Pericardial calcification in tuberculous constrictive pericarditis: a marker of chronicity unassociated with early postoperative outcomes
Original Article

Pericardial calcification in tuberculous constrictive pericarditis: a marker of chronicity unassociated with early postoperative outcomes

Zhengkai Zhao1# ORCID logo, Qiuyi Cai1#, Jing Guo2#, Shuangshuang Yan2, Shuzhen Wang2, Lijuan Zhang2, Li Zhang2, Qiuyu Xiao2, Kunyue Tan2, Feng Xiong2

1Department of Radiology, The Third People’s Hospital of Chengdu, The Affiliated Hospital of Southwest Jiaotong University, Chengdu, China; 2Department of Cardiology, The Third People’s Hospital of Chengdu, The Affiliated Hospital of Southwest Jiaotong University, Chengdu, China

Contributions: (I) Conception and design: Z Zhao, F Xiong; (II) Administrative support: None; (III) Provision of study materials or patients: Z Zhao, J Guo, Q Cai; (IV) Collection and assembly of data: Z Zhao, Q Cai, J Guo, S Yan, S Wang, Lijuan Zhang, Li Zhang, Q Xiao, K Tan; (V) Data analysis and interpretation: Z Zhao, Q Cai; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

#These authors contributed equally to this work as co-first authors.

Correspondence to: Feng Xiong, MD. Department of Cardiology, The Third People’s Hospital of Chengdu, The Affiliated Hospital of Southwest Jiaotong University, No. 82 Qinglong Street, Qingyang District, Chengdu 610031, China. Email: 496884618@qq.com.

Background: Tuberculous constrictive pericarditis (TCP) can progress to a chronic, calcific stage, restricting cardiac function. The role of pericardial calcification, best assessed by cardiac computed tomography (CT), in predicting surgical outcomes is unclear. We aimed to evaluate the association of pericardial calcification with clinical features, cardiac structural/functional alterations, and early postoperative outcomes in TCP patients undergoing pericardiectomy.

Methods: In this retrospective study, 104 consecutive patients with TCP who underwent pericardiectomy were classified into calcification (n=34) and non-calcification (n=70) groups based on preoperative cardiac CT. Clinical data, laboratory results, echocardiographic parameters, and CT imaging variables were compared between groups. The impact of various pericardial calcification indicators on early postoperative adverse outcomes (a composite of low cardiac output syndrome or in-hospital mortality) was analyzed. Multivariate linear regression was performed to identify factors independently associated with the duration of postoperative intensive care unit (ICU) stay.

Results: Patients with pericardial calcification had a longer disease duration, more severe bilateral atrial enlargement, greater dilation of the venae cavae, and a higher peak early diastolic mitral inflow velocity (E), alongside significantly lower C-reactive protein (CRP) levels and less pericardial thickening (all P<0.05). Postoperatively, both groups showed decreases in peak early diastolic mitral annular velocity (e'), ventricular septal bounce incidence, and left atrial (LA) size compared to preoperative values (all P<0.05). There were no significant differences in various pericardial calcification indicators between patients with and without early postoperative adverse outcomes (all P>0.05). Multivariate linear regression analysis identified ejection fraction (EF) (β=−0.278, P=0.004) and the presence of pleural effusion (β=0.205, P=0.037) as independent correlates of postoperative ICU stay, whereas the extent of pericardial calcification [ln(calcium score +1)] (β=−0.062, P=0.558) showed no independent association.

Conclusions: Pericardial calcification in TCP signifies a chronic disease state, characterized by attenuated inflammation but more pronounced cardiac remodeling and diastolic dysfunction. However, it is not associated with an increased risk of early adverse outcomes nor with the duration of postoperative ICU stay after pericardiectomy.

Keywords: Tuberculous constrictive pericarditis (TCP); calcification; computed tomography (CT); echocardiography (ECHO); intensive care unit (ICU)


Submitted Nov 12, 2025. Accepted for publication Mar 09, 2026. Published online Apr 08, 2026.

doi: 10.21037/qims-2025-aw-2402


Introduction

Tuberculous constrictive pericarditis (TCP) is a condition caused by the infection of the pericardium with Mycobacterium tuberculosis. The pathological process involves the deposition of proteins and fibrin after the absorption of pericardial effusion, leading to pericardial thickening, adhesion, and calcification. These changes restrict cardiac diastolic function, ultimately inducing severe heart failure and circulatory disturbances (1). The clinical features of TCP include a slow onset and prolonged course, with low-grade fever, fatigue, and night sweats resulting from chronic infection. It also presents with neck vein distention, hepatomegaly, ascites, lower extremity edema, hypotension, and even debility and dyspnea due to pericardial constriction. However, whether the clinical manifestations of TCP with pericardial calcification are more severe remains unproven. Multimodal imaging, including computed tomography (CT), echocardiography (ECHO), and cardiac magnetic resonance imaging (CMR), is becoming increasingly prevalent in the diagnosis and treatment of TCP (2,3). As a distinctive feature of TCP, pericardial calcification is primarily assessed using CT prior to surgical planning (4,5). The primary changes in cardiac structure and function caused by TCP include pericardial thickening and adhesions, atrial enlargement, diastolic dysfunction, and even the development of arrhythmias and myocardial atrophy. TCP accompanied by pericardial calcification suggests that prolonged diastolic restriction may result in greater damage to cardiac structure and function, although further confirmation is required. Pericardiectomy is the preferred treatment for TCP. However, the impact of pericardial calcification on survival rates after surgery for constrictive pericarditis (CP) remains controversial. Ling et al. (6) proposed that pericardial calcification serves as an independent predictor of unfavorable perioperative outcomes in patients with CP, yet it exerts no influence on long-term survival rates. However, other studies have indicated that pericardial calcification is unable to predict early clinical outcomes in CP (7) and has a negative impact on long-term survival (8). Additionally, there are also research findings suggesting that a low burden of pericardial calcification was associated with a high rate of mid-term clinical events after pericardiectomy to treat CP (9). The impact of pericardial calcification on early postoperative clinical outcomes in CP caused by Mycobacterium tuberculosis infection has not yet been evaluated. Therefore, this study aimed to comprehensively evaluate the association of pericardial calcification with the clinical presentation, cardiac structural and functional alterations, and early postoperative outcomes—including the duration of intensive care unit (ICU) stay—in patients undergoing pericardiectomy for TCP. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-aw-2402/rc).


Methods

Study population

This retrospective study analyzed data from the medical records of patients who underwent pericardiectomy for TCP at our institution between January 2013 and June 2024. Based on the presence or absence of pericardial calcification on preoperative CT images, patients were divided into two groups: the calcification group and the non-calcification group. Inclusion criteria were as follows: (I) definitive evidence of tuberculosis included: acid-fast smear positivity or Mycobacterium tuberculosis culture positivity from sputum/respiratory tract specimens or extrapulmonary specimens, or positive Mycobacterium tuberculosis nucleic acid (DNA/RNA) detection; or characteristic clinical and imaging features combined with a positive tuberculin skin test [purified protein derivative (PPD) test] or positive interferon-gamma release assay (IGRA); (II) preoperative transthoracic ECHO and chest CT confirming pericardial thickening or calcification indicative of pericarditis; (III) intraoperative confirmation of pericardial constriction necessitating pericardiectomy; (IV) pathological examination of the resected pericardium confirmed the presence of characteristic granulomas and caseating necrosis, with acid-fast bacilli identified on Ziehl-Neelsen staining. The exclusion criteria are as follows: (I) absence of preoperative contrast-enhanced cardiac CT scanning; (II) poor quality of CT images. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Institutional Review Board of The Third People’s Hospital of Chengdu (No. 2024-S-361), and the requirement for written informed consent was waived due to the retrospective nature of the study.

Clinical information

Preoperative baseline data included age, gender, body mass index (BMI), disease duration, preoperative heart rate, presence of comorbidities such as atrial fibrillation, hypertension, and diabetes, as well as the preoperative New York Heart Association (NYHA) functional classification for patients with TCP. Laboratory test indicators encompassed white blood cell count (WBC), C-reactive protein (CRP), serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total protein (TP), albumin (ALB), prealbumin (PA), and cholinesterase (CHE). Data collected from surgery to discharge included the incidence of postoperative low cardiac output syndrome (LCOS), ICU and total hospital length of stay, and in-hospital mortality. LCOS was defined by a cardiac index (CI) of less than 2.2 L/min/m2. The criteria for ICU discharge were as follows: acute organ or system failure had been essentially corrected, vital signs were relatively stable, and the patient was conscious. All pericardial stripping procedures were performed via sternotomy. Early postoperative adverse outcomes were defined as the occurrence of at least one of the following: LCOS after surgery or in-hospital mortality.

Ultrasound image acquisition and protocols

Echocardiographic examinations were conducted using ultrasound equipment (Siemens, Forchheim, Germany; Philips, Amsterdam, The Netherlands; and GE, Chicago, IL, USA) on two occasions: once within the week prior to pericardial decortication surgery, and again between 3 to 7 days after the surgery, once the patient was hemodynamically stable. Left atrial diameter (LAD), left ventricular end-diastolic diameter (LVEDD), and right ventricular diameter (RVD) were obtained from the parasternal long-axis view, while the right atrial transverse diameter (RAD) and early diastolic peak flow velocity of the mitral valve (E) were acquired from the apical four-chamber view. Tissue Doppler imaging was utilized to measure the early diastolic peak velocity of the mitral annulus (e'), and the E/e' ratio was calculated. The left ventricular ejection fraction (LVEF) was determined using the Simpson’s method. The severity of tricuspid and mitral regurgitation was graded based on the regurgitant area: <2 cm2 as minimal, 2-4 cm2 as mild, 4-8 cm2 as moderate, and >8 cm2 as severe.

CT image acquisition and evaluation of pericardial calcification

Prior to pericardial stripping, all patients underwent retrospective electrocardiogram gated cardiac CT enhanced scan using CT scanners (Siemens and Philips) with breath-holding after deep inspiration. The CT images were reconstructed with a slice thickness of 1.5 mm and analyzed on a picture archiving and communication system (PACS) workstation. The pericardial calcification score and volume were calculated using the Agatston score with commercial software (Terarecon Intuition). Due to the large values and skewed distribution of the calcification scores, the natural logarithm (ln) of the calcification score plus one [ln(calcium score +1)] was used to mitigate the influence of extreme values.

CT image analysis

For the measurement of the left ventricular apical angle, multiplanar reconstruction (MPR) was employed to obtain a four-chamber heart view from the retrospectively gated contrast-enhanced CT images at end-diastole. The distance from the apical vertex to the midpoint of the line connecting the mitral annulus was measured as the longitudinal long-axis diameter (Ld) at end-diastole. The Ld was divided into three equal parts by two short axes (D1, D2) perpendicular to Ld. The angle between the line connecting the apical vertex and the intersections of D1 with the left ventricular myocardium was measured as the end-diastolic left ventricular apical angle (Figure 1A). The same method was applied to measure the end-systolic left ventricular apical angle. The perpendicular distance from the midpoint of the apical long-axis diameter to the intersection of the left ventricular myocardium was measured as the end-diastolic apical diameter (Dap), and the apical sphericity index was calculated as Dap/(Ld/3) (Figure 1B). The thickness of the pericardium was measured at its thickest point around the left and right ventricles, apex, anterior interventricular grooves, left and right atria, superior and inferior vena cava, and right ventricular outflow tract. All measurements were performed by the same experienced CT diagnostician and averaged over three repetitions. Thirty cases were randomly selected, and another CT diagnostician, blinded to the study, measured the apical sphericity index on CT images to analyze inter-observer variability. The inter-observer correlation coefficient was 0.89 (P<0.01), indicating good agreement. Pericardial crescent sign is defined as local thickening of the visceral and parietal layers of the pericardium, with a low-density, incompletely absorbed pericardial effusion in between, resembling a crescent-shaped change on imaging.

Figure 1 Measurement of variables in enhanced cardiac CT imaging. (A) The angle between the line connecting the apex of the heart and the intersections of D1 with the left ventricular myocardium is measured as the left ventricular apical angle at end-diastole. (B) The apical sphericity index is calculated as Dap divided by (Ld/3). CT, computed tomography; Dap, end-diastolic apical diameter; Ld, longitudinal long-axis diameter.

Statistical analysis

Statistical analysis was performed using SPSS 21.0 software, with P<0.05 considered statistically significant. Continuous variables are expressed as mean ± standard deviation. For normally distributed continuous variables, comparisons between groups were conducted using independent sample t-tests or paired sample t-tests; for non-normally distributed variables, Mann-Whitney U tests were employed. Categorical variables are presented as frequencies (%) and compared using Chi-squared (χ2) tests. The correlation between postoperative ICU stay and continuous variables was analyzed using Pearson or Spearman statistics, while the point-biserial correlation was used for binary variables. Based on clinical experience, relevant variables including age, NYHA class 3 or 4, disease duration, and variables showing significant correlations were included in a subsequent multivariate linear regression analysis to identify independent factors influencing postoperative ICU stay. An interaction test was then performed on the identified independent factors affecting postoperative ICU stay.


Results

Patient characteristics

This study included 104 consecutive patients undergoing pericardiectomy. Baseline clinical characteristics of the pericardial calcification group (n=34) and the non-calcification group (n=70) among 104 consecutive patients are summarized in Table 1. Compared to the non-calcification group, the calcification group had a longer disease duration, a higher incidence of atrial fibrillation, and higher levels of ALB and CHE, with statistically significant differences (P<0.05). The CRP level was significantly higher in the non-calcification group than in the calcification group (P<0.05).

Table 1

Comparison of baseline clinical characteristics between the two groups

Variable Calcification group (N=34) Non-calcification group (N=70) t/Z/χ2 P value
Age (years) 48.09±16.07 44.52±19.84 −0.83 0.40
Male 22 (64.7) 48 (68.5) 0.15 0.69
BMI (kg/m2) 23.89±3.59 22.30±3.18 −1.92 0.06
Heart rate (beats/min) 80.33±21.21 87.44±12.74 0.99 0.32
Disease duration (months) 31.17±49.42 8.62±16.13 2.59 0.01
Atrial fibrillation 12 (35.3) 0 27.92 <0.01
Hypertension 2 (5.9) 8 (11.4) 2.46 0.11
Diabetes 2 (5.9) 4 (5.7) 0.27 0.59
NYHA 3 or 4 22 (64.7) 33 (47.1) 2.83 0.09
WBC (103/μL) 5.98±2.25 5.71±2.35 −0.44 0.65
CRP (mg/dL) 7.35±18.19 21±27.21 2.17 0.01
ALT (IU/L) 26.55±27.09 20.17±15.59 −1.32 0.18
AST (IU/L) 32.95±23.77 27.43±12.61 −0.99 0.32
TP (g/L) 63.18±10.28 60.03±9.45 −1.27 0.20
ALB (g/L) 35±6.94 32±5.09 3.16 0.01
PA (mg/L) 200±103.86 156±68.78 1.72 0.08
CHE (IU/L) 6,893±2,040.31 4,943±1,922.42 2.94 <0.01

Data are presented as mean ± standard deviation or number (%). ALB, albumin; ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; CHE, cholinesterase; CRP, C-reactive protein; NYHA, New York Heart Association; PA, prealbumin; TP, total protein; WBC, white blood cell count.

Comparison of enhanced cardiac CT imaging variables

Preoperative CT indicators for both groups are compared in Table 2. The calcification group exhibited wider superior and inferior venae cavae compared to the non-calcification group, while the non-calcification group had a significantly higher incidence of pericardial effusion, with statistically significant differences (P<0.05). The pericardial thickness at various locations was lower in the calcification group than in the non-calcification group (P<0.05). A typical image of TCP with calcified constrictive rings is shown in Figure 2.

Table 2

Comparison of preoperative CT indicators between the two groups

Variable Calcification group (N=34) Non-calcification group (N=70) t/Z/χ2 P value
End-diastolic left ventricular apical angle (°) 60.60±8.48 61.88±11.80 −0.27 0.78
End-systolic left ventricular apical angle (°) 52.00±12.97 54.44±10.78 −0.44 0.66
Apical sphericity index (%) 78.17±28.46 79.02±20.37 −0.15 0.87
Pericardial crescent sign 8 (23.5) 16 (22.8) 0.01 0.93
Superior vena cava (mm) 32.47±6.79 24.90±4.32 5.93 <0.01
Inferior vena cava (mm) 42.70±9.15 36.12±5.45 3.86 <0.01
Pericardial effusion 8 (23.5) 52 (74.3) 24.15 <0.01
Pleural effusion 21 (61.7) 55 (78.5) 3.28 0.06
Ascites 12 (35.3) 39 (55.7) 3.81 0.05
Pericardial thickness (mm)
   Left ventricle 7.55±3.90 11.11±6.62 −3.43 <0.01
   Right ventricle 8.08±5.51 11.17±6.14 −2.48 0.01
   Apex of heart 1.94±1.20 5.58±5.32 −5.45 <0.01
   Anterior interventricular groove 4.52±4.52 7.47±5.89 −2.70 0.01
   Left atrial 2.91±2.78 4.62±3.60 −2.44 0.02
   Right atrium 4.35±3.25 9.07±5.58 −5.42 <0.01
   Superior vena cava 1.79±1.38 3.65±3.19 −4.14 <0.01
   Inferior vena cava 2.67±2.01 5.47±4.55 −4.33 <0.01
   Right ventricular outflow tract 4.58±3.19 6.64±4.01 −2.60 0.01

Data are presented as mean ± standard deviation or number (%). CT, computed tomography.

Figure 2 Enhanced cardiac CT scan of a 30-year-old female with TCP. (A) The four-chamber view shows compressed and deformed ventricles. (B) The short-axis view of the ventricles reveals a constrictive ring of pericardial calcification surrounding the heart, with thickening of the right ventricular wall and intramyocardial calcification visible (arrow). (C) The view of the right atrium and right ventricle shows the compression of the right ventricle by pericardial calcification (arrows). (D-F) A three-dimensional image provides a comprehensive visualization of the constrictive ring of pericardial calcification (arrows). CT, computed tomography; TCP, tuberculous constrictive pericarditis.

Comparison of echocardiographic variables

Preoperative and postoperative echocardiographic indicators for both groups are compared in Table 3, and intra-group comparisons of preoperative and postoperative echocardiographic indicators are presented in Table 4. In both preoperative and postoperative assessments, the calcification group had larger left and right atrial dimensions and higher peak early diastolic mitral inflow velocity (E) than the non-calcification group (P<0.05). The calcification group also had a higher incidence of ventricular septal bounce preoperatively, with statistically significant differences (P<0.05). Postoperatively, the calcification group showed reductions in left atrial (LA) dimension, peak early diastolic mitral annular velocity (e'), and ventricular septal bounce compared to preoperative values, all with statistically significant differences (P<0.05). The non-calcification group also experienced reductions in both atrial dimensions, e', and ventricular septal bounce postoperatively, but an increase in E compared to preoperative values, all with statistically significant differences (P<0.05). The E/e' ratio increased postoperatively in both groups, with statistically significant differences (P<0.05).

Table 3

Comparison of preoperative and postoperative echocardiographic indicators between the two groups

Variable Preoperative Postoperative
Calcification group (N=34) Non-calcification group (N=70) t/Z/χ2 P value Calcification group (N=34) Non-calcification group (N=70) t/Z/χ2 P value
LAD (mm) 45.25±7.86 38.26±5.15 −3.78 <0.01 40.90±5.83 36.09±5.83 −2.93 <0.01
LVEDD (mm) 42.85±6.08 41.30±3.99 1.32 0.18 43.25±4.21 41.92±3.84 1.31 0.19
RAD (mm) 42.33±6.90 39.04±5.22 2.68 <0.01 41.71±7.41 37.46±4.63 2.97 <0.01
RVD (mm) 20.60±4.17 19.60±2.44 1.01 0.31 21.05±2.89 19.95±2.41 1.68 0.09
EF (%) 58.60±6.15 57.80±6.74 0.47 0.63 60.15±5.00 59.50±7.60 0.35 0.72
E (cm/s) 88.53±20.57 67.44±21.00 4.78 <0.01 85.37±16.05 76.49±24.80 −2.46 0.01
e' (cm/s) 10.80±3.63 10.93±4.29 −0.13 0.89 8.55±2.83 8.75±3.06 −0.27 0.78
E/e' ratio 8.52±2.65 7.58±5.21 0.77 0.43 11.13±3.97 10.01±5.42 0.84 0.39
Ventricular septal bounce 33 (97.1) 57 (81.2) 4.79 0.03 3 (8.8) 5 (7.1) 0.09 0.76
Mitral regurgitation 15 (46.8) 18 (33.3) 1.55 0.21 12 (37.5) 12 (21.8) 2.49 0.11
Tricuspid regurgitation 16 (50) 31 (56.4) 0.44 0.50 14 (43.7) 28 (50.9) 0.41 0.51

Data are presented as mean ± standard deviation or number (%). E, early diastolic peak flow velocity of the mitral valve; e', early diastolic peak velocity of the mitral annulus; EF, ejection fraction; LAD, left atrial diameter; LVEDD, left ventricular end-diastolic diameter; RAD, right atrial transverse diameter; RVD, right ventricular diameter.

Table 4

Comparison of preoperative and postoperative echocardiographic indicators within each group

Variable Calcification group (N=34) Non-calcification group (N=70)
Preoperative Postoperative t/Z/χ2 P value Preoperative Postoperative t/Z/χ2 P value
LAD (mm) 45.25±7.86 40.90±5.83 2.75 0.01 38.26±5.15 36.09±5.83 3.72 <0.01
LVEDD (mm) 42.85±6.08 43.25±4.21 −0.42 0.67 41.30±3.99 41.92±3.84 −0.85 0.39
RAD (mm) 42.33±6.90 41.71±7.41 0.70 0.49 39.04±5.22 37.46±4.63 2.39 0.02
RVD (mm) 20.60±4.17 21.05±2.89 −0.77 0.44 19.60±2.44 19.95±2.41 −0.81 0.41
EF (%) 58.60±6.15 60.15±5.00 −1.19 0.24 57.80±6.74 59.50±7.60 −1.55 0.10
E (cm/s) 88.53±20.57 85.37±16.05 0.84 0.40 67.44±21.00 76.49±24.80 −3.51 <0.01
e' (cm/s) 11.80±3.63 8.55±2.83 2.84 0.01 10.93±4.29 8.75±3.06 4.58 <0.01
E/e' ratio 8.52±2.65 11.13±3.97 −2.71 0.01 7.58±5.21 10.01±5.42 −4.70 <0.01
Ventricular septal bounce 33 (97.1) 3 (8.8) 19.08 <0.01 57 (81.4) 5 (7.1) 10.2 <0.01
Mitral regurgitation 15 (46.8) 12 (37.5) 0.02 0.88 18 (32.7) 12 (21.8) 1.64 0.25
Tricuspid regurgitation 16 (50) 14 (43.7) 0.50 0.47 31 (56.4) 28 (50.9) 0.18 0.67

Data are presented as mean ± standard deviation or number (%). E, early diastolic peak flow velocity of the mitral valve; e', early diastolic peak velocity of the mitral annulus; EF, ejection fraction; LAD, left atrial diameter; LVEDD, left ventricular end-diastolic diameter; RAD, right atrial transverse diameter; RVD, right ventricular diameter.

Calcification and clinical indicators, early postoperative adverse outcomes

There were no statistically significant differences (P>0.05) in various perioperative clinical indicators between the pericardial calcification and non-calcification groups, as shown in Table 5. The mean ICU stay was 3.48±2.50 days, and the total hospital stay was 23.73±8.54 days for the 104 patients, with an in-hospital mortality rate of 3.8% (4 of 104 patients). Table 6 shows no statistically significant differences (P>0.05) in the pericardial calcification, calcification volume, or the ln(calcium score +1) between patients with and without early postoperative adverse outcomes.

Table 5

Comparison of clinical indicators between the two groups

Variable Calcification group (N=34) Non-calcification group (N=70) t/Z/χ2 P value
Postoperative low cardiac output syndrome 3 (8.8) 12 (17.1) 1.28 0.25
Postoperative ICU stay (days) 3.24±2.34 3.60±2.59 0.69 0.49
Total length of hospital stay (days) 24.32±7.36 23.44±9.10 −0.49 0.62
In-hospital death 1 (2.9) 3 (4.3) 0.11 0.73

Data are presented as mean ± standard deviation or number (%). ICU, intensive care unit.

Table 6

Comparison of calcification indicators between patients with and without early postoperative adverse outcomes

Variable Early postoperative adverse outcomes t/Z/χ2 P value
Yes (N=15) No (N=89)
Pericardial calcification 3 (20.0) 31 (34.8) 1.28 0.25
Calcification volume (mm2) 8,648.90±14,232.71 12,611.13±14,143.06 −0.55 0.57
Ln(calcium score +1) 7.06±3.15 8.45±2.49 0.09 0.76

Data are presented as mean ± standard deviation or number (%). Ln(calcium score +1), natural logarithm (ln) of the calcification score plus one.

Factors associated with postoperative ICU stay

Correlation analysis revealed that postoperative ICU stay was significantly correlated with ejection fraction (EF) (r=−0.24, P=0.02), ln(calcium score +1) (r=−0.51, P=0.01), and pleural effusion (r=0.25, P=0.01) (Table 7). Multivariate linear regression analysis further identified EF (β=−0.278, P=0.004) and pleural effusion (β=0.205, P=0.037) as independent and significant correlates of postoperative ICU stay (Table 7). The interaction test results indicated that there was no multiplicative interaction between EF and pleural effusion on postoperative ICU stay (F=0.261, P>0.05).

Table 7

Correlation analysis and multivariate linear regression analysis of postoperative ICU stay

Variable Correlation analysis Multivariate analysis
Number of patients r value P value B β P value
Age 104 −0.06 0.50 −0.004 −0.029 0.766
Disease duration 104 −0.05 0.62 −0.006 0.001 0.999
NYHA 3 or 4 104 0.09 0.38 0.590 0.118 0.226
Atrial fibrillation 104 −0.07 0.48
CRP 104 0.11 0.26
EF 104 −0.24 0.02 −0.108 −0.278 0.004
E 104 −0.01 0.97
e' 104 0.10 0.32
E/e' 104 −0.13 0.20
Ventricular septal bounce 104 0.06 0.51
Tricuspid regurgitation 86 0.04 0.72
Pericardial calcification 104 −0.07 0.49
Calcification volume 104 −0.25 0.19
Ln(calcium score +1) 104 −0.51 0.01 −0.040 −0.062 0.558
Apical sphericity index 104 0.10 0.28
Pericardial crescent sign 104 −0.05 0.61
Pericardial effusion 104 0.08 0.42
Pleural effusion 104 0.25 0.01 1.154 0.205 0.037
Ascites 104 0.17 0.09

CRP, C-reactive protein; E, early diastolic peak flow velocity of the mitral valve; e', early diastolic peak velocity of the mitral annulus; EF, ejection fraction; ln(calcium score +1), natural logarithm (ln) of the calcification score plus one; ICU, intensive care unit; NYHA, New York Heart Association.


Discussion

Our study delineates a distinct clinical phenotype for TCP with pericardial calcification, characterized by a more protracted disease course and more severe diastolic dysfunction, yet paradoxically attenuated systemic inflammation and pericardial thickening compared to non-calcific TCP. Following pericardiectomy, both phenotypes showed improvements in atrial dimensions and diastolic functions. Notably, pericardial calcification was not significantly associated with early postoperative adverse outcomes or with the duration of ICU stay. This finding reinforces the concept that calcification per se, while indicative of chronicity and advanced remodeling, does not independently portend a more complicated early postoperative course.

The natural history of tuberculous pericarditis initially involves a strong hypersensitivity reaction of the pericardial tissue to tuberculin protein, leading to inflammatory exudation (10). As it progresses to the subacute phase, the pericardial mesothelium is disrupted, with granulation tissue proliferation and potential formation of tuberculous nodules, and in severe cases, caseous necrosis may occur. In the chronic phase, pericardial fibrosis and calcification are the primary features (11). Cardiac CT can accurately assess the presence and distribution of pericardial calcification, providing crucial information for the diagnosis of TCP and preoperative planning for pericardiectomy (5). Our study results suggest that TCP with pericardial calcification has a prolonged course, reduced pericardial thickening, and milder inflammatory reactions, indicating a chronic phase. TCP without pericardial calcification shows marked pericardial thickening, a higher incidence of pericardial effusion, and more severe inflammatory reactions, suggesting an acute or subacute inflammatory phase. In our study, all cases of atrial fibrillation were confined to the calcification group. This may be attributed to long-standing restricted cardiac filling promoting myocardial atrophy and interstitial fibrosis, which in turn can disrupt atrial electrophysiology and precipitate atrial fibrillation.

ECHO has been widely used to assess cardiac function and hemodynamics in TCP (12). The two mechanisms of TCP are: pericardial thickening, which may be accompanied by calcification, leading to impaired diastolic cardiac filling; or significant fluid accumulation within the pericardial space, compressing the ventricles throughout the cardiac cycle and hindering cardiac filling and contraction (11). Both groups in our study exhibited pericardial thickening, with some accompanying pericardial effusion, compressing the ventricles and resulting in restricted diastolic function, manifesting as bilateral atrial enlargement and widened inferior vena cava, indicating diastolic dysfunction in both groups. Preoperatively, the calcified group had greater atrial and vena cava widths than the non-calcified group, suggesting more pronounced ventricular compression and severer diastolic dysfunction in the calcified group. Postoperatively, with the relief of compression from thickened and constricted pericardium, both groups experienced a reduction in atrial enlargement. The decreased early diastolic peak velocity of the mitral annulus (e') after surgery indicates a reduction in left ventricular end-diastolic pressure, a smaller atrioventricular pressure gradient, increased left ventricular blood flow filling, improved restricted cardiac filling, and some recovery of left ventricular diastolic function. Kumar et al. (13) also reported a decrease in postoperative inferior vena cava width, LA size, and medial mitral annulus velocity (e') compared to preoperative values. Our study results showed a significant reduction in the incidence of ventricular septal bounce after surgery compared to before. Welch et al. (14) demonstrated that ventricular septal bounce reflects the dissociation between intrapleural and intracardiac pressures and the interventricular dependence within a fixed space; this sign is a characteristic manifestation of TCP in echocardiographic diagnosis. The EF in TCP is generally normal, with the primary hemodynamic abnormality being the loss of pericardial compliance, which leads the heart to rely on elevated ventricular pressure to maintain its filling state and ensure adequate blood output.

Pericardiectomy is the preferred treatment for TCP, but the surgical mortality rate can reach 2.3–12% (15). A meta-analysis showed (16) that the average ICU stay after TCP pericardiectomy was 1.93±3.26 days, with an average in-hospital mortality rate of 7%; notably, mortality associated with pericardiectomy has gradually declined over the past few decades (17-19). In this study, the postoperative ICU stay was 3.48±2.50 days, and the in-hospital mortality rate was 3.8%. Studies have indicated that poor preoperative NYHA functional class and high preoperative central venous pressure are risk factors for postoperative complications in TCP, and postoperative complications are risk factors for prolonged ICU stays (20). Acharya et al. (21) demonstrated that low preoperative EF, atrial fibrillation, and poor NYHA functional class lead to medium-term adverse outcomes after pericardiectomy for TCP. Jung et al. (22) reported that tuberculous pericarditis patients with low serum ALB, large pericardial effusion, and absence of cardiovascular disease have a higher risk of medium-term adverse outcomes. Bozbuga et al. (23) found that advanced age, atrial fibrillation, concurrent tricuspid insufficiency, and low cardiac output are significant negative predictors of long-term survival in TCP. In our study, the quantitative extent of pericardial calcification was not an independent predictor of postoperative ICU stay, nor was it associated with early postoperative adverse outcomes. This may align with the interpretation that pericardial calcification represents a stabilized, chronic phase of the disease. The inflammatory activity is low, and the pathological process may have reached a plateau. During surgery, although calcified plaques can be technically challenging, they often present with clearer dissection planes compared to the edematous and adherent tissues in acute inflammation, potentially allowing for a more definitive pericardiectomy. Consequently, the anticipated technical difficulty of calcification does not necessarily translate into worse early hemodynamics or prolonged intensive care need, provided the surgery is performed thoroughly. The identification of independent predictors such as lower EF and pleural effusion underscores that early recovery is influenced more by the patient’s baseline cardiac function and systemic comorbidities than by the mere presence or extent of pericardial calcification.

Study limitations

The retrospective single-center design with n=34 in the calcification group limits power for subgroups and likely introduces selection bias (only surgical cases). The postoperative follow-up period was short, and the study only investigated the impact of pericardial calcification on early postoperative cardiac structure and function, as well as its correlation with early adverse outcomes and postoperative ICU stay. Future research will be expanded to a multi-center prospective design with long-term follow-up.


Conclusions

In conclusion, pericardial calcification in TCP signifies a chronic disease state, characterized by attenuated inflammation but more pronounced cardiac remodeling and diastolic dysfunction. It is not associated with an increased risk of early adverse outcomes after pericardiectomy, nor does its quantitative extent independently predict the duration of postoperative ICU stay. These findings suggest that while pericardial calcification is a robust imaging marker of disease chronicity, it does not appear to be a decisive factor for early postoperative prognosis. Perioperative risk stratification should instead incorporate factors such as left ventricular EF and the presence of pleural effusion.


Acknowledgments

None.


Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-aw-2402/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-aw-2402/dss

Funding: This work was supported by Sichuan Natural Science Foundation (No. 24NSFC0262).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-aw-2402/coif). All authors declared that this study was supported by Sichuan Natural Science Foundation (No. 24NSFC0262). The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Institutional Review Board of The Third People’s Hospital of Chengdu (No. 2024-S-361), and the requirement for written informed consent was waived due to the retrospective nature of the study.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.


References

  1. Klein AL, Abbara S, Agler DA, Appleton CP, Asher CR, Hoit B, Hung J, Garcia MJ, Kronzon I, Oh JK, Rodriguez ER, Schaff HV, Schoenhagen P, Tan CD, White RD. American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease: endorsed by the Society for Cardiovascular Magnetic Resonance and Society of Cardiovascular Computed Tomography. J Am Soc Echocardiogr 2013;26:965-1012.e15. [Crossref] [PubMed]
  2. Welch TD. Constrictive pericarditis: diagnosis, management and clinical outcomes. Heart 2018;104:725-31. [Crossref] [PubMed]
  3. Miranda WR, Oh JK. Constrictive Pericarditis: A Practical Clinical Approach. Prog Cardiovasc Dis 2017;59:369-79. [Crossref] [PubMed]
  4. Suh SY, Rha SW, Kim JW, Park CG, Seo HS, Oh DJ, Ro YM. The usefulness of three-dimensional multidetector computed tomography to delineate pericardial calcification in constrictive pericarditis. Int J Cardiol 2006;113:414-6. [Crossref] [PubMed]
  5. Conte E, Agalbato C, Melotti E, Marchetti D, Schillaci M, Ratti A, Ippolito S, Pancrazi M, Perone F, Dalla Cia A, Pepi M, Pontone G, Imazio M, Brucato A, Chetrit M, Klein A, Andreini D. The Contemporary Role of Cardiac Computed Tomography and Cardiac Magnetic Resonance Imaging in the Diagnosis and Management of Pericardial Diseases. Can J Cardiol 2023;39:1111-20. [Crossref] [PubMed]
  6. Ling LH, Oh JK, Breen JF, Schaff HV, Danielson GK, Mahoney DW, Seward JB, Tajik AJ. Calcific constrictive pericarditis: is it still with us? Ann Intern Med 2000;132:444-50. [Crossref] [PubMed]
  7. Senapati A, Isma'eel HA, Kumar A, Ayache A, Ala CK, Phelan D, Schoenhagen P, Johnston D, Klein AL. Disparity in spatial distribution of pericardial calcifications in constrictive pericarditis. Open Heart 2018;5:e000835. [Crossref] [PubMed]
  8. Chowdhury UK, Subramaniam GK, Kumar AS, Airan B, Singh R, Talwar S, Seth S, Mishra PK, Pradeep KK, Sathia S, Venugopal P. Pericardiectomy for constrictive pericarditis: a clinical, echocardiographic, and hemodynamic evaluation of two surgical techniques. Ann Thorac Surg 2006;81:522-9. [Crossref] [PubMed]
  9. Lee YH, Kim SM, Kim EK, Park SJ, Lee SC, Park SW, Jeong DS, Chang SA. Pattern of pericardial calcification determines mid-term postoperative outcomes after pericardiectomy in chronic constrictive pericarditis. Int J Cardiol 2023;387:131133. [Crossref] [PubMed]
  10. Ntsekhe M, Matthews K, Syed FF, Deffur A, Badri M, Commerford PJ, Gersh BJ, Wilkinson KA, Wilkinson RJ, Mayosi BM. Prevalence, hemodynamics, and cytokine profile of effusive-constrictive pericarditis in patients with tuberculous pericardial effusion. PLoS One 2013;8:e77532. [Crossref] [PubMed]
  11. Isiguzo G, Du Bruyn E, Howlett P, Ntsekhe M. Diagnosis and Management of Tuberculous Pericarditis: What Is New? Curr Cardiol Rep 2020;22:2. [Crossref] [PubMed]
  12. Kim MS, Chang SA, Kim EK, Choi JO, Park SJ, Lee SC, Park SW, Oh JK. The Clinical Course of Tuberculous Pericarditis in Immunocompetent Hosts Based on Serial Echocardiography. Korean Circ J 2020;50:599-609. [Crossref] [PubMed]
  13. Kumar M, Padhy A, Munjal R, Gupta A. Short term clinical and echocardiography outcomes of pericardiectomy in constrictive pericarditis. J Cardiovasc Thorac Res 2021;13:169-73. [Crossref] [PubMed]
  14. Welch TD, Ling LH, Espinosa RE, Anavekar NS, Wiste HJ, Lahr BD, Schaff HV, Oh JK. Echocardiographic diagnosis of constrictive pericarditis: Mayo Clinic criteria. Circ Cardiovasc Imaging 2014;7:526-34. [Crossref] [PubMed]
  15. Dybowska M, Błasińska K, Gątarek J, Klatt M, Augustynowicz-Kopeć E, Tomkowski W, Szturmowicz M. Tuberculous Pericarditis-Own Experiences and Recent Recommendations. Diagnostics (Basel) 2022;12:619. [Crossref] [PubMed]
  16. Yadav S, Shah S, Iqbal Z, Alharbi MG, Kalra HS, Suri M, Soni N, Okpaleke N, Hamid P. Pericardiectomy for Constrictive Tuberculous Pericarditis: A Systematic Review and Meta-analysis on the Etiology, Patients' Characteristics, and the Outcomes. Cureus 2021;13:e18252. [Crossref] [PubMed]
  17. Pessinaba S, Sonhaye L, Agbétiafa M, Wossinu Quacoe M, Aloumon M, Yayehd K, Amadou L, d'Alméida R, Damorou F. La péricardite chronique constrictive, une véritable gangue calcifiée réalisant un goulot d’étranglement médio-ventriculaire : à propos d’un cas Ann Cardiol Angeiol (Paris) 2019;68:125-8. [The chronic constrictive pericarditis, a real calcified gangue realizing a mid-ventricular bottleneck: A case report].
  18. Djafarou Boubacar R, Mohamed Aden F, Ekhya Amoumoune F, Diallo TH, Faraj R, Baba OEM, El Khadir L, Atteyeh M, Tahirou Oumarou H, Sow S, Mouine N, Asfalou I, Moutakiallah Y, Benyass A. Severe calcification in chronic constrictive pericarditis of tuberculous-related a case report and literature review. Radiol Case Rep 2024;19:5882-7. [Crossref] [PubMed]
  19. Syed FF, Mayosi BM. A modern approach to tuberculous pericarditis. Prog Cardiovasc Dis 2007;50:218-36. [Crossref] [PubMed]
  20. Fang L, Yu G, Huang J, Zhao W, Ye B. Predictors of postoperative complication and prolonged intensive care unit stay after complete pericardiectomy in tuberculous constrictive pericarditis. J Cardiothorac Surg 2020;15:148. [Crossref] [PubMed]
  21. Acharya A, Koirala R, Rajbhandari N, Sharma J, Rajbanshi B. Anterior Pericardiectomy for Postinfective Constrictive Pericarditis: Intermediate-Term Outcomes. Ann Thorac Surg 2018;106:1178-81. [Crossref] [PubMed]
  22. Jung IY, Song YG, Choi JY, Kim MH, Jeong WY, Oh DH, Kim YC, Song JE, Kim EJ, Lee JU, Jeong SJ, Ku NS, Kim JM. Predictive factors for unfavorable outcomes of tuberculous pericarditis in human immunodeficiency virus-uninfected patients in an intermediate tuberculosis burden country. BMC Infect Dis 2016;16:719. [Crossref] [PubMed]
  23. Bozbuga N, Erentug V, Eren E, Erdogan HB, Kirali K, Antal A, Akinci E, Yakut C. Pericardiectomy for chronic constrictive tuberculous pericarditis: risks and predictors of survival. Tex Heart Inst J 2003;30:180-5.
Cite this article as: Zhao Z, Cai Q, Guo J, Yan S, Wang S, Zhang L, Zhang L, Xiao Q, Tan K, Xiong F. Pericardial calcification in tuberculous constrictive pericarditis: a marker of chronicity unassociated with early postoperative outcomes. Quant Imaging Med Surg 2026;16(5):396. doi: 10.21037/qims-2025-aw-2402

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