(Circulation. 2000;101:2817.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Short-Term Clinical Outcome of Patients With Acute Pulmonary Embolism, Normal Blood Pressure, and Echocardiographic Right Ventricular Dysfunction
From the Emergency Department (S.G., I.O., P.C., F.P., A. Camaiti, A. Conti, G.B.) and S. Luca Cardiology Unit (G.S.), Azienda Ospedaliera Careggi, Florence, and the Institute of Internal and Vascular Medicine, University of Perugia (G.A.), Perugia, Italy.
Correspondence to Dr Iacopo Olivotto, Via Pier Capponi 46, 50132 Firenze, Italy. E-mail jacoli{at}flownet.it
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Abstract |
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Background—The role of echocardiographic right ventricular (RV) dysfunction in predicting clinical outcome in clinically stable patients with pulmonary embolism (PE) is undefined. In this study, we assessed the prevalence and clinical outcome of normotensive patients with RV dysfunction among a broad spectrum of PE patients.
Methods and Results—This prospective clinical outcome study
included cohort of 209 consecutive patients (age, 65±15 years) with
documented PE. Acute RV dysfunction was diagnosed in the presence of
1 of the following: RV dilatation (without hypertrophy),
paradox septal systolic motion, and Doppler evidence of
pulmonary hypertension. Four groups were identified: 28
patients presenting with shock or cardiac arrest (13%), 19
hypotensive patients without shock (9%), 65 normotensive patients with
echocardiographic RV dysfunction (31%), and 97
normotensive patients without RV dysfunction (47%). Among normotensive
patients with RV dysfunction, 6 (10%) developed PE-related shock after
admission: 3 of these patients died, and 3 were successfully treated
with thrombolytic agents. In comparison, none of the 97
normotensive patients without RV dysfunction developed shock or died as
a result of PE.
Conclusions—A significant proportion (31%) of normotensive patients with acute PE presents with RV dysfunction; these patients with latent hemodynamic impairment have a 10% rate of PE-related shock and 5% in-hospital mortality and may require aggressive therapeutic strategies. Conversely, normotensive patients without echocardiographic RV dysfunction have a benign short-term prognosis. Thus, early detection of echocardiographic RV dysfunction is of major importance in the risk stratification of normotensive patients with acute PE.
Key Words: embolism • shock • echocardiography
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Introduction |
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Acorrelation has been reported between echocardiographic right ventricular (RV) dysfunction and clinical outcome in patients with objectively confirmed pulmonary embolism (PE).1 2 3 4 5 6 7 8 9 10 11 12 Patients with echocardiographic RV dysfunction are known to be at risk of subsequent clinical worsening and PE-related death and may benefit from more aggressive therapeutic strategies, including thrombolytic treatment.13 14 However, the prognostic value of RV dysfunction in patients with PE and normal blood pressure has not been specifically assessed. Because normotensive patients with RV dysfunction represent a large proportion of patients with PE, the benefits of extending thrombolytic treatment to this subgroup need to be weighted against potential disadvantages in terms of bleeding risk and added costs.15 The aim of this study was to evaluate the prevalence and short-term prognosis of patients with objectively confirmed PE, normal blood pressure, and echocardiographic RV dysfunction.
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Methods |
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Patients
Between 1994 and 1997, 388 consecutive patients with clinical suspicion of PE were examined at the Emergency Department of the Azienda Ospedaliera Careggi in Florence, Italy. The initial assessment included clinical history and physical examination, chest radiograph, 12-lead ECG, arterial blood gas analysis, echocardiography, and lower-limb venous ultrasonography. A subsequent evaluation was performed with lung perfusion scan and/or spiral CT scan; pulmonary angiography was performed in those patients lacking a definite PE diagnosis at this stage. Autopsy was performed in patients who died without a definite diagnosis of PE. Thus, PE was excluded in 179 of the 388 patients (46%). The remaining 209 patients (age, 65±15 years; range, 18 to 90 years; 84 men, 125 women) with objectively confirmed PE were included in this prospective clinical outcome study.
Echocardiographic Examination
Standard 2-dimensional echo Doppler examination was
performed 
1 hour from admission with Toshiba SSH140A equipment with
2- and 3.75-MHz probes. Patients with 1 of the following were
considered to have acute RV dysfunction12 : (1) RV
dilatation (end-diastolic diameter >30 mm or RV/left
ventricular end-diastolic diameter ratio >1 in
4-chamber view), (2) paradox septal systolic motion, and (3)
pulmonary hypertension (Doppler pulmonary
acceleration time <90 ms or the presence of an RV/atrial gradient
>30 mm Hg). However, these signs of RV overload were not
considered acute in the presence of RV wall hypertrophy
(free wall thickness >7 mm).
Color Venous Duplex Scanning
Examination was performed 3 hours from hospital admission with
Toshiba SSA 270A equipment with 5- and 7.5-MHz probes. Lack of vein
compressibility was interpreted as a positive result and was confirmed
with color-flow imaging and pulsed-wave Doppler
analysis.16 17 Absent or reduced flow, lack of
respiratory variation, and failure to increase flow with calf
compression were used to confirm the diagnosis. Pelvic and upper limb
veins were routinely examined in patients with a negative lower-limb
scan.
Perfusion Lung Scan
Lung scans were performed with
99mTc-labeled human albumin
microspheres. Six views were required. A normal or near-normal
lung scan excluded PE, and a high-probability scan (clear-cut perfusion
defects of 1 pulmonary segments, mismatched at chest
radiograph) confirmed the diagnosis.1 18 Patients with
intermediate-probability scans underwent CT scan and/or
angiography.
High-Resolution CT
A direct scan of the lungs was obtained with a Somatom
Plus 4 CT scanner (Siemens) with 1-mm slices every 20 mm and
standard sequential acquisition technique. After injection of contrast
material, adjacent 3-mm slices were obtained over the hilar region with
the spiral acquisition technique. Total scan time ranged from 5 to 10
minutes.
Pulmonary Angiography
Nonionic contrast material was injected into the main
pulmonary artery. In patients with uncertain PE diagnosis,
selective injections were performed with oblique views. The diagnosis
of PE required direct visualization of the embolus or an intraluminal
filling defect constant in 2 different views or after repeated
injections.
Management Strategies
Intravenous heparin was started as soon as PE was
suspected with a bolus dose of 80 IU/kg, followed by an 18-IU ·
kg-1 · h-1
infusion rate, later adjusted to maintain the activated partial
thromboplastin time between 60 and 90 seconds in patients with
confirmed diagnosis. All patients with clinical signs of
hemodynamic impairment or
echocardiographic RV dysfunction were observed for 24
hours in a short-observation unit within the Emergency Department and
underwent continuous monitoring of ECG, oxymetry, respiratory rate, and
arterial blood pressure. Conversely, all normotensive
patients without RV dysfunction were transferred to nonemergency wards.
Thrombolytic treatment was instituted in patients with
confirmed PE and hemodynamic impairment as deemed
appropriate by the attending physician. Recombinant tissue-type
plasminogen activator (rtPA) was used at a dose
rate of 100 mg IV over 2 hours; urokinase was used at a dose rate of
4400-IU/kg bolus injection, followed by a 4400–IU ·
kg-1 · h-1
maintenance dose for 24 to 48 hours.1 Moreover, in
selected patients with a floating proximal vein thrombus,
thrombolysis protected by temporary caval filters
(Cordis) was performed. After filter insertion, urokinase infusion was
started with a bolus of 100 000 to 300 000 IU, followed by a dose
adjusted to maintain fibrinogen levels between 120 and 150 mg/dL until
lysis of the floating component of the thrombus was documented. After
acute treatment, all patients were started on oral warfarin, which was
continued for 6 months, with the dose adjusted to maintain the
international normalized ratio between 2 and 3.
Definition of Patient Subgroups Based on Clinical
Presentation
At initial evaluation, patients were defined as hypotensive and
normotensive if they had a systolic pressure <100 mm Hg
or 100 mm Hg, respectively. Hypotensive patients
were defined as being in shock only if presenting with associated
signs of systemic hypoperfusion (clouded sensorium, oliguria, cold and
clammy skin, and lactic acidosis at arterial blood gas
analysis). Thus, on the basis of the combination of clinical
and echocardiographic findings, 4 different patient
profiles were defined for prognostic assessment: (1) patients
presenting with shock (or cardiac arrest), (2) hypotensive patients
without shock, (3) normotensive patients with RV dysfunction, and (4)
normotensive patients without RV dysfunction.
Statistical Analysis
Data were expressed as mean±SD. We used Student’s t
test for comparison of normally distributed data and the
2 test for comparison of noncontinuous
variables expressed as proportions. Univariate and
multivariate analyses for the assessment of
independent risk predictors were performed by use of the Cox regression
model.19
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Diagnosis of PE
In the 209 patients, the diagnosis of PE was obtained on the basis of a high-probability lung scan in 145 (69%), a positive CT scan in 31 (15%), and a positive pulmonary angiography in 29 (14%). In 4 patients who died on admission (2%), PE was diagnosed at autopsy: in 3, PE had been strongly suspected from the clinical and echocardiographic findings, whereas in 1 patient, a ruptured abdominal aortic aneurysm had been suspected.
Clinical and Echocardiographic Profiles on
Admission
The clinical presentation of PE ranged from severe
shock and respiratory failure to only mild symptoms (Table 1
). Of the 209 study patients, 162
(78%) were clinically stable and normotensive, whereas 47 (22%)
presented a systolic blood pressure <100 mm Hg
(the Figure). Of the latter, 28 were
judged to be in shock, including the 4 patients who presented
with cardiac arrest or died shortly after admission. The remaining 19
patients presented with hypotension but no indications of shock
(the Figure).
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Echocardiographic examination was performed in all
patients except 2 who presented with cardiac arrest. Adequate
2-dimensional images were obtained for all patients, whereas an
accurate Doppler evaluation was technically feasible in 161 (77%).
A total of 110 patients (53%) were judged to have acute RV dysfunction
with 1 of the following: RV dilatation (n= 89), systolic
flattening of the interventricular septum (n=48), and
Doppler evidence of pulmonary hypertension (n=62). Six
normotensive patients with chronic respiratory disease and evidence of
RV dysfunction associated with RV free wall hypertrophy
(>7 mm) were considered to have chronic rather than acute RV
dysfunction. Interobserver and intraobserver agreement for the
definition of RV dysfunction was 94% and 96%, respectively.
From the clinical and echocardiographic findings on
admission, the patients were categorized as follows (the
Figure
): (1) patients presenting with shock or cardiac
arrest (n=28, 13%), (2) hypotensive patients without shock (n=19,
9%), (3) normotensive patients with RV dysfunction (n=65, 31%), and
(4) normotensive patients without RV dysfunction (n=97, 47%).
The clinical features of normotensive patients with and without
RV dysfunction are compared in Table 2.
On average, patients with RV dysfunction had a lower systolic
blood pressure and were more tachycardic, hypoxic, and hypocarbic on
presentation. There was no difference in the prevalence of
smoking history or chronic lung disease between the 2 groups (Table 2).
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Treatment
Intravenous heparin was immediately started in
all patients at the time PE was suspected. In 2 of the 4 patients who
died suddenly (<1 hour after admission), heparin treatment was not
implemented because of lack of time (n=1) or a wrong initial diagnosis
(n=1). Thrombolytic treatment was initially administered to
31 patients (15%), including 16 patients presenting with shock, 5
patients with minor hemodynamic impairment, and 10
normotensive patients with floating venous thrombosis after
percutaneous vena cava filter insertion. Three
additional normotensive patients with RV dysfunction and subsequent
clinical deterioration received rtPA (n=2) or urokinase (n=1) 4 to 7
hours after the diagnosis of PE (the Figure and Table 3). Of the 34 patients treated with
thrombolytic agents, 2 (6%) had severe
treatment-related complications, including 1 nonfatal cerebral
hemorrhage and 1 hematuria requiring urgent transfusion; 8
additional patients (24%) suffered minor extracerebral bleeding not
requiring transfusion.
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In the 12 patients presenting with shock who did not receive thrombolytic treatment, the following reasons were given: advanced age (>85 years; n=4), advanced cancer (n=3), sudden death (n=2), recent surgery (n=1), recent stroke (n=1), and misdiagnosis (n=1).
In-Hospital Mortality and PE-Related Clinical Outcome
Of the 209 study patients, 17 (8%) died during admission. Of
these 17 deaths, 13 were judged to be directly related to PE; the
remaining 4 were due to cancer (n=3) and heart failure (n=1; the
Figure). The 13 PE-related deaths were distributed as follows
(the Figure): 9 among the 28 patients with shock (32%), 1 among
the 19 patients with minor hemodynamic impairment
(5%), 3 among the 65 normotensive patients with RV dysfunction (5%),
and 0 among the 97 normotensive patients without RV dysfunction (the
Figure). Echocardiography thus showed a
100% negative predictive value for PE-related death, although its
positive predictive value was very low (Table 4). Of the 13 PE-related deaths, only 2
occurred in patients receiving urgent thrombolysis in
the group presenting with shock; the remaining 11 were among those
patients in whom thrombolysis had not been instituted
by the physician in charge.
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Among the 65 patients with RV dysfunction who were normotensive on
presentation, a total of 6 patients (10%) experienced
clinical deterioration and developed shock during the acute phase
judged to be caused by PE despite adequate anticoagulation with heparin
(Table 3). Of these 6 patients, 3 died shortly after the event,
as mentioned above, whereas 3 were successfully treated with urgent
thrombolysis instituted at the time of clinical
deterioration (Table 3). Of note, 2 of the 3 patients who died
had absolute contraindications to thrombolytic
treatment, and 1 was an elderly patient with metastatic cancer. At
multivariate analysis, the following
variables were associated with short-term clinical worsening and/or
PE-related death among the 65 normotensive patients with RV
dysfunction: advanced age, recent trauma or orthopedic treatment, and
lower systolic blood pressure and dizziness at
presentation (Table 5).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Role of Echocardiography in Risk Stratification of Patients With PE
Echocardiography has progressively achieved a prominent role in the diagnosis and clinical assessment of patients with PE.1 2 3 4 5 6 7 8 9 10 11 12 13 In patients with normal blood pressure and no signs of shock on presentation, RV dysfunction provides indirect evidence of severe pulmonary artery obstruction and impending hemodynamic failure1 2 13 20 (Table 2
). Among normotensive patients, only the subgroup with
evidence of RV dysfunction experienced adverse PE-related outcome (the
Figure). Hence, the negative predictive value of
echocardiography for PE-related death proved to be
100% in this particular patient population, although its positive
predictive value was low (Table 4). From these results,
echocardiographic examination of normotensive patients
with PE is mandatory for early detection of latent
hemodynamic impairment, provides valuable information
for risk stratification, and appears to be most relevant as a screening
test for the identification of low-risk
patients.1 3 4 6
Prevalence and Prognosis of Latent Hemodynamic Impairment
In the heterogeneous spectrum of PE, normotensive
patients with RV dysfunction represent the wide gray area
between mild disease and severe hemodynamic
impairment.1 2 3 4 5 6 8 In our study, normotensive patients
presenting with RV dysfunction represented 31% of the
total cohort and 40% of all normotensive patients with PE. These
findings are in agreement with the existing literature, indicating that
patients with latent hemodynamic impairment
represent a substantial subgroup among unselected patients with
PE.1 15 20
During the hospital admission, 10% of the 65 patients with latent
hemodynamic impairment (n=6) developed shock as a
result of PE recurrence, half of whom died soon after admission
(the Figure). In the remaining 3 patients, life-saving delayed
thrombolysis was successfully instituted. Of note, the
3 patients who died were not considered candidates for
thrombolysis because of specific contraindications and
general clinical conditions (Table 3). At
multivariate analysis, the clinical
variables associated with the development of shock after admission
were represented by advanced age, recent trauma or
orthopedic treatment, and dizziness and lower systolic blood
pressure at presentation.
PE-related mortality among the 65 patients with latent
hemodynamic impairment (5%) was significantly lower
than that of patients presenting with shock (32%;
P<0,0005; the Figure); however, it was not
negligible, especially compared with the absent PE-related mortality
among normotensive patients without RV dysfunction. In particular, the
5% mortality rate was identical to that of patients with minor
clinical manifestations of hemodynamic impairment (the
Figure) and similar to those observed in patients with major PE
and no evidence of cardiogenic shock by other
researchers.21 22 Therefore, once patients
with shock are excluded, the detection of RV dysfunction defines a
large subgroup of patients at intermediate short-term risk of
PE-related mortality that seems to be independent of the clinical
manifestations of hemodynamic impairment.
Other studies have addressed the relevance of RV dysfunction as a predictor of adverse outcome in patients with PE. However, to the best of our knowledge, ours is the first prospective study to analyze the issue specifically in patients who are clinically stable on presentation. This is of primary importance because aggressive therapeutic strategies (including widespread use of thrombolysis) have been advocated for patients with RV dysfunction, although their potential benefit in the absence of overt cardiogenic shock is still unresolved. At present, the available data on the prognosis of patients with pulmonary embolism and RV dysfunction emanate from multicenter registries with potential patient selection bias,23 24 originate from studies designed for other purposes,21 22 or have been described regardless of their clinical presentation, as in Reference 25 . In this last study, among patients with RV dysfunction, no distinction is made between patients presenting in shock who are known to have a severe prognosis and definitely require thrombolysis and those who are clinically stable on presentation and may benefit from conservative treatment. As a consequence, the reported mortality figure of 14% in patients with PE and RV dysfunction is misleading in that it presumably represents an average value between the high mortality rate of patients presenting with shock (32% mortality in our study) and the lower mortality rate of stable patients with RV dysfunction (5% in our study).
Relevance of Latent Hemodynamic Impairment on
Management Strategies
The finding that all normotensive patients without evidence of RV
dysfunction had a favorable prognosis on standard heparin treatment is
relevant because of its potential implications in disease
management.25 Although caution is still required at this
stage,24 our data support the possibility of less
aggressive treatment for patients with PE but no clinical or
echocardiographic signs of instability. Particularly
appealing is the possibility of considering home treatment with
low-molecular-weight heparin in these patients, following the existing
guidelines for the treatment of deep venous thrombosis, with
considerable economic and lifestyle benefits.26
The optimal acute management strategy for clinically stable patients with evidence of RV dysfunction is as yet unclear, and although it has been suggested that thrombolysis may improve the outcome in this particular subgroup,14 23 such hypotheses are still under debate.15 Results of the present study suggest that the detection of RV dysfunction represents an important prognostic determinant and is associated with a significant prevalence of severe adverse PE-related outcome. However, its positive predictive value may be too low to warrant aggressive treatment in all normotensive patients with RV dysfunction. According to our study, the decision of extending thrombolytic treatment to all patients with RV dysfunction would lead to a 5-fold increase in the use of such treatment among patients with PE and presumably to a comparable rise in treatment-related complications. Therefore, such decision needs to be supported by prospective randomized trials, which are still not available.
At present, all patients with PE and latent
hemodynamic impairment should be carefully monitored
during the initial phase of the hospital admission, and patients with
low bleeding risk should probably be considered for immediate
thrombolysis.21 23 27 This decision,
however, becomes more challenging for the substantial subgroup of
patients with 1 contraindications (including advanced age). In these
patients at high bleeding risk, it may be wiser to postpone the
decision of initiating thrombolysis and to select
candidate patients for "delayed" thrombolysis on
the basis of the short-term clinical course, as can be inferred by the
MAPPET study (Management strategy And Prognosis of Pulmonary
Embolism Trial)23 and the present study (Table 3).
Study Limitations
Our results are confined to the in-hospital period. Therefore, no
conclusion can be drawn as to the long-term consequences of latent
hemodynamic impairment in patients with PE. However, a
recent study by Ribeiro et al25 reported a 3-fold increase
in mortality at 1 year in patients with RV dysfunction at
presentation compared with those without, suggesting that
the prognostic implications of RV dysfunction in patients with acute PE
may be extended long term.
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Acknowledgments |
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We are indebted to Professor Vieri Boddi for statistical advice.
Received September 16, 1999; revision received December 15, 1999; accepted January 25, 2000.
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B. Fremont, G. Pacouret, D. Jacobi, R. Puglisi, B. Charbonnier, and A. de Labriolle Prognostic Value of Echocardiographic Right/Left Ventricular End-Diastolic Diameter Ratio in Patients With Acute Pulmonary Embolism: Results From a Monocenter Registry of 1,416 Patients Chest, February 1, 2008; 133(2): 358 - 362. [Abstract] [Full Text] [PDF]
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V. Palmieri, E. A. Palmieri, and A. Celentano Functional limitation and right ventricular dysfunction at 6-month follow-up in patients with non-massive pulmonary embolism: useful outcomes for testing therapy of acute submassive pulmonary embolism? Eur. Heart J., October 2, 2007; 28(20): 2430 - 2431. [Full Text] [PDF]
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C. Becattini, M. C. Vedovati, and G. Agnelli Prognostic Value of Troponins in Acute Pulmonary Embolism: A Meta-Analysis Circulation, July 24, 2007; 116(4): 427 - 433. [Abstract] [Full Text] [PDF]
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H. Dogan, L. J. M. Kroft, M. V. Huisman, R. J. van der Geest, and A. de Roos Right Ventricular Function in Patients with Acute Pulmonary Embolism: Analysis with Electrocardiography-synchronized Multi-Detector Row CT Radiology, November 7, 2006; (2006) 2421052089. [Abstract] [Full Text]
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S. Grifoni, S. Vanni, S. Magazzini, I. Olivotto, A. Conti, M. Zanobetti, G. Polidori, F. Pieralli, N. Peiman, C. Becattini, et al. Association of persistent right ventricular dysfunction at hospital discharge after acute pulmonary embolism with recurrent thromboembolic events. Arch Intern Med, October 23, 2006; 166(19): 2151 - 2156. [Abstract] [Full Text] [PDF]
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B. Ghaye, A. Ghuysen, V. Willems, B. Lambermont, P. Gerard, V. D'Orio, P. A. Gevenois, and R. F. Dondelinger Severe Pulmonary Embolism:Pulmonary Artery Clot Load Scores and Cardiovascular Parameters as Predictors of Mortality Radiology, June 1, 2006; 239(3): 884 - 891. [Abstract] [Full Text] [PDF]
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N. Meneveau, M.-F. Seronde, M.-C. Blonde, P. Legalery, K. Didier-Petit, F. Briand, F. Caulfield, F. Schiele, Y. Bernard, and J.-P. Bassand Management of unsuccessful thrombolysis in acute massive pulmonary embolism. Chest, April 1, 2006; 129(4): 1043 - 1050. [Abstract] [Full Text] [PDF]
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P. D. Maldjian, A. Anis, and M. Saric Radiological reasoning: pulmonary embolism--thinking beyond the clots. Am. J. Roentgenol., March 1, 2006; 186(3 Suppl): S219 - S223. [Abstract] [Full Text] [PDF]
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D. Aujesky, P.-M. Roy, C. P. Le Manach, F. Verschuren, G. Meyer, D. S. Obrosky, R. A. Stone, J. Cornuz, and M. J. Fine Validation of a model to predict adverse outcomes in patients with pulmonary embolism Eur. Heart J., February 2, 2006; 27(4): 476 - 481. [Abstract] [Full Text] [PDF]
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D. Aujesky, D. S. Obrosky, R. A. Stone, T. E. Auble, A. Perrier, J. Cornuz, P.-M. Roy, and M. J. Fine A Prediction Rule to Identify Low-Risk Patients With Pulmonary Embolism Arch Intern Med, January 23, 2006; 166(2): 169 - 175. [Abstract] [Full Text] [PDF]
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S. Z. Goldhaber Thrombolytic Therapy for Patients With Pulmonary Embolism Who Are Hemodynamically Stable But Have Right Ventricular Dysfunction: Pro Arch Intern Med, October 24, 2005; 165(19): 2197 - 2199. [Full Text] [PDF]
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