Enlarged Right Ventricle Without Shock in Acute Pulmonary Embolism: Prognosis

Article Outline

• Abstract
• Materials and Methods
  • Statistical Methods
• Results
• Discussion
• Conclusions
• References
• Copyright

Abstract 

Objective

An unsettled issue is the use of thrombolytic agents in patients with acute pulmonary embolism (PE) who are hemodynamically stable but have right ventricular (RV) enlargement. We assessed the in-hospital mortality of hemodynamically stable patients with PE and RV enlargement.

Methods

Patients were enrolled in the Prospective Investigation of Pulmonary Embolism Diagnosis II. Exclusions included shock, critical illness, ventilatory support, or myocardial infarction within 1 month, and ventricular tachycardia or ventricular fibrillation within 24 hours. We evaluated the ratio of the RV minor axis to the left ventricular minor axis measured on transverse images during computed tomographic angiography.

Results

Among 76 patients with RV enlargement treated with anticoagulants and/or inferior vena cava filters, in-hospital deaths from PE were 0 of 76 (0%) and all-cause mortality was 2 of 76 (2.6%). No septal motion abnormality was observed in 49 patients (64%), septal flattening was observed in 25 patients (33%), and septal deviation was observed in 2 patients (3%). No patients required ventilatory support, vasopressor therapy, rescue thrombolytic therapy, or catheter embolectomy. There were no in-hospital deaths caused by PE. There was no difference in all-cause mortality between patients with and without RV enlargement (relative risk=1.04).

Conclusion

In-hospital prognosis is good in patients with PE and RV enlargement if they are not in shock, acutely ill, or on ventilatory support, or had a recent myocardial infarction or life-threatening arrhythmia. RV enlargement alone in patients with PE, therefore, does not seem to indicate a poor prognosis or the need for thrombolytic therapy.

Keywords: Pulmonary embolism, Right ventricular dysfunction, Venous thromboembolism

An unsettled issue is the prognosis and use of thrombolytic agents in hemodynamically stable patients with acute pulmonary embolism (PE) who have evidence of right ventricular (RV) dysfunction.¹ RV dysfunction in a patient with PE and normal systolic blood pressure has been classified as “impending hemodynamic instability.”² At one university, thrombolytic therapy is given to all patients with PE who have RV dysfunction unless contraindicated.³ RV dysfunction has been used as an indication for surgical embolectomy in normotensive patients with PE.⁴ RV dysfunction was defined as an RV to left ventricular (LV) end-diastolic diastolic diameter ratio greater than 1 in the apical 4-chamber view, RV end-diastolic diameter greater than 30 mm, or paradoxical septal systolic motion.⁴ The need for a randomized trial in such patients, however, is recognized.¹, ³, ⁵ In view of diverse opinion about the prognosis or whether thrombolytic therapy should be administered to stable patients with acute PE who have RV enlargement,⁵ we evaluated such patients who were enrolled in the Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) investigation. We tested the hypothesis that in-hospital mortality and the rate of life-threatening adverse events among patients with PE treated with anticoagulants and/or inferior vena cava filters may be higher in those with RV enlargement than in those without RV enlargement.

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Materials and Methods 

Data are from the PIOPED II, which was a multicenter national collaborative investigation of the accuracy of multidetector computed tomographic (CT) angiography alone with venous phase imaging of the veins of the pelvis and thigh for the diagnosis of acute PE.⁶ The data allow a retrospective cohort comparison of outcome between those with and those without RV enlargement. In PIOPED II, 181 patients had a reference test diagnosis of PE and a CT angiogram that was of adequate quality for interpretation.⁶ Among these patients, CT angiograms were available for analysis of RV enlargement in 160 patients. All patients in PIOPED II were aged 18 years or more. Exclusions included shock, critical illness, ventilatory support, or myocardial infarction within 1 month, and ventricular tachycardia or ventricular fibrillation within 24 hours.

We evaluated the ratio of the RV minor axis to the LV minor axis measured on transverse images of contrast-enhanced multidetector CT angiograms obtained for the evaluation of suspected acute PE⁷, ⁸, ⁹, ¹⁰, ¹¹ (Figure 1, Figure 2). We did not perform multiplanar reformatted reconstructions.¹², ¹³ The minor axes of the right ventricle and left ventricle were measured at their widest points between the inner surface of the free wall and the surface of the interventricular septum.¹⁴ The maximum dimensions of the right ventricle and left ventricle may be found at slightly different levels.¹¹, ¹⁴ Typically, the maximum RV dimension was measured at the level of the tricuspid valve, and the maximum LV dimension was measured at the level of the mitral valve.⁸ Papillary muscles were excluded from the measurement of LV dimension.¹⁴ Assessment of the RV/LV dimension ratio was made independently by 2 readers (FM and AB). An RV/LV dimension ratio greater than 1 was defined as RV enlargement.¹⁰, ¹⁵, ¹⁶, ¹⁷, ¹⁸, ¹⁹ The combination of septal dyskinesis with RV enlargement also was evaluated. In patients with RV enlargement, readers evaluated images for the presence of septal displacement, shown as either flattening¹⁴, ²⁰ or leftward displacement of the interventricular septum.⁸, ¹⁰, ¹⁴, ²⁰ These categories of septal displacement served as a surrogate for septal dyskinesis as seen on echocardiography²¹ and were evaluated separately.

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• Figure 1. 

  Patient with RV/LV dimension ratio<1 shown on transverse image of contrast-enhanced multidetector CT angiogram. Minor axis of right ventricle is shown by dotted line at top, and minor axis of left ventricle is shown at bottom.

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• Figure 2. 

  Patient with RV/LV dimension ratio>1 shown on transverse image of contrast-enhanced multidetector CT angiogram. Minor axis of right ventricle is shown by dotted line at top, and minor axis of LV is shown at bottom. Flattening of the interventricular septum is shown.

Because of the possibility that comorbid conditions may have caused RV enlargement, we evaluated patients with no prior cardiopulmonary disease, as well as all patients. No prior cardiopulmonary disease was defined as no current asthma, pneumonia, history of chronic bronchitis, emphysema, chronic obstructive pulmonary disease, current or history of right or left-sided heart failure, lung cancer, or prior PE.

Statistical Methods 

Confidence intervals (CIs) were calculated using the binomial distribution. Mortality rates were compared by the chi-square test. The single unweighted kappa statistic was used to test for agreement between readers.²² Relative risk and its 95% CI was calculated with the program at www.sign.Ac.uk/methodlogy/risk.xls.

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Results 

Among 160 patients with PE, by the reference standard in PIOPED II who had a CT angiogram adequate for interpretation of whether PE was present and whose images were available for review for this study, 157 (98%) showed the left and right ventricles with adequate clarity for evaluation of the diastolic dimensions (Figure 3). Two of these received thrombolytic therapy. One of these patients was normotensive but was treated with thrombolytic therapy because of the perceived high risk of RV enlargement and hypokinesis of the right ventricle. The other patient was treated with thrombolytic therapy because of hypoxia despite the administration of oxygen. Treatment in the remaining 155 patients was with only anticoagulants in 138, anticoagulants plus inferior vena cava filter in 15, and inferior vena cava filter alone in 2.

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• Figure 3. 

  Enrollment and outcome. IVC=inferior vena cava. Data are based on measurements of reader 1.

The age and sex of the patients treated with anticoagulants and/or an inferior vena cava filter according to whether ventricular enlargement was present and whether they had prior cardiopulmonary disease are shown in Table 1. The age and sex of patients with and without RV enlargement were similar. The Wells’ objective clinical assessment score in these patients is shown in Table 2.²³ Patients with an enlarged right ventricle more often had a high probability clinical assessment than those who did not have RV enlargement (P ≤.05).

Table 1. Age and Sex of Patients Treated with Anticoagulants and/or Inferior Vena Cava Filter

	RV/LV Dimension Ratio>1			RV/LV Dimension Ratio≤1
	No Prior CPD	Prior CPD	All Patients	No Prior CPD	Prior CPD	All Patients
Age (y)	57±16	60±16	58±16	54±15	59±20	55±17
Males	22/55(40)	9/23(39)	31/78(40)	21/56(38)	13/23(57)	34/79(43)

RV/LV=right ventricular to left ventricular; CPD=cardiopulmonary disease.

All differences not significant.

Data are based on measurements of reader 1.

Table 2. Wells Clinical Assessment Score in Patients Treated With Anticoagulants and/or Inferior Vena Cava Filter

	RV/LV Dimension Ratio>1			RV/LV Dimension Ratio≤1
Wells score⁎	No Prior CPD N=48	Prior CPD N=21	All Patients N=69	No Prior CPD N=54	Prior CPD N=20	All Patients N=74
<2	8(17)	5(24)	13(19)	9(17)	3(15)	12(16)
2-6	30(63)	10(48)	40(58)	40(74)	14(70)	54(73)
>6	10(21)	6(29)	16(23)†	5(9)	3(15)	8(11)

RV/LV=right ventricular to left ventricular; CPD=cardiopulmonary disease.

Data are based on measurements of reader 1.

The following results are those of reader 1. RV enlargement was observed in 78 of 157 patients (50%) with PE. Among those treated with anticoagulants and/or inferior vena cava filters, RV enlargement was observed in 76. In these patients, in-hospital death from PE was 0 of 76 (0%) (95% CI, 0-3.9) and all-cause mortality was 2 of 76 (2.6%) (95% CI, 0.3-9.2) (Figure 3; Table 3). One patient died of glioblastoma multiforme, and 1 patient died of carcinoma of the lung. No septal motion abnormality was observed in 49 patients (64%), septal flattening was observed in 25 patients (33%), and septal deviation toward the left ventricle was observed in 2 patients (3%). Among the 76 patients who had an enlarged right ventricle who were treated with anticoagulants and/or an inferior vena cava filter, the RV/LV dimension ratio was ≥1.1 in 56 (74%),≥1.2 in 36 (47%),≥1.3 in 24 (32%),≥1.4 in 16 (21%), and≥1.5 in 11 (14%) (Table 4). The association with interventricular septal motion abnormalities is shown in Table 4. None of the patients had an in-hospital life-threatening adverse event that required ventilatory support, vasopressor therapy, rescue thrombolytic therapy, or catheter embolectomy. Even if the patient who was treated with thrombolytic therapy because of RV enlargement and hypokinesis would have died after treatment with anticoagulants, the death rate from PE in those with RV enlargement would have been 1 of 80 (1.3%) and all-cause mortality would have been 3 of 80 (3.8%).

Table 3. Patients Treated with Anticoagulants and/or Inferior Vena Cava Filter

	RV/LV Dimension Ratio>1			RV/LV Dimension Ratio≤1
Outcome	No Prior CPD n/N (%)	Prior CPD n/N (%)	All Patients n/N (%)	No Prior CPD n/N (%)	Prior CPD n/N (%)	All Patients n/N (%)
PE deaths	0/54(0)	0/22(0)	0/76(0)	1/56(1.8)	0/23(0)	1/79(1.3)
All-cause deaths	0/54(0)	2/22(9)⁎	2/76(2.6)	1/56(1.8)	1/23(4.3)	2/79(2.5)
Life-threatening adverse events	0/54(0)	0/22(0)	0/76(0)	0/56(0)	0/23(0)	0/79(0)

RV/LV=right ventricular to left ventricular; CPD=cardiopulmonary disease; PE=pulmonary embolism.

All differences not significant.

Data are based on measurements of reader 1.

Table 4. Right Ventricular/Left Ventricular Dimension Ratios and Interventricular Septal Motion in All Patients Treated with Anticoagulants and/or Inferior Vena Cava Filter

RV/LV=right ventricular to left ventricular.

Data are based on measurements of reader 1.

Among patients with PE and no RV enlargement who were treated with anticoagulants and/or an inferior vena cava filter, in-hospital death from PE occurred in 1 of 79 (1.3%) (95% CI, 0.03-6.9) and all-cause mortality was 2 of 79 (2.5%) (95% CI, 0.3-8.9). The patient who died, but not of PE, died of respiratory failure from pneumocystis pneumonia associated with human immunodeficiency virus. There was no difference in the rate of death from PE or all-cause mortality between patients with RV enlargement and those without RV enlargement. The relative risk of all-cause mortality in patients with RV enlargement compared with patients without RV enlargement was 1.04 (95% CI, 0.15-7.19).

In regard to patients with no prior cardiopulmonary disease and PE, 54 had RV enlargement and were treated with anticoagulants or an inferior vena cava filter. There were no in-hospital deaths among these 54 patients. RV enlargement was accompanied by septal flattening in 19 patients (35%) and by septal deviation to the left in 1 patient (2%) (Table 5). The RV/LV dimension ratio was ≥1.2 in 27 of these patients and≥1.3 in 17 patients with no prior cardiopulmonary disease (Table 5).

Table 5. Right Ventricular/Left Ventricular Dimension Ratios and Interventricular Septal Motion in Patients with No Prior Cardiopulmonary Disease Treated with Anticoagulants and/or Inferior Vena Cava Filter

RV/LV=right ventricular to left ventricular.

Data are based on measurements of reader 1.

The kappa statistic for agreement between readers of whether there was RV enlargement was 0.745, indicating good agreement. The kappa statistic for agreement on flattening or leftward displacement of the interventricular septum was 0.165, indicating only slight agreement. Reader 2 measured an RV/LV dimension ratio greater than 1 in 66 of 157 patients (42%). Among those treated with anticoagulants and/or an inferior vena cava filter, RV enlargement was observed in 64 patients. In-hospital death from PE was 0 of 64 (0%) (95% CI, 0-7.1), and all-cause mortality was 2 of 64 (3.1%) (95% CI, 0.6-11.8). Among patients treated with anticoagulants and/or an inferior vena cava filter in whom both readers agreed that there was RV enlargement, death from PE was 0 of 60 (0%) (95% CI, 0-7.5), and all-cause mortality was 2 of 60 (3.3%) (95% CI, 0.6-12.5).

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Discussion 

The data do not support the hypothesis that an enlarged right ventricle in stable patients with acute PE may lead to a higher in-hospital mortality or higher rate of life-threatening adverse events. There was no difference in the rate of death from PE or all-cause mortality between patients with RV enlargement and patients without RV enlargement. In the patients with no prior cardiopulmonary disease, those with possible prior RV enlargement were excluded. None of the patients with RV enlargement had an in-hospital adverse event that required ventilatory support, vasopressor therapy, rescue thrombolytic therapy, or catheter embolectomy.

Selection of an RV/LV dimension ratio greater than 1 as indicative of RV enlargement was conservative and has been used by several investigators.¹⁰, ¹⁵, ¹⁶, ¹⁷, ¹⁸, ¹⁹ Others defined RV enlargement or dysfunction on the basis of an RV/LV dimension ratio greater than 0.9, although measurements were made from a reconstructed CT 4-chamber view.¹³, ²⁴ An RV/LV dimension ratio greater than 0.6 also has been used to define RV overload.⁵ Irrespective of the RV/LV dimension ratio that ranged from greater than 1.0 to 2.9 in our study, there were no deaths from PE.

The agreement between readers 1 and 2 of interpretation of RV enlargement was good (kappa = 0.745). Others, using a similar method with 3 readers, showed an intraclass correlation of 0.51.⁹ The kappa statistic that we showed for agreement of whether there was flattening or bowing of the interventricular septum showed only slight agreement (kappa = 0.165). Others showed fair agreement on the presence of septal bowing (kappa = 0.54).⁹

Without electrocardiographic gating, transverse images of the heart may not be truly diastolic images. However, the positive predictive value of measurements on CT transverse sections of an RV/LV dimension ratio greater than 1 or septal deviation was 7 of 7 (100%), based on echocardiography as a reference standard in 23 patients and pulmonary angiography in 2 patients.¹⁰ Sensitivity was 7 of 9 (78%), and specificity was 16 of 16 (100%).¹⁰ In another investigation, similar comparisons were made in 14 patients with massive PE.¹⁸ The positive predictive value for RV dilatation or septal deviation was 11 of 11 (100%). RV dilation or septal deviation was shown by CT in 11 of 12 patients (92%).¹⁸ Specificity was 2 of 2 (100%).

Definitions of RV dysfunction vary (Table 6, Table 7). Goldhaber and associates²⁵ and Wolfe and associates²⁶ defined RV dysfunction as RV hypokinesis on the basis of echocardiograms. Others used RV enlargement as one of the criteria.⁴, ⁵, ¹¹, ¹³, ¹⁵, ¹⁶, ¹⁷, ²⁷, ²⁸, ²⁹ Some used only RV enlargement to define RV dysfunction.⁵, ¹¹, ²⁷, ²⁸ Others used RV enlargement or dyskinesia of the interventricular septum.⁴, ¹⁵ Konstantinides and associates²⁸ also required the absence of inspiratory collapse of the inferior vena cava. Some evaluated prognosis by RV enlargement, without defining it as dysfunction.¹³ Others evaluated prognosis by RV enlargement and other findings as indicators of RV afterload stress and/or pulmonary hypertension.¹⁵, ¹⁶, ¹⁷ Some evaluated prognosis by RV enlargement and interventricular septal dyskinesis as indicators of acute cor pulmonale.²⁹

Table 6. Mortality and Adverse Events: Pulmonary Embolism and Right Ventricular Enlargement

Reference	RV Enlargement and Dysfunction Definition	Patient Group	Duration	All-cause Mortality RV Large n/N (%)	All-cause Mortality RV Not Large n/N (%)	PE Mortality; RV Large n/N (%)	PE Mortality RV Not Large n/N (%)
Schoepf et al.13	RV/LV>0.9 Reformatted CT 4-chamber view	All PE	30 d	43/276(15.6)	12/155(7.7)†
Van der Meer et al.11	RV/LV>1 and≤1.5	All PE	90 d⁎			4/51(7.8)	0/51(0)‡
Van der Meer et al.11	RV/LV>1.5	All PE	90 d⁎			3/18(16.7)
Kasper et al.16	RV/LV>1 or RVEDD>30 mm or≥2 of the following: TR jet>2.8 m/s or>2.5 m/s if no inspiratory collapse of IVC, RPA>12 mm/m2, RV wall>5 mm, no inspiratory collapse of IVC	All PE	In-hospital	16/87(18.4)	13/230(5.7)§	11/87(12.6)	2/230(0.9)§
Vieillard-Baron et al.29	RV/LV area>0.6 plus septal dyskinesia	No prior CPD	In-hospital	22/98(22.5)

RV/LV=right ventricular to left ventricular; RVEDD=right ventricular end-diastolic dimension; PE=pulmonary embolism; CT=computed tomographic; TR=tricuspid regurgitation; RPA=right pulmonary artery; IVC=inferior vena cava; CPD=cardiopulmonary disease.

Table 7. Mortality and Adverse Events: Pulmonary Embolism and Right Ventricular Enlargement Not in Shock

Reference	RV Enlargement and Dysfunction Definition	Follow-up Duration	All-cause Mortality Anticoagulants n/N (%)	All-cause Mortality Thrombolytic Agents n/N (%)	PE Mortality Anticoagulants n/N (%)	PE Mortality Thrombolytic Agents n/N (%)	In-hospital Adverse Events† Anticoagulants n/N (%)	In-hospital Adverse Events Thrombolytic Agents n/N (%)
Konstantinides et al.28	RV enlargement+no inspiratory collapse of IVC⁎	30 d	3/138(2.2)	4/118(3.4)			34/138(24.6)	12/118(10.2)‡
Sukhija et al.27	RV/LV area>0.9 or RV≥4.5 cm	In-hospital	17/40(43)	2/6(33)
Hamel et al.5	RV/LV dimension>0.6	In-hospital	0/64(0)	4/64(6.3)	0/64(0)	1/64(1.6)
Goldhaber et al.25	RV ED area enlarged RV hypokinesis	14 d	2/18(11.1)	0/18(0)	2/18(11.1)	0/18(0)
Konstantinides et al.17	RV/LV>1, paradoxical septal wall motion, no inspiratory collapse of IVC, or TR jet>2.8 m/s or>2.5 m/s if no inspiratory collapse of IVC	30 d	61/550(11.1)	8/169(4.7)§
Vieillard-Baron et al.29	RV/LV area>0.6 +septal dyskinesis No prior cardiopulmonary disease	In-hospital	1/32(3.1%)
Grifoni et al.15	RV/LV dimension>1 or RVEDD>30 mm or paradoxical septal systolic motion or pulmonary acceleration time<90 ms or RV/atrial gradient>30 mm Hg	In-hospital			3/65(4.6)		3/65(4.6)

RV/LV=right ventricular to left ventricular; PE=pulmonary embolism; TR=tricuspid regurgitation; IVC=inferior vena cava; ED=end diastolic; RVEDD=right ventricular end-diastolic dimension.

Among patients with PE who died in hospital, the RV dimension on average was larger and the LV dimension was smaller than among those who survived.⁷, ³⁰ The reported mortality rate from PE among patients with an enlarged right ventricle ranged from 7.8% to 16.7%¹¹, ¹⁶ and depended on the severity of RV enlargement¹¹ (Table 6). In a study of patients in an intensive care unit who had severe PE-related conditions, Ghaye and associates⁷ showed a 5% all cause in-hospital mortality among patients with an RV/LV dimension ratio of 1.0, a 10% mortality among patients with an RV/LV dimension ratio of 1.3, 20% mortality with an RV/LV dimension ratio of 1.7, and a 30% mortality among patients with an RV/LV dimension ratio of 1.9. All-cause mortality in patients with PE and RV enlargement has been reported to range from 15.6% to 23.5%.¹³, ¹⁶, ²⁹ However, some showed that RV enlargement was not a predictor of mortality.⁹ In-hospital adverse events (escalation of therapy including cardiopulmonary resuscitation, mechanical respiratory support, catecholamine treatment for hypotension, rescue thrombolysis, or surgical embolectomy)¹² or admission to an intensive care unit⁸ were observed more frequently in patients with RV enlargement or dysfunction than in those without.

It is controversial whether patients with RV enlargement and/or dysfunction who are not in shock and are treated only with anticoagulants have a higher death rate from PE, all-cause mortality, or higher rate of in-hospital adverse events than those treated with thrombolytic agents. Previous literature showed mixed results (Table 6). Mortality from PE in such patients who were treated with anticoagulants ranged from 0% to 11.1%,⁵, ¹⁵, ²⁵ and all cause mortality in the 2 studies in which it was reported was the same as the mortality from PE.⁵, ²⁵ No statistically different mortality rate was shown in those treated with thrombolytic agents,⁵, ²⁵ although Goldhaber and associates²⁵ showed a favorable trend with thrombolytic agents. All-cause mortality in patients with an enlarged right ventricle and/or RV dysfunction who were not in shock in general ranged from 0% to 11.1% (Table 7).⁵, ¹⁷, ²⁵, ²⁹ One group, however, found a 43% all-cause mortality in those treated with anticoagulants.²⁷ Only 1 group showed a significantly lower all cause mortality among patients treated with thrombolytic agents.¹⁷ In-hospital adverse events were less frequent in those treated with thrombolytic agents (24.6% vs 10.2%) (Table 7).²⁸ A lower rate of adverse events (4.6%) among surviving patients with RV enlargement who were treated with anticoagulants was reported by Grifoni and associates¹⁵ than by Konstantinides et al.²⁸

The strengths of this investigation are the incorporation of all of the Standards for Reporting Diagnostic Accuracy criteria.³¹, ³² Recruited patients were inpatients and outpatients of both sexes with a wide range of ages and associated illnesses. Therefore, the Standards for Reporting Diagnostic Accuracy criteria for a representative population were met.³¹

A weakness is that we did not follow patients with PE. Therefore, the rates of recurrent PE and mortality after hospital discharge are not known. Recurrent PE was observed more frequently in hemodynamically stable patients with RV dysfunction treated with anticoagulants than in patients treated with thrombolytic agents.²⁵ Another weakness was the inability to assess RV hypokinesis from the CT images. RV hypokinesis was used in the assessment of RV dysfunction in the patients evaluated by Goldhaber and associates²⁵ and Wolfe and associates.²⁶

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Conclusions 

In-hospital prognosis is good in patients with PE and RV enlargement, providing they are not in shock, acutely ill, or receiving ventilatory support, or had a recent myocardial infarction or life-threatening arrhythmia. In patients with PE, RV enlargement alone does not seem to adversely affect prognosis or be an indication for thrombolytic therapy.

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