Orthotopic heart transplantation (OHT) has become anccepted form of therapy for end-stage heart disease with 5-nd 10-year survival rates of 75% and 55%, respectively.1
cute rejection, infection, and cardiac allograft vasculopathyave been recognized as the major causes of morbidity andortality in these patients. Constrictive pericarditis may follow
ny cardiac surgical procedure, including coronary bypass,alvular replacement surgery and corrective surgery for con-enital heart disease.2–8 Cardiac surgery is reported to be theeading cause of pericardial constriction in patients with andentifiable etiology.2–6 The incidence of pericardial constric-ion after cardiac surgery varies from 0.1% to 0.3%.5 Thereave also been rare case reports of constrictive pericarditisfter cardiac transplantation surgery; several of these haveescribed constriction in association with purulent pericarditisnd mediastinitis.9–16 In this report, we describe the largestlinical experience of post-transplant pericardial constriction of
Reprint requests: Ramesh C. Bansal, MD, Adult Echocardiographyaboratory, Loma Linda University School of Medicine, 11234 Andersontreet, Room 4404, Loma Linda, CA 92354. Telephone: 909-558-7675.ax: 909-558-0903.
on-infectious etiology. We review the literature and report thencidence, etiology, diagnostic features, and management ofhis condition.
ethods
e performed a search of our institution’s echocardio-raphic database and identified all patients who had evi-ence of pericardial constriction after orthotopic heart trans-lantation. Our surgical database was also searched toapture cases that had undergone peri-cardiectomy for post-ransplant constriction. We then proceeded to review theiredical and surgical records and collected information re-
arding clinical, imaging, hemodynamic, and pathologicesults. The number of diagnosed and treated rejection ep-sodes were obtained. All patients received intravenous ste-oids peri-operatively and were continued on a taperingose of oral prednisone as part of a triple-drug immunosup-ressive regimen. The follow-up period ranged from 7
372 The Journal of Heart and Lung Transplantation, Vol 29, No 3, March 2010
urgical technique
urgical management of the pericardium at the time of OHTonsisted of excision of a generous segment of the anteriorericardium after excision of the native heart and prior tomplantation of the donor organ. This window ends approx-mately 2 cm anterior to the left phrenic nerve. This com-unication between the pericardial and the left pleural
paces reduces the incidence of large pericardial fluid col-ection. Such partial peri-cardiectomy is routinely per-ormed in patients with first-time sternotomy; however, inatients with multiple previous sternotomies and/or cardiacperations, the presence of fibrous adhesions within theiddle mediastinum and the pleural spaces may not allowuch pericardial resection. In such cases when the medias-
inal tissue is fixed or indurated with extensive adhesions,e opt not to take down the adhesions. Routinely, however,
arge chest tubes are used to drain the pericardial and leftleural spaces. Primary closure of the sternotomy is per-ormed after the transplantation procedure and no attempt isade to close the pericardium over the grafted organ.When pericardial constriction occurs after heart trans-
lantation, re-operation is performed via re-do sternotomy.ardiopulmonary bypass may be necessary for completend adequate pericardiectomy. Surgical bleeding duringericardiectomy is usually controlled after reversal of hep-rinization.
esults
etween January 1986 and May 2009, 127 adult OHTrocedures were performed at our institution. After OHT,erial echocardiographic studies are performed per institu-ional protocol. Review of this database revealed the pres-nce of pericardial effusions of varying sizes in 53 patients42% of all cases) in the early post-operative period (aver-ge 27 days). In the great majority of cases, the effusionesolved spontaneously in the subsequent 3 months withoutonsequences. Five patients developed diagnostic featuresf pericardial constriction (4% of all transplant recipients;% of patients developing effusions) and constitute theasis of this report. In 4 cases, surgical findings and patho-ogic specimens at pericardiectomy confirmed the clinicaliagnosis.
Table 1 Patients’ Salient Clinical Characteristics and Outcome
Patient
Age at the timeof diagnosis(years) Gender
Post-transplantpericardialeffusion
Pericardprior topericard
1 (A.J.) 49 M Yes 22 (M.M.) 57 M Yes 03 (N.R.) 47 F Yes 04 (A.L.) 35 M Yes 05 (P.D.) 28 M Yes 0
A summary of our patients’ demographics, clinical andurgical characteristics, and ancillary data is presented inable 1.
Time to development of constriction varied from 3eeks to 11 years after OHT. All patients presented withrogressive symptoms of right-sided heart failure. Echocar-iography was the initial imaging study to suspect pericar-ial constriction in all patients. Hemodynamic studies wereerformed in 4 and computed tomography in 2 patients.ndomyocardial biopsy at variable intervals was performedn all individuals; low-grade rejection requiring adjustmentf immunosuppressant drugs was found in 4 of 5 cases.
Four patients underwent successful pericardiectomy withatisfactory intra-operative results. However, despite clearvidence of restoration of near-normal hemodynamics andardiac function, 1 patient died 30 days after pericardiec-omy as a consequence of widespread, extensive, multifocalerpetic ulcerations involving the entire gastrointestinalract.
Summaries of our 5 cases are presented in what follows.
ase 1
49-year-old man with severe ischemic cardiomyopathy un-erwent OHT. A follow-up echocardiogram 3 months laterevealed a large pericardial effusion with features of tampon-de that led to prompt pericardiocentesis; the effusion re-ccumulated and led to a second pericardiocentesis 6 weeksater. He remained clinically stable until 14 months after theransplant when he presented with right-sided heart failure withower extremity edema and ascites. Echocardiographic exam-nation revealed a thick pericardium overlying the right atriumnd right ventricle with markedly elevated right atrial (RA)ressure, features consistent with pericardial constriction.
During pericardiectomy, the thick, fibrotic pericardium wasonfirmed and epicardial decortication completed the proce-ure. The patient was discharged home 2 days later. At hisost recent visit 5.7 years after pericardiectomy, he was
symptomatic and echocardiography showed normal graftunction and filling pressures.
ase 2
56-year-old man with dilated cardiomyopathy underwentHT. An echocardiogram 2 months later showed a small- to
esis
yRejectionepisodes
Time toconstrictiondevelopment Outcome
Long-termfollow-up afterpericardiectomy
2 14 months NYHA I 5.7 years5 13 months NYHA I 8.9 years0 3 weeks NYHA II 9.4 years9 5 years Expired N/A2 (humoral) 11 years N/A N/A
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373Bansal et al. Constrictive Pericarditis in Cardiac Transplant
oderate-sized localized pericardial effusion that resolvedpontaneously. Severe constriction was diagnosed by echo-ardiography 13 months after OHT. Diagnosis was sup-orted by hemodynamic studies.
During radical pericardiectomy, a thickened pericardiumnd a dense epicardial peel over the right atrium and ven-ricle were found. The patient had a favorable postoperativeourse and was discharged 5 days after pericardiectomy.
He was most recently seen 8.9 years after pericardiec-omy and has continued to have no cardiac symptoms; hischocardiogram showed normal ventricular function andlling pressures.
ase 3
much earlier presentation of constriction was seen in ourhird case, a 47-year-old woman who had undergone trans-lant for sarcoid-related cardiomyopathy. Only 3 weeksfter OHT, she presented with hypotension, leg edema, andscites. Echocardiogram revealed bloody effusion, clottedlood circumferentially in the pericardium with thickenednd fused pericardial layers, and high RA pressure. Shenderwent urgent phrenic-to-phrenic pericardiectomy. Im-ediately after resection, an improvement in blood pressure
nd a drop in central venous pressure (CVP) were noted. Aericardial pathologic specimen showed sarcoid granuloma-ous lesions and pericardial thickness of up to 1.5 cm. Sheas discharged in stable condition 2 days after pericardiec-
omy.On a recent visit at 9.4 years after OHT, she reported
oderate exertional dyspnea related to diastolic dysfunc-ion, severe tricuspid regurgitation, and pulmonary hyper-ension.
ase 4
29-year-old man with palliated complex congenital heartisease underwent OHT. Several Grade 2R rejection episodes
igure 1 Apical 4-chamber views with left ventricle displayed aanel shows marked leftward septal shift (arrow) in inspiration du
ight ventricle.
ere managed with intensification of immunosuppressants. Aelf-resolving, small pericardial effusion was noted as early as9 days after OHT. Five years after transplant, heart failureymptoms developed and chest X-ray showed a new pleuralffusion. Echo-Doppler studies showed normal systolic func-ion and evidence of pericardial thickening and enhanced ven-ricular interdependence by 2-dimensional echocardiographynd respirophasic valvar flow changes (Figures 1 and 2). Echo-ardiography also showed left pleural effusion. Right heartatheterization demonstrated classical hemodynamics of con-triction (Figure 3). A cardiac computerized tomography (CT)can showed regional pericardial thickening of up to 6 mmFigure 4).
Myocardial biopsy showed no evidence of rejection. Athe time of pericardiectomy, the patient was critically ill as
consequence of marked coagulopathy secondary to liverysfunction (INR 7.0), decreased renal function (creatinine.9 mg/dl), nutritional depletion, oliguria, hypotension, andypoxemia. Marked pericardial thickening (up to 8 mm)ith dense epicardial peel causing extreme cardiac constric-
ion was noted during pericardiectomy (Figure 5). Pericar-iectomy and epicardial decortication were performed usingardiopulmonary bypass, after which a drop in CVP from 42o 15 cm H2O and a brisk increase in urine output wereoted. He was extubated 72 hours after pericardiectomyith marked improvement in hemodynamics and heart fail-re symptoms. Intermittent hemodialysis was required.hree weeks after, he developed a surgical abdomen with
efractory shock; despite resuscitative efforts, he died 31ays after pericardiectomy. Post-mortem examination re-ealed widespread multifocal herpetic ulcerations involvinghe entire gastrointestinal tract.
ase 5
29-year-old man with viral cardiomyopathy underwentHT and developed a spontaneously resolving pericardial
ffusion 2 weeks after transplantation. Incipient echocardio-
ericardial thickening is shown in the left panel (arrow). The rightntricular interdependence. LA, left atrium; LV, left ventricle; RV,
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374 The Journal of Heart and Lung Transplantation, Vol 29, No 3, March 2010
raphic evidence of pericardial constriction was first noted1 years after OHT, as evidenced by preserved left ventric-lar systolic function, normal valve function, a non-collaps-ble inferior vena cava, pleural effusion (Figure 6), andncreased transvalvar respirophasic flow variation. The peri-ardium was only minimally thickened by echocardiogra-hy and showed normal systolic function and preservedystolic and E= velocities by Doppler tissue imaging (Figure). These findings favored constriction rather than restric-ion or rejection. Chest CT showed normal thickness peri-ardium (Figure 7); however, the CT showed other featuresf volume overload, including dilation of inferior vena cavand pleural effusion (Figure 7).
He was recently admitted with an episode of syncope dueo complete heart block, presumably due to humoral rejec-ion and allograft vasculopathy. In addition to plasmaphere-
igure 2 Pulsed Doppler examination of aortic valve (AV) flowxpiration as compared with 60 cm/s in inspiration.
igure 3 Right heart pressure tracings show high right atrialressure (RA) with a rapid “y” descent. Right ventricular (RV)racing shows dip-and-plateau pattern, with an inspiratory (Ins)ncrease and expiratory (Exp) decrease in RV systolic pressure.ortic tracing shows reciprocal rise in aortic pressure in expira-
ion. v
is and intensification of immunosuppressants, he has beenait-listed for re-do heart transplant.
iscussion
ost-transplant constrictive pericarditis
onstrictive pericarditis is an infrequent, but well-docu-ented complication of cardiac surgery.2–8 It was first re-
orted in 19722 and may develop after any cardiac surgicalrocedure, including coronary bypass grafting, valve sur-ery, and repair of congenital lesions.2–8 The incidence of
5-chamber view shows marked increase in velocity to 90 cm/s in
igure 4 Computed tomography of chest shows marked peri-ardial thickening (arrow) and left pleural effusion (LPE). LV, left
from
entricle; RV, right ventricle.
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375Bansal et al. Constrictive Pericarditis in Cardiac Transplant
ost-surgical constriction ranges from 0.1% to 0.3%.5–7 Ineveloping countries, the most common etiology of con-triction continues to be tuberculosis.8 In the United States,owever, cardiac surgery has become the leading cause ofonstriction and accounts for 18%7 to 37%5 of cases with andentifiable etiology.
Constriction has also rarely been reported after cardiacransplantation.9–16 Review of the transplant literature re-eals a total of 17 cases of pericardial constriction reportedn 8 publications (Table 2). In previous reports, the time toecognition of constriction ranged from 1 month to 2ears9–16; we observed its development as early as 3 weeksnd as late as 11 years after OHT. This condition affectedpproximately 1.5% of cases in previous clinical10,13 and.6% in post-mortem11 reports. In our series, it developed inof 127 (4%) of adult cardiac transplants. The true inci-
ence of post–cardiac transplant constriction remains elu-ive; patients with pericardial constriction causing mildeart failure may respond to diuretics and are unlikely tondergo testing to establish the diagnosis. Similarly, refrac-ory heart failure in transplant recipients may be treated asejection and restrictive cardiomyopathy rather than con-triction. This uncertainty may have delayed the diagnosisn Patients 4 and 5 in the present series, and has beenecognized previously.15
igure 6 Select echo-Doppler images from Patient 5 showing dnd right pleural effusion (PE) is noted in the middle panel. Tissue
= tissue velocities. The pericardium was minimally thickened and fuse
athogenesis
t has been suggested that pericardial constriction after car-iac surgery is related to peri-operative pericardial injury ornflammation and exposure of the injured serosal surface tontra-pericardial bleeding.3 In addition, pericardial irrigationith povidone–iodine in the presence of serosal injury mayrecipitate a pericardial fibrotic reaction.2,3 Clinical featuresuggestive of the post–pericardiotomy syndrome were notedn 62% of cases in one large series of post-surgical pericar-ial constriction.3 Pericardial injury, irritation, bleeding,nd mediastinal infections initiate a fibrotic reaction thatredisposes to the subsequent development of constrictionn heart transplant recipients. A review of the 17 reportedases of post-transplant constriction showed that 4 cases hadediastinal or wound infection, and 2 had infected and 10
on-infected pericardial effusion after OHT. In our series,ll 5 cases developed a non-infected pericardial effusion orematoma after surgery. Pericardiocentesis was performedn 1 patient.
iagnosis
he diagnosis of constrictive pericarditis should be stronglyonsidered in cardiac transplant recipients who present with
igure 7 Computed tomography image of the chest shows nor-al pericardial thickness (arrow) and right pleural effusion (PE).
inferior vena cava (IVC) in the left panel. The liver is congesteder imaging from lateral mitral annulus shows high systolic (S) and
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376 The Journal of Heart and Lung Transplantation, Vol 29, No 3, March 2010
ymptoms of predominant right heart failure and a history ofarly post-operative pericardial effusion, bleeding, hema-oma, or mediastinal infection. In patients with heart trans-lant, however, rejection and restriction must be exclud-d.17–19 Echocardiography is usually the first studyerformed and provides guidance regarding selection ofppropriate complimentary procedures such as CT, mag-etic resonance, and cardiac catheterization. The detectionf thickened pericardium of �3 mm may be of help iniagnosing pericardial constriction.20,21 Pericardial thick-ess can be measured by transthoracic and transesophagealchocardiography (Figure 1), and also by CT (Figures 4 and). Of note, an isolated thickened pericardium in the ab-ence of abnormal hemodynamics does not imply constric-ion. On the contrary, in 21% of patients with post-surgicalonstriction, a normal pericardial thickness was encoun-ered on cardiac CT.3 Talreja et al described a normal peri-ardial thickness in 18% of patients undergoing pericardiec-omy for constriction.21 Clinical, echo-Doppler andemodynamic features of constriction but normal pericardialhickness on cardiac CT (Figure 7) were found in 1 patient inur series.
Patients with constrictive pericarditis demonstrate theharacteristic features of dissociation of intracardiac andntrathoracic pressures and enhanced ventricular interdepen-ence. These abnormalities lead to inspiratory leftward sep-al shift on 2-dimensional echocardiography (Figure 1) andynamic respirophasic flow variation in intracardiac flowelocities. Doppler echocardiography demonstrates an in-rease in mitral and aortic flow velocities in excess of 25%uring expiration compared with inspiration (Figure 2).
Table 2 Previously Reported Constricted Pericarditis After Ort
Investigators(date) n Incidence Wounda
Data from Copeland(1986)
1 NA Serratia effusionpericardial (1 of 1)
Data from Carrier(1994)
2 1.5% (2 of 133) NA
Data from Loire(1994)
5 2.6% (5 of 191) NA
Data from Hinkamp(1994)
4 1.4% (4 of 295) Staphylococcal pericardeffusion (1 of 4)
Data from Roca(1995)
2 NA Staphylococcalmediastinitis (1 of 2)
Empyema (1 of 2)Data from Rose
(2002)1 NA Pseudomonas
mediastinitis (1 of 1)Data from Ramana
(2005)1 NA Wound infection (1 of 1
Data from Kumar(2008)
1 NA NA
NYHA, New York Heart Association (heart failure classification); NA,aInfection/mediastinitis/pericarditis/empyema.
levated right atrial pressure produces inferior vena cava d
ilation and lack of inspiratory collapse. High cardiac fillingressures cause pleural effusion and ascites (Figures 4, 6,nd 7). Cardiac catheterization shows high right atrial meanressure with a rapid “y” descent and lack of respiratoryariation (Figures 3 and 8). Right ventricular pressure trac-ng shows a characteristic dip-and-plateau, or square-rootattern (Figure 3). Enhanced ventricular interdependenceeads to a rise in right ventricular systolic pressure due toncreased right ventricular filling during inspiration and aeciprocal decrease in left ventricular22–24 and aortic pres-ures (Figures 3 and 8).
anagement and outcomes
ericardiectomy and epicardial decortication relieve the re-traint on cardiac filling and result in marked symptomatic
c Heart Transplantation
t-transplanticardial effusion
Time to constrictiondevelopment Outcome
15 months NYHA I
icardial hematoma2 of 2)
1 and 12 months NYHA I (1) persistentsymptoms and SCD(1)
igure 8 Right atrial (RA) pressure tracing (left panel) showsapid “y” descent and high mean pressure. Simultaneous rightRV) and left ventricular (LV) tracings in the right panel show
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377Bansal et al. Constrictive Pericarditis in Cardiac Transplant
mprovement in the majority of patients. Peri-operativeortality appears to be related to etiology; it was reported to
e 2.7% in idiopathic, 8.3% in post-surgical, and 21.4% inost-radiation pericardial constriction.5 Long-term survivals adversely impacted by post-radiation etiology, advancedonstriction, calcification, older age, left ventricular systolicysfunction, higher pulmonary pressure, and renal dysfunc-ion.5,7
In post-transplant pericardial constriction, good out-omes after pericardiectomy are related to an early diagno-is. It is evident that the coexistence of post-transplantestrictive cardiomyopathy is associated with poor long-erm results even after pericardiectomy is performed.13
Previous reports in which postoperative clinical data arevailable have demonstrated that approximately 50% of pa-ients enjoy satisfactory, long-term, symptom-free surviv-l.9,10,12–16 Our results confirm the potential for excellent long-erm outcomes when the condition is diagnosed and treatedarly. When the diagnosis is delayed or recognized late, thisondition is associated with malnutrition, coagulopathy, andiver and kidney insufficiency. These patients can be criticallyll and their post-pericardiectomy outcome may be poor. Con-ervative management with clinical and echocardiographicurveillance appears to be a safe strategy in minimally symp-omatic individuals.
In conclusion, constrictive pericarditis should be stronglyonsidered in heart transplant patients presenting with heartailure with preserved systolic function. The index of sus-icion should be higher in transplant recipients with a his-ory of post-operative pericardial effusion, hematoma, orediastinal infection. A complete echo-Doppler examina-
ion will provide definitive information in the majority ofatients. CT and cardiac catheterization provide comple-entary information. Pericardiectomy with epicardial de-
ortication should be considered early in symptomatic casesnd is generally associated with favorable long-term results.
isclosure Statement
he authors have no conflicts of interest to disclose.
eferences
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