Clinical Characteristics, Treatment Response, and Prognosis Between Saddle and Non-Saddle Pulmonary Embolism in Intermediate- to High-Risk Acute Pulmonary Embolism

By Qihong Chen^1,2, Jinqi Huang^1,2

Affiliations

1. The School of Clinical Medicine, Fujian Medical University, Fuzhou, China
2. Department of Interventional Vascular Surgery, The First Hospital of Putian City, Putian, China.

doi: 10.29271/jcpsp.2026.08.1063

Abstract
Objective: To investigate the clinical characteristics of patients with saddle pulmonary embolism (SPE) among those with intermediate- to high-risk acute pulmonary embolism (APE).
Study Design: A comparative study.
Place and Duration of the Study: Department of Interventional Vascular Surgery, the First Hospital of Putian City, Putian, China, from May 2017 to October 2024.
Methodology: Combined anticoagulation and interventional therapy was administered to all enrolled intermediate- to high-risk APE patients (with right ventricular dysfunction and/or elevated cardiac biomarkers, or haemodynamic instability) per the study protocol. Based on whether SPE was identified on computed tomography pulmonary angiography, patients were divided into the SPE group and the non-SPE group. Clinical characteristics, cardiac biomarkers, imaging features, and clinical outcomes were compared between the two groups.
Results: When comparing the groups, no significant differences were observed in N-terminal pro-B-type natriuretic peptide, right ventricular diameter/left ventricular diameter, and peripheral pulmonary artery obstruction index before and after treatment (p >0.05). However, the SPE group had higher levels of cardiac troponin I than the non-SPE group before and after treatment (p <0.05). There was no significant difference in in-hospital mortality between the two groups (p = 0.653). In the SPE group, the saddle embolism resolved completely in 94.74% of patients after treatment.
Conclusion: Patients with SPE may experience more severe myocardial injury. The short-term resolution of the saddle embolism after treatment appears not to be a critical factor affecting treatment response.

Key Words: Intermediate- to high-risk, Acute pulmonary embolism, Computed tomography pulmonary angiography, Saddle pulmonary embolism, Clinical characteristics.

Introduction

Acute pulmonary embolism (APE) is a potentially life-threatening condition and represents the third most common cause of car- diovascular death, following myocardial infarction and stroke.¹ Computed tomography pulmonary angiography (CTPA) is the primary diagnostic and assessment tool for APE, capable of not only confirming the presence and extent of APE but also providing relevant information on right ventricular (RV) dys- function.^2,3 Saddle pulmonary embolism (SPE) specifically refers to a thromboembolism that extends to the bifurcation of the pulmonary trunk into the right and left pulmonary arteries.

The presence of a saddle embolism in CTPA often raises con- cerns about severe illness. However, regarding the specific impact of SPE on the severity and clinical outcomes of patients with intermediate- to high-risk APE, existing research is limi- ted, and conclusions are inconsistent. For example, one study found no statistically significant difference in in-hospital mortality between the SPE and non-SPE groups (2.1% vs. 4.9%, p = 0.32), while another study reached the opposite conclusion.^4,5

This uncertainty highlights the need to clarify further the cli- nical significance of SPE in specific populations, such as intermediate- to high-risk patients. Therefore, the primary objective of this retrospective study was to compare the clinical characteristics of patients with SPE and non-SPE among those with intermediate- to high-risk APE who underwent interventional therapy. In addition, treatment responses and short-term clinical outcomes were compared between the two groups.
 

METHODOLOGY

Consecutive patients with intermediate- to high-risk APE who were admitted to the Department of Interventional Vascular Surgery, the First Hospital of Putian City, Putian, China, from May 2017 to October 2024. The inclusion criteria were receipt of anticoagulant therapy and interventional treatment; symptom onset within 15 days before presentation; and classification as intermediate-risk APE with imaging evidence of RV dysfunction or elevated cardiac biomarkers, or as high-risk APE with hypotension or shock. The exclusion criteria were low-risk patients, i.e., those without hypotension, shock, imaging evidence of RV dysfunction, or elevated cardiac biomarkers; patients with pre-existing multi-organ failure before the onset of APE; and patients without a CTPA examination before treatment. Based on admission CTPA findings, patients were independently evaluated by two inter-ventional vascular surgeons with 5–7 years of experience and classified into the SPE group if a saddle pulmonary embo-lism was identified or into the non-SPE group otherwise.

The interventional procedure was primarily performed via a femoral vein approach. A 5F pigtail catheter was inserted into the affected pulmonary artery for direct catheter-directed thrombolysis. Depending on the treatment phase, either low-molecular-weight heparin or unfractionated heparin was administered. The specific methods and drug dosages refe-renced previously published research from the centre.⁶ In the later stage of the study, a small subset of patients also underwent mechanical thrombectomy and intraoperative catheter-directed infusion of alteplase.

Data collection was completed by retrospectively review-ing the electronic medical record system. Laboratory para-meters, such as N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI), and imaging exa- mination results before and after interventional treatment during hospitalisation were recorded. On the axial CTPA images, the maximum right ventricular diameter (RVD) was measured perpendicular to the interventricular septum, and the left ventricular diameter (LVD) was measured using the same method (Figure 1). The peripheral pulmonary embolism index (PPEI) was calculated as follows: each lung was divided into 10 segmental arteries on CTPA, with a score of 0 for patent arteries, 1 for partially occluded arteries, and 2 for completely occluded arteries. The total score for each patient ranged from 0 to 40, and the PPEI was calcu-lated as (total score / 40) × 100%.

Table I: Comparison of general clinical characteristics between the two patient groups.
 

Clinical characteristics	SPE group (n = 23)	Non-SPE group (n = 104)	c2/Z	p-values
Gender	-	-	-	-
Male (n = 36)	10	26	3.166	0.075*
Female (n = 91)	13	78
Age (years)	66 (61-71)	65 (58-74)	-0.122	0.903+
Onset time (days)	1 (1-4)	3 (1-7)	-1.375	0.169+
Lower extremity DVT	-	-	-	-
None (n = 22)	2	20	2.277	0.517*
Left side (n = 38)	8	30
Right side (n = 29)	7	22
Bilateral (n = 38)	6	32
Syncopea	-	-	-	-
No (n = 95)	15	80	1.369	0.242*
Yes (n = 32)	8	24
Hypertension	-	-	-	-
No (n = 80)	11	69	2.771	0.096*
Yes (n = 47)	12	35
Diabetes	-	-	-	-
No (n = 107)	19	88	<0.001	>0.999*
Yes (n = 20)	4	16
Coronary heart disease	-	-	-	-
No (n = 105)	21	84	0.817	0.366*
Yes (n = 22)	2	20
Hyperlipidaemia	-	-	-	-
No (n = 62)	7	55	3.799	0.051*
Yes (n = 65)	16	49
History of VTE	-	-	-	-
No (n = 109)	20	89	<0.001	>0.999*
Yes (n = 18)	3	15
Trauma or surgeryb	-	-	-	-
No (n = 103)	17	86	0.461	0.497*
Yes (n = 24)	6	18
Malignant tumour	-	-	-	-
No (n = 118)	21	97	<0.001	>0.999*
Yes (n = 9)	2	7
Length of hospital stay (days)	9 (5-17)	8 (6-16)	-0.075	0.940+
Thrombolysis time (days)	2 (1-3)	2 (2-3)	-1.425	0.154+
aThere is a definite history of syncope during the onset of this APE; bThere is a history of trauma or surgery within two months before admission. *Chi-square test; +Mann-Whitney U test. SPE: Saddle pulmonary embolism; DVT: Deep venous thrombosis; VTE: Venous thromboembolism.

Table II: Comparison of NT-proBNP, cTnI, RVD/LVD, and PPEI between groups before and after treatment.

Variables	n	Pre-treatment NT-proBNP (ng/L)	n	Post-treatment NT-proBNP (ng/L)
SPE group	20	964.45 (601.50-2009.75)	11	150.00 (74.00-238.00)
Non-SPE group	66	862.50 (400.87-2987.70)	40	272.00 (70.75-2882.50)
Z		-0.271	-	-1.226
p-values		0.786*	-	0.220*
-		Pre-treatment cTnI (μg/L)	-	Post-treatment cTnI (μg/L)
SPE group	21	0.14 (0.06-0.52)	12	0.03 (0.02-0.06)
Non-SPE group	59	0.04 (0.01-0.23)	37	0.01 (0.01-0.02)
Z		-2.581	-	-2.535
p-values		0.010*	-	0.011*
-		Pre-treatment RVD/LVD	-	Post-treatment RVD/LVD
SPE group	22	1.49 (1.09-1.69)	16	1.09 (1.02-1.36)
Non-SPE group	98	1.40 (1.16-1.71)	77	1.12 (1.01-1.32)
Z		-0.170	-	-0.275
p-values		0.865*	-	0.783*
-		Pre-treatment PPEI (%)	-	Post-treatment PPEI (%)
SPE group	22	62.50 (51.88-70.00)	19	30.00 (15.00-35.00)
Non-SPE group	104	57.50 (47.50-66.88)	84	30.00 (17.50-45.00)
Z		-1.069	-	-0.451
p-values		0.285*	-	0.652*
Some patients lacked NT-proBNP and cTnI data; in the SPE group, one patient was incidentally found to have a SPE during a carotid computed tomography angiography examination and did not undergo CTPA; in some patients, the left ventricle was not opacified with contrast on CTPA, making it impossible to calculate the RVD/LVD. *Mann-Whitney U test. SPE: Saddle pulmonary embolism; NT-proBNP: N-terminal pro-B-type natriuretic peptide; cTnI: Cardiac troponin I; RVD: Right ventricular diameter; LVD: Left ventricular diameter; PPEI: Peripheral pulmonary embolism index; CTPA: Computed tomography pulmonary angiography.

Table III: Intra-group comparison of NT-proBNP, cTnI, RVD/LVD, and PPEI before and after treatment.

Variables	n	Pre-treatment NT-proBNP (ng/L)	Post-treatment NT-proBNP (ng/L)	Z	p-values
SPE group	10	913.13 (276.83-6117.50)	152.00 (72.75-676.00)	-1.478	0.139*
Non-SPE group	25	2133.00 (536.11-6457.00)	276.00 (70.86-3291.73)	-2.857	0.004*
		Pre-treatment cTnI (μg/L)	Post-treatment cTnI (μg/L)
SPE group	12	0.22 (0.08-0.88)	0.03 (0.02-0.06)	-3.059	0.002*
Non-SPE group	20	0.08 (0.03-0.23)	0.01 (<0.01-0.02)	-3.584	<0.001*
		Pre-treatment RVD/LVD	Post-treatment RVD/LVD
SPE group	16	1.49 (1.05-1.74)	1.09 (1.02-1.36)	-2.457	0.014*
Non-SPE group	72	1.33 (1.15-1.58)	1.09 (1.00-1.32)	-3.516	<0.001*
		Pre-treatment PPEI (%)	Post-treatment PPEI (%)
SPE group	19	62.50 (50.00-70.00)	30.00 (15.00-35.00)	-3.828	<0.001*
Non-SPE group	84	57.50 (48.13-67.50)	30.00 (17.50-45.00)	-7.787	<0.001*
Data for NT-proBNP and cTnI were unavailable for some patients. In the SPE group, one case of SPE was incidentally discovered during carotid computed tomography angiography examination without subsequent CTPA; left ventricular contrast opacification was insufficient in some CTPA studies, precluding RVD/LVD calculation. *Wilcoxon signed-rank test. SPE: Saddle pulmonary embolism; NT-proBNP: N-terminal pro-B-type natriuretic peptide; cTnI: Cardiac troponin I; RVD: Right ventricular diameter; LVD: Left ventricular diameter; PPEI: Peripheral pulmonary embolism index; CTPA: Computed tomography pulmonary angiography.

SPSS version 23.0 software was used for statistical analysis. Continuous variables were confirmed to be non-normally distributed through frequency histograms and the Kolmo-gorov-Smirnov normality test, and are therefore expressed as median (IQR). For inter-group comparisons, the Mann-Whitney U test was employed, while for intra-group compa-risons before and after treatment, the Wilcoxon signed-rank test was utilised. Categorical variables are expressed as numbers (percentages), and intergroup comparisons were conducted using the chi-square test. A p-value of <0.05 was considered statistically significant.

Results

A total of 127 patients with APE were ultimately included in this study. CTPA revealed that 23 patients (18.11%) had SPE. The patients were divided into the SPE group (n = 23) and the non-SPE group (n = 104). There were no significant differences in general clinical characteristics between the two groups (p >0.05; Table I).

Intergroup comparisons revealed no significant differences in NT-proBNP, RVD/LVD, or PPEI between the two groups before and after treatment (p >0.05). However, the cTnI level in the SPE group was higher than that in the non-SPE group (p <0.05; Table II).

Compared with pre-treatment levels, both groups showed significant reductions in cTnI, RVD/LVD, and PPEI after treat-ment (p <0.05). In the SPE group, NT-proBNP showed a decreasing trend post-treatment but without statistical significance (p = 0.139), whereas the non-SPE group demons-trated a significant reduction in NT-proBNP (p <0.05; Table III).

No statistically significant difference was found in in-hospital mortality between the SPE group (2/23, 8.70%) and the non-SPE group (4/104, 3.85%; c² = 0.202, p = 0.653). During the hospitalisation period, 19 patients in the SPE group underwent post-treatment CTPA examinations, of which 18 patients (94.74%) showed complete resolution of their saddle embolism (Figure 2).

Figure 1: A 69-year-old male patient with SPE. (A) Saddle embolism of the pulmonary trunk. (B, C) The maximum RV and LV internal diameters measured perpendicular to the interventricular septum were 56.8 mm and 37.7 mm, respectively, yielding an RV/LV diameter ratio of 1.51.

Figure 2: A 65-year-old female patient with SPE. (A) Saddle embolism visible before treatment. (B, C) The multiplanar technique reveals that the cord-like thrombus evolves into a large thrombus at the distal end of the left and right pulmonary arteries. (D) Nine days after the completion of interventional therapy, the saddle embolism disappeared.

Discussion

There is ongoing controversy regarding whether saddle embolism signifies a higher risk of severity or deterioration in patients with APE. Before the widespread use of CTPA, saddle embolism was predominantly identified through autopsy, and thus traditionally associated with haemodynamic instability and death.⁷ Some studies have suggested that saddle embolism may indicate an unstable clinical condition, thus recommending a more aggressive therapeutic approach.^8,9 However, other studies have indicated that peripheral APE has a more significant impact on haemodynamics compared to central APE, and there is no direct correlation between the location of the thrombus and prognosis; patients with haemodynamically stable SPE respond well to conventional anticoagulant therapy.^10,11 The incidence of SPE in this study was 18.11%, which is generally consistent with previous research findings. For instance, Ibrahim et al. identified 73 cases (16.9%) of SPE among 432 patients with APE.¹² Hajizadeh et al. also identified 70 cases (14.2%) of SPE among 492 consecutive patients with APE.⁵ However, in a large-scale national survey, SPE accounted for only 1.2% of all APE cases.⁹ This discrepancy may partly be attributed to the fact that the present study focused on intermediate- to high-risk patients, whereas the survey included APE patients across all risk stratifications. A study by Enzweiler et al. demonstrated that saddle embolism is an early manifestation of APE, and as the duration of illness increases, the incidence of visible SPE on CTPA gradually decreases because of thrombus fragmentation and detachment from the pulmonary artery bifurcation.¹³ The duration of illness was shorter in the SPE group compared to the non-SPE group, although the difference was not statis-tically significant (p = 0.169).

Due to the retrospective nature of this study, to more accu-rately reflect the patients' conditions, easily accessible indi-cators (NT-proBNP, cTnI, and RVD/LVD) to assess the severity of APE rather than variable and unreliable para-meters such as blood pressure, heart rate, blood oxygen saturation, and respiratory rate. Circulatory failure is a significant factor contributing to the deterioration of APE patients, and the indicators used in this study are all effective predictors of circulatory failure.^14-16 The results of this study showed no significant differences in NT-proBNP levels or RVD/LVD ratios between the SPE and non-SPE groups before or after treatment, suggesting comparable degrees of RV functional impairment in the two groups. This finding is consistent with the results of the study by Isath et al.⁴ This study shows that cTnI levels in the SPE group were higher than those in the non-SPE group both before and after treatment, indicating more severe myocardial injury in the SPE group. This may be related to a more severe degree of embolism, as well as higher pulmonary artery pressure and RV afterload. Consistent with the present results, Hajizadeh et al. found that cTnI levels in the SPE group were significantly higher than those in the non-SPE group (p <0.05).⁵ In the study by Alkinj et al., the positive rate of troponin was higher in the SPE group (p <0.001).¹⁷

It is generally believed that effective treatment can alleviate the elevations in cTnI and NT-proBNP associated with APE.¹⁸ In this study, compared to pre-treatment levels, there was a trend towards a decrease in NT-proBNP in the SPE group after treatment; however, this was not statistically significant (p = 0.139). This finding may be attributable to the small sample size and the wide variability in NT-proBNP levels. Regarding the pre-treatment PPEI results, it was found that both the SPE and non-SPE groups had significant involvement of the peripheral pulmonary arteries, with no significant difference between the two groups. This result may be associated with the inclusion of intermediate- to high-risk patients in this study. Intermediate- to high-risk APE patients often have more extensive pulmonary artery involvement, particularly in the peripheral pulmonary arteries.

The primary innovation of this study lies in its first report of the documentation of dynamic changes in key indicators (cTnI, NT-proBNP, RVD/LVD, and PPEI) before and after inter-ventional therapy combined with anticoagulant treatment in patients with APE, as well as the differences observed bet-ween the SPE and non-SPE groups. This is of significant impor-tance for assessing treatment efficacy and disease status. The findings reveal that, compared to pre-treatment levels, all indicators showed marked improvement post-treatment, demonstrating good consistency. This result robustly reflects the efficacy of the combined interventional and anticoagulant therapy. Specifically, the decrease in cTnI suggests reduced myocardial injury, the decline in NT-proBNP reflects improved cardiac function, and the reduction in RVD/LVD and PPEI indicates alleviation of RV dilation and pulmonary artery obstruction. The concurrent improvement in these indicators signifies a substantial overall improvement in the patients' condition. Notably, the study also found no significant diffe-rence in response to the combined interventional and anti-coagulant therapy between the SPE and non-SPE groups. This result may imply that saddle embolism is not a crucial factor influencing treatment response, or the consistency in treat-ment response could be attributed to similarities between the two groups in other aspects, such as widespread involvement of the peripheral pulmonary arteries.

However, some findings from previous studies are inconsis-tent with those of the present study. Studies by Ibrahim and Alkinj et al. have shown that patients with SPE exhibit significantly greater RV dilatation on echocardiography than those with non-SPE (p <0.001).^12,17 One possible explanation is that assessment of RV dilatation on echocardiography does not fully align with the measurement indices (such as RVD/LVD) obtained from CTPA, which may affect the interpretation of the results. In the study by Isath et al., there was no significant difference in troponin levels bet-ween the SPE and non-SPE groups (p = 0.314).⁴

It remains unclear whether saddle embolism in APE is associated with haemodynamic compromise and affects the clinical outcomes of patients with APE. This study reported no statistically significant difference in in-hospital mortality bet-ween the SPE and non-SPE groups (8.70% vs. 3.85%, p = 0.653), consistent with findings of multiple studies. For instance, a Cox regression analysis revealed that saddle embolism does not necessarily imply a high risk of short-term adverse events in non-high-risk APE patients.¹⁹ Due to the limited number of cases in this study, further research is needed to determine whether saddle embolism affects prognosis. Regarding the mortality rate of patients with SPE, Wong et al. reported a 9.2% in-hospital mortality rate among 120 SPE patients, whereas Hajizadeh et al. reported a significantly higher morta-lity rate of 28.6% among 70 SPE patients.^20,5

Interestingly, the location with the greatest thrombus burden in saddle embolism was often in the distal branches of the left and right pulmonary arteries rather than at the proximal saddle site. When studying saddle embolism, it is important to distinguish it from central APE. A study by Choi et al. demonstrated that central APE, including saddle embolism and bilateral pulmonary artery embolism, rather than isolated saddle embolism, is an independent predictor of adverse prognosis.²¹ In the study by Enzweiler et al., a similar phenomenon of short-term disappearance of saddle embolism was observed.¹³ Follow-up studies with an average interval of 7.5 days showed that saddle embolism disappeared in 8 out of 12 SPE patients (66.7%).¹³

The limitations of this study include the small sample size, retrospective single-centre design, observation limited to the in-hospital period, and potential confounding effects of pre-existing cardiopulmonary diseases.

Conclusion

Patients with SPE may experience more severe myocardial injury. Following effective treatment, the SPE resolved rapidly, suggesting that its presence itself may not be the key factor influencing treatment response. Whether saddle embolism impacts prognosis requires further investigation.

ETHICAL APPROVAL:
This study is a retrospective analysis of clinical charac-teristics and has been approved by the Ethics Committee of The First Hospital of Putian City, Putian, China (Approval No. 2024-156; dated: December 5, 2024).

PATIENTS’ CONSENT:
All treatment protocols were performed with patient/guardian informed consent. As this was a retrospective observational study, patient consent for study participation was waived by the Ethics Committee.

COMPETING INTEREST:
The authors declared no conflict of interest.

AUTHORS’ CONTRIBUTIONS:
QC: Conception, design, data collection, statistical analysis, interpretation of the results, and manuscript writing.
JH: Study design, data collection, and manuscript review.
Both authors approved the final version of the manuscript to be published.

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