- Email: [email protected]
Treating Constrictive Pericarditis in a Chinese Single-Center Study: A Five-Year Experience
Yiyun Lin, MD,* Mi Zhou, MMS,* Jian Xiao, MD, Bin Wang, MD, and Zhinong Wang, MD Department of Cardiothoracic Surgery, Changzheng Hospital, the Second Military Medical University, Shanghai, China
Background. Constrictive pericarditis is a rare and disabling disease that can result in chronic fibrous thickening of the pericardium. Prompt treatment of constrictive pericarditis is necessary to limit morbidity and mortality. Methods. We analyzed the clinical details of 51 constrictive pericarditis patients who underwent surgery from January 2005 to December 2010 at our center. Results. Of the patients, 33 (65%) had tuberculous constrictive pericarditis, 13 (25%) had idiopathic pericarditis, 3 (6%) had previous cardiac surgery, and 1 (2%) had connective tissue disease. All patients underwent total pericardiectomy by midline sternotomy. The in-hospital mortality rate was 3.9% (2 of 51 patients). The cause of death was severe low cardiac output syndrome in 1 patient and acute renal failure in the other patient. There
were 2 cases of recurrent constrictive pericarditis after discharge. The actuarial 1-year survival rate was 93.7%. One-year follow-up revealed that an initial higher erythrocyte sedimentation rate, abnormal creatinine value, postoperative low output syndrome, and pleural effusion were all associated with increased mortality. Conclusions. Rapid diagnosis and treatment of constrictive pericarditis are crucial to reduce mortality and morbidity. Pericardiectomy should be performed early after diagnosis, in order to prevent chronic illness. After surgery, inotropes, diuretics, salt restriction, and nutrition supply are also critical to improve the prognosis. The inflammation marker erythrocyte sedimentation rate should be evaluated during follow-up. (Ann Thorac Surg 2012;94:1235– 40) © 2012 by The Society of Thoracic Surgeons
C
Patients and Methods
onstrictive pericarditis, a rare and disabling disease, involves chronic fibrous thickening of the pericardium [1–3]. In the past, the main cause of constrictive pericarditis was tuberculosis (Tb) [1]. With widely use of antituberculosis drugs, the etiology of this disease has evolved. The most frequent indications of pericarditis in developed countries are prior cardiac surgery, irradiation therapy, and idiopathic pericarditis [4, 5]. In developing countries, however, Tb remains the most common cause of constrictive pericarditis [4 –9]. Constrictive pericarditis presents most frequently as a result of chronic fibrous pericardial thickening, calcification of the pericardium, or a combination of both. The constricting pericardial envelope surrounds the entire heart and impairs filling of all the cardiac chambers. In patients with cardiac dysfunction, the definitive treatment is surgical pericardiectomy [10 –12]. Prompt treatment of constrictive pericarditis can prevent mortality. The present article is based on our experience over the past 5 years with Chinese patients in our single-center hospital. And our focus is to advance the understanding of the pathogenesis, diagnosis, management, and follow-up of constrictive pericarditis.
Accepted for publication May 2, 2012. *Yiyun Lin and Mi Zhou contributed equally to this article. Address correspondence to Dr Wang, Department of Cardiothoracic Surgery Changzheng Hospital, Fengyang Rd 415, Shanghai, China 200003; e-mail: [email protected].
© 2012 by The Society of Thoracic Surgeons Published by Elsevier Inc
We retrospectively analyzed the clinical reports of 51 consecutive patients (38 males, 13 females; age 40.1 ⫾ 15.5 years; range 13 to 73 years) with constrictive pericarditis who underwent surgery from January 2005 to January 2011 in our single-center institution. Our institutional ethics committee approved the present study and all patients gave written informed consent. The diagnosis of constrictive pericarditis was made according to the combination of Doppler echocardiography (thickened or calcified pericardium), cardiac catheterization (elevated end-diastolic pressure and the “square root sign” of right ventricular pressure tracing) [13, 14], or pericardial biopsy [3]. The definite diagnosis of Tb constrictive pericarditis was based on the above criteria and one of the following: (1) a positive Tb culture from pericardial effusion or pericardial tissue; (2) a positive acid-fast stain bacilli or typical caseous granuloma on pericardial biopsy specimen; or (3) a positive Tb polymerase chain reaction in the pericardial biopsy specimen [15, 16]. Indications for pericardiectomy were preoperative clear diagnosis of constrictive pericarditis, patients with poor condition (eg, heart rate ⬎ 120/minute, albumin ⬍ 25 g/L, severe hepatic or renal failure, or severe ascites) who did not improve after medical treatment, and patients who had pericardial fenestration before the condition improved. In-hospital mortality was defined as death in-hospital or within 30 days after surgery. Results are expressed as number (percentages), mean (standard 0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2012.05.002
ADULT CARDIAC
Treating Constrictive Pericarditis in a Chinese Single-Center Study: A Five-Year Experience
1236
LIN ET AL CHINESE EXPERIENCE OF CONSTRICTIVE PERICARDITIS
ADULT CARDIAC
deviation), or as median (range) when the distribution of variables was not normal. The Student t test or the Mann-Whitney test was used for continuous variables and the Fisher exact test or 2 test was used for categoric variables. A p value of less than 0.05 was considered statistically significant. Analyses were performed by using SPSS version 17.0 (SPSS Inc, Chicago, IL).
Results Table 1 lists the causes of constriction in the series. Of the 51 patients, 33 patients (65%) had Tb constrictive pericarditis and 13 (25%) had idiopathic constrictive pericarditis. Underlying conditions were previous cardiac surgery for 3 patients (6%) and connective tissue disease for 1 patient (2%). The remaining patient had chest trauma 40years ago. The average pulse pressure was 34 ⫾ 8 mm Hg, and the mean heart rate was 100 ⫾ 14 beats per minute. When classifying patients using the preoperative New York Heart Association functional class, 24 (47%) were in class II, 19 (37%) were in class III, and 8 (16%) were in class IV. The median duration of symptoms was 6 months (range 1 to 480 months). The most common symptoms were lower limb edema (67%), shortness of breath (65%), exertional dyspnea (59%), abdominal distension (43%), palpitation (30%), and cough (26%). On physical examination, the most prominent clinical signs were raised jugular vein distension (65%), increased cardiac dullness (61%), distant heart sounds (57%), hepatomegaly (46%), tachycardia (37%), and ascites (36%). Table 2 summarizes the main features. Initial laboratory assessment showed increases in serum total and direct bilirubin, alkaline phosphatase, and markers of inflammation (erythrocyte sedimentation rate [ESR] and C-reactive protein). Among the 33 patients with Tb constrictive pericarditis, not all patients had pulmonary infection (7 patients still had Tb pleuritis or lymph-node Tb and 2 patients had a definite past history of pulmonary Tb); however, none had bone and joint Tb. Of these patients, the most common symptoms and signs were exertional dyspnea (64%), lower leg edema (64%), raised jugular vein distension (61%), and distant heart sounds (56%). None of the patients had a positive acidfast stain, Tb-DNA test, or Tb antibody test while in the hospital. On the electrocardiograms, nonspecific T wave changes were detected in 18 patients (35%), ST segment
Table 1. Etiology of Constrictive Pericarditis in Our SingleCenter Site Etiologic Factors Mycobacterium tuberculosis Idiopathic Post cardiac surgery Connective tissue disease Chest trauma history
No.
%
33 13 3 1 1
65 25 6 2 2
Ann Thorac Surg 2012;94:1235– 40
Table 2. Preoperative Clinical Details of Constrictive Pericarditis Variable Age, years Males Pulse pressure, mm Hg NYHA functional class II III IV Symptoms: Lower limb edema Shortness of breath Exertional dyspnea Abdominal distension Palpitation Cough Paroxysmal nocturnal dyspnea Fever Fatigue Chest pain Night sweat Signs: Raised jugular vein distension Peripheral edema Increased cardiac dullness Distant heart sounds Hepatomegaly Tachycardia Splenomegaly Ascites Pericardial knock sound Pulsus paradoxus S3
Result 40.1 ⫾ 15.5 38 (75%) 33.8 ⫾ 7.8 24 (47%) 19 (37%) 8 (16%) 33 (67%) 32 (65%) 29 (59%) 21 (43%) 15 (30%) 13 (26%) 12 (25%) 12 (25%) 12 (25%) 8 (16%) 6 (12%) 32 (65%) 33 (65%) 30 (61%) 28 (57%) 23 (46%) 19 (37%) 18 (36%) 18 (36%) 15 (31%) 11 (22%) 6 (12%)
Results of qualitative variables are expressed in absolute values (percentages) and results of continuous variables as mean (SD). NYHA ⫽ New York Heart Association.
depression was seen in 13 (25%) patients, low-voltage was observed in 13 (25%) patients, and atrial arrhythmias or fibrillations were found in 15 (29%) patients. Imaging examinations revealed a thickened pericardium in 92%, calcification of pericardium in 47%, cardiomegaly in 87%, pleural effusion in 51%, congestive liver in 65%, splenomegaly in 43%, and ascites in 36% patients. The chest radiograms revealed changes suggestive of pulmonary Tb in 13 (25%) patients. By Doppler echocardiography, the mean ejection fraction value was 0.59 ⫾ 0.06, pericardial thickening and calcification were found in 75% and 47%, respectively, and diastolic dysfunction was seen in almost all of the patients. Biatrial enlargement was also frequently observed; left atrium 84 ⫾ 28 mL and right atrium 69 ⫾ 27 mL (compared with normal left atrial volume 47 ⫾ 17 mL and normal right atrial volume 39 ⫾ 12 mL) [17–19]. In addition, there were mild to severe tricuspid and mitral valve incompetence in 5 and 4
LIN ET AL CHINESE EXPERIENCE OF CONSTRICTIVE PERICARDITIS
patients, respectively. A detailed list of patient characteristics is reported in Table 3. All patients underwent pericardiectomy and a midline sternotomy was performed in all cases. Constricting layers of epicardium were removed when possible. The dissection was started at the base of the aorta, followed by the lateral and posterior walls of the left ventricle and the pulmonary veins and the pulmonary artery, and extended downward to the diaphragmatic pericardium. Finally, the pericardium was resected over the free wall of the right ventricle and then over the vena cavae. We Table 3. Preoperative Examination of 51 Patients with Constrictive Pericarditis Variable Biochemical variables in blood: Hemoglobin, g/L Platelets, ⫻109/L Total bilirubin, mol/L Direct bilirubin, mol/L Albumin, g/L Alanine aminotransferase, U/L Aspartate aminotransferase, U/L Lactate dehydrogenase, U/L Alkaline phosphatase, U/L Creatinine, mol/L Urea, mmol/L Prothrombin time, seconds Erythrocyte sedimentation rate, mm/H C-reactive protein, mg/L Electrocardiogram variables: Heart rate, beats/minute Atrial arrhythmias or fibrillation T wave changes ST-segment depression Low-voltage Imaging variables: Thickened pericardium Calcification of pericardium Cardiomegaly Congestive liver Pleural effusion Splenomegaly Ascites Changes of pulmonary Tb Echocardiographic variables: Left ventricular ejection fraction Pericardial thickening Pericardial calcification Volume of left atrium, ml Volume of right atrium, ml Mild to severe tricuspid valve incompetence Mild to severe mitral valve incompetence
Result 133 ⫾ 17 151 ⫾ 57 24.8 ⫾ 10.1 12.9 ⫾ 6.3 36 ⫾ 4 26 ⫾ 12 36 ⫾ 14 221 ⫾ 54 131 ⫾ 53 81 ⫾ 20 6.2 ⫾ 1.9 14.5 ⫾ 1.4 18 ⫾ 16 11.5 ⫾ 6.9 100 ⫾ 14 15 (29%) 18 (35%) 13 (25%) 13 (25%) 47 (92%) 24 (47%) 44 (87%) 32 (65%) 26 (51%) 21 (43%) 18 (36%) 13 (25%) 0.59 ⫾ 0.06 38 (75%) 24 (47%) 84 ⫾ 28 69 ⫾ 27 5 (10%) 4 (8%)
The results of qualitative variables are expressed in absolute values (percentages) and the results of continuous variables are expressed as mean (SD).
1237
did not remove inaccessible areas, including the base of the heart where it is adherent to the diaphragm. Calcified plaques were often very difficult to remove. Cardiopulmonary bypass was not commonly used during surgery, except for 4 patients as a safe method for removing calcified pericardium, 2 patients who had concomitant mitral replacement, and 1 patient for removal of myxomas in the right atrium. Operative findings included markedly thickened pericardium (65%), adhesions (54%), and calcification (50%). The preoperative average central venous pressure was 20.2 ⫾ 5.1 mm Hg and declined to 7.4 ⫾ 3.1 mm Hg postsurgically (p ⬍ 0.001). Likewise, pulse pressure increased from 30 mm Hg to 50 to 60 mm Hg. The mean duration of the operation was 172 ⫾ 61 minutes. Pathological changes, which included caseous necrosis, fibrosis, calcification, inflammation, and hyaline plaque formation, occurred in some but not all patients. All of the bacteria cultures were negative. In-hospital mortality was 3.9% (2 of 51 patients). The cause of death was severe low cardiac output syndrome due to right heart failure, with elevated ventricular filling pressure in 1 patient and acute renal failure in the context of preoperative chronic renal failure in the other patient. There were several postsurgical complications in the surviving patients, which included pleural effusion in 23 patients, low output syndrome in 15 patients, pulmonary infection in 5 patients, and diarrhea in 1 patient. None of the patients had recurrence of heart failure before discharge. The median duration of mechanical ventilation was 10.2 ⫾ 2.8 hours. In 14 patients, blood transfusions were given during or after surgery. The average volume of perioperative transfusion was 1,286 ⫾ 698 mL. The median intensive care unit stay was 2.4 ⫾ 1.4 days. The median hospital stay was 21.9 ⫾ 3.5 days (range 8 to 39 days). For the patients in whom Tb constrictive pericarditis was diagnosed, they would receive antituberculosis agents (isoniazid, rifampicin, and ethambutol daily for 6 months, or pyrazinamide daily for 2 months). After first discharge, 2 patients were rehospitalized to undergo redo surgery for recurrent Tb constrictive pericarditis, at 3 and 10 months of follow-up. The first patient died from heart failure as a complication of the disseminated disease in 2 months after the redo surgery and the second patient died from postoperative multiple organ dysfunction syndrome in the hospital. A third patient died of scleroderma by the 6-month follow-up. The actuarial 1-year survival rate in 49 patients was 93.7% (Fig 1). Univariate analyses showed that a preoperative higher level of ESR (p ⫽ 0.006), abnormal creatinine value (p ⫽ 0.029), postoperative low output syndrome (p ⫽ 0.001), and pleural effusion (p ⫽ 0.035) were each positively associated with increased mortality.
Comment Constrictive pericarditis is an uncommon condition involving impaired mid and late ventricular filling due to a thickened or noncompliant pericardium. The most important findings of our evaluation were that clinical
ADULT CARDIAC
Ann Thorac Surg 2012;94:1235– 40
1238
LIN ET AL CHINESE EXPERIENCE OF CONSTRICTIVE PERICARDITIS
Ann Thorac Surg 2012;94:1235– 40
Fig 1. Kaplan-Meier curve showing survival for the 49 constrictive pericarditis patients. (Cum ⫽ cumulative.)
ADULT CARDIAC
manifestations could worsen, even with short durations of symptoms, and thus timely diagnosis and prompt treatment are important to improved prognosis. Our results are consistent with previous studies, which showed that constriction was more common in males [7, 12, 20]. While there is no clear explanation for the sex differences, previous studies have found male to female preponderances varying from 1.7:1 to 4:1 [3]. Our study showed almost 3 times as many males as females were subjects. The normal pericardium is approximately 3-mm thick. With chronic constriction, especially from Tb, the pericardium may double to 6 mm or more, calcify, and intimately involve the epicardium. In the classic form, fibrous scarring and adhesions of both pericardial layers lead to obliteration of the pericardial cavity. Thus, while early ventricular filling is unimpeded, diastolic filling is subsequently reduced abruptly as a result of the inability of the ventricles to fill due to physical constraints imposed by the structurally altered pericardium. Cardiac output is reduced, likely due to the inadequate diastolic filling of the ventricles. In our experience, the predominant symptoms of constrictive pericarditis are lower limb edema, shortness of breath, and exertional dyspnea; abdominal symptoms, palpitation, and cough are also common. The most frequent signs are raised jugular vein distension, increased cardiac dullness, and distant heart sounds. Other findings include hepatomegaly, tachycardia, pleural effusion, and ascites. Increased heart rate and elevated venous pressure are compensatory mechanisms that offset the increase in intrapericardial pressure. At times, however, patients may not present with sufficient signs or symptoms for the clinician to make a definite diagnosis. In these cases, additional imaging is required and recommended. Echocardiography is essential for the diagnosis of the pericardial syndrome. Compared with echocardiogra-
phy, cardiac computed tomography and magnetic resonance imaging offer the advantage of better imaging of the pericardium, with more accurate measurements of pericardial thickening [21]. Cardiac computed tomography and magnetic resonance imaging can delineate abnormal pericardial thickness found in constrictive pericarditis [10]. The association between the characteristic hemodynamic changes with increases of pericardial thickness more than 3 mm always confirms the diagnosis [22]. This is an important point because Tb pericardial constriction is almost always associated with pericardial thickening [23]. Constrictive pericarditis must be diagnosed early because cardiac tamponade can occur in the acute phase and constrictive pericardia may subsequently develop. Decreased cardiac output resulting from a chronic constrictive process may require surgical intervention. Currently, pericardiectomy is the only accepted curative treatment for improving cardiac hemodynamics in constrictive pericarditis [24]. In our center, surgery occurs within 1 week of diagnosis. In cases where this is a delay due to the difficultly in gaining a clear diagnosis, however, surgery should be undertaken as soon as possible, before clinical manifestations become worse. As to thoracotomy, Chen and Lai [13] often found it difficult to remove the pericardium overlying the thinwalled right atrium and vena cava by left anterolateral thoracotomy, but Lachman and colleagues [11] reported that the left anterolateral approach allowed wider access to the left ventricle, which was a significantly improved approach. In our series, all procedures were done through median sternotomy, which provides good operative exposure and is the preferred surgical approach. Cardiopulmonary bypass can be used as a safe method for removing calcified pericardium. The objective of the procedure is to release the ventricles from the densely adherent pericardial shell. The lack of a surgical plane
LIN ET AL CHINESE EXPERIENCE OF CONSTRICTIVE PERICARDITIS
can make this an operation with high blood loss, and attention must be paid to salvage and reinfuse blood. Epicardial coronary vessels are at risk in this dissection and particular care must be taken when dissecting in the regions of these vessels. After surgery, care should be taken to remove every constrictive layer to avoid persistent pericardial constriction, and cardiac performance immediately improves after incision of the pericardium [10]. In this series, pleural effusion, low output syndrome, and pulmonary infection were the most common postoperative complications (Table 4). Because diastolic filling recovers (especially filling of the right atrium), inotropes, diuretics, and salt restriction are important to avoid low cardiac output and right heart failure. However, the overzealous use of diuretics is not recommended and could possibly lead to sudden death [25]. On the other hand, Tb may cause long-term malnutrition and constrictive pericarditis leads to cardiogenic nutrient deprivation. Clinicians, therefore, attach great importance to nutrition supply and will give a blood transfusion if needed.
Table 4. Intraoperative and Postoperative Information of 51 Patients With Constrictive Pericarditis Variable Intraoperative information: Duration of the operation, minutes Cardiopulmonary bypass used Concurrent operation Mitral replacement Removal of myxomas Central venous pressure (CVP) change Preoperative CVP, mm Hg Postoperative CVP, mm Hg Operative findings: Markedly thickened pericardium Pericardium adhesions Pericardium calcification Postoperative information: Duration of mechanical ventilation, hours Blood transfusions (including during or after surgery): Number of patients Volume of transfusion, mL Postsurgical complications (49 surviving patients): Pleural effusion Low output syndrome Pulmonary infection Diarrhea Intensive care unit stay, days Hospital stay, days In-hospital mortality
Result 172 ⫾ 61 7 (14%) 2 (4%) 1 (2%) 20.2 ⫾ 5.1 7.4 ⫾ 3.1 32 (65%) 28 (54%) 26 (50%) 10.2 ⫾ 2.8
14 (27%) 1,286 ⫾ 698
23 (47%) 15 (31%) 5 (10%) 1 (2%) 2.4 ⫾ 1.4 21.9 ⫾ 3.5 2 (3.9%)
The results of qualitative variables are expressed in absolute values (percentages) and the results of continuous variables are expressed as mean (SD).
1239
In our single-center institution, Tb counted for 65% of the causes of constrictive pericarditis. The diagnosis of Tb in constrictive pericarditis in this series was almost always confirmed by pathological diagnosis. Atypical for pulmonary Tb, however, some of our patients did not suffer from any respiratory symptoms. All examinations to test for Tb (for example, sputum acid-fast stain, Tb-DNA test, and Tb antibody tests) were negative. It is thought that Tb constrictive pericarditis occurs much later after active Tb pulmonary infection or ineffective therapy of the pulmonary infection [24]. For patients with suspected Tb constriction, we recommend that antituberculosis therapy be started before and continued after pericardial surgery. As for the conservative treatment option, the use of corticosteroids is still controversial. Some view that a course of glucocorticoid treatment (eg, prednisone, 20 to 60 mg/day for up to 6 weeks [9]) is useful to manage the acute disease, reduce effusion, facilitate hemodynamic recovery, and thus decrease mortality rates [26]. However, it is uncertain whether adjunctive corticosteroids are effective in reducing mortality or pericardial constriction [21]. Progression to chronic constrictive pericarditis, however, does not seem affected by such therapy. As a general case, we did not give corticosteroid therapy to Tb constrictive pericarditis patients because those who received surgical treatment experienced chronic pericardial changes and did not show any obvious symptoms of poisoning. Furthermore, long-term use of glucocorticoid could increase the risk of postoperative infection. From the 1-year follow-up, our results demonstrate that an initial higher ESR and abnormal preoperative creatinine value, postoperative low output syndrome, and pleural effusion predict mortality. Because reversible constrictive pericarditis was associated with pericardial and systemic inflammation [27], some inflammation markers, such as ESR, should be included during follow-up.
Limitations This study is unique in that it summarizes the Chinese experience of treating constrictive pericarditis over the past 5 years. However, there were a few limitations that warrant mentioning. Only a few patients underwent preoperative hemodynamic cardiac catheterization and hence there was an increased difficulty to differentiate between constriction and restrictive cardiomyopathy. We routinely made the differential diagnosis according to cardiac computed tomography and magnetic resonance imaging, which were considered as excellent methods for differentiating [20]. Further, although the etiology of constrictive pericarditis varies geographically and resistant TB strains have appeared gradually [28], we lacked a special test to find out the definite strain of Tb that caused 2 recurrent cases in our follow-up. Lastly, we need to continue our follow-up to determine the long-term outcomes in this cohort.
Conclusions Rapid diagnosis and treatment of constrictive pericarditis are crucial to reduce mortality. We suggest that pericardial stripping should be performed early and as radically as possible in an effort to prevent chronic illness. After surgery, nutritional supply and proper fluid infusion are
ADULT CARDIAC
Ann Thorac Surg 2012;94:1235– 40
1240
LIN ET AL CHINESE EXPERIENCE OF CONSTRICTIVE PERICARDITIS
also critical for a good prognosis. Inflammation markers, such as ESR, should also be included during follow-up.
References ADULT CARDIAC
1. Fowler NO. Tuberculous pericarditis. JAMA 1991;266:99 – 103. 2. Clare GC, Troughton RW. Management of constrictive pericarditis in the 21st century. Curr Treat Options Cardiovasc Med 2007;9:436 – 42. 3. Schwefer M, Aschenbach R, Heidemann J, Mey C, Lapp H. Constrictive pericarditis, still a diagnostic challenge: Comprehensive review of clinical management. Eur J Cardiothorac Surg 2009;36:502–10. 4. Chowdhury UK, Subramaniam GK, Kumar AS, et al. Pericardiectomy for constrictive pericarditis: A clinical, echocardiographic, and hemodynamic evaluation of two surgical techniques. Ann Thorac Surg 2006;81:522–9. 5. Peset AM, Marti V, Cardona M, et al. Outcome of pericardiectomy for chronic constrictive pericarditis. [Article in Spanish] Rev Esp Cardiol 2007;60:1097–101. 6. Russell JB, Syed FF, Ntsekhe M, et al. Tuberculous effusiveconstrictive pericarditis. Cardiovasc J Afr 2008;19:200 –1. 7. Zheng SY, Zhu P, Zhuang J, et al. Surgical treatment of 128 cases of constrictive pericarditis. [Article in Chinese] Nan Fang Yi Ke Da Xue Xue Bao 2010;30:535–7. 8. Murray JF. A century of tuberculosis. Am J Respir Crit Care Med 2004;169:1181– 6. 9. Reuter H, Burgess LJ, Louw VJ, Doubell AF. The management of tuberculous pericardial effusion: experience in 233 consecutive patients. Cardiovasc J S Afr 2007;18:20 –5. 10. Bozbuga N, Erentug V, Eren E, et al. Pericardiectomy for chronic constrictive tuberculous pericarditis: risks and predictors of survival. Tex Heart Inst J 2003;30:180 –5. 11. Lachman N, Vanker EA, Christensen KN, Satyapal KS, Fennell WM. Pericardiectomy: a functional anatomical perspective for the choice of left anterolateral thoracotomy. J Card Surg 2009;24:411–3. 12. Imazio M, Brucato A, Maestroni S, et al. Risk of constrictive pericarditis after acute pericarditis. Circulation 2011;124: 1270 –5. 13. Chen RF, Lai CP. Clinical characteristics and treatment of constrictive pericarditis in taiwan. Circ J 2005;69:458 – 60. 14. Imazio M, Spodick DH, Brucato A, Trinchero R, Markel G, Adler Y. Diagnostic issues in the clinical management of pericarditis. Int J Clin Pract 2010;64:1384 –92.
Ann Thorac Surg 2012;94:1235– 40
15. Fowler NO. Constrictive pericarditis: its history and current status. Clin Cardiol 1995;18:341–50. 16. Bathoorn E, Limburg A, Bouwman JJ, Bossink AW, Thijsen SF. Diagnostic potential of an enzyme-linked immunospot assay in tuberculous pericarditis. Clin Vaccine Immunol 2011;18:874 –7. 17. Pritchett AM, Jacobsen SJ, Mahoney DW, Rodeheffer RJ, Bailey KR, Redfield MM. Left atrial volume as an index of left atrial size: a population-based study. J Am Coll Cardiol 2003;41:1036 – 43. 18. Wang Y, Gutman JM, Heilbron D, Wahr D, Schiller NB. Atrial volume in a normal adult population by twodimensional echocardiography. Chest 1984;86:595– 601. 19. Aune E, Baekkevar M, Roislien J, Rodevand O, Otterstad JE. Normal reference ranges for left and right atrial volume indexes and ejection fractions obtained with real-time threedimensional echocardiography. Eur J Echocardiogr 2009;10: 738 – 44. 20. Mookadam F, Jiamsripong P, Raslan SF, Panse PM, Tajik AJ. Constrictive pericarditis and restrictive cardiomyopathy in the modern era. Future Cardiol 2011;7:471– 83. 21. Syed FF, Mayosi BM. A modern approach to tuberculous pericarditis. Prog Cardiovasc Dis 2007;50:218 –36. 22. Cinar B, Enç Y, Göksel O, et al. Chronic constrictive tuberculous pericarditis: Risk factors and outcome of pericardiectomy. Int J Tuberc Lung Dis 2006;10:701– 6. 23. Talreja DR, Edwards WD, Danielson GK, et al. Constrictive pericarditis in 26 patients with histologically normal pericardial thickness. Circulation 2003;108:1852–7. 24. Augustin P, Desmard M, Mordant P, et al. Clinical review: intrapericardial fibrinolysis in management of purulent pericarditis. Crit Care 2011;15:220. 25. Marshall A, Ring N, Lewis T. Constrictive pericarditis: lessons from the past five years’ experience in the south west cardiothoracic centre. Clin Med 2006;6:592–7. 26. Strang JI, Nunn AJ, Johnson DA, Casbard A, Gibson DG, Girling DJ. Management of tuberculous constrictive pericarditis and tuberculous pericardial effusion in transkei: results at 10 years follow-up. QJM 2004;97:525–35. 27. Feng D, Glockner J, Kim K, et al. Cardiac magnetic resonance imaging pericardial late gadolinium enhancement and elevated inflammatory markers can predict the reversibility of constrictive pericarditis after antiinflammatory medical therapy: a pilot study. Circulation 2011;124:1830 –7. 28. Mayosi BM, Burgess LJ, Doubell AF. Tuberculous pericarditis. Circulation 2005;112:3608 –16.
Background. Constrictive pericarditis is a rare and disabling disease that can result in chronic fibrous thickening of the pericardium. Prompt treatment of constrictive pericarditis is necessary to limit morbidity and mortality. Methods. We analyzed the clinical details of 51 constrictive pericarditis patients who underwent surgery from January 2005 to December 2010 at our center. Results. Of the patients, 33 (65%) had tuberculous constrictive pericarditis, 13 (25%) had idiopathic pericarditis, 3 (6%) had previous cardiac surgery, and 1 (2%) had connective tissue disease. All patients underwent total pericardiectomy by midline sternotomy. The in-hospital mortality rate was 3.9% (2 of 51 patients). The cause of death was severe low cardiac output syndrome in 1 patient and acute renal failure in the other patient. There
were 2 cases of recurrent constrictive pericarditis after discharge. The actuarial 1-year survival rate was 93.7%. One-year follow-up revealed that an initial higher erythrocyte sedimentation rate, abnormal creatinine value, postoperative low output syndrome, and pleural effusion were all associated with increased mortality. Conclusions. Rapid diagnosis and treatment of constrictive pericarditis are crucial to reduce mortality and morbidity. Pericardiectomy should be performed early after diagnosis, in order to prevent chronic illness. After surgery, inotropes, diuretics, salt restriction, and nutrition supply are also critical to improve the prognosis. The inflammation marker erythrocyte sedimentation rate should be evaluated during follow-up. (Ann Thorac Surg 2012;94:1235– 40) © 2012 by The Society of Thoracic Surgeons
C
Patients and Methods
onstrictive pericarditis, a rare and disabling disease, involves chronic fibrous thickening of the pericardium [1–3]. In the past, the main cause of constrictive pericarditis was tuberculosis (Tb) [1]. With widely use of antituberculosis drugs, the etiology of this disease has evolved. The most frequent indications of pericarditis in developed countries are prior cardiac surgery, irradiation therapy, and idiopathic pericarditis [4, 5]. In developing countries, however, Tb remains the most common cause of constrictive pericarditis [4 –9]. Constrictive pericarditis presents most frequently as a result of chronic fibrous pericardial thickening, calcification of the pericardium, or a combination of both. The constricting pericardial envelope surrounds the entire heart and impairs filling of all the cardiac chambers. In patients with cardiac dysfunction, the definitive treatment is surgical pericardiectomy [10 –12]. Prompt treatment of constrictive pericarditis can prevent mortality. The present article is based on our experience over the past 5 years with Chinese patients in our single-center hospital. And our focus is to advance the understanding of the pathogenesis, diagnosis, management, and follow-up of constrictive pericarditis.
Accepted for publication May 2, 2012. *Yiyun Lin and Mi Zhou contributed equally to this article. Address correspondence to Dr Wang, Department of Cardiothoracic Surgery Changzheng Hospital, Fengyang Rd 415, Shanghai, China 200003; e-mail: [email protected].
© 2012 by The Society of Thoracic Surgeons Published by Elsevier Inc
We retrospectively analyzed the clinical reports of 51 consecutive patients (38 males, 13 females; age 40.1 ⫾ 15.5 years; range 13 to 73 years) with constrictive pericarditis who underwent surgery from January 2005 to January 2011 in our single-center institution. Our institutional ethics committee approved the present study and all patients gave written informed consent. The diagnosis of constrictive pericarditis was made according to the combination of Doppler echocardiography (thickened or calcified pericardium), cardiac catheterization (elevated end-diastolic pressure and the “square root sign” of right ventricular pressure tracing) [13, 14], or pericardial biopsy [3]. The definite diagnosis of Tb constrictive pericarditis was based on the above criteria and one of the following: (1) a positive Tb culture from pericardial effusion or pericardial tissue; (2) a positive acid-fast stain bacilli or typical caseous granuloma on pericardial biopsy specimen; or (3) a positive Tb polymerase chain reaction in the pericardial biopsy specimen [15, 16]. Indications for pericardiectomy were preoperative clear diagnosis of constrictive pericarditis, patients with poor condition (eg, heart rate ⬎ 120/minute, albumin ⬍ 25 g/L, severe hepatic or renal failure, or severe ascites) who did not improve after medical treatment, and patients who had pericardial fenestration before the condition improved. In-hospital mortality was defined as death in-hospital or within 30 days after surgery. Results are expressed as number (percentages), mean (standard 0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2012.05.002
ADULT CARDIAC
Treating Constrictive Pericarditis in a Chinese Single-Center Study: A Five-Year Experience
1236
LIN ET AL CHINESE EXPERIENCE OF CONSTRICTIVE PERICARDITIS
ADULT CARDIAC
deviation), or as median (range) when the distribution of variables was not normal. The Student t test or the Mann-Whitney test was used for continuous variables and the Fisher exact test or 2 test was used for categoric variables. A p value of less than 0.05 was considered statistically significant. Analyses were performed by using SPSS version 17.0 (SPSS Inc, Chicago, IL).
Results Table 1 lists the causes of constriction in the series. Of the 51 patients, 33 patients (65%) had Tb constrictive pericarditis and 13 (25%) had idiopathic constrictive pericarditis. Underlying conditions were previous cardiac surgery for 3 patients (6%) and connective tissue disease for 1 patient (2%). The remaining patient had chest trauma 40years ago. The average pulse pressure was 34 ⫾ 8 mm Hg, and the mean heart rate was 100 ⫾ 14 beats per minute. When classifying patients using the preoperative New York Heart Association functional class, 24 (47%) were in class II, 19 (37%) were in class III, and 8 (16%) were in class IV. The median duration of symptoms was 6 months (range 1 to 480 months). The most common symptoms were lower limb edema (67%), shortness of breath (65%), exertional dyspnea (59%), abdominal distension (43%), palpitation (30%), and cough (26%). On physical examination, the most prominent clinical signs were raised jugular vein distension (65%), increased cardiac dullness (61%), distant heart sounds (57%), hepatomegaly (46%), tachycardia (37%), and ascites (36%). Table 2 summarizes the main features. Initial laboratory assessment showed increases in serum total and direct bilirubin, alkaline phosphatase, and markers of inflammation (erythrocyte sedimentation rate [ESR] and C-reactive protein). Among the 33 patients with Tb constrictive pericarditis, not all patients had pulmonary infection (7 patients still had Tb pleuritis or lymph-node Tb and 2 patients had a definite past history of pulmonary Tb); however, none had bone and joint Tb. Of these patients, the most common symptoms and signs were exertional dyspnea (64%), lower leg edema (64%), raised jugular vein distension (61%), and distant heart sounds (56%). None of the patients had a positive acidfast stain, Tb-DNA test, or Tb antibody test while in the hospital. On the electrocardiograms, nonspecific T wave changes were detected in 18 patients (35%), ST segment
Table 1. Etiology of Constrictive Pericarditis in Our SingleCenter Site Etiologic Factors Mycobacterium tuberculosis Idiopathic Post cardiac surgery Connective tissue disease Chest trauma history
No.
%
33 13 3 1 1
65 25 6 2 2
Ann Thorac Surg 2012;94:1235– 40
Table 2. Preoperative Clinical Details of Constrictive Pericarditis Variable Age, years Males Pulse pressure, mm Hg NYHA functional class II III IV Symptoms: Lower limb edema Shortness of breath Exertional dyspnea Abdominal distension Palpitation Cough Paroxysmal nocturnal dyspnea Fever Fatigue Chest pain Night sweat Signs: Raised jugular vein distension Peripheral edema Increased cardiac dullness Distant heart sounds Hepatomegaly Tachycardia Splenomegaly Ascites Pericardial knock sound Pulsus paradoxus S3
Result 40.1 ⫾ 15.5 38 (75%) 33.8 ⫾ 7.8 24 (47%) 19 (37%) 8 (16%) 33 (67%) 32 (65%) 29 (59%) 21 (43%) 15 (30%) 13 (26%) 12 (25%) 12 (25%) 12 (25%) 8 (16%) 6 (12%) 32 (65%) 33 (65%) 30 (61%) 28 (57%) 23 (46%) 19 (37%) 18 (36%) 18 (36%) 15 (31%) 11 (22%) 6 (12%)
Results of qualitative variables are expressed in absolute values (percentages) and results of continuous variables as mean (SD). NYHA ⫽ New York Heart Association.
depression was seen in 13 (25%) patients, low-voltage was observed in 13 (25%) patients, and atrial arrhythmias or fibrillations were found in 15 (29%) patients. Imaging examinations revealed a thickened pericardium in 92%, calcification of pericardium in 47%, cardiomegaly in 87%, pleural effusion in 51%, congestive liver in 65%, splenomegaly in 43%, and ascites in 36% patients. The chest radiograms revealed changes suggestive of pulmonary Tb in 13 (25%) patients. By Doppler echocardiography, the mean ejection fraction value was 0.59 ⫾ 0.06, pericardial thickening and calcification were found in 75% and 47%, respectively, and diastolic dysfunction was seen in almost all of the patients. Biatrial enlargement was also frequently observed; left atrium 84 ⫾ 28 mL and right atrium 69 ⫾ 27 mL (compared with normal left atrial volume 47 ⫾ 17 mL and normal right atrial volume 39 ⫾ 12 mL) [17–19]. In addition, there were mild to severe tricuspid and mitral valve incompetence in 5 and 4
LIN ET AL CHINESE EXPERIENCE OF CONSTRICTIVE PERICARDITIS
patients, respectively. A detailed list of patient characteristics is reported in Table 3. All patients underwent pericardiectomy and a midline sternotomy was performed in all cases. Constricting layers of epicardium were removed when possible. The dissection was started at the base of the aorta, followed by the lateral and posterior walls of the left ventricle and the pulmonary veins and the pulmonary artery, and extended downward to the diaphragmatic pericardium. Finally, the pericardium was resected over the free wall of the right ventricle and then over the vena cavae. We Table 3. Preoperative Examination of 51 Patients with Constrictive Pericarditis Variable Biochemical variables in blood: Hemoglobin, g/L Platelets, ⫻109/L Total bilirubin, mol/L Direct bilirubin, mol/L Albumin, g/L Alanine aminotransferase, U/L Aspartate aminotransferase, U/L Lactate dehydrogenase, U/L Alkaline phosphatase, U/L Creatinine, mol/L Urea, mmol/L Prothrombin time, seconds Erythrocyte sedimentation rate, mm/H C-reactive protein, mg/L Electrocardiogram variables: Heart rate, beats/minute Atrial arrhythmias or fibrillation T wave changes ST-segment depression Low-voltage Imaging variables: Thickened pericardium Calcification of pericardium Cardiomegaly Congestive liver Pleural effusion Splenomegaly Ascites Changes of pulmonary Tb Echocardiographic variables: Left ventricular ejection fraction Pericardial thickening Pericardial calcification Volume of left atrium, ml Volume of right atrium, ml Mild to severe tricuspid valve incompetence Mild to severe mitral valve incompetence
Result 133 ⫾ 17 151 ⫾ 57 24.8 ⫾ 10.1 12.9 ⫾ 6.3 36 ⫾ 4 26 ⫾ 12 36 ⫾ 14 221 ⫾ 54 131 ⫾ 53 81 ⫾ 20 6.2 ⫾ 1.9 14.5 ⫾ 1.4 18 ⫾ 16 11.5 ⫾ 6.9 100 ⫾ 14 15 (29%) 18 (35%) 13 (25%) 13 (25%) 47 (92%) 24 (47%) 44 (87%) 32 (65%) 26 (51%) 21 (43%) 18 (36%) 13 (25%) 0.59 ⫾ 0.06 38 (75%) 24 (47%) 84 ⫾ 28 69 ⫾ 27 5 (10%) 4 (8%)
The results of qualitative variables are expressed in absolute values (percentages) and the results of continuous variables are expressed as mean (SD).
1237
did not remove inaccessible areas, including the base of the heart where it is adherent to the diaphragm. Calcified plaques were often very difficult to remove. Cardiopulmonary bypass was not commonly used during surgery, except for 4 patients as a safe method for removing calcified pericardium, 2 patients who had concomitant mitral replacement, and 1 patient for removal of myxomas in the right atrium. Operative findings included markedly thickened pericardium (65%), adhesions (54%), and calcification (50%). The preoperative average central venous pressure was 20.2 ⫾ 5.1 mm Hg and declined to 7.4 ⫾ 3.1 mm Hg postsurgically (p ⬍ 0.001). Likewise, pulse pressure increased from 30 mm Hg to 50 to 60 mm Hg. The mean duration of the operation was 172 ⫾ 61 minutes. Pathological changes, which included caseous necrosis, fibrosis, calcification, inflammation, and hyaline plaque formation, occurred in some but not all patients. All of the bacteria cultures were negative. In-hospital mortality was 3.9% (2 of 51 patients). The cause of death was severe low cardiac output syndrome due to right heart failure, with elevated ventricular filling pressure in 1 patient and acute renal failure in the context of preoperative chronic renal failure in the other patient. There were several postsurgical complications in the surviving patients, which included pleural effusion in 23 patients, low output syndrome in 15 patients, pulmonary infection in 5 patients, and diarrhea in 1 patient. None of the patients had recurrence of heart failure before discharge. The median duration of mechanical ventilation was 10.2 ⫾ 2.8 hours. In 14 patients, blood transfusions were given during or after surgery. The average volume of perioperative transfusion was 1,286 ⫾ 698 mL. The median intensive care unit stay was 2.4 ⫾ 1.4 days. The median hospital stay was 21.9 ⫾ 3.5 days (range 8 to 39 days). For the patients in whom Tb constrictive pericarditis was diagnosed, they would receive antituberculosis agents (isoniazid, rifampicin, and ethambutol daily for 6 months, or pyrazinamide daily for 2 months). After first discharge, 2 patients were rehospitalized to undergo redo surgery for recurrent Tb constrictive pericarditis, at 3 and 10 months of follow-up. The first patient died from heart failure as a complication of the disseminated disease in 2 months after the redo surgery and the second patient died from postoperative multiple organ dysfunction syndrome in the hospital. A third patient died of scleroderma by the 6-month follow-up. The actuarial 1-year survival rate in 49 patients was 93.7% (Fig 1). Univariate analyses showed that a preoperative higher level of ESR (p ⫽ 0.006), abnormal creatinine value (p ⫽ 0.029), postoperative low output syndrome (p ⫽ 0.001), and pleural effusion (p ⫽ 0.035) were each positively associated with increased mortality.
Comment Constrictive pericarditis is an uncommon condition involving impaired mid and late ventricular filling due to a thickened or noncompliant pericardium. The most important findings of our evaluation were that clinical
ADULT CARDIAC
Ann Thorac Surg 2012;94:1235– 40
1238
LIN ET AL CHINESE EXPERIENCE OF CONSTRICTIVE PERICARDITIS
Ann Thorac Surg 2012;94:1235– 40
Fig 1. Kaplan-Meier curve showing survival for the 49 constrictive pericarditis patients. (Cum ⫽ cumulative.)
ADULT CARDIAC
manifestations could worsen, even with short durations of symptoms, and thus timely diagnosis and prompt treatment are important to improved prognosis. Our results are consistent with previous studies, which showed that constriction was more common in males [7, 12, 20]. While there is no clear explanation for the sex differences, previous studies have found male to female preponderances varying from 1.7:1 to 4:1 [3]. Our study showed almost 3 times as many males as females were subjects. The normal pericardium is approximately 3-mm thick. With chronic constriction, especially from Tb, the pericardium may double to 6 mm or more, calcify, and intimately involve the epicardium. In the classic form, fibrous scarring and adhesions of both pericardial layers lead to obliteration of the pericardial cavity. Thus, while early ventricular filling is unimpeded, diastolic filling is subsequently reduced abruptly as a result of the inability of the ventricles to fill due to physical constraints imposed by the structurally altered pericardium. Cardiac output is reduced, likely due to the inadequate diastolic filling of the ventricles. In our experience, the predominant symptoms of constrictive pericarditis are lower limb edema, shortness of breath, and exertional dyspnea; abdominal symptoms, palpitation, and cough are also common. The most frequent signs are raised jugular vein distension, increased cardiac dullness, and distant heart sounds. Other findings include hepatomegaly, tachycardia, pleural effusion, and ascites. Increased heart rate and elevated venous pressure are compensatory mechanisms that offset the increase in intrapericardial pressure. At times, however, patients may not present with sufficient signs or symptoms for the clinician to make a definite diagnosis. In these cases, additional imaging is required and recommended. Echocardiography is essential for the diagnosis of the pericardial syndrome. Compared with echocardiogra-
phy, cardiac computed tomography and magnetic resonance imaging offer the advantage of better imaging of the pericardium, with more accurate measurements of pericardial thickening [21]. Cardiac computed tomography and magnetic resonance imaging can delineate abnormal pericardial thickness found in constrictive pericarditis [10]. The association between the characteristic hemodynamic changes with increases of pericardial thickness more than 3 mm always confirms the diagnosis [22]. This is an important point because Tb pericardial constriction is almost always associated with pericardial thickening [23]. Constrictive pericarditis must be diagnosed early because cardiac tamponade can occur in the acute phase and constrictive pericardia may subsequently develop. Decreased cardiac output resulting from a chronic constrictive process may require surgical intervention. Currently, pericardiectomy is the only accepted curative treatment for improving cardiac hemodynamics in constrictive pericarditis [24]. In our center, surgery occurs within 1 week of diagnosis. In cases where this is a delay due to the difficultly in gaining a clear diagnosis, however, surgery should be undertaken as soon as possible, before clinical manifestations become worse. As to thoracotomy, Chen and Lai [13] often found it difficult to remove the pericardium overlying the thinwalled right atrium and vena cava by left anterolateral thoracotomy, but Lachman and colleagues [11] reported that the left anterolateral approach allowed wider access to the left ventricle, which was a significantly improved approach. In our series, all procedures were done through median sternotomy, which provides good operative exposure and is the preferred surgical approach. Cardiopulmonary bypass can be used as a safe method for removing calcified pericardium. The objective of the procedure is to release the ventricles from the densely adherent pericardial shell. The lack of a surgical plane
LIN ET AL CHINESE EXPERIENCE OF CONSTRICTIVE PERICARDITIS
can make this an operation with high blood loss, and attention must be paid to salvage and reinfuse blood. Epicardial coronary vessels are at risk in this dissection and particular care must be taken when dissecting in the regions of these vessels. After surgery, care should be taken to remove every constrictive layer to avoid persistent pericardial constriction, and cardiac performance immediately improves after incision of the pericardium [10]. In this series, pleural effusion, low output syndrome, and pulmonary infection were the most common postoperative complications (Table 4). Because diastolic filling recovers (especially filling of the right atrium), inotropes, diuretics, and salt restriction are important to avoid low cardiac output and right heart failure. However, the overzealous use of diuretics is not recommended and could possibly lead to sudden death [25]. On the other hand, Tb may cause long-term malnutrition and constrictive pericarditis leads to cardiogenic nutrient deprivation. Clinicians, therefore, attach great importance to nutrition supply and will give a blood transfusion if needed.
Table 4. Intraoperative and Postoperative Information of 51 Patients With Constrictive Pericarditis Variable Intraoperative information: Duration of the operation, minutes Cardiopulmonary bypass used Concurrent operation Mitral replacement Removal of myxomas Central venous pressure (CVP) change Preoperative CVP, mm Hg Postoperative CVP, mm Hg Operative findings: Markedly thickened pericardium Pericardium adhesions Pericardium calcification Postoperative information: Duration of mechanical ventilation, hours Blood transfusions (including during or after surgery): Number of patients Volume of transfusion, mL Postsurgical complications (49 surviving patients): Pleural effusion Low output syndrome Pulmonary infection Diarrhea Intensive care unit stay, days Hospital stay, days In-hospital mortality
Result 172 ⫾ 61 7 (14%) 2 (4%) 1 (2%) 20.2 ⫾ 5.1 7.4 ⫾ 3.1 32 (65%) 28 (54%) 26 (50%) 10.2 ⫾ 2.8
14 (27%) 1,286 ⫾ 698
23 (47%) 15 (31%) 5 (10%) 1 (2%) 2.4 ⫾ 1.4 21.9 ⫾ 3.5 2 (3.9%)
The results of qualitative variables are expressed in absolute values (percentages) and the results of continuous variables are expressed as mean (SD).
1239
In our single-center institution, Tb counted for 65% of the causes of constrictive pericarditis. The diagnosis of Tb in constrictive pericarditis in this series was almost always confirmed by pathological diagnosis. Atypical for pulmonary Tb, however, some of our patients did not suffer from any respiratory symptoms. All examinations to test for Tb (for example, sputum acid-fast stain, Tb-DNA test, and Tb antibody tests) were negative. It is thought that Tb constrictive pericarditis occurs much later after active Tb pulmonary infection or ineffective therapy of the pulmonary infection [24]. For patients with suspected Tb constriction, we recommend that antituberculosis therapy be started before and continued after pericardial surgery. As for the conservative treatment option, the use of corticosteroids is still controversial. Some view that a course of glucocorticoid treatment (eg, prednisone, 20 to 60 mg/day for up to 6 weeks [9]) is useful to manage the acute disease, reduce effusion, facilitate hemodynamic recovery, and thus decrease mortality rates [26]. However, it is uncertain whether adjunctive corticosteroids are effective in reducing mortality or pericardial constriction [21]. Progression to chronic constrictive pericarditis, however, does not seem affected by such therapy. As a general case, we did not give corticosteroid therapy to Tb constrictive pericarditis patients because those who received surgical treatment experienced chronic pericardial changes and did not show any obvious symptoms of poisoning. Furthermore, long-term use of glucocorticoid could increase the risk of postoperative infection. From the 1-year follow-up, our results demonstrate that an initial higher ESR and abnormal preoperative creatinine value, postoperative low output syndrome, and pleural effusion predict mortality. Because reversible constrictive pericarditis was associated with pericardial and systemic inflammation [27], some inflammation markers, such as ESR, should be included during follow-up.
Limitations This study is unique in that it summarizes the Chinese experience of treating constrictive pericarditis over the past 5 years. However, there were a few limitations that warrant mentioning. Only a few patients underwent preoperative hemodynamic cardiac catheterization and hence there was an increased difficulty to differentiate between constriction and restrictive cardiomyopathy. We routinely made the differential diagnosis according to cardiac computed tomography and magnetic resonance imaging, which were considered as excellent methods for differentiating [20]. Further, although the etiology of constrictive pericarditis varies geographically and resistant TB strains have appeared gradually [28], we lacked a special test to find out the definite strain of Tb that caused 2 recurrent cases in our follow-up. Lastly, we need to continue our follow-up to determine the long-term outcomes in this cohort.
Conclusions Rapid diagnosis and treatment of constrictive pericarditis are crucial to reduce mortality. We suggest that pericardial stripping should be performed early and as radically as possible in an effort to prevent chronic illness. After surgery, nutritional supply and proper fluid infusion are
ADULT CARDIAC
Ann Thorac Surg 2012;94:1235– 40
1240
LIN ET AL CHINESE EXPERIENCE OF CONSTRICTIVE PERICARDITIS
also critical for a good prognosis. Inflammation markers, such as ESR, should also be included during follow-up.
References ADULT CARDIAC
1. Fowler NO. Tuberculous pericarditis. JAMA 1991;266:99 – 103. 2. Clare GC, Troughton RW. Management of constrictive pericarditis in the 21st century. Curr Treat Options Cardiovasc Med 2007;9:436 – 42. 3. Schwefer M, Aschenbach R, Heidemann J, Mey C, Lapp H. Constrictive pericarditis, still a diagnostic challenge: Comprehensive review of clinical management. Eur J Cardiothorac Surg 2009;36:502–10. 4. Chowdhury UK, Subramaniam GK, Kumar AS, et al. Pericardiectomy for constrictive pericarditis: A clinical, echocardiographic, and hemodynamic evaluation of two surgical techniques. Ann Thorac Surg 2006;81:522–9. 5. Peset AM, Marti V, Cardona M, et al. Outcome of pericardiectomy for chronic constrictive pericarditis. [Article in Spanish] Rev Esp Cardiol 2007;60:1097–101. 6. Russell JB, Syed FF, Ntsekhe M, et al. Tuberculous effusiveconstrictive pericarditis. Cardiovasc J Afr 2008;19:200 –1. 7. Zheng SY, Zhu P, Zhuang J, et al. Surgical treatment of 128 cases of constrictive pericarditis. [Article in Chinese] Nan Fang Yi Ke Da Xue Xue Bao 2010;30:535–7. 8. Murray JF. A century of tuberculosis. Am J Respir Crit Care Med 2004;169:1181– 6. 9. Reuter H, Burgess LJ, Louw VJ, Doubell AF. The management of tuberculous pericardial effusion: experience in 233 consecutive patients. Cardiovasc J S Afr 2007;18:20 –5. 10. Bozbuga N, Erentug V, Eren E, et al. Pericardiectomy for chronic constrictive tuberculous pericarditis: risks and predictors of survival. Tex Heart Inst J 2003;30:180 –5. 11. Lachman N, Vanker EA, Christensen KN, Satyapal KS, Fennell WM. Pericardiectomy: a functional anatomical perspective for the choice of left anterolateral thoracotomy. J Card Surg 2009;24:411–3. 12. Imazio M, Brucato A, Maestroni S, et al. Risk of constrictive pericarditis after acute pericarditis. Circulation 2011;124: 1270 –5. 13. Chen RF, Lai CP. Clinical characteristics and treatment of constrictive pericarditis in taiwan. Circ J 2005;69:458 – 60. 14. Imazio M, Spodick DH, Brucato A, Trinchero R, Markel G, Adler Y. Diagnostic issues in the clinical management of pericarditis. Int J Clin Pract 2010;64:1384 –92.
Ann Thorac Surg 2012;94:1235– 40
15. Fowler NO. Constrictive pericarditis: its history and current status. Clin Cardiol 1995;18:341–50. 16. Bathoorn E, Limburg A, Bouwman JJ, Bossink AW, Thijsen SF. Diagnostic potential of an enzyme-linked immunospot assay in tuberculous pericarditis. Clin Vaccine Immunol 2011;18:874 –7. 17. Pritchett AM, Jacobsen SJ, Mahoney DW, Rodeheffer RJ, Bailey KR, Redfield MM. Left atrial volume as an index of left atrial size: a population-based study. J Am Coll Cardiol 2003;41:1036 – 43. 18. Wang Y, Gutman JM, Heilbron D, Wahr D, Schiller NB. Atrial volume in a normal adult population by twodimensional echocardiography. Chest 1984;86:595– 601. 19. Aune E, Baekkevar M, Roislien J, Rodevand O, Otterstad JE. Normal reference ranges for left and right atrial volume indexes and ejection fractions obtained with real-time threedimensional echocardiography. Eur J Echocardiogr 2009;10: 738 – 44. 20. Mookadam F, Jiamsripong P, Raslan SF, Panse PM, Tajik AJ. Constrictive pericarditis and restrictive cardiomyopathy in the modern era. Future Cardiol 2011;7:471– 83. 21. Syed FF, Mayosi BM. A modern approach to tuberculous pericarditis. Prog Cardiovasc Dis 2007;50:218 –36. 22. Cinar B, Enç Y, Göksel O, et al. Chronic constrictive tuberculous pericarditis: Risk factors and outcome of pericardiectomy. Int J Tuberc Lung Dis 2006;10:701– 6. 23. Talreja DR, Edwards WD, Danielson GK, et al. Constrictive pericarditis in 26 patients with histologically normal pericardial thickness. Circulation 2003;108:1852–7. 24. Augustin P, Desmard M, Mordant P, et al. Clinical review: intrapericardial fibrinolysis in management of purulent pericarditis. Crit Care 2011;15:220. 25. Marshall A, Ring N, Lewis T. Constrictive pericarditis: lessons from the past five years’ experience in the south west cardiothoracic centre. Clin Med 2006;6:592–7. 26. Strang JI, Nunn AJ, Johnson DA, Casbard A, Gibson DG, Girling DJ. Management of tuberculous constrictive pericarditis and tuberculous pericardial effusion in transkei: results at 10 years follow-up. QJM 2004;97:525–35. 27. Feng D, Glockner J, Kim K, et al. Cardiac magnetic resonance imaging pericardial late gadolinium enhancement and elevated inflammatory markers can predict the reversibility of constrictive pericarditis after antiinflammatory medical therapy: a pilot study. Circulation 2011;124:1830 –7. 28. Mayosi BM, Burgess LJ, Doubell AF. Tuberculous pericarditis. Circulation 2005;112:3608 –16.