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. 2019;26(4):191–198. doi: 10.6001/actamedica.v26i4.4203

Prognostic value of Mastora obstruction score in acute pulmonary embolism

Jolita Račkauskienė 1,2,*,**, Vaida Gedvilaitė 3,**, Mindaugas Matačiūnas 4,5, Mažvilė Abrutytė 6, Edvardas Danila 1,2
PMCID: PMC7180411  PMID: 32355456

Abstract

Background

To evaluate the clinical significance of Mastora obstruction score in hemodynamically stable patients with acute pulmonary embolism (aPE).

Materials and methods

One-hundred-and-six patients with newly diagnosed aPE, confirmed by computed tomography pulmonary angiography (CTPA), were included in the study and prospectively examined. aPE severity was assessed by using Mastora obstruction score. According to the Mastora index, patients were divided into “non-massive” and “massive” groups. The  patients’ medical histories and blood laboratory data were collected, and instrumental tests were performed and analyzed.

Results

Eighty-two (77%) of the patients had “non-massive” aPE. Cough (48%), fever (44%), and pleural effusion (48%) occurred significantly more often in the  “non-massive” PE group, while syncope (42%) and right ventricular dysfunction (86%) were more frequent in the  “massive” PE group. The  probability of the  right ventricular dysfunction was significantly higher in the  presence of increased pulmonary artery pressure (Cramer’s V = 0.410; p < 0.0001) and respiratory failure (Cramer’s V = 0.247; p = 0.032). Increased CRP level was found in the majority of the patients (90%). D-dimer level <500 μg/L (lower than the commonly recommended cut-off level) was found in 5% of cases.

Conclusions

The clinical manifestation depends on the massiveness of aPE. Division of aPE cases into two groups suggests two possible subtypes of aPE: cardiovascular and respiratory. The “non-massive” aPE was associated with respiratory symptoms and an inflammatory response. The  “massive” aPE is associated with an increased D-dimer level and leads to cardiovascular disorders. However, the “massive” aPE may be presented by normal D-dimer concentration level.

Keywords: pulmonary embolism, Mastora, chest CTPA, CRP, D-dimer

INTRODUCTION

Acute pulmonary embolism (aPE) is a life-threatening fatal disease with an annual incidence of 70 cases per 100 000 inhabitants (1, 2). It is the third most frequent cardiovascular disease with an overall annual incidence of 100–200 per 100 000 people (3). Mortality rate of patients not diagnosed and treated in a timely manner for aPE is as high as 30% and the risk of death is higher at 30 and 90 days after the first episode of PE (4–6). In addition, near 40% of cases of aPE and DVT are prone to recur (4, 7). The prognosis for aPE depends on many factors, such as individual response, the size and location of the clot, and comorbidities (8). Traditionally, massiveness of aPE has been defined on the basis of angiographic burden of emboli by use of the radiologic indexes designed for PE severity, such as Qanadli, Miller, or Mastora score (9, 10). The Mastora score is one of the latest radiologic indexes. The aim of the study was to analyze the  significance of Mastora obstruction score in hemodynamically stable aPE.

MATERIALS AND METHODS

Study population

The study population consisted of 106 patients (43% males; mean age 68 ± 14 years) with newly diagnosed aPE between January 2010 and April 2013. All patients were examined at Vilnius University Hospital Santaros Klinikos. Inclusion criteria were legal age (≥18 years), an acute, symptomatic, and newly diagnosed PE with objective confirmation by chest CTPA. Exclusion criteria were hemodynamic instability, sepsis (which was diagnosed before aPE), recurrence of PE, surgery or trauma during the acute period (the last four weeks). During the  study, the  patients’ medical histories was collected, blood laboratory (D-dimer and CRP level concentration) and instrumental tests such as transthoracic echocardiography, deep venous ultrasonography of the legs (duplex scanning), and chest CTPA data were performed and evaluated. The demographic features of the study population are shown in Table 1.

Table 1.

The demographic features of the population

Risk factors Number of patients %
Age > 65 years 64 (60.4)
Smoking history 22 20.8
Deep venous thrombosis 71 67
Congestive heart failure * 33 31.1
Rhythm disturbances * 28 26.4
Malignancy 25 23.6
Obesity 23 21.7
Congestive respiratory failure 19 17.9
Bed rest 16 15.1
Surgery ** (during the last 3 months) 10 9.4
Trauma * (during the last 3 months) 7 6.6
Oral contraceptive therapy/Hormone replacement therapy 3 2.8
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* 16 (15.1%) patients suffered from congestive heart failure and arrhythmias.

** 4 (3.8%) patients, who underwent surgery and had trauma (excluding patients who underwent surgery or trauma during last 4 weeks).

According to the Mastora score, patients were allocated to one of two groups: group I (“non-massive” aPE)  –  when pulmonary vascular obstruction was less than 50%, and group II (“massive” aPE group) – when pulmonary vascular obstruction was ≥ 50% of the pulmonary artery bed (9). A  signed informed consent form was obtained from all participants. The study was approved by the local Bioethics Committee.

Methods

All study tests were performed within one week after aPE confirmation. During the  study, chest CTPA was applied to all 106 (100%) patients. Chest CTPA was carried out with 64 computed tomography scans GE VCT (General Electric Healthcare, Milwaukee, WI, USA) using Omnipaque 350 intravenous contrast. aPE scope was evaluated using Mastora method (GE Advantage Workstation software, version 4.4_04.05_EXT_ CTT_5.X) for all the study patients. For the purpose of evaluating the CT score of severity of aPE, the scoring system was applied to five mediastinal, six lobar, and 20 segmental arteries. The five mediastinal arteries comprised the pulmonary artery trunk, the right and left main pulmonary arteries, and the right and left interlobar arteries. The six lobar arteries included the right truncus anterior, the left upper lobe pulmonary artery (upper arterial branch, i.e., the culminal branch), the right middle lobe pulmonary artery, the left upper lobe pulmonary artery (the lower arterial branch, i.e., the lingular artery), and the  right and left lower lobe pulmonary arteries. The 20 segmental pulmonary arteries consisted of the three right and left upper lobe (upper division) segmental arteries, the  two right middle lobe and left upper lobe (lower division) segmental arteries, and the  five right and left lower lobe segmental arteries. The  CT severity score was based on the  percentage of the  obstructed surface of each central and peripheral pulmonary arterial section using a 5-point scale (1: <25%; 2: 25–49%; 3: 50–74%; 4: 75–99%; 5: 100%). The  maximum Mastora obstruction score value was 155 (9). All patients underwent deep venous ultrasonography of the legs (GE Logiq 6 ultrasound system) and 76  (71.6%) of them transthoracic echocardiography (GE Vivid 7 ultrasound system). The echocardiographic severity of aPE was defined by the presence of signs of right heart dysfunction, paradoxical movement of the interventricular septum and/or systolic pulmonary hypertension (11). The  systolic pressure in the  pulmonary artery on cardiac ultrasound was measured in 42  (55.3%) patients. The  D-dimer concentration level was evaluated with quantitative immune-turbid-metric (latex agglutination) method. A concentration was considered to be increased when D-dimer >500 mcg/L 1). CRP was explored with a method of latex immune-analysis and the level was consider to be increased when CRP 5 mg/L (1).

Statistical analysis

Statistical analysis was performed with SPSS 20.0. Variables were derived and tested to confirm normal distribution using the  Kolmogorov-Smirnov test. Comparisons were made by x test, between the  two groups which were evaluated using Student’s t-test or the Mann-Whitney U test. All correlation analyses were performed using Pearson’s coefficient of rank correlation. Cramer’s V test was used to detect the measure of association. Cramer’s V is a measure of association between two nominal variables, giving a value between 0 and +1. This measure varies from 0 (corresponding to no association between the variables) to 1 (complete association) and can reach 1 only when the two variables are equal to each other. A value of p < 0.05 was accepted as statistically significant.

RESULTS

The Mastora obstruction score varied highly: from 0.65 to 100. Eighty-two (77%) of the patients had “non-massive” aPE, whereas 24 (23%) had “massive” aPE. Cough, fever, and pleural effusion occurred significantly more often in the “non-massive” aPE group. Syncope and right ventricular dysfunction were more frequent in the “massive” aPE group. Some clinical symptoms, such as dyspnea, weakness, and chest pain were statistically observed equally often in both groups (Table 2).

Table 2.

Demographics and clinical features of aPE. Blood laboratory data and instrumental tests of patients of “non-massive aPE” and “massive aPE” groups

“Non-massive aPE” group (n = 82) “Massive aPE” group (n = 24) p
Age (years) Min 38 Max 93 Min 37 Max 89 0.935
Mean 67.5 ± 14.6 Mean 69 ± 14
D-dimer (μg/L) Min 265 Max 25150 Min 1035 Max 20500 0.638
Mean 4531 ± 4685 Mean 6872 ± 5775
CRP (mg/L) Min 1.1 Max 216 Min 9.5 Max 99 0.130
Mean 60 ± 52 Mean 36 ± 28
Dyspnea 72 (88%) 23 (96%) 0.257
Weakness 51 (62%) 16 (67%) 0.690
Chest pain 46 (56%) 10 (42%) 0.121
Cough 39 (48%) 4 (17%) 0.007
Fever 36 (44%) 3 (13%) 0.005
Haemoptysis 16 (20%) 1 (4%) 0.072
Syncope 9 (11%) 10 (42%) 0.001
Right ventricular dysfunction 27 (50%) 19 (86%) 0.003
Pleural effusion 39 (48%) 6 (25%) 0.049
Opacity/consolidation on chest CT 26 (32%) 5 (21%) 0.303
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The Mastora obstruction score had a relatively weak association with right ventricular dysfunction (Cramer’s V  =  0.335; p  =  0.022), syncope (Cramer’s V = 0.369; p = 0.002) and paradoxical movement of the interventricular septum (Cramer’s V = 0.4; p = 0.007). The Mastora index correlated positively with D-dimer level (r  =  0.249; p = 0.011), but negatively with CRP (r = –0.259; p = 0.012). D-dimer concentration was in a range from 265 μg/L to 25150 μg/L (average 5059 μg/L). Ninety-seven (95%) of all the  study patients had D-dimer level higher than 500  μg/L (above commonly recommended cut-off level). D-dimer concentration was significantly higher in the “massive” aPE group compared to the  “non-massive” PE group. Importantly, five (5%) of all the patients had D-dimer level below 500 μg/L. One of these patients had thrombosis of the main pulmonary arteries, another one – of the lobar pulmonary arteries, while the remaining three – of the segmental and (or) sub-segmental pulmonary artery branches. Higher D-dimer concentration was associated with obesity (Cramer’s V = 0.345; p = 0.033) and cancer (Cramer’s V  =  0.529; p  <  0.0001). Increased CRP level was found in 85 patients (80% of all the study patients). CRP level was significantly higher in the “non-massive” PE group comparing with the “massive” aPE group patients. When CRP level was increased (>5  mg/L), 35 patients (41%) had fever. Only one patient had fever while CRP level was in the  normal range (<5 mg/L). When CRP >5 mg/L, the opacity/consolidation was found in 27 (31.7%) cases, whereas CRP <5 mg/L – opacity/consolidation was found in one (4%) case. The CRP level is associated with fever (Cramer’s V = 0.439; p = 0.001), hemoptysis (Cramer’s V = 0.35; p = 0.021), CRP and opacities/consolidation on the  chest CT scans (Cramer’s V = 0.419; p = 0.002). For 31 (29%) of the patients, opacities or consolidation on the chest CTPA scans and for 45 (42%) pleural effusion were found. Pleural effusion was statistically significantly associated with fever (Cramer’s V = 0.295; p = 0.002), but there was no reliable association to CRP. Hemoptysis occurred more frequently when opacities/consolidation were found in CT scans (Cramer’s V = 0.228; p = 0.019). Pleural effusion increased the  probability of fever (Cramer’s V = 0.295; p = 0.002), but there was no reliable correlation with CRP. Patients with pleural effusion had a higher probability of rhythm disorders (Cramer’s V = 0.221; p = 0.023) and respiratory failure (Cramer’s V = 0.246; p = 0.011). The systolic pressure in the pulmonary artery on cardiac ultrasound was elevated in 85% cases. The  mean pressure of the pulmonary artery was 47 mmHg. Right ventricular dysfunction was detected for 46 (74%) patients, paradoxical motion of interventricular septum for 6 (8%) patients. A higher pulmonary artery systolic pressure was associated with a higher probability of the right ventricular dysfunction (Cramer’s V = 0.410; p < 0.0001) and the paradoxical motion of interventricular septum (Cramer’s V  =  0.236; p  =  0.039). Patients with rhythm disorders had a higher probability of dyspnea (Cramer’s V = 0.204; p = 0.036). The higher probability of the right ventricular dysfunction was relatively moderately associated with increased pulmonary artery pressure (Cramer’s V = 0.410; p < 0.0001) and presented with respiratory failure (Cramer’s V = 0.247; p = 0.032). During the study period, PE resulted in the death of two (2%) patients. One patient died on the 7th day (Mastora score 6.45), and the second patient on the 20th day (Mastora score 0.65) after the PE diagnosis was confirmed. There was a statistically higher probability of death when there was congestive heart failure (Cramer’s V = 0.206; p = 0.034), DVT (Cramer’s V = 0.198; p = 0.042), opacities/consolidation in CT scans (Cramer’s V = 0.216; p = 0.026), or smoking in a life history (Cramer’s V = 0.271; p = 0.005) and aPE.

DISCUSSION

For decades, clinicians have been taught that aPE – defined by the National Institute of Health as a “sudden blockage in a lung artery” – always matters and to be vigilant because a missed embolism can be fatal. When a patient presents with shortness of breath, pleuritic chest pain, tachycardia, or signs of right heart strain, clinicians are trained to think “it may be the pulmonary embolism” (12). The fear of missing a diagnosis of this life-threatening disease has led to increased application of invasive diagnostic strategies, with a  significant rise in the use of CTPA over the last decade (13). Therefore, increased accessibility of chest CTPA led to the detection of more PE cases (12). After a while, clinicians noticed that clinical manifestation of aPE may have no symptoms and manifest in different ways (14). The  aim of the  study was to evaluate the  role of the  Mastora obstruction score in hemodynamically-stable aPE patients. According to the Mastora obstruction score, aPE was classified into two groups (“non-massive – less than 50% obstruction and “massive”  –  50% and more obstruction) and compared. The  key findings in our study are: (i) clinical and laboratory manifestation of aPE depends on “massiveness” of the thrombosis of the pulmonary arteries; (ii) “massive” aPE more often presented with syncope, right ventricular dysfunction, higher level of D-dimer; (iii) “non-massive” aPE mostly presented with cough, fever, pleural effusion, higher level of CRP; (iv) the normal level of D-dimer did not exclude aPE, even massive one. Our study showed statistically significant differences between clinical features of “massive” aPE compared with the  “non-massive” PE group. Some symptoms such as syncope, dyspnea, weakness, chest pain, cough, fever, or hemopthysis can occur in both groups, but some of them are detected more often when emboli have obstructed the pulmonary trunk or its main branches (8). We noticed that syncope, dyspnea, and weakness more often occurred in the “massive” PE group whereas cough, chest pain and fever in the “non-massive” group. Some authors have shown that clinical cardiac consequences become apparent when >30–50% of the pulmonary arterial bed is occluded by emboli (3, 8). The current opinion suggests replacing potentially misleading terms such as “massive”, “submassive”, and “non-massive” with the estimated level of the risk of aPE-related early death (3). However, our study showed that clinical manifestation depends on the massiveness of the thrombosis. We noticed that there were some clinical and laboratory mismatches between the “massive” and “non-massive” PE groups. According to the scope of the thrombosis, we found different clinical manifestation of PE: “massive” PE is more often associated with an increased D-dimer level and leads to cardiovascular disorders such as syncope and right ventricular dysfunction. Pulmonary artery pressure and pulmonary vascular resistance increase proportionately to the increased flow when a main pulmonary artery or pulmonary trunk is acutely obstructed by emboli and as a consequence we could have violent response – right heart failure (15, 16). Duplyakov et al. found that syncope may be a criterion of a high risk of fatal complications of PE, influenced by emboli (8). Comparing “massive” PE group with the “non-massive” group, patients in the  first group had a  higher level of D-dimer, but a lower CRP level. These clinical and laboratory findings were suspected. The  level of D-dimer concentration shows what is happening during thrombosis: if a higher percentage of pulmonary arteries are obstructed, then fibrinolysis occurs more intensively and, as a result, we have a  higher D-dimer level (17, 18). Meanwhile, our study clarified that “non-massive” PE is more associated with respiratory symptoms (such as a cough, hemoptysis, and pleural effusion) and an elevated CRP level. When the pulmonary artery is occluded by emboli, venous blood pressure increases in the preocluded region and may cause hemorrhage in the alveoli and cough with hemoptysis occurs as a response. If embolus occludes only distal or sub-segmental branch of the  pulmonary artery, it does not disturb the  main blood flow and has no effect on the pressure in the main pulmonary artery, it could still increase systemic inflammatory reaction. Elevated CRP is an inflammatory response to the process of the thrombosis, influenced by released cytokines and neurohumoral factors (16). Folsom showed that elevated CRP is independently associated with an increased risk of VTE (19, 20). It is our accidental study finding: we did not investigate the neurohumoral way during our research and it needs further investigations. All these findings reveal two possible subtypes of PE: respiratory and cardiovascular, respectively. Our study showed that in a  small number of cases PE could be diagnosed when D-dimer concentration was below 500 μg/L. This finding was comparable to Wouter’s and Goldhaber’s data that emboli in subsegmental artery branches may be misdiagnosed when D-dimer concentration level is used as a single test to exclude thrombosis (17, 21). The controversial study by Pierrer and others showed that plasma D-dimer concentration below 500 μg/L allows the exclusion of PE (22).

Our study has several limitations. Firstly, it had a relatively low number of patients. Nevertheless, it was prospectively investigated and the study population was typical of everyday practice. Secondly, we did not use cardio-specific biomarkers such as TNI and BNP at the beginning of the study because it was not a standard procedure in our clinic several years ago. Since these biomarkers were performed for minority of the  study patients, we could not make any further calculations and evaluate them as predictive markers for the mortality rate.

CONCLUSIONS

This study shows that clinical manifestation depends on the  massiveness of PE. Moreover, in a  small number of cases “massive” aPE may be presented by normal D-dimer concentration level. Dividing aPE cases into two groups (less or more than 50% of the  pulmonary artery bed) suggests two possible subtypes of aPE: cardiovascular and respiratory. “Non-massive” aPE was associated with respiratory symptoms and an  inflammatory response. “Massive” aPE is associated with increased D-dimer level and leads to cardiovascular disorders, such as syncope and right ventricular dysfunction. Further investigations are needed to clarify this suggestion. However, it should be taken into account that, at present, the Mastora obstruction index itself does not impact the choice for antithrombotic treatment.

Acknowledgments

We would like to thank all the departments that participated in this survey and all the  patients who gave their consent to participate.

CONFLICT OF INTEREST

The authors declare no conflict of interest.

FINANCIAL DISCLOSURE

The authors have no funding to disclose.

Jolita Račkauskienė, Vaida Gedvilaitė, Mindaugas Matačiūnas, Mažvilė Abrutytė, Edvardas Danila

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