voltage, RBBB, and STsegment elevation in lead V1 (Table 4). Because a minority of patients with APE had low QRS voltage (8%) or RBBB (12%) on their admission ECG, we built a “model 2,” excluding these parameters from “model 1.” In “model 2”, independent ECG parameters predicting CS in a multivariate regression analysis were QR sign in lead V1, fragmented QRS in lead V1, ST-segment elevation in lead aVR, and ST-segment depression in leads V4 to V6 (Table 5).

Table 4 Model 1 ECG parameters independently associated with CS in multivariate regression analysis Parameters

OR

95 % CI

P

Low QRS voltage RBBB ST-segment elevation in lead V1

3.44 2.95 7.62

1.57-7.56 1.47-5.91 4.50-12.90

.002 .002 .000

Bayesian Information Criterion = 398.1, AUC = 0.75.

4.1. Depolarization abnormalities Recent publications have shown that the incidence of RBBB is 11% to 29% in patients with APE [12-16]. In the present study, RBBB was detected in 12.6% of our population. In the International Cooperative Pulmonary Embolism Registry, 16% of APE patients presented with complete or incomplete RBBB [12]. In a study by Escobar et al [13] in patients with hemodynamically stable, symptomatic APE, RBBB was present in 16% of patients who survived and in 11% patients who died during the 30-day follow-up period. In our study, RBBB was observed

Table 5 Model 2. ECG parameters independently associated with CS in multivariate regression analysis Parameters

OR

95% CI

P

QR sign in lead V1 ST-segment elevation in lead aVR ST-segment depression in leads V4-V6 Fragmented QRS in lead V1

2.66 2.49 2.24 3.00

1.38-5.10 1.41-4.39 1.27-3.96 1.48-6.05

.003 .002 .006 .002

Abbreviation: CI, confidence interval. Bayesian Information Criterion = 421.5, AUC = 0.75.

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in 22.2% of high-risk patients and was more frequent in high-risk vs non–high-risk APE patients. The presence of RBBB in high-risk patients was not associated with death. In the study of Janata et al [11], mortality in high-risk patients with RBBB was 50% and did not differ statistically from mortality of patients without RBBB.

most centers involved in this study receive referrals from small centers with less available technology. Presented data do not address either the sensitivity or specificity of the individual criteria because no control group was included.

4.2. Repolarization abnormalities

6. Conclusion

4.2.1. ST-segment elevation Acute pulmonary embolism can mimic an acute coronary syndrome in the presence of ST-segment elevation. This is especially frequent for ST-segment elevation in leads III and aVF, replicating an inferior myocardial infarction. In addition, ST elevation may also be observed in lead V1 because this lead reflects electrical processes of the anterior free right ventricular wall, and lead III reflects processes from the inferior region of the right ventricle [17]. In the present study, ST-segment elevation in lead III was found in 12.5% of the entire population and in 28.9% of high-risk patients. In APE, ST-segment elevation can also be observed in leads V1 to V4 [18-20]. In the present study, ST-segment elevation in lead V1 was found in 23.6% of the patients and in 56.7 % of the high-risk patients [21]. Similarly, Kucher et al [22] observed STsegment elevation in lead V1 in 20% of APE patients. Janata et al [11] in a population of 396 patients with APE showed that mortality was significantly higher in patients with ST-segment elevation in lead V1 as compared with those without (12.9% vs 5.1%, P = .009) and tends to be higher in patients with ST-segment elevation in lead aVR (10.3 % vs 5.4%, P = not significant). In the high-risk group in the study by Janata et al [11], the mortality rate was 30.4% in patients with ST-segment elevation in lead aVR and 41.2% in patients with ST-segment elevation in lead V1. In our study, ST-segment elevation in lead aVR was detected in 36.2% of our APE patients and in 64.8% of the high-risk patients. The aforementioned ST-segment abnormalities, however, did not predict mortality in high-risk APE patients.

Electrocardiographic abnormalities in patients with APE allow identifying a subgroup of patients with worse evolution due to CS. These ECG parameters do not identify higher mortality in patients with APE and CS.

4.2.2. ST-segment depression Geibel et al [14] reported ST-segment depression in leads I, II, and/ or V4 to V6 in 39% of APE patients. In the present study, ST-segment depression in leads V4 to V6 was found in 24.5% of all patients and in 51.6% of high-risk patients. Kaczynska et al [23] reported ST-segment depression in 24% of APE patients and showed that these changes were significantly more common in a subgroup of patients with increased troponin levels (41.4% vs 0%, P = .004). Janata et al [11] reported that the mortality rate in high-risk patients with ST-segment depression was 35.7% but did not differ from those at low risk. In our study, ST-segment depression in lateral leads was more frequently seen in high-risk patients but did not predict mortality. 4.2.3. Negative T waves Ferrari et al [24] reported negative T waves in the precordial leads of 68% of APE patients and concluded that this was the best predictor of worse outcome. Similarly, Geibel et al [14] reported negative T waves in leads V2 to V3 in 45% of APE patients, and Punkullu et al [6] reported T waves in leads V1 to V3 in 43% of APE patients. In the study of Janata et al [11], the mortality rate in high-risk patients with negative T waves was 31.6% and did not differ from mortality in patients without negative T waves. In the present study, negative T waves in leads V2 to V4 were found in 40.3% of APE patients and in 52.2% of high-risk patients but did not predict mortality in this group. 5. Study limitations The main limitation of the study is its retrospective design that can introduce some bias. The proportion of high-risk patients is higher in our study than in previously reported series. This could be related that

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