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Chapter 21
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Short- andLong-Term Results
21.1 Part 1
21.2 Perioperative Mortality andLow Cardiac Output
Syndrome, Long-Term Survival Following
Pericardiectomy intheCurrent Era
Despite advancement in cardiac surgery, pericardiectomy is still associated with
widely ranging adverse outcomes, with perioperative mortality ranging from 5.6 to
11% [1, 2, 6, 7, 16–23, 36, 40, 59, 60, 63, 64, 83–85, 93, 107]. Analysis of the pub-
lished literature substantiates advanced NewYork Heart Association presentation,
preoperative chronic obstructive airway disease, hyperbilirubinemia, renal failure,
previous cardiac surgery, and requirement of cardiopulmonary bypass as predictors
of worse outcomes [1, 2, 6, 7, 16–23, 36, 40, 59, 60, 63, 64, 83–85, 93, 107].
The published literature documents 24–28% incidence of low cardiac output
syndrome following pericardiectomy, and another 24–28% mortality secondary to
low cardiac output syndrome following pericardiectomy [1, 2, 6, 7, 16–22, 24, 26,
27, 36, 40, 59, 60, 63, 64, 83–85, 93, 107].
Perioperative mortality appears to be closely related to delayed presentation at
operation, hepatorenal dysfunction and post operative low cardiac output syndrome.
It has been observed that, regardless of the extent of pericardial resection or surgical
technique, a subset of patients with constrictive pericarditis will develop low output
syndrome in the post operative period [16, 36, 63, 64, 86].
Various factors implicated in low output syndrome following pericardiectomy
are incomplete or ineffective decortication, myocardial involvement by the same
pathology, myocardial atrophy due to prolonged inmobilisation, ventricular
Ltd. 2023
U. K. Chowdhury, L. K. Sankhyan, Surgical Treatment of Chronic Constrictive
Pericarditis, https://doi.org/10.1007/978-981-99-5808-5_21
355© The Author(s), under exclusive license to Springer Nature Singapore Pte
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21 Short- andLong-Term Results
remodelling, and abnormal diastolic lling, worsening tricuspid regurgitation, post
operative mitral regurgitation due to papillary muscle elongation [14, 16, 37, 41,
59–61, 63, 64, 73, 86].
Severe low cardiac output state is commonly seen in patients presenting late for
surgical intervention. Morphometric and morphological analysis of surgical biopsies from the left ventricle of patients suffering from constrictive pericarditis have
shown oedematous bres containing abnormal nuclei, sarcoplasmic organelles and
myobrillar dissolution (type B bres) suggestive of myocardial ischemia [42, 43,
78, 79]. Additionally, in constrictive pericarditis, prolonged cardiac compression is
thought to predispose the heart to disuse atrophy. Thus, in constrictive pericarditis,
myocardial ischemia and disuse atrophy may both be the etiologic factors of myocardial dysfunction and it is indeed difcult to ascertain the degree of pericardial
constriction and myocardial restriction [37, 42–44, 63, 65, 78, 86].
Therefore, based on the available evidence in the literature, pericardiectomy
should be considered early, before a patient develops NewYork Heart Association
class III symptoms, patients with a mild degree of ventricular discordance during
the respiratory cycle, right atrial pressure more than 24mmHg, evidence of hepatorenal dysfunction, massive ascites, pericardial calcication, and signs of progressive systemic congestion [3, 6, 7, 16–33, 63, 65],
The importance of an early diagnosis and indications for the operation has been
addressed in previously published guidelines [3, 6, 7, 16, 18, 25, 27, 33, 65].
Although the diagnosis of constrictive pericarditis can be a challenging process, it
seems conceivable that constrictive pericarditis should be considered in patients
with cardiac failure with preserved left ventricular function. Interestingly, although
both ventricular diastolic pressures are equal in this disease, symptoms and signs of
right-sided cardiac failure usually dominate. A careful physical examination with
judicious use of multimodality imaging including, Doppler echocardiography, computed tomography, cardiac magnetic resonance with or without hemodynamic
assessment studies facilitates early diagnosis [3, 65].
Hyperbiluribinemia is a surrogate for a cardiac failure caused by mechanical
cardiac entrapment. Such cardiac failure likely results in hepatic congestion and
cardiac cirrhosis at Terminal stage. Recently, several institutions have demonstrated
hyperbiluribinemia as an incremental risk factor for perioperative mortality following cardiac transplantation [50, 102–104]. Similarly, severe hypoalbuminemia, a
predictor of malnutrition and poor health have also been demonstrated to be associated with increased perioperative and long-term mortality [8, 9, 16, 18, 25, 27, 32,
33, 40].
Over the past few decades, the aetiological spectrum of constrictive pericarditis
has also changed in different parts of the world, resulting in diagnostic uncertainities and commensurable changes in the indications and complexity of pericardial
excision. While the incidence of post surgical and post irradiation pericarditis continue to increase in developed countries, tuberculosis remains dominant in developing countries [1–6, 9, 16–22, 36, 59, 60, 63, 64, 70, 72].
Analysis of the published literature reveals that aetiology of constrictive pericarditis inuences both short and long-term outcomes following pericardiectomy [1].
21.2 Perioperative Mortality and Low Cardiac Output Syndrome, Long-Term Survival…
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Idiopathic and inammatory pathogenesis is reported to be associated with best
short and long-term outcomes, while post irradiation pericarditis is associated with
high operative mortality and poor late results. The survival curve of post- cardiotomy
patients is between that of idiopathic patients and post-radiation patients [1–6, 9,
16–25, 48, 59, 60, 63, 93].
The higher mortality associated with pericardiectomy for post-radiation (21.4%)
and post-surgical constriction (8.3%) is probably related to the fact that constriction
is not the sole factor producing cardiac failure in these subgroups [1–6, 9, 16–22,
60, 63, 93], In 2012, The Johns Hopkins Medical Institute reported that 7-year sur-
vival ranged from 88% for patients with an idiopathic aetiology to 27% for those
with post-radiation aetiology [40].
In the Cleveland Clinic series, idiopathic constrictive pericarditis had the best
prognosis with a 7-year actuarial survival of 88%, followed by post-surgical constrictive pericarditis with 66%, and post-radiation constrictive pericarditis with 27%
[9]. In the Mayo Clinic series, the independent predictors of poor long-term outcomes were older age, advanced NewYork Heart Association class, and previous
radiation [59, 60].
In a German series reported by Szabo and associates, none of the patients with
radiation-induced pericarditis survived over six years [83]. In the series from Johns
Hopkins Medical Institutions reported by George T and associates, survival differed
sharply by aetiology, with idiopathic, post-operative, and post-irradiation 5-year
survivals of 79.8%, 55.9%, and 11% respectively (p<0.0001) [40].
In a collective review of literature on 54 patients with radiation-induced constrictive pericarditis undergoing pericardiectomy, the early mortality in the compiled
series was 29.6% (16 of 54) and late mortality was 35%. Only 20 patients (43%)
were long-term survivors [70]. The poor results in these patients compared with
patients having pericardiectomy for other reasons seem to be due mainly to the various kinds of radiation-induced damage to the heart as a whole, including accelerated atherosclerosis, premature coronary artery disease, myocardial brosis,
cardiomyopathies, atrioventricular conduction disturbances, and valvular dysfunction, with the result that complete relief by pericardiectomy may not be technically
feasible [4, 5, 22–26, 44, 55, 70, 85]. Radiation-induced heart disease becomes
clinically apparent 10–15years after radiation exposure [87, 99, 105].
In cases of post-radiation, the disease is not restricted to the pericardium alone,
but also affects the myocardium and/or endocardium. The pathogenesis of postirradiation myocardial brosis could be related to capillary endothelial cell injury
leading to a quantitative loss of capillaries, failure of the microcirculation, and ischemia [89]. Microvascular dysfunction and interstitial brosis may reduce exercise
tolerance and exercise capacity. Analysis of the cited reports of radiation doses suggest that severe cardiac damage (potentially leading to death) has to be expected in
patients who receive doses around 4000 rads, not just in those patients receiving
excessive irradiation [4, 5, 22, 28, 44, 45, 55, 70, 71, 87, 89, 99, 105].
Tokuda and associates in Japan Adult Cardiovascular Surgery Database, and
other investigators, have demonstrated chronic lung disease having negative effect
on patients undergoing pericardiectomy [93]. The involvement of adjacent
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pleuro- pulmonary structures by the constrictive disease process, radiation-induced
pulmonary and chest wall brosis, and tuberculous involvement in the lungs could
limit functional recovery after pericardiectomy [59, 60, 93]. The prevalence of
tuberculosis in developing countries, and history of vast over-use of asbestos in the
1970s in Japan, may result in constrictive pericarditis complicated with restrictive
respiratory dysfunction [38, 66, 94]. These country-specic issues should be taken
into consideration when optimizing the management of pericardiectomy. Therefore,
careful pre-operative evaluation of respiratory function, and aggressive perioperative interventions against respiratory complications, are deemed essential for
patients undergoing pericardiectomy.
21 Short- andLong-Term Results
21.3 Surgical Approach, Extent ofPericardiectomy andUse
ofExtracorporeal Circulation
Literature is divided on the degree of pericardial excision necessary to achieve an
optimal post surgical outcome. Quicker normalization of hemodynamics have been
reported after radical pericardiectomy decorticating the heart from right to left phrenovascular pedicle, pericardium posterior to the phrenic nerve, and the diaphragmatic pericardium.
While Viola suggested that pericardial resection over the superior and inferior
caval veins and right atrium is not essential for improvement of hemodynamics
[99], Culliford demonstrated that persistent symptoms right sided congestion and
delayed clinical improvement are commonly the results of incomplete decortication
[22]. However, the outcome is related not only to the extent of pericardial resection
but also to myocardial involvement in the disease process [23, 100].
In a large series of patients from India, the long term mortality risk was 4.5 times
higher (95% CI: 2.05, 9.75) in patients undergoing partial pericardiectomy via conventional left anterolateral thoracotomy as compared with total pericardiectomy. In
the same series, the risk of death was 9.09 (95% CI, 3.94–22) times higher in
patients with pericardial calcication undergoing pericardiectomy [16].
Copeland and co-workers routinely used cardiopulmonary bypass in pericardiectomy [27]. It is pertinent to highlight the great majority of the patients in Stanford
and Mayo Clinic series were either post surgical or post irradiation, thereby justifying routine use of cardiopulmonary bypass during pericardiectomy. Omoto’s team
also used cardiopulmonary bypass in almost all their patients, but concomitant operations undertaken to repair congenital or acquired heart disease made its use necessary in one-third patients undergoing pericardiectomy [72]. Although
cardiopulmonary bypass facilitates surgical dissection by emptying the ventricular
cavities and also helps in managing in advertent cardiac injury, its routine use to
facilitate pericardial resection remain controversial [16–23, 26, 27, 40, 72].
Without the assistance of cardiopulmonary bypass, gaining access to the lateral
wall of the left ventricle is indeed difcult through a median sternotomy. Thus,
21.4 Constrictive Pericarditis Following Cardiac Transplantation
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without the assistance of cardiopulmonary bypass, the procedure could end up with
an incomplete pericardiectomy of the left side. Incomplete pericardiectomy has
been reported as a risk factor for a poor outcome by several investigators [16–23,
40, 46, 93].
In the Japan Adult Cardiovascular Surgery Database, cardiopulmonary bypass
was used in 28.9% of cases undergoing pericardiectomy [93]. The result of multivariate analysis in the Japan Adult Cardiovascular Surgery Database indicated that
the use cardiopulmonary bypass was not merely a surrogate of disease severity but
the use of cardiopulmonary bypass itself was a risk factor for a poor outcome. The
drawbacks of routine usage of cardiopulmonary bypass was the potential for
increased perioperative bleeding and bypass-related complications [93, 95].
This Japanese study conrmed an increased reoperation rate for bleeding and
increased ICU stay exceeding 8days in the bypass group than those without cardiopulmonary bypass. Therefore the risk- benet ratio should be carefully assessed for
each patient [93, 95].
Although left anterolateral thoracotomy is useful to perform pericardiectomy. it
is important to consider the negative effect of thoracotomy on the patient’s respiratory function intra and postoperatively [10]. A thorough assessment of pulmonary
function including the adverse effect of signicant pleural effusion is essential to
decide on the desirable surgical approach.
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21.4 Constrictive Pericarditis Following
Cardiac Transplantation
Constrictive pericarditis may follow cardiac surgical procedure with an incidence
ranging from 0.1 to 0.3% [9, 56, 59, 60]. Constrictive pericarditis is a rare complica-
tion in cardiac transplantation, with a reported incidence of 1.4–3.9% [11, 51, 52,
56–58, 96]. The time from cardiac transplantation to evolution of constrictive peri-
carditis ranges from 3weeks to 11 years [11, 25–27, 29, 51, 52, 56–58, 61, 79–
81, 96].
A high incidence of pericardial effusion among cardiac transplantation recipients
has been reported by several investigators [11, 25–29, 41, 51, 52, 59, 60, 62, 96].
Factors contributing to the development of pericardial effusion after cardiac transplantation include: (i) large residual pericardial cavity after cardiac transplantation,
(ii) preoperative use of anticoagulants, (iii) postoperative coagulopathy in terminally ill patients, (iv) hypoproteinemia from malnutrition associated with end-stage
cardiac disease, (vi) asymptomatic perforation of the right ventricular wall by the
bioptome, and (vii) acute allograft rejection [12, 13, 25, 52, 57, 58, 100, 101].
The diagnosis of constrictive pericarditis in cardiac transplantation with symptoms of right sided heart failure, with preserved systemic ventricular function,
should be borne in mind. Attention should specially be paid to cardiac
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transplantation with a history of postoperative pericarditis, and those with rejection
episodes [12, 13, 25, 52, 57, 58, 61, 100, 101].
An integration of clinical data and multimodality imaging (echocardiography,
cardiac computed tomography scan and hemodynamic data) is essential to establish
the diagnosis of post-transplant constrictive pericarditis. European Society of
Cardiology advocates an initial echocardiography followed by appropriate multimodality imaging studies, namely cardiac computed tomography, magnetic resonance imaging and invasive catheterization studies [3, 15, 65].
For early diagnosis, nuclear magnetic resonance is the best imaging technique to
demonstrate pericardial thickening, mediastinal hematoma, and right atrial/right
ventricular constriction. Periodic echocardiographic examination of the transplanted
heart contributes to the early detection and follow-up of pericardial effusion. When
signs of cardiac tamponade develop, a subxiphoid pericardiotomy should be performed and maintained for 48–72hours. An early diagnosis followed by a radical
pericardiectomy is the recommended procedure for post transplant constrictive
pericarditis.
21 Short- andLong-Term Results
21.5 Calcic Constrictive Pericarditis andSurvival
In two different studies, the overall incidence of pericardial calcication detected on
chest roentgenogram ranged between 5% and 27% [22, 59, 60]. Bozbuga and associates found pericardial calcication in 44% of patients with tuberculous pericarditis [7]. In the series reported by Ghavidel and associates, pericardial calcication
was detected on chest roentgenogram in 20% of all patients, and in 30% of patients
with tubercular pericarditis [47].
The incidence of pericardial calcication in tubercular pericarditis ranges from 5
to 76% [1, 7, 9, 16–23, 40, 59, 60, 72]. In the cumulative series of 547 patients from
All India Institute of Medical Sciences, New Delhi, 37% of patients had radiologically and intraoperatively demonstrable calcication. This is comparable to 39% in
nine previous studies with a total of 803 patients [9, 16–23, 63, 64, 70–72, 87, 88,
97, 98]. In the Western series, pericardial calcication was more commonly associ-
ated with idiopathic constrictive pericarditis, while in developing countries a majority of patients of calcic pericarditis exhibited evidence of tuberculosis [9, 16, 23,
63, 64, 70–72, 87, 88, 97, 98].
The exact pathogenesis of calcic pericarditis in the present era remains unclear.
The role of calcic constrictive pericarditis in postoperative outcomes remains controversial [59, 60]. Although constrictive pericarditis was not associated with
adverse postoperative outcomes in some studies, it has been implicated in other
studies as a predictor of perioperative and postoperative mortality [6, 9, 16–23, 40,
43, 46, 48, 49, 59, 60, 73–75].
Contrary to the observations of these single-centre studies, Gopaldas and associates in US Nationwide sample studies on 13,593 patients undergoing
21.6 Re-Operations Following Pericardiectomy
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pericardiectomy noted the presence of calcied pericardium in 15% of patients,
independently associated with a lesser requirement for cardiopulmonary bypass
and quicker discharge from hospital without ancillary home support. Their analysis exhibited a 52% lower in-hospital mortality in patients with calcic pericarditis [46].
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21.6 Re-Operations Following Pericardiectomy
Re-operations for recurrent constrictive pericarditis following pericardiectomy are
common [16, 22, 89]. Published reports attest to the unpredictable and variable pattern of constrictive pericarditis and lend support to radical decortication. In 1962,
Saidi and Scannell performed four such procedures [90]. In 1971, the Mayo clinic
group reported 8 reoperations among 27 patients after incomplete decortication [106].
In one of the largest series (n=395) from India, 9 patients with partial pericardiectomy required reoperation for recurrent symptoms of right sided cardiac failures
with one hospital death. These data indicate that adequate pericardiectomy involves
resection of the entire pericardium from all surfaces of the heart and major intrapericardial vessels.
Following pericardiectomy, worsening mitral regurgitation and tricuspid regurgitation have been reported by several investigators [14–23, 41, 53, 54]. Buckingham
and associates proposed two hypotheses for the evolving pattern of mitral valvular
dysfunction following pericardiectomy: (i) the increased mobility of the lateral wall
of the left ventricular and anterolateral papillary muscle following pericardiectomy
allows an increased inward movement of the wall during systole, that shortens the
distance between the papillary muscle and attachment points of the chordae on the
mitral valve. This decreased distance lengthens the anterolateral papillary muscle
apparatus for systolic valvular coaptation; (ii) alternatively, the return of the interventricular septum and posterior left ventricular wall after pericardiectomy effectively increases the distance from the posteromedial papillary muscle to the chordal
attachment of the mitral valve [15–23, 41, 53, 54, 90].
In order to analyse the country-wise aetiologic spectrum and varied institutional
protocol of performing pericardiectomy, we are narrating the short- and long-term
results following pericardiectomy as stated under.
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21 Short- andLong-Term Results
21.7 Part 2
21.8 Mayo Clinic Series
A contemporary spectrum of proven constrictive pericarditis in 135 patients evaluated at the Mayo Clinic from 1985 through 1995 was compared with that of a historic cohort of 231 patients from 1936 through 1982. Notable trends were an
increasing frequency of constrictive pericarditis following mediastinal irradiation
(13%) for breast carcinoma and Hodgkin’s lymphoma, cardiac surgery (18%), purulent pericarditis (16%), and presentation in older patients (median age 61, range
11–78years) vs 45, (range 0.8–83years). The median duration of symptoms in this
study group before pericardiectomy was 11.7months (range 3days to 29.1years).
Perioperative mortality decreased signicantly as compared to the historic cohort
(6% vs 14%; p= 0.01), but late survival was inferior to that of an age- and sexmatched US population (p < 0.001). Actuarial survival at 5 and 10 years was
78±5% and 57±8%, respectively [59, 60, 63].
Cox regression analysis identied older age, advanced NewYork heart association functional class and post irradiation constrictive pericarditis as incremental risk
factors for death in the late post operative period. At 10years, 83 percent were in
NYHA functional class I/II.
These authors concluded that radical pericardiectomy was associated with lower
perioperative and late mortality and improved functional status in the great majority.
However, long-term results of pericardiectomy are disappointing in elderly patients
and those with post irradiation constrictive pericarditis. According to the Mayo
Clinic recommendation, cardiac transplantation could be considered in selected
patients with coexisting severe valvular disease with good pulmonary function and
without a recurrent tumour [59, 60].
21.9 Cleveland Clinic Foundation Series
In 2004, Bertog SC and associates investigated a total of 163 patients who underwent pericardiectomy for constrictive pericarditis over a 24-year period at the
Cleveland Clinic Foundation. Aetiology of constrictive pericarditis was idiopathic
(46%), post cardiac surgery (37%), and radiotherapy (9%). The median duration
between pericardiectomy and preceding surgeries was 16months. The median duration between pericardiectomy and preceding radiation was 11 years (range
2–30years). Thirty (18.4%) patients underwent pericardiectomy under cardiopulmonary bypass. Perioperative mortality was 6%. Median follow-up among survivors was 6.9years (range 0.8 to 24.5years) [9].
Idiopathic constrictive pericarditis had the best prognosis (7years survival 88%)
followed by post-surgical (66%) and post-radiation constrictive pericarditis (27%).
In bootstrap-validated Cox proportional hazard analysis, incremental risk factors
21.11 German Series
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for late death were older age, radiation induced constrictive pericarditis, hepatorenal dysfunction, poor ventricular function,and high pulmonary artery pressure.
Interestingly, Pericardial calcication had no impact on survival.
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21.10 Stanford Series
Culliford and associates from Stanford University, reported95 patients with constrictive pericarditis from 1970 to 1985. A trend similar to the Mayo Clinic series
cited above was seen regarding post-surgical constrictive pericarditis, and post
radiotherapy. Post-surgical constrictive pericarditis emerged as an important aetiology after 1980, constituting 29% of cases during 1980–1985 [22].
In cases of post-radiotherapy constrictive pericarditis, cases presenting between
1980 and 1985 were associated with a signicantly longer period of presentation
than that for cases presenting between 1970 and 1979 (11 years vs 4.7 years,
p<0.05).
For post-surgical constrictive pericarditis, the latent period was 2 years
11months±3years 6months, which was signicantly shorter than the post- radiation
group (p < 0.01). Effusive-constrictive pericarditis occurred in 24% overall with
similar prevalence in all aetiologic groups. Overall perioperative mortality was
12%; it was low in the idiopathic group (8%), and high in the post radiotherapy
group (21%) [22].
21.11 German Series
In 2013, Szabo G and associates reported the 24-years’ experience of a single
European centre regarding contemporary indications, risk factors, short and long
term outcomes following pericardiectomy for constrictive pericarditis [83].
Among 89 patients undergoing pericardiectomy between 1988 and 2012, the
mean age was 57.9±15.6years. The predominant aetiology was idiopathic in more
than half of the cases (n=49, 55%) followed by post-cardiotomy (n=21, 23.6%),
and post-radiation (n=5, 5.6%). All patients underwent pericardiectomy via median
sternotomy; 35 (39.3%) patients needed cardiopulmonary bypass support for successful surgical resection. Perioperative mortality was 7%, with over 60% survival
after 20years. Idiopathic constrictive pericarditis had the best survival (5-year actuarial survival, 79.6%) followed by post-surgical (47.7%, p<0.05) and post- radiation
pericarditis (no survivors after 5years, p<0.05) [83].
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21 Short- andLong-Term Results
21.12 Spanish Series
In 2007, Peset and associates presented their 23years’ experience on 31 consecutive
patients undergoing pericardiectomy for constrictive pericarditis. The aetiology of
pericarditis was idiopathic (48.%), tuberculosis (29%), post- radiotherapy (9%),
neoplasia (6%) and post-cardiac surgery (6%). Post-surgical constriction presented
clinically at more than 14years after cardiac surgery; pericarditis following radiotherapy was after 6years of treatment for Hodgkin’s disease. In-hospital mortality
was 16%. At a median follow-up of 5.3years (range 1–22years), the actuarial survival was 82% at 6months, 82% at 1–9years, and 64% at 10years [76].
Despite surgical intervention, the functional class did not improve in 6 of 26
survivors and worsened progressively in 1 patient who had undergone radiotherapy.
Post operatively, there was incomplete recovery of diastolic function because of
adjacent brotic myocardial alterations.
21.13 Chinese Series
In 2012, Lin Y and associates published a series of 51 consecutive patients who
underwent pericardiectomy from 2005 to December 2010. The aetiology was tuberculosis (65%), idiopathic (25%), post-cardiac surgery (6%), and connective tissue
disease (2%). All patients underwent pericardiectomy via median sternotomy.
Perioperative mortality was 3.9%. The actuarial 1-year survival rate was 93.7% [62].
21.14 All India Institute ofMedical Sciences Series
Part A: Chowdhury UK and associates from All India Institute of Medical Sciences,
New Delhi, compared the outcomes after total versus partial pericardiectomy, clinically, echocardiographically and haemodynamically, on a consecutive series of 395
patients operated on between 1985 and 2004. This single centre study incidentally
evaluated the postoperative outcomes on the largest number of patients undergoing
pericardiectomy from a single institution in the published literature. The median age
was 24years (range 10months to 71years). The interval between pericardial effusion and development of pericardial constriction ranged from 1 to 12months (mean,
6.3±3.6) months.
Duration of symptoms ranged from 15days to 6years (mean 20±8.6months).
The majority (n=389, 98.2%) were in NewYork Heart Association class III/IV.A
specic aetiologic factor was identied in 380 (96.2%) patients.
The indications for operation were: tubercular and non-tubercular constrictive
pericarditis (n = 254, 64.3%), purulent constrictive pericarditis (n = 25, 6.3%),
effusive- constrictive pericarditis (n=42, 10.6%), annular constrictive pericarditis
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