Significance of Syncope at Presentation among Patients With Pulmonary Emboli

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Significance of Syncope at Presentation among Patients with Pulmonary Emboli Sharon Shalom Natanzon MD , Shlomi Matetzky MD , Fernando Chernomordik MD , Israel Mazin MD , Romana Herscovici MD , Orly Goitein MD , Sagit Ben-Zekry MD , Nir Shlomo Msc , Avishay Grupper MD , Roy Beigel MD PII: DOI: Reference:

S0002-9149(19)31487-0 https://doi.org/10.1016/j.amjcard.2019.12.018 AJC 24346

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The American Journal of Cardiology

Received date: Revised date: Accepted date:

30 September 2019 8 December 2019 13 December 2019

Please cite this article as: Sharon Shalom Natanzon MD , Shlomi Matetzky MD , Fernando Chernomordik MD , Israel Mazin MD , Romana Herscovici MD , Orly Goitein MD , Sagit Ben-Zekry MD , Nir Shlomo Msc , Avishay Grupper MD , Roy Beigel MD , Significance of Syncope at Presentation among Patients with Pulmonary Emboli, The American Journal of Cardiology (2019), doi: https://doi.org/10.1016/j.amjcard.2019.12.018

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Significance of Syncope at Presentation among Patients with Pulmonary Emboli

Sharon Shalom Natanzon MDa*, Shlomi Matetzky MDa*, Fernando Chernomordik MDa, Israel Mazin MDa, Romana Herscovici MDa, Orly Goitein MDb, Sagit Ben-Zekry MDa, Nir Shlomo Msca, Avishay Grupper MDa, and Roy Beigel MDa

a

The Intensive Cardiac Care Unit, Cardiovascular Division, and bCardiovascular

Imaging Unit, Sheba Medical Center, Tel Hashomer, The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel Running Head: Syncope in Intermediate-Risk Pulmonary Embolism *Both authors contributed equally to the writing of this manuscript

Declaration of interests: None

Corresponding Author: Sharon Shalom Natanzon M.D. Intensive Cardiac Care Unit Cardiovascular Division, Sheba Medical Center Tel Hashomer, 52621, Israel Tel: +972-3-5302504; Fax: +972-3-5302171 E-mail: [email protected]

The following authors participated in the current study and their contribution is as follows: S. S. Natanzon contributed toward the conceptualization, methodology design and performance of the study, analysis of the data, and preparation of the manuscript. S. Matetzky contributed toward the design and performance of the study, analysis of the data, and preparation of the manuscript. F. Chernomordick contributed toward the design and performance of the study, analysis of the data. I. Mazin contributed toward the design and performance of the study, R. Herscovici contributed toward analysis of the data, investigation and preparation of the manuscript. O.Goitein contributed toward the design and performance of the study,. S. Ben-Zekry contributed toward the design and performance of the study, N. Shlomo contributed toward the design and performance of the study, analysis of the data. A. Grupper contributed toward the design and performance of the study. R. Beigel contributed toward the design and performance of the study, preparation of the manuscript, reviewing and editing. All authors were involved in interpretation of data and the final approval of the report

Patients with intermediate-risk pulmonary emboli (PE) present a challenging clinical problem. While syncope has been suggested as a marker for adverse outcomes in these patients, data remain scarce. We aimed to investigate the clinical outcomes of intermediate risk PE patients presenting with syncope. We performed a retrospective cohort study comprised of consecutive, normotensive, PE patients, with evidence of right ventricular involvement. The primary outcome of major adverse clinical events (MACE) included either one or a combination of: mechanical ventilation, hemodynamic instability and need for inotropic support, reperfusion therapy, and in-hospital mortality. Secondary outcomes included: each of the above individual components including major bleeding and renal failure. Overall, 212 patients were evaluated, 40 (19%) presented with syncope, and had a higher prevalence of MACE (29% vs 9.4%, p=0.003), as well as each of the individual secondary endpoints: mechanical ventilation (10% vs 1.8%, p=0.026), hemodynamic instability (18% vs 2.9%, p=0.02), increased need of inotropic support (10% vs 0.6%, p=0.005), and bleeding (15% vs 2.4%, p=0.004). The prevalence of in-hospital mortality was very low (0.5%) with no significant difference between those with and without syncope. There was no significant difference in the need for reperfusion therapy. Upon multivariable analysis, syncope was found to be an independent predictor of adverse clinical outcomes (OR 3.8, C.I 1.48-9.76, p=0.005). In conclusion, among intermediate-risk PE patients with RV involvement, the presence of syncope is associated with a more complicated in-hospital course. Key words: pulmonary embolism, intermediate risk, syncope, prognosis

Introduction

Pulmonary embolism (PE) is a common disease with a wide clinical presentation and course ranging from mild symptoms to a life-threatening condition. Current classification of PE is based on mortality risk1. While the initial therapeutic approach for patients with intermediate-risk PE consists initially of anticoagulation1, some of these patients may deteriorate2 and eventually require reperfusion therapy. Thus, further risk stratification is warranted. While Syncope has been identified as one of the many presentations of PE with a prevalence of 10-35%3-5, limited and conflicting data exist regarding its prognostic significance6-8, especially in the subgroup of patients with right ventricular (RV) involvement. The aim of the current study was to evaluate the significance of syncope in PE patients presenting with evidence of RV involvement (intermediate risk according to European guidelines1 and submassive according to U.S guidelines9). Methods We retrospectively analyzed consecutive patients with intermediate-risk PE with evidence of RV involvement admitted to the intensive cardiac care unit of the Sheba Medical Center between 2008 and 2017. Patients were included if they were: >18 years of age, diagnosed with PE, were hemodynamically stable upon presentation, and demonstrated at least one of the following: 1) evidence of RV enlargement upon computed tomography and/or evidence of RV dysfunction upon echocardiography; 2) evidence of elevated cardiac troponin levels suggesting myocardial damage. RV involvement on CT was defined as one of the following: a) RV/left ventricular (LV) ratio of ≥0.9; b) a shift of the interventricular septum towards the LV; or c) backflow of contrast to the inferior vena cava. RV involvement on echocardiography was defined as one of the following: a) RV/LV≥1 ratio; b) enlarged RV diameter of >35 mm at the mid-ventricular level or >41 mm at the base of the RV; or c) RV contractile dysfunction. The severity of RV dysfunction was estimated

quantitively by experienced echocardiographers mostly based on 2-dimensional echocardiography and categorized as either normal, mild, moderate, or severe RV dysfunction. Collected data included: prior medical history, presenting signs and symptoms, clinical findings, treatment administered, and in-hospital course including clinical deterioration, as well as in-hospital and 90 days mortality which was obtained from the ministry of interior records. Syncope was defined as an abrupt, transient loss of consciousness with spontaneous resolution. A composite of major adverse clinical events (MACE) consisting of clinical deterioration during hospitalization was defined as any one of the following: 1) either a drop in systolic blood pressure to <90 mmHg for at least 15 minutes with signs of end organ hypo-perfusion, or the need for vasopressor support to maintain adequate blood pressure of >90 mmHg, as well as the need for cardiopulmonary resuscitation; 2) the need for mechanical ventilation; 3) the need for reperfusion therapy after admission (either by systemic thrombolysis or surgical embolectomy); 4) in-hospital mortality. A comparison between patients presenting with and without syncope prior to or upon admission was evaluated. The study was approved by the Sheba medical center institutional review board (IRB), project number 2258-15-SMC. We applied the Kolmogorov- Smirnov test and found that our cohort did not follow the normal distribution pattern. Thus, we used the Mann-Whitney U test for comparing continuous variables which were cited as mean ± SD. Chi-square test or Fisher exact test was used for comparing categorical variables, cited as percentages. Multivariate analysis was performed using binary logistic regression to assess the association between syncope and in-hospital clinical deterioration adjusted for age, body mass index and RV/LV diameter. Results are presented in Odds Ratio with 95% confidence interval.

Results A total of 212 intermediate-risk PE patients were evaluated, of whom 40 (19%) presented with syncope. These patients did not differ regarding their baseline clinical characteristics, including cardiovascular risk factors and the presence of malignancy, or a prior venous thromboembolism event, as well as the use of oral anticoagulants at presentation (Table 1). As shown in table 2, There was a higher prevalence of S1Q3T3 pattern in patients presenting with syncope compared to those without (33% vs. 26%, p<0.001). Upon computed tomography the mean RV/LV diameter ratio was significantly higher among patients presenting with syncope (1.7±0.6 vs. 1.4±0.4, p= 0.01). Echocardiography demonstrated a trend towards a higher prevalence of either moderate or severe RV dysfunction (58% vs.40%, p=0.08) in patients presenting with syncope compared to their non-syncope counterparts. Patients presenting with syncope had a significantly more complicated inhospital course (Table 3) with more than 3 times higher incidence of MACE (29% vs 9.4%, p=0.003). The increase in MACE arose from a significantly higher incidence of hemodynamic instability (18% vs 3%, p=0.02), an increased need for inotropic support (10% vs 0.6%, p=0.005), and mechanical ventilation (10% vs. 1.8%, p=0.03). In contrast, there was no significant difference in the need for reperfusion therapy, both surgical (5% vs. 0.6%, p=0.093) and pharmacological (8% vs 6%, p=0.73) among patients with and without a history of syncope. Interestingly, patients presenting with syncope also had higher bleeding rates (15% vs 2.4%, p=0.004). The prevalence of both in-hospital and 90 days mortality were low without significant difference between the two groups. (Figure 1). Upon multi-variable analysis, after adjusting for potential confounders including differences in baseline characteristics and imaging results suggestive of more extensive RV involvement, syncope was found to be an independent predictor of a MACE (OR 3.8, C.I 1.48-9.76, p=0.005). A greater RV/LV

diameter ratio was the only other independent predictor of adverse clinical outcome (OR 3.37, C.I 1.52-7.46, p=0.003) (Figure 2). Discussion In the current study, we demonstrated that intermediate-risk PE patients with evidence of RV involvement who present with syncope are at higher risk for clinical deterioration during hospitalization, compared with intermediate-risk PE patients without syncope. Intermediate-risk PE patients present a rather heterogenous group of patients. While most will suffice with anticoagulation therapy, some will have a poorer prognosis in the acute phase2,10 requiring advanced and reperfusion therapy, compared to their low-risk/uncomplicated PE counterparts. Accordingly, there is a need for improved stratification of intermediate-risk PE patients in an attempt to identify prognostic markers of clinical deterioration. Currently, the prognostic significance of syncope in patients with PE has been inconclusive with only very limited data available3,4,6. The unique nature of the current study is the focus on a selective subgroup of intermediate-risk PE patients, especially those with evidence of RV involvement, where there is concern regarding further deterioration. In the current study, we found that patients with, compared to those without syncope, had a significantly larger RV/LV diameter on computed tomography, demonstrating a trend towards a higher prevalence of moderatesevere RV dysfunction. This supports the hypothesis, which was previously reported by others11, that the presence of syncope places a higher thrombotic burden on the RV, causing transient RV failure leading to hemodynamic decompensation. Our findings might also explain the association between syncope and RV strain, together with the fact that patients with syncope had a more complicated in-hospital clinical course and adverse outcomes, mainly necessitating a greater need for escalation

therapy, including more frequent hemodynamic instability, need for mechanical ventilation, and ionotropic support. Our findings suggest that syncope in PE patients, with evidence of RV involvement, should be addressed to some extent as hypotension or hemodynamic compromise, mandating a more aggressive approach, and therefore should be integrated into algorithms for the triage of patients presenting with acute PE. Syncope patients didn't differ in their baseline characteristics, laboratory findings or the majority of ECG features. The higher prevalence of S1Q3T3 on ECG among syncope patients is in accordance with our findings. This pattern is strongly suggestive of RV dysfunction (high specificity, low sensitivity)13, and has been suggested as a predictor of mortality among PE patients14. In accord with our findings, Omar et al7 demonstrated that syncope was associated with a worse in-hospital clinical course but was not associated with higher in-hospital mortality. Iqbal et al8 and Roncon et al6 demonstrated that 30-day mortality was higher in PE patients presenting with syncope. Importantly, in a recent study by Barco et al15, syncope at presentation was found to be associated with signs of hemodynamic instability and/or RV dysfunction, as well as increased risk for adverse outcomes in a general non-selective cohort of PE patients. However, this association was attenuated and became no longer significant when focusing on normotensive patients compared to a mixed population. In contrast, we focused on a more specific homogeneous group of intermediate-risk who exhibited objective evidence of RV involvement but were nevertheless defined as hemodynamically stable. It is specifically in these patients where the therapeutic dilemma is greatest. According to current guidelines1, these patients should be monitored rigorously with any sign of hemodynamic instability warranting consideration of active reperfusion.

In accord with our findings a prior analysis by Duplyakov et al, evaluating high- and intermediate-risk PE patients suggested that the history of syncope in patients with suspected PE might be considered as a criterion for high-risk of fatal complications during hospitalization, due to the tight association between syncope and embolism of the pulmonary trunk and its main branches12. While the Pulmonary Embolism Thrombolysis (PEITHO) trial showed that intermediate high-risk patients were unlikely to derive any net clinical benefit from routine use of systemic thrombolysis in view of the high risk for major bleeding 16, it has been hypothesized that perhaps in a selected sub-group of these normotensive patients, intravenous thrombolysis or even reduced-dose thrombolysis and/or pharmaco-mechanical catheter-directed reperfusion techniques (which are associated with very low life-threatening rates, particularly intracranial bleeding complications), might be beneficial17. Thus, syncope might point to the more vulnerable intermediaterisk PE patients who are more likely to deteriorate and therefore could benefit more from intensive monitoring, as well as a more aggressive therapeutic approach, which could include thrombolysis and/or mechanical thrombectomy. Our study is limited by its retrospective single center registry, and as such it can only be addressed as hypothesis-generating. Prospective randomized studies are needed to evaluate whether a more aggressive therapeutic approach in this patient population is warranted. In conclusion, in intermediate-risk PE patients, the presence of syncope at presentation is associated with a more complicated in-hospital clinical course. Our findings suggest that intermediate-risk PE patients presenting with syncope might benefit from an interim intensive surveillance, including continuous monitoring and ongoing assessment for consideration of escalation therapy beyond anticoagulation.

[1] Konstantinides SV, Meyer G, Becattini C, Bueno H, Geersing GJ, Harjola VP, Huisman MV, Humbert M, Jennings CS, Jiménez D, Kucher N, Lang IM, Lankeit M, Lorusso R, Mazzolai L, Meneveau N, Ní Áinle F, Prandoni P, Pruszczyk P, Righini M, Torbicki A, Van Belle E, Zamorano JL. 2019 ESC Guidelines for the Diagnosis and Management of Acute Pulmonary Embolism Developed in Collaboration with the European Respiratory Society (ERS); The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Eur Heart J 2019. Epub ahead of print. [2] Becattini C, Agnelli G, Lankeit M, Masotti L, Pruszczyk P, Casazza F, Vanni S, Nitti C, Kamphuisen P, Vedovati MC, De Natale MG, Konstantinides S. Acute pulmonary embolism: mortality prediction by the 2014 European Society of Cardiology risk stratification model. Eur Respir J 2016;48(3):780–786. [3] Altınsoy B, Erboy F, Tanriverdi H, Uygur F, Örnek T, Atalay F, Tor M. Syncope as a presentation of acute pulmonary embolism. Ther Clin Risk Manag 2016;12:1023–1028. [4] Calvo-Romero JM, Pérez-Miranda M , Bureo-Dacal P. Syncope in acute pulmonary embolism. Eur J Emerg Med 2004;11(4):208–209. [5] Kasper W, Konstantinides SV, Geibel A, Olschewski M, Heinrich F, Grosser KD, Rauber K, Iversen S, Redecker M, Kienast J. Management strategies and determinants of outcome in acute major pulmonary embolism: results of a multicenter registry. J Am Coll Cardiol 1997;30(5):1165–1171. [6] Roncon L, Zuin M, Casazza F, Becattini C, Bilato C, and P. Zonzin. Impact of syncope and pre-syncope on short-term mortality in patients with acute pulmonary embolism. Eur J Intern Med 2018;54:27-33. [7] Omar HR, Mirsaeidi M, Weinstock MB, Enten G, Mangar D, and Camporesi EM. Syncope on presentation is a surrogate for submassive and massive acute pulmonary embolism. Am J Emerg Med 2018;36(2):297–300. [8] Iqbal U, Jameel A, Anwar H, Scribani MB, Bischof E, and Chaudhary A. Does syncope predict mortality in patients with acute pulmonary embolism? A retrospective review. J Clin Med Res 2017;9(6):516–519. [9] Kearon C, Akl EA, Comerota AJ, Prandoni P, Bounameaux H, Goldhaber SZ, Nelson ME, Wells PS, Gould MK, Dentali F, Crowther M, Kahn SR. Antithrombotic therapy for VTE

disease: Antithrombotic Therapy and Prevention of Thrombosis,9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012; 141(2): e4195-e4965. [10] Grifoni S, Olivotto L, Cecchini P, Pieralli F, Camaiti A, Santoro G, Conti A, Agnelli G, Berni G. Short-term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction. Circulation 2000;101(24):2817–2822. [11] Konstantinides S, Geibel A, Olschewski M, Görnandt L, Roskamm H, Spillner G, Just H, Kasper W. Association between thrombolytic treatment and the prognosis of hemodynamically stable patients with major pulmonary embolism: results of a multicenter registry. Circulation 1997;96(3):882–888. [12] Duplyakov D, Kurakina E, Pavlova T, Khokhlunov S, and Surkova E. Value of syncope in patients with high-to-intermediate risk pulmonary artery embolism. Eur Heart J Acute Cardiovasc Care 2015;4(4):353–358. [13] Punukollu G, Gowda R.M, Vasavada B.C, and Khan I.A, Role of electrocardiography in identifying right ventricular dysfunction in acute pulmonary embolism. Am J Cardiol 2005;96(3):450–452 [14] Qaddoura A, Digby GC, Kabali C, Kukla P, Zhan ZQ, and Baranchuk AM, The value of electrocardiography in prognosticating clinical deterioration and mortality in acute pulmonary embolism: A systematic review and meta-analysis. Clin Cardiol 2017; 40(10):814-824 [15] Barco S, Ende-Verhaar YM, Becattini C, Jimenez D, Lankeit M, Huisman MV, Konstantinides SV, Klok FA. Differential impact of syncope on the prognosis of patients with acute pulmonary embolism: a systematic review and meta-analysis. Eur Heart J 2018;39(47):4186–4195 [16] Meyer G, Vicaut E, Danays T, Agnelli G, Becattini C, Beyer-Westendorf J, Bluhmki E, Bouvaist H, Brenner B, Couturaud F, Dellas C, Empen K, Franca A, Galiè N, Geibel A, Goldhaber SZ, Jimenez D, Kozak M, Kupatt C, Kucher N, Lang IM, Lankeit M, Meneveau N, Pacouret G, Palazzini M, Petris A, Pruszczyk P, Rugolotto M, Salvi A, Schellong S, Sebbane M, Sobkowicz B, Stefanovic BS, Thiele H, Torbicki A, Verschuren F, Konstantinides SV; PEITHO Investigators. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med 2014;370(15):1402–1411.

[17] Barco S, Vicaut E, Klok FA, Lankeit M, Meyer G, Konstantinides S. Improved identification of thrombolysis candidates amongst intermediate-risk pulmonary embolism patients: implications for future trials. Eur Respir J 2018;51(1)

Figure Legends

Figure 1: Clinical outcomes of pulmonary embolism patients presenting with syncope

Figure 2: Clinical predictors of complicated in-hospital course RV = Right ventricle/Right ventricular; LV = Left ventricle; BMI = Body mass index

Table 1: Baseline characteristics of Intermediate risk patients

Syncope Total

No (N=172)

Yes (N=40)

Age (Years ± SD)

(N=212) 65.1±16

64.6±17.2

67.3±12.7

0.35

Women

118 (56%)

97 (56%)

21 (53%)

0.72

Smoker

32 (15%)

27 (17%)

5 (13%)

0.63

Body mass index (Mean±SD)

30 ± 7

30 ± 7

28± 5

0.11

Hypertension

109 (52%)

88 (52%)

21 (52%)

0.99

Hyperlipidemia

80 (38%)

62 (36%)

18 (45%)

0.37

Diabetes Mellitus

53 (25%)

44(26%)

9 (23%)

0.84

Coronary artery disease

26 (13%)

20 (12%)

6 (15%)

0.59

Malignancy

46 (22%)

36 (21%)

10 (25%)

0.60

Immobilization

76 (36%)

60 (36%)

16 (40%)

0.59

Prior oral anti coagulation

32 (15%)

27 (16%)

5 (13%)

0.81

Prior venous thromboembolism

39 (18%)

32(19%)

7 (18%)

0.96

Heart rate (BPM, mean±SD)

98 ± 20

98 ± 20

99 ±19

0.74

Systolic blood pressure (mmHg,

128 ± 23

129 ± 22

127 ± 27

0.63

95% ± 13

95% ± 11

93% ± 18

0.40

Variable

P*

(Kg/m2)

Mean±SD) O2 Saturation (Mean±SD)

*P value between the syncope and non-syncope groups

Table 2: ECG, Laboratory and imaging findings Syncope Total Variable

No

Yes

P*

(N=212)

(N=172)

(N=40)

Sinus tachycardia

114 (54%)

89 (52%)

25 (63%)

0.39

New onset atrial fibrillation

9 (4.3%)

8 (4.7%)

1 (2.5%)

0.68

T-wave inversion V1-4

68 (32%)

55 (32%)

13 (32%)

0.55

S1Q3T3

57 (28%)

44 (26%)

13 (33%)

<0.001

New ICRBBB

27 (13%)

18 (11%)

9 (23%)

0.07

New CRBBB

20 (10%)

16 (9%)

4 (10%)

0.49

D-Dimer (ng/ml)(Mean±SD)

4650±8726

4134±7795

6898±11855

0.1

Troponin(µg/l)(Mean±SD)

1.02±1.96

1.00±2.08

1.12±1.38

0.71

Lactate(mg/dl) (Mean±SD)

22.82±13.42

22.45±13.13

24.33±14.63

0.45

Enlarged right ventricle

119 (56%)

95 (55%)

24 (60%)

0.52

Interventricular septal shift

154 (75%)

124 (72%)

30 (75%)

0.35

Main pulmonary artery thrombus

121 (57%)

97 (56%)

24 (60%)

0.61

Inferior vena cava backflow

100 (47%)

80 (47%)

20 (50%)

0.32

RV/LV diameter ratio (Mean±SD)

1.49±0.51

1.44±0.46

1.69±0.66

0.01

Moderate or severe RV Dysfunction 91 (44%)

68 (40%)

23 (58%)

0.08

Tricuspid regurgitation grade ≥2

71 (34%)

59 (36%)

12 (31%)

0.71

Systolic pulmonary artery pressure

50 ± 14

50 ± 14

53 ± 12

0.24

ECG Findings

Laboratory Findings

CTA Findings

Echocardiographic Findings

(mmHG, mean±SD) Systolic pulmonary artery pressure

27 (13%)

25 (15%)

2 (5%)

>35mmHg *P value between the syncope and non-syncope groups

Table 3: Clinical Outcomes

Syncope Variable

Total

No (N=172)

Yes (N=40)

P*

N=212 Clinical deterioration

27 (13%)

16 (9%)

11 (29%)

0.003

Amines

5(2.4%)

1(0.6%)

4 (10%)

0.005

Hemodynamic instability

12 (6%)

5 (3%)

7 (18%)

0.002

Mechanical ventilation

7 (3%)

3 (2%)

4 (10%)

0.03

Thrombolysis

14 (7%)

11 (6%)

3 (8%)

0.73

Surgery

2(1.4%)

1 (0.6%)

1(5%)

0.09

Reperfusion therapy

16 (7.5%)

12 (7%)

4 (10%)

0.81

All bleeding

24 (11%)

15 (9%)

9 (23%)

0.02

Major bleeding

14 (7%)

11 (7%)

3 (8%)

0.73

Acute kidney injury

17 (8%)

10 (6%)

7 (18%)

0.02

In-hospital mortality

1 (0.5%)

0 (0.0)

1 (2.5%)

0.19

3 (1%)

2 (1%)

1 (3%)

0.46

Mortality 90 days

*P value between the syncope and non-syncope groups

0.14