Abstract
Context:
Although computed tomography pulmonary angiography (CTPA) can confirm a diagnosis of acute pulmonary thromboembolism (PTE), its use may not be feasible in hemodynamically unstable patients. Transthoracic echocardiography (TTE) is useful to diagnose such cases but lacks specific, easily identifiable signs for differentiating acute PTE from other causes of right heart strain.
Aims:
We investigated the effectiveness of the “SRC” sign, a nondilated main pulmonary artery with a dilated right atrium (RA) and right ventricle (RV), for diagnosing acute PTE.
Settings and Design:
This was an observational, retrospective, single-center study.
Subjects and Methods:
Patients with acute dyspnea and dilated RA and RV, with or without dilated pulmonary artery (PA), and those suspected of PTE according to the Wells criteria were included. Blood tests, electrocardiography, and CTPA were performed to confirm PTE diagnosis. Patients were divided into a nondilated PA and dilated RA and RV group and a dilated PA, RA, and RV group.
Statistical Analysis Used:
Chi-square test with Yates’s correction was used for statistical analysis.
Results:
Forty-one patients (27 men) with suspected PTE were included, with 36 showing a dilated RA and RV on echocardiography. The SRC sign was present in 22 patients, all of whom were confirmed via CTPA to have acute PTE. The SRC sign demonstrated 100% specificity, 100% positive predictive value, and 92.86% negative predictive value.
Conclusions:
TTE is valuable for assessing patients with acute dyspnea. Although RA and RV dilatation may indicate acute PTE, they are insufficient for diagnosis confirmation. The SRC sign shows high specificity for major acute PTE and may aid in decision-making.
Keywords: Acute pulmonary thromboembolism, dilated right atrium, dilated right ventricle, pulmonary thromboembolism diagnosis, SRC sign, transthoracic echocardiography
INTRODUCTION
Among cardiovascular-related fatalities, pulmonary thromboembolism (PTE) ranks as the third leading cause, following myocardial infarction and stroke in terms of prevalence.[1] The annual reported incidence of PTE is 39–115 per 100,000 cohorts.[2] The mortality rate for acute PTE is high, with almost a third of patients dying within hours of their initial symptoms. This is often attributed to the challenges in promptly diagnosing and treating the condition, which may even go undetected.[3] An autopsy study from northern India reported PTE as the primary cause of mortality in 16% of hospitalized patients.[4] An epidemiological study on Asian patients reported that the rate of symptomatic venous thromboembolism (VTE) or sudden death due to VTE was 2.3% higher in Asian than in Western countries.[5] Bĕlohlávek et al. noted that pulmonary embolism had a 30% mortality rate if untreated; the rate decreased to between 3% and 7% in treated patients.[6] Considering the associated fatality rate, PTE should be diagnosed rapidly and accurately.
PTE diagnosis and treatment are based on determining pretest probability, analyzing electrocardiogram readings, assessing D-dimer levels, utilizing transthoracic echocardiography (TTE), evaluating chest radiography findings, and performing computed tomography pulmonary angiography (CTPA).[7] A high index of suspicion is needed to diagnose PTE because of its nonspecific signs and symptoms and to differentiate it from other conditions causing right heart strain such as chronic obstructive pulmonary disease (COPD) with cor pulmonale, atrial septal defect (ASD), restrictive cardiomyopathy, and right ventricular cardiomyopathy. CTPA is the diagnostic modality of choice for PTE, but its use may not be feasible in hemodynamically unstable patients.[8]
Along with clinical evaluation, TTE serves as a crucial portable bedside supportive tool for PTE diagnosis. TTE is a readily available, noninvasive, and reproducible tool. Various echocardiographic findings, including the right atrium (RA)/RV size, RV dysfunction, McConnell’s sign, 60/60 sign, and presence of a thrombus in the RA or RV, have been reported to be useful for diagnosis, risk stratification, and prognostic prediction in PTE.[7] Nevertheless, specific, easily identifiable echocardiographic signs for diagnosing acute PTE using TTE are lacking. Moreover, while TTE is recognized as a useful bedside diagnostic tool, a more precise and reliable indicator is needed to differentiate acute PTE from other conditions that can cause right heart strain. The novel “SRC” sign (nondilated pulmonary artery [PA], with dilated RA and RV) as depicted in Figure 1 might address this gap by providing a potentially more specific echocardiographic marker for acute PTE. This sign may offer several advantages: (1) improved diagnostic accuracy for acute PTE, (2) easier and faster identification during bedside TTE examinations, and (3) potential to differentiate acute PTE from chronic conditions affecting the right heart. Previous studies have shown the correlation of pulmonary hypertension with PA size; however, they rarely evaluated the role of PA size in diagnosing acute PTE on TTE.[8,9,10]
Figure 1.
Representative transthoracic echocardiography images of the SRC sign. (a) Normal sized pulmonary artery. (b) Dilated right atrium/right ventricle
In this study, we investigated the effectiveness of a dilated RA/RV with a nondilated main pulmonary artery (MPA) for diagnosing acute PTE. Evaluating the effectiveness of this SRC sign for detecting PTE may enhance the diagnostic capabilities of TTE for acute PTE, potentially leading to more timely and accurate diagnoses in clinical settings.
SUBJECTS AND METHODS
Study design
This pilot study aimed to explore the potential of a novel diagnostic sign for the rapid and accurate diagnosis of acute PTE. We employed a nonrandomized, investigator-initiated, observational study design at a single institution, with retrospective data analysis. The study was conducted at our institute from January 2014 to September 2024, and the protocol was approved by the regional ethics committee. The study was conducted in compliance with the principles of the Declaration of Helsinki, and written informed consent was obtained from all participants prior to the start of the study. The study adhered to the STROBE guidelines.
All consecutive patients above 18 years of age diagnosed with acute dyspnea and a dilated RA and RV, with or without a dilated MPA on TTE, and those suggested of having PTE according to Wells criteria were enrolled.[11] Those patients presenting with acute dyspnea but not fulfilling Wells criteria were excluded.
Considering the limited research available on the association between PA size and acute PTE diagnosis, our sample size of 41 participants from a single center and recruited over a period of 129 months was deemed to be appropriate for an initial proof-of-concept study.
Study procedures
Patients presenting with acute dyspnea and suspected of having PTE according to Wells criteria were clinically evaluated in the emergency department. Blood tests, including D-dimer tests, and electrocardiograms (ECGs) were performed after clinical evaluation. A pulse oximeter (Accusure YK011) was applied to the finger, and oxygen saturation was recorded. TTE (VVID E95, GE Healthcare, Chicago, IL, USA) and CTPA (Resolution ACTs, GE Healthcare Waukesha, WI, USA) were performed for all participants, as was the venous Doppler test. Forty-one eligible patients suspected of having PTE and with a dilated RA and RV, irrespective of the size of the MPA, on TTE were enrolled. PTE cases confirmed with CTPA were classified as massive, submassive, or low risk and treated according to the American Heart Association guidelines (2011).[12] PTE-mimicking cases were treated as per their respective current standard practice guidelines. Comorbidities such as hypertension, diabetes mellitus, and coronary artery disease were managed as per current standard practice guidelines.
Transthoracic echocardiography
TTE was performed using all standard views. RA and RV assessment was conducted as per standard guidelines by the American Society of Echocardiography.[13] RA, tricuspid regurgitation (TR) jet assessment, tricuspid annular plane systolic excursion (TAPSE), and pulmonary arterial hypertension (PAH) estimation were conducted in the apical four-chamber view. An RA area above 18 cm2 was considered an indicator of dilated RA. RV size was assessed qualitatively and quantitatively as per standard guidelines from the American Society of Echocardiography.[13] RV dimensions were obtained from the apical four-chamber RV-focused view at the end of the diastole. Dilated RV was considered to be present if the RV diameter was >42 mm at the base, >35 mm at mid-level, and >86 mm longitudinally. Two-dimensional fractional area change <35% and TAPSE below 16 were considered abnormal, suggesting RV dysfunction.[13]
PA dilation on TTE was determined by comparing the diameter of the MPA with that of the proximal ascending aorta. The MPA diameter was measured in the parasternal short-axis view of the right ventricular outflow tract using the inner edge method, at a point halfway between the pulmonary valve and PA bifurcation. The ascending aorta diameter was assessed in the parasternal long-axis view, above the sinotubular junction, also utilizing the inner edge method.[9] The diameters of the PA and aorta were recorded, and the ratio between the two diameters was calculated. An MPA diameter greater than that of the ascending aorta was considered evidence of dilatation (ratio >1).[14] Systolic pulmonary artery pressure (SPAP) was calculated from TR jet velocity in the apical four-chamber view. SPAP was classified as mild (35–50 mmHg), moderate (50–70 mmHg), or severe (>70 mmHg).[15] CTPA was conducted on all but one patient to confirm PTE. Patients were divided into two groups: the first group included patients with a nondilated PA but dilated RA and RV, while patients in the second group had a dilated PA, RA, and RV. The “SRC sign” was defined as the presence of a nondilated PA with a dilated RA and RV.
Data collection
Demographic information, including age and sex, was recorded for all participants. Information regarding comorbid conditions, such as diabetes mellitus, hypertension, coronary artery disease, cerebrovascular accidents, deep vein thrombosis, or recent surgery, was recorded for all patients. The TTE and CTPA results were recorded for each patient. Information about thrombolysis, thrombophilia profile, and ECG evaluation was recorded as well.
Data analysis
We utilized OpenEpi version 3.01 (https://www.openepi.com/) for the statistical analysis. Descriptive statistics were used to present the study outcomes, with continuous variables expressed as mean and standard deviation (SD) and categorical variables represented as numbers and percentages. The Chi-square test with Yates’s correction and a one-tailed P value was used to study the association between nondilated PA and dilated RA/RV for the diagnosis of acute PTE. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated using standard formulae. P <0.05 indicated statistical significance.
RESULTS
Patient characteristics
Forty-one patients presenting with dyspnea or suspected signs of PTE were included in this study. Their characteristics are summarized in Tables 1 and 2. Thirty (73.17%) of the sample population were men. Hypertension was the most common comorbid condition in 9 (21.95%). Submassive PTE cases were predominant, accounting for 15 (36.58%) more followed by acute massive PTE, with minor PTE being the least common. PTE-mimicking illnesses such as ASD were the most commonly seen in 6 (14.63%), followed by COPD with cor pulmonale and restrictive cardiomyopathy. Sinus tachycardia was the most common ECG presentation seen in 15 (36.58%), affecting more than one-third of the patients, followed by the S1Q1T3 pattern. Thrombolysis was administered to fewer than half of the patients, with tenecteplase being the most frequently used agent in 16 (39.02%). Hypoxia was the most common indication for thrombolysis. Lower limb deep vein thrombosis (DVT) was observed in 29 (70.73%) cases, upper limb DVT in 1 case, and a hypercoagulable state in 13 (31.70%), with four cases having undergone major surgery as risk factors for PTE.
Table 1.
Patient characteristics
| Parameters | Dilated PA group (n=14), n (%) | Normal size PA group (n=27), n (%) | Total patients (n=41), n (%) |
|---|---|---|---|
| Sex | |||
| Male | 7 (50) | 23 (85.18) | 30 (73.17) |
| Female | 7 (50) | 4 (14.81) | 11 (26.82) |
| Comorbidities | |||
| DM | 1 (7.14) | 3 (11.11) | 3 (7.31) |
| HTN | 4 (28.57) | 5 (18.51) | 9 (21.95) |
| Obesity | 1 (7.14) | 4 (14.81) | 5 (12.19) |
| PTE mimicking diseases | |||
| Anemia | 1 (7.14) | 1 (3.70) | 1 (2.43) |
| ASD | 6 (42.85) | 0 | 6 (14.63) |
| RCM with LVF | 2 (14.28) | 0 | 2 (4.87) |
| COPD with acute exacerbation | 0 | 1 (3.70) | 1 (2.43) |
| COPD with Cor pulmonale | 4 (28.57) | 0 | 4 (9.75) |
| Postpartum sepsis, ARF with RV cardiomyopathy | 1 (7.14) | 0 | 1 (2.43) |
| Clinical presentation | 0 | ||
| Cardiogenic shock | 2 (14.28) | 7 (25.92) | 9 (21.95) |
| Hypoxia | 5 (35.71) | 24 (88.88) | 29 (70.73) |
| Syncope | 0 | 1 (3.70) | 1 (2.4) |
| ECG presentation | |||
| Sinus tachycardia | 3 (21.42) | 12 (44.44) | 15 (36.58) |
| Sinus tachycardia with complete RBBB | 1 (7.14) | 1 (3.70) | 2 (4.87) |
| Sinus tachycardia with S1Q3T3 | 0 | 6 (22.22) | 6 (14.63) |
| Incomplete RBBB with sinus tachycardia | 0 | 2 (7.40) | 2 (4.87) |
| Atrial fibrillation | 2 (14.28) | 1 (3.70) | 3 (7.31) |
| Normal | 4 (28.57) | 1 (3.70) | 5 (12.19) |
| RBBB | 4 (28.57) | 0 | 4 (9.75) |
| Sinus tachycardia with T wave inversion in V1-4 | 0 | 4 (14.81) | 4 (9.75) |
| Thrombophilia profile | |||
| Protein S deficiency | 0 | 5 (18.51) | 5 (12.19) |
| Protein C deficiency | 0 | 2 (7.40) | 2 (4.87) |
| Hyperhomocysteinemia | 0 | 6 (22.22) | 6 (14.63) |
| Antithrombin III deficiency | 0 | 0 | 0 |
| Factor V Leiden mutation | 0 | 0 | 0 |
| Major surgery | 0 | 4 (14.81) | 4 (9.75) |
| Thrombolytic agents used | |||
| Tenecteplase | 0 | 16 (59.25) | 16 (39.02) |
| Streptokinase | 0 | 3 (11.11) | 3 (7.31) |
| Anticoagulants used | |||
| Fondaparinux | 0 | 5 (18.51) | 5 (12.19) |
| Low molecular weight heparin | 0 | 2 (7.40) | 2 (4.87) |
| Rivaroxaban | 0 | 15 (55.55) | 15 (36.58) |
| Warfarin | 1 (7.14) | 11 (40.74) | 11 (26.82) |
PTE=Pulmonary thromboembolism, DM=Diabetes mellitus, HTN=Hypertension, RCM=Restrictive cardiomyopathy, LVF=Left ventricular failure, ARF=Acute renal failure, RV=Right ventricle, RBBB=Right bundle branch block, PA=Pulmonary artery
Table 2.
Transthoracic echocardiography findings, pulmonary thromboembolism severity, and deep vein thrombosis cases
| TTE findings | Dilated PA (n=14), n (%) | Normal size PA (n=27), n (%) | Total patients (n=41), n (%) |
|---|---|---|---|
| Tricuspid regurgitation | |||
| Mild | 5 (35.71) | 10 (37.03) | 15 (36.58) |
| Moderate | 4 (28.57) | 14 (51.85) | 18 (43.90) |
| Severe | 5 (35.71) | 3 (11.11) | 8 (14.63) |
| PAH | 12 (85.71) | 24 (88.88) | 36 (87.80) |
| RV dysfunction (TAPSE <16 mm) | 5 (35.71) | 6 (22.22) | 11 (26.8) |
| McConnell’s sign | 0 | 17 (62.96) | 17 (41.46) |
| RA/RV/IVC thrombus | 0 | 0 | 0 |
| Mean PA size in mm | 32 | 22.126 | |
| Mean PA/Aorta ratio | 1.33 | 0.922068483 | |
| PTE severity | |||
| Acute massive PTE | 0 | 7 (25.92) | 7 (17.07) |
| Acute Submassive PTE | 0 | 15 (55.55) | 15 (36.58) |
| Acute small PTE | 0 | 3 (11.11) | 3 (7.32) |
| Chronic PTE | 1 (7.14) | 0 | 1 (2.43) |
| Associated DVT | |||
| Bilateral DVT | 0 | 2 (7.40) | 2 (4.87) |
| Right lower limb DVT | 0 | 5 (18.51) | 5 (12.19) |
| Left lower limb DVT | 0 | 5 (18.51) | 5 (12.19) |
| Left upper limb DVT | 0 | 1 (3.70) | 1 (2.43) |
PTE=Pulmonary thromboembolism, PA=Pulmonary artery, PAH=Pulmonary arterial hypertension, RV=Right ventricle, TAPSE=Tricuspid annular plane systolic excursion, RA=Right atrium, DVT=Deep vein thrombosis, IVC=Inferior vena cava
TTE evaluation revealed moderate tricuspid regurgitation in 18 (43.90%) cases, PAH in 36 (87.80%), and RV dysfunction in 11 (26.8%) cases. There were no cases of thrombus in the RA, RV, PA, or inferior vena cava. Thirty-six participants exhibited a dilated RA and RV on TTE. The “SRC sign” was present in 23 patients, all of whom were confirmed via CTPA to have acute PTE. Conversely, among patients with a dilated RA, RV, and PA, only one patient had confirmed acute PTE.
Moreover, one patient presenting with dyspnea in the postpartum period exhibited dilated RA, RV, and PA, along with elevated creatinine levels. CTPA was deferred based on the SRC sign. The patient subsequently died of sepsis. An autopsy study revealed no evidence of PTE.
Validity of the SRC for pulmonary thromboembolism identification
Our observations revealed that the presence of dilated RA and RV, regardless of MPA dimensions, exhibited 86.67% specificity (P < 0.001) for acute PTE diagnosis [Table 3]. Notably, when a nondilated PA was observed in conjunction with a dilated RA and RV (i.e., the SRC sign), the specificity increased to 100% (P < 0.001) for acute PTE diagnosis [Table 3]. The NPV for this sign was 92.86%. Thus, the SRC sign demonstrated remarkable effectiveness in ruling out PTE.
Table 3.
Effectiveness of the SRC sign for pulmonary thromboembolism identification
| PTE | No PTE | P | Specificity (%) | 95% CI | PPV (%) | NPV (%) | |
|---|---|---|---|---|---|---|---|
| Normal PA with or without dilated RA/RV | 25 | 2 | 0.000000454* | 86.67 | 59.54–98.34 | 92.59 | 92.86 |
| Dilated PA with dilated RA/RV (n=41) | 1 | 13 | |||||
| Dilated RA/RV (n=36) | |||||||
| Normal PA with dilated RA/RV (SRC sign) | 22 | 0 | 0.000000272* | 100 | 75.29–100 | 100 | 92.86 |
| Dilated PA with dilated RA/RV | 1 | 13 |
*Dilated RA and RV suggestive of RV strain is strongly associated with major PTE in acute dysponea evaluation. PA=Pulmonary artery, RA=Right atrium, RV=Right ventricle, PTE=Pulmonary thromboembolism, CI=Confidence interval, PPV=Positive predictive value, NPV=Negative predictive value, (n=41) indicates total participants, (n=36) indicates participants with dilated RA/RV irrespective of PA size
DISCUSSION
In the present study, we investigated the association of a nondilated MPA along with a dilated RA and RV with acute PTE. We showed that the presence of a dilated RA and RV, regardless of MPA dimensions, exhibited 86.67% specificity for acute PTE diagnosis and that the specificity increased to 100% when a nondilated PA was observed in conjunction with dilated RA and RV (i.e., the SRC sign). Moreover, the NPV for the SRC sign was 92.86%, allowing for effective identification of non-PTE cases. Along with a higher specificity and NPV, the SRC sign has several other advantages over other signs, including improved diagnostic accuracy, better ability to differentiate from other RV strain conditions, and rapid noninvasive evaluation, and may help clinicians to make more confident decisions regarding patient management and treatment. Typically, acute PTE is associated with right heart strain, leading to dilation of the right-side cardiac chambers and PA. The acute obstruction of the pulmonary arterial bed, caused by thromboemboli, coupled with the release of chemical mediators and hypoxic vasoconstriction in the affected lung, contributes to an elevation in pulmonary vascular resistance.[16] Most studies of echocardiography in acute PTE have mentioned the evaluation of qualitative and quantitative RV function, size of the RA and RV, and thrombus in the cardiac chambers but have provided very little information regarding the association between the size of the PA and a diagnosis of acute PTE.
Pathological factors influencing PA size and potentially leading to dilatation may be congenital or acquired. From a hemodynamic perspective, the most significant pathological factor is the prolonged presence of elevated PA pressure, which results in increased wall shear stress and chronic vascular remodeling.[17] However, the observation of a nondilated PA alongside a dilated RA and RV suggests that a more complex pathophysiological process is at work.
Several factors may contribute to this phenomenon. First, the rapid onset of obstruction of pulmonary blood flow may not allow sufficient time for PA dilation, while the right heart chambers respond more quickly to increased afterload. Second, the PA may undergo acute vasoconstriction in response to the embolic event, potentially masking any dilation. Third, patient-specific factors, such as preexisting cardiopulmonary conditions or genetic predispositions, may influence the manifestation of this sign.[10] Fourth, the timing of the observation may play a role: the nondilated PA might represent an early stage in the progression of acute PTE, captured before significant PA dilation occurs.
Xi et al. investigated PA dilatation in PAH of various etiologies, such as congenital heart disease, chronic PTE, and idiopathic PAH. However, the dilatation of the PA in acute PTE was not addressed in their research.[10] O’Corragain et al. examined the relationship between pulmonary artery diameter (PAD) and echocardiographic indicators of RV dysfunction in individuals experiencing acute PTE and demonstrated that increased PAD in patients with acute PTE was significantly associated with echocardiographic markers of RV dysfunction.[8] However, it is worth noting that this investigation did not assess for preexisting chronic PAH or RV dysfunction.[8] Previous studies have primarily focused on the dilation of the RA and RV as a key indicator of acute PTE, often overlooking the role of the PA.
The current study focused on the association of a nondilated PA and concomitant dilated RA and RV in diagnosing acute PTE. Analysis of our data showed that the SRC sign is a highly specific echocardiographic sign to diagnose acute PTE. This novel sign could have significant implications for early diagnosis and management of acute PTE. It may become particularly valuable in cases where traditional diagnostic criteria are equivocal or when rapid decision-making is crucial. To the best of our knowledge, such an association has not been described in the literature.
Limitations
Our sample size of 41 participants limits the generalizability of the study findings. While our findings are compelling, caution should be exercised owing to this limitation, and further research to validate these results is warranted. Nevertheless, despite the small sample size, our study provides valuable preliminary data on the association between PA size and acute PTE, laying the groundwork for future research.
CONCLUSIONS
The observation of a nondilated PA with concomitant RA and RV dilation (i.e., the SRC sign) as an indicator of acute massive PTE represents a potentially valuable addition to the echocardiographer diagnostic toolkit. This sign provides an important clue for the diagnosis of acute PTE. However, robust clinical studies are necessary to validate its utility, understand its mechanistic underpinnings, and determine its potential application for the improvement of patient outcomes in acute PTE management. Nevertheless, this novel sign may contribute to more timely and accurate diagnoses in cases of suspected PTE, ultimately enhancing the care of patients affected by this life-threatening condition.
Ethical statement
The study was approved by GMCYIEC, Yavatmal and approval no. is 28/2015.
Conflicts of interest
There are no conflicts of interest.
Acknowledgments
We appreciate the cooperation from Dr. Swapnil Sune for the CTPA and venous Doppler tests. We would like to acknowledge the support provided by Editage (www.editage.com) for English language editing of the manuscript.
Funding Statement
Nil.
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