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Asian Cardiovasc Thorac Ann 2001;9:286-290
© 2001 Asia Publishing EXchange Pte Ltd

ORIGINAL CONTRIBUTION

Radical Pericardiectomy for Chronic Constrictive Pericarditis

Tadashi Omoto, MD, Kazutomo Minami, MD, Dimitrios Varvaras, MD, Dietmer Böthig, MD, Reiner Körfer, MD

Department of Thoracic and Cardiovascular Surgery Heart Center North-Rhine-Westphalia Ruhr-University of Bochum Bad Oeynhausen, Germany
For reprint information contact: Tadashi Omoto, MD Tel: 49 5731 97 0 Fax: 49 5731 97 2300 email: omoto{at}kddnet.de Department of Thoracic and Cardiovascular Surgery, Heart Center North-Rhine-Westphalia, Ruhr-University of Bochum, Georgstraße 11, Bad Oeynhausen D-32545, Germany.

   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
A retrospective analysis was undertaken in 79 patients who underwent pericardiectomy for chronic constrictive pericarditis from January 1985 to February 1999. Most operations (77) were carried out with cardiopulmonary bypass, with subtotal pericardiectomy in 75 patients, and concomitant operations in 25. Postoperative complications occurred in 8 patients: cerebrovascular accident in 2, renal insufficiency in 5, bleeding in 2, low output syndrome in 4, and respiratory insufficiency in 2. The operative mortality was 5%; causes of death were cardiac-related in all cases. Actuarial survival at 1, 5, and 10 years was 89.9% ± 3.4%, 74.9% ± 5.7%, and 55.4% ± 13.5%, respectively. Regression analysis was performed using 53 clinical variables. Female gender, renal insufficiency, concomitant coronary artery bypass grafting, and preoperative right ventricular end-diastolic pressure > 20 mm Hg were found to be predictors of poor survival. At follow-up, improved functional status was noted in 88% of patients. Subtotal pericardiectomy can be performed on cardiopulmonary bypass with low mortality and good long-term survival.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Pericardiectomy is the only accepted curative treatment for chronic constrictive pericarditis. Good results have been reported by institutions using different surgical approaches; with or without cardiopulmonary bypass (CPB), and subtotal or partial pericardiectomy.1–4 The optimal surgical therapy has not been established with regard to the extent of pericardial resection and the need for CPB. In view of the increasing number of redo cardiac operations, pericardiectomy with a median sternotomy using CPB has become the standard operative technique in our institute. The purpose of this study was to determine early and long-term survival, and to examine the risks of this operative approach and the functional outcome in patients.


   PATIENTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
The study group consisted of 79 consecutive patients with chronic constrictive pericarditis who were treated from January 1985 to February 1999 at the Heart Center North-Rhine-Westphalia. There were 61 men (77%) and 18 women (23%); their ages ranged from 22 to 77 years (median age, 56.6 ± 2.5 years). Preoperative and follow-up New York Heart Association (NYHA) functional class was determined using questions adopted from a study by Goldman and colleagues.5 Preoperatively, there were no patients in NYHA functional class I, 4 (5%) were in class II, 48 (61%) were in class III, and 27 (34%) were in class IV. The etiology of the pericardial disease was tuberculosis in 4, radiation-induced in 5, previous cardiac operation in 13, previous incomplete pericardiectomy in 4 (performed in other institutes), and unclear in 52 patients (66%). The presenting symptoms are summarized in Table 1Go. On electrocardiography, low voltage was detected in 16 patients (20%), and atrial fibrillation was found in 31 (39%). Chest radiography showed pericardial calcification in 36 patients (46%) and pleural effusion in 30 (38%). The mean cardiothoracic ratio was 0.49 ± 0.06. Seventy-six patients (96%) underwent catheterization. Their hemodynamics are summarized in Table 2Go. Ejection fraction was 65% ± 11% (range, 33% to 84%) by echo-cardiography.


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  		Table 1. Presenting Symptoms in 79 Patients
 

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  		Table 2. Preoperative Hemodynamics in 76 Patients
 
Pericardiectomy was performed using a median ster-notomy in all cases. The extent of pericardiectomy was classified into two categories: subtotal pericardiectomy was defined as wide excision of the pericardium from all surfaces of the heart and major intrapericardial vessels, with the phrenic nerves defining the posterior extent of pericardial resection; and partial pericardiectomy which did not include the pericardium overlying the right atrium, pulmonary veins, venae cavae, or the left atrium. The dissection was generally started at the ascending aorta and the right atrium, continued over the diaphragmatic surface of the pericardium, the pulmonary artery, and free wall of the right ventricle, and then the lateral and posterior walls of the left ventricle and the pulmonary veins. CPB was used in 77 patients (97%). The ascending aorta and right appendage were cannulated in the usual fashion. Additional venous cannulation was performed in the right atrium. Subtotal pericardiectomy was carried out in 75 patients (95%). In 4 patients (5%), partial pericardiectomy was performed according to intraoperative findings. Concomitant operations to repair congenital or acquired heart disease were undertaken in 25 patients (Table 3Go).


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  		Table 3. Concomitant Operations in 25 Patients
 
Follow-up was conducted using hospital records and telephone calls to the patients, their relatives, and physicians. Data were analyzed using SPSS version 9.0 (SPSS Inc, Chicago, IL, USA). Fifty-three clinical variables (Table 4Go) were analyzed using the Cox proportional hazards method to determine negative predictors of long-term survival. Actuarial survival was calculated by the Kaplan-Meier method. These data are presented as the mean ± standard deviation. A p value < 0.05 was considered significant for all statistical calculations.


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  		Table 4. Preoperative, Postoperative, and Follow-Up Variables
 

   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Median intensive care unit stay was 2.7 ± 3.4 days. Median hospital stay was 7 ± 2 days. Median ventilation time was 6 ± 1.5 hours. Median volume of blood transfused was 3.4 ± 4.5 units. The 30-day operative mortality rate was 5% (4 patients). One patient who underwent a concomitant coronary artery bypass graft operation and had a history of right heart failure on 3 occasions, died intraoperatively because of failure to wean from CPB due to severe low output syndrome. Another patient who had previous coronary grafting, mitral valve replacement, and a history of liver insufficiency and chronic obstructive lung disease, suffered low output syndrome and persistent respiratory insufficiency postoperatively and died on the 7th day. The 3rd patient who died had a history of renal and liver insufficiency preoperatively, and succumbed to low output syndrome on the 11th day due to multiple organ failure. The 4th patient had an uneventful post-operative course but died on postoperative day 18 due to ventricular fibrillation and circulatory collapse.

Nonfatal intraoperative complications affected 7 patients (9%). Intraoperative bleeding occurred in 6 due to laceration of the right atrium in 2, the ascending aorta in 2, the pulmonary artery in 1, and the right ventricle in 1. Another patient was difficult to wean from CPB, and an intraaortic balloon pump was used. There were 19 postoperative complications in 8 (10%) patients (Table 5Go). Catecholamines were used in 51 patients (65%), mostly low-dose dopamine as a prophylaxis against low output syndrome.


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  		Table 5. Postoperative Complications and Comorbidity
 
During a median follow-up of 47.52 ± 35.4 months with 4 patients lost to follow-up, there were 15 deaths (20%) including 9 from cardiac-related causes, 2 from malignancy, and 1 from pneumonia after a lower limb fracture (Table 6Go). Of the 75 surviving patients, none required reoperation for recurrent pericarditis. Figure 1Go depicts the relationship between preoperative and postoperative NYHA class. Improved functional capacity was recorded in 66/75 (88%), and 60 (80%) were in NYHA class I or II postoperatively. The overall survival rate is represented in Figure 2Go. Actuarial survival at 1, 5, and 10 years was 89.9% ± 3.4%, 74.9% ± 5.7%, and 55.4% ± 13.5%, respectively. Female gender (p = 0.0349), valvular heart disease (p = 0.0191), renal insufficiency (p = 0.003), concomitant coronary bypass surgery (p = 0.0086), concomitant valvular surgery (p = 0.0123), and pre-operative right atrial end-diastolic pressure > 20 mm Hg (p = 0.0074) were significant negative predictors of long-term survival.


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  		Table 6. Late Mortality
 


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  		Figure 1. Preoperative and postoperative New York Heart Association (NYHA) functional status of 75 surviving patients.

 


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  		Figure 2. Actuarial survival for all patients who underwent pericardiectomy (including operative deaths).

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Chronic constrictive pericarditis is an inflammatory process that involves both fibrous and serous layers of the pericardium, leading to pericardial thickening and constriction of the ventricles.6 The etiologic spectrum of constrictive pericarditis comprises post-radiotherapy, postoperative and postinfectious sequelae, as well as neoplasia, connective tissue disease, and autoimmune disease.7 In 1929, Churchill8 performed the first successful pericardiectomy for constrictive pericarditis. Subsequently, a number of different operative techniques and approaches have been described.1–4 Good late results have been reported in many large series. However, defining the best surgical approach for pericardiectomy has been a problem. The degree and duration of improvement following a variety of recommended procedures are difficult to determine as this disease is relatively uncommon. Two main conclusions have emerged from retrospective studies: good results can be obtained by subtotal pericardiectomy; and in a small but significant portion of patients with constrictive pericarditis, low output syndrome will develop after pericardiectomy, regardless of operative approach or the extent of pericardial resection.1–4,9,10

Controversy still remains as to whether diseased peri-cardium overlying the atria and major vessels contributes to the impairment of cardiac function observed in constrictive pericarditis. The initial clinical and hemo-dynamic responses after pericardiectomy are not always substantial, and continued improvement has been noted in some patients over many months.11–13 A decrease in central venous pressure tends to occur after 2 to 4 days postoperatively, becoming normal by 4 weeks.11 Senni and colleagues14 demonstrated that left ventricular diastolic filling remained abnormal in 43% of patients on late follow-up Doppler echocardiography. It has been suggested that the abnormal ventricular compliance is due to myocardial alterations.15 The etiology of persistent abnormal ventricular end-diastolic pressure in the early postoperative period is unclear; however, inadequate operations cannot be excluded. By studying left ventricular pressure-volume loops, total pericardiectomy was found to achieve normalization of the diastolic filling pattern as well as systolic function.16 Piehler and colleagues17 reported that late complications after pericardiectomy for effusion were related to the amount of remaining pericardium. These studies emphasize the importance of the extent of the pericardiectomy.

Previously, a left anterolateral thoracotomy was used.2,18 However, with this approach, it is not easy to institute CPB and avoid accidental bleeding. More recently, median sternotomy for pericardiectomy has provided good results.1,4,19 Median sternotomy gives good exposure of the right atrium and the venae cavae, and it allows extensive removal of parietal pericardium using CPB. CPB aids surgical dissection by emptying the ventricular cavities to define clearly the appropriate plane of dissection, and facilitating the management of inadvertent cardiac injury. Although potential bleeding after CPB was anticipated, only 2 patients suffered postoperative bleeding in this study.

Despite extensive pericardiectomy, there have always been some early deaths due to low output syndrome: 3/79 in our study compared to 22/231 in a Mayo Clinic study, and 4/71 in a report from Stanford University.3,4 Myocardial dysfunction can result from myocardial involvement in the disease process that led to constrictive pericarditis. The myocardial dysfunction can result from myocardial atrophy. Restrictive cardiomyopathy and constrictive pericarditis can coexist if they have a common cause such as radiation fibrosis.20,21 Low output syndrome may also be caused by changes in cardiac architecture. Worsening tricuspid regurgitation can be observed as a result of postoperative right ventricular dilatation.22 Buckingham and colleagues23 demonstrated mitral insufficiency by transesophageal echocardiography after pericardiectomy, which was thought to be due to elongation of the papillary muscles. A low output state after pericardiectomy gradually improves during hospitalization in most cases.

DeValeria and colleagues9 reported preoperative NYHA class IV, history of malignancy, and previous pericardial procedures to be negative predictors of long-term survival. McCaughan and colleagues3 found a significant correlation between preoperative functional class and in-hospital mortality and low output syndrome. However, NYHA class III or IV status was not a predictor of poor survival in this study which found that long-term outcome was significantly influenced by right ventricular end-diastolic pressure (> 20 mm Hg), but not by left ventricular end-diastolic pressure. It was concluded that right ventricular end-diastolic pressure is a useful parameter for predicting survival. As no patient required reoperation for symptoms or signs of pericardial disease, subtotal pericardiectomy using CPB is recommended as a safe and effective procedure for chronic constrictive pericarditis.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Copeland JG, Stinson EB, Griepp RB, Shumway NE. Surgical treatment of chronic constrictive pericarditis using cardiopulmonary bypass. J Thorac Cardiovasc Surg 1975; 69:236–8.[Abstract]

  2. Culliford AT, Lipton M, Spencer FC. Operation for chronic constrictive pericarditis: do the surgical approach and degree of pericardial resection influence the outcome significantly? Ann Thorac Surg 1980;29:146–52.[Abstract]

  3. McCaughan BC, Schaff HV, Piehler JM, Danielson GK, Orszulak TA, Puga FJ, et al. Early and late results of pericardiectomy for constrictive pericarditis. J Thorac Cardiovasc Surg 1985;89:340–50.[Abstract]

  4. Seifert FC, Miller DG, Oesterl SN, Oyer PE, Stinson EB, Shumway NE. Surgical treatment of constrictive pericarditis: analysis of outcome and diagnostic error. Circulation 1985:72(Suppl II):264–73.

  5. Goldman L, Hashimoto B, Cook EF, Loscalzo A. Comparative reproducibility and validity of systems for assessing cardiovascular functional class: advantages of a new specific activity scale. Circulation 1981;64:1227–34.[Abstract/Free Full Text]

  6. Kirklin JW, Barrett-Boyes BG. Cardiac surgery: pericardial disease. New York: John Wiley & Sons, 1986:1433.

  7. Cameron J, Oesterle SN, Baldwin JC, Hancock EW. The etiologic spectrum of constrictive pericarditis. Am Heart J 1987;113:354–60.[Medline]

  8. Churchill ED. Decortication of the heart (Delorme) for adhesive pericarditis. Arch Surg 1929;19:1457–67.[Abstract/Free Full Text]

  9. DeValeria PA, Baumgartner WA, Casale AS, Greene PS, Cameron DE, Gardner TJ, et al. Current indications, risks, and outcome after pericardiectomy. Ann Thorac Surg 1991;52:219–24.[Abstract]

  10. Bashi VV, John S, Ravikumar E, Jairaj PS, Shyamsunder K, Krishnaswami S. Early and late results of pericardiectomy in 118 cases of constrictive pericarditis. Thorax 1988;43:637–41.[Abstract/Free Full Text]

  11. Viola AR. The influence of pericardiectomy on hemodynamics of chronic constrictive pericarditis. Circulation 1973;48:1038–42.[Abstract/Free Full Text]

  12. Harrison EC, Crawford DW, Lau FY. Sequential left ventricular function studies before and after peri-cardiectomy for constrictive pericarditis: delayed resolution of residual restriction. Am J Cardiol 1970;26:319–23.[Medline]

  13. Bhatia ML, Grover DN, Roy SB. Haemodynamic effects of exercise in patients with constrictive pericarditis before and after pericardiectomy. Indian Heart J 1977;44: 177–83.

  14. Senni M, Redfield MM, King LH, Danielson GK, Tajik AJ, Oh JK. Left ventricular systolic and diastolic function after pericardiectomy in patients with constrictive pericarditis. J Am Coll Cardiol 1999;33:1182–8.[Abstract/Free Full Text]

  15. Deterling RA, Humphreys GH. Factors in the etiology of constrictive pericarditis. Circulation 1955;12:30–43.[Medline]

  16. Kuroda H, Sakagucchi M, Takano T, Tsunemoto H, Shinohara M, Fukaya Y, et al. Intraoperative monitoring of pressure-volume loops of the left ventricle in pericardiectomy for constrictive pericarditis. Ann Thorac Surg 1996;112:198–9.

  17. Piehler JM, Pluth JR, Schaff HV, Danielson GK, Orszulak TA, Puga FJ. Surgical management of effusive pericardial disease. Influence of extent of pericardial resection on clinical course. J Thorac Cardiovasc Surg 1985;90: 506–16.[Abstract]

  18. Cooly JC, Clagett OT, Kirklin JW. Surgical aspects of chronic constrictive pericarditis. A review of 72 operative causes. Ann Surg 1958;147:488–93.[Medline]

  19. Pugliese P, Bernabei M, Eufrate S. Total pericardiectomy for chronic constrictive pericarditis using femoro-femoral bypass. Int Surg 1984;69:39–40.[Medline]

  20. Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation 1989;79: 357–70.[Abstract/Free Full Text]

  21. Fowles RE, Mason JW. Role of cardiac biopsy in the diagnosis and management of cardiac disease. Prog Cardiovasc Dis 1984;27:153–72.[Medline]

  22. Johnson TL, Bauman WB, Josephson RA. Worsening tricuspid regurgitation following pericardiectomy for constrictive pericarditis. Chest 1993;104:79–81.[Abstract/Free Full Text]

  23. Buckingham RE Jr, Furnary AP, Weaver MT, Floten HS, Davis RF. Mitral insufficiency after pericardiectomy for constrictive pericarditis. Ann Thorac Surg 1994;58: 1171–4.[Abstract]




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