Constrictive Pericardial Disease Research Articles

A Patient-Centered Mobile Intervention to Promote Self-Management and Improve Patient Outcomes in Chronic Heart Failure: The ManageHF Trial

Introduction Heart failure (HF) is the most common hospital discharge diagnosis among older adults. As a result, the management of HF is moving toward a proactive real-time technological model of assisting patients with monitoring and self-management. Hypothesis Our hypothesis was that a patient-centered mobile application, ManageHF, would reduce Minnesota Living with Heart Failure Questionnaire (MLHFQ) at 6 and 12 weeks post-hospital discharge compared to usual care. Methods A single-center randomized controlled trial was performed. Patients were included if they were greater than 45 years of age, had a left ventricular ejection fraction (LVEF) 40% (with LA size >40 mm or BNP > 200 pg/ml or NT-proBNP > 800 pg/ml) and were currently admitted or recently discharged for acute on chronic decompensated HF. Patients were excluded for any of the following: unstable coronary syndromes within 8 weeks, primary valvular heart disease, constrictive pericardial disease, uncorrected thyroid disease, dialysis or creatinine >4.0 mg/dL, a hospice candidate, active cancer, pulmonary fibrosis, discharged to a setting other than home, or required a chronic inotrope. The intervention group used a mobile application, ManageHF, along with a Fitbit wearable and scale. The mobile application prompted active self-monitoring and provided a health status indicator to promote self-management. The control group received usual care. The primary outcome was the change in MLHFQ from baseline to 6 and 12 weeks using mixed models. Secondary outcomes were the Self-Care Heart Failure Index (SCHFI) questionnaire and HF admissions. Results Eighty-two patients were enrolled and completed all baseline assessments. Baseline characteristics were similar between groups with the exception of HF type. The intervention group had a reduced MLHFQ at 6 weeks (p=0.026) but not at 12 weeks (p=0.61) compared to control (Figure). There was no effect of the intervention on the SCHFI or any of its subcomponents at 6 or 12 weeks. The time to first HF admission was not statistically different between the two groups (HR 0.85, 95% CI 0.36-2.0, p=0.71). Median number of days the intervention group performed self-monitoring was 63 days. Conclusion ManageHF improved MLHFQ at 6 weeks, but did not sustain its effects at 12 weeks. No effect was seen on self-care measured by SCHFI. Further research is needed to enhance engagement in the app for a longer period of time and to determine if the app can reduce HF admissions in a larger study.

Effusive-constrictive pericarditis: current perspectives

Effusive-constrictive pericarditis: current perspectives Bernhard Maisch Faculty of Medicine, Philipps-University Marburg and Center for Heart and Vessels, Marburg, Germany Abstract: Effusive-constrictive pericarditis (ECP) is defined by concurrent pericardial effusion and pericardial constriction. Whereas the pericardial cavity is typically obliterated in patients with constrictive pericarditis without any effusion, in patients with ECP the scarred pericardium not only constricts the cardiac volume but can also put pericardial fluid under increased pressure, leading to signs suggestive of cardiac tamponade. These hemodynamic features can persist even after the pericardial effusion is removed. The underlying pathogenetic process predominantly involves the visceral pericardium or epicardium. It combines visceral pericardial constriction with pericardial inflammation. Its etiology may be as variable as the causes of effusive or constrictive pericardial disease, which may be infective (e.g., bacterial or viral), malignant or autoreactive. The label idiopathic ECP should be avoided and restricted to only those cases in whom, after thorough clinical and pathological workup including PCR for microbial agents in pericardial fluid and cardiac tissue from peri- and epicardial or endomyocardial biopsies and the assessment of autoimmune processes, no definite diagnosis can be made. Since a considerable number of ECP patients have an inflammatory and reversible pericardial reaction, they can improve under causal and/or anti-inflammatory treatment. The treatment should therefore be based first on eradicating the underlying etiological factors. If such a treatment course remains ineffective, pericardiectomy including the removal of the visceral pericardium is the remaining therapeutic option. Keywords: pericarditis, etiology, constriction, hemodynamics of ECP, treatment&nbsp

Occult constrictive pericardial disease emerging 40\xa0years after chest radiation therapy: a case report

BackgroundThe main etiology of constrictive pericarditis (CP) has changed from tuberculosis to therapeutic mediastinal radiation and cardiac surgery. Occult constrictive pericardial disease (OCPD) is a covert disease in which CP is manifested in a condition of volume overload.Case presentationA 60-year-old patient with a history of thoracic radiation therapy for non-Hodgkin’s lymphoma (40 years earlier) was transferred to our hospital for treatment of repeated congestive heart failure. For a preoperative hemodynamic study, pre-hydration with intravenous normal saline (50 mL/hour) was used to manifest the pericardial disease and prevent contrast-induced nephropathy. The hemodynamic study showed a right ventricular dip-plateau pattern and discordance of right and left ventricular systolic pressures during inspiration, which was not seen in the volume-controlled state. These responses were concordant with OCPD. A pericardiectomy, aortic valve replacement, and mitral and tricuspid valve repair were performed. Postoperatively, the heart failure was controlled with standard medication.ConclusionsThis case revealed a volume-induced change in hemodynamics in OCPD with severe combined valvular heart disease, which suggests the importance of considering OCPD in patients who had undergone radiation therapy 40 years before.

Idiopathic Constrictive Pericardial Disease in a Patient with Cystic Fibrosis

Introduction We report on a case of a patient with cystic fibrosis and co-existent constrictive pericardial disease. This unique presentation has been presented only once before in the literature. Our case is the first documented case where a patient with cystic fibrosis has undergone curative pericardial stripping. Case The case is about a patient who was diagnosed with cystic fibrosis at the age of 45. His sweat chloride level was 77.0mmol/L and genotype heterozygous for RII7H and delta F508. His FEV1 was 75% predicted at the time of admission. The patient was hospitalized for a presumed pulmonary exacerbation of his cystic fibrosis. He presented with cough with scant mucous production and no hemoptysis. He also noted dyspnea on exertion and new onset peripheral edema. He was treated for a pulmonary exacerbation with intravenous antibiotics and airway clearance measures and discharged home after two days. He worsened despite optimal therapy for a pulmonary exacerbation. A simultaneous right and left heart catheterization was performed that was suggestive of constrictive pericardial disease. The patient underwent a pericardial stripping that resolved his symptoms. He was discharged home after surgery and has been doing well. Discussion Constrictive pericardial disease is an extremely rare complication that is not frequently seen in cystic fibrosis. Simultaneous left and right heart catheterization can be used to make the diagnosis. Surgery is curative. Although pulmonary exacerbation is the most common cause of shortness of breath in patients with cystic fibrosis other diagnosis should be considered.

Constrictive pericarditis – still an overlooked entity

Constrictive pericarditis still remains a challenge for clinicians because it is a rare disease, with a long symptom-free period that can make it difficult to establish the relation between etiology and first clinical presentation. Multimodality imaging is the modern approach for diagnostic work-up and clinical management. In this context, we report a typical case of constrictive pericardial disease, first misconstrued as decompensated liver cirrhosis, and later unsuccessfully treated as congestive heart failure, without a clear etiology. By reporting this case, we also aimed to highlight the importance of some complementary diagnostic techniques in refining the preoperative assessment, in order to adequately address a patient to pericardiectomy, the only curative treatment.

Mechanical Support for the Failing Right Ventricle in Patients With Precapillary Pulmonary Hypertension.

Right ventricular (RV) dysfunction is the principal predictor of adverse outcome in pulmonary hypertension (PH).1,2 For those PH patients requiring inpatient intensive care because of acutely decompensated heart failure, mortality estimates can range as high as 30% to 48%.3–5 Hyponatremia, renal insufficiency, systemic hypotension, and severe tricuspid regurgitation are worrisome clinical characteristics that prognosticate poor outcome in this PH patient subpopulation.3,5,6 Effective strategies to optimize cardiopulmonary hemodynamics and support RV function are paramount; clinical responsiveness to pulmonary vascular/RV-specific treatment is likely to decrease the probability of requiring surgical intervention and, ultimately, improve outcome. This review will discuss existing evidence pertaining to the timing and utility of mechanical support in patients with RV failure attributable to pulmonary vascular disease. Constrictive pericardial disease, selected forms of congenital heart disease, inflow obstruction, primary myocardial disease, and pressure or volume overload are each well-described causes of adverse RV remodeling, RV systolic dysfunction, and cor pulmonale.7 Among patients with RV dysfunction as a result of pressure overload, precapillary PH and left-sided heart failure are the most common etiologies. The first adaptive response of the RV to pressure overload is hypertrophy. If untreated, the RV dilates to compensate for increased RV preload and, according to the Frank-Starling principle, to maintain stroke volume. When further increases in RV end-diastolic filling volume do not offset progressive RV contractile dysfunction, clinically evident RV failure ensues. In advanced stages, RV cavitary dilation may also impair left ventricular (LV) diastolic filling kinetics and contribute further to global pump dysfunction and, consequently, to the congestive heart failure syndrome. Mechanical support in the setting of RV dysfunction aims to stabilize and therapeutically improve several key mechanisms underpinning RV decompensation and heart failure by reducing RV preload and afterload, and by improving …

Ascites with Elevated Protein Content as the Presenting Sign of Constrictive Pericardial Disease

Two men, one 63 and one 52 years old, presented with ascites. Analysis of the ascitic fluid in both patients revealed a high protein content and an elevated serum-ascites gradient. Various studies showed the cause of the ascites to be constrictive pericardial disease. Total excision of their parietal pericardia relieved their symptoms, decreased their cardiac filling pressures, and increased their cardiac indices. These cases highlight the importance of suspecting pericardial constriction as an etiology for high-protein-count ascites.

Association of the Metabolic Syndrome With Pulmonary Venous Hypertension

Pulmonary venous hypertension (PVH) is a well-described cause of pulmonary hypertension (PH) in patients with left heart disease associated with elevated left heart filling pressure. PVH results from a number of processes, including left-sided valvular disease, constrictive pericardial disease, restrictive cardiomyopathies, and left ventricular (LV) systolic dysfunction. PVH in patients with normal LV systolic function, commonly referred to as diastolic dysfunction, is not well characterized. We observed that many patients with PH due to PVH have obesity, hypertension, diabetes mellitus, and hypercholesterolemia, which are clinical features of the metabolic syndrome (MS), a previously identified cause for systemic vascular disease. We evaluated 122 consecutive patients referred for diagnosis and treatment of PH and compared the prevalence of features of the MS between patients with PVH and those with pulmonary arterial hypertension (PAH). We also compared clinical and hemodynamic characteristics between these two groups. Compared to patients with PAH, patients with PVH had a higher frequency of hypertension, obesity, diabetes mellitus, and hyperlipidemia. Two or more features of the MS were found in 16 of 17 patients with PVH (94.1%) compared with 34.3% of patients with PAH (p < 0.001; odds ratio, 30.7; 95% confidence interval, 3.6 to 260.0). PH was substantial, but less severe overall, in patients with PVH compared to those with PAH (mean pulmonary artery pressure, 45 +/- 17 mm Hg [range, 26 to 71 mm Hg] vs 53 +/- 10 [range, 33 to 72 mm Hg], respectively [p = 0.041]; and pulmonary vascular resistance, 4.4 +/- 2.9 units [range, 1.2 to 10.8 units] vs 10.8 +/- 4.7 units [range, 4.8 to 21.9 units], respectively [p < 0.001]). PVH is highly associated with the MS. Our results suggest that the MS may predispose patients to develop pulmonary vascular disease.

The Utility of Cardiovascular Magnetic Resonance in Constrictive Pericardial Disease

Cardiovascular magnetic resonance (CMR) has a high diagnostic accuracy for constrictive pericarditis (CP). CMR allows for high-resolution imaging of the pericardium and associated structures in any imaging plane compared with that provided by other imaging modalities. We briefly discuss the specific quantitative and qualitative CMR sequences that can be tailored to answer the clinical questions pertaining to CP, where the diagnostic yield has been proven when characteristic CMR features of CP are present. Such features allow for differentiation of CP from restrictive cardiomyopathy, where the clinical differentiation between the 2 can often be challenging.

Acute Isolated Viral Pericarditis With Rapid Progression to Constrictive Pericardial Disease

A previously healthy 42-year-old man presented with fatigue and progressive dyspnea 6 weeks after an episode of massive diarrhea that required supportive intravenous therapy. A chest x-ray showed bilateral pleural effusion and echocardiography demonstrated extensive pericardial effusion, whereas global systolic right and left ventricular function appeared preserved (Figure 1A). Figure 1. Echocardiographic still frames of a four-chamber view at endsystole. (A) During initial presentation, extensive pericardial effusion (white arrow) and a “swinging heart” pattern were seen. (B) Six months later, paradoxical motion of the interventricular septum and an echo-intense pericardium were found (white arrowheads). The patient was referred to cardiac magnetic resonance imaging for suspected inflammatory involvement of the myocardium; cardiac magnetic resonance imaging demonstrated acute inflammation confined to the visceral and parietal pericardial layers (Figure 2A through …

Right atrial inflow obstruction of the inferior vena cava due to atrial septal aneurysm and an elongated Eustachian valve

We describe a patient with oedema of the legs and ascites due to right atrial (RA) inflow obstruction, caused by atrial septal aneurysm (ASA) and an elongated Eustachian valve (EV). Both structural abnormalities created a narrow inflow channel to the free RA cavity. RA inflow obstruction is usually related to constrictive pericardial disease and pericardial tamponade. Other cardiac causes of RA inflow obstruction are rare and include lipomatous hypertrophy of interatrial septum, tumour or thrombus in the right atrium (RA). Reports, describing inflow obstruction in the RA as a consequence of an elongated EV or an ASA, are extremely rare.

Comparison of Usefulness of Tissue Doppler Imaging Versus Brain Natriuretic Peptide for Differentiation of Constrictive Pericardial Disease from Restrictive Cardiomyopathy

Brain (B-type) natriuretic peptide (BNP) and tissue Doppler imaging may distinguish restrictive cardiomyopathy (RCMP) from idiopathic constrictive pericardial disease (CP). However, their comparative efficacy is unknown for patients with CP from secondary causes (e.g., surgery or radiotherapy). We compared the efficacy of tissue Doppler imaging and BNP for differentiation of RCMP (n = 15) and CP (n = 16) were compared. BNP was higher in patients with RCMP than CP (p = 0.008), but the groups overlapped, particularly for BNP <400 pg/ml. BNP was lower with idiopathic CP than secondary CP (139 +/- 50 vs 293 +/- 69 pg/ml; p <0.001) or RCMP (139 +/- 50 vs 595 +/- 499 pg/ml; p <0.001), but not significantly different between those with secondary CP and RCMP (293 +/- 69 vs 595 +/- 499 pg/ml; p = 0.1). Patients with CP and RCMP had less overlap in early diastolic and isovolumic contraction tissue Doppler imaging velocities compared with BNP, with clear separation of groups evident with mean early diastolic annular velocities (averaged from 4 walls). Early diastolic tissue Doppler imaging velocity was superior to BNP for differentiation of CP and RCMP (area under the curve 0.97 vs 0.76, respectively; p = 0.01). In conclusion, mean early diastolic mitral annular velocity correctly distinguished CP from RCMP even when there was a large overlap of BNP between the 2 groups.

Management of Effusive and Constrictive Pericardial Heart Disease

Case study: A 69-year-old white male was referred for transesophageal echocardiography (TEE) two days after urgent coronary artery bypass grafting. In the first 24 postoperative hours, pleural and pericardial drainage was nearly 3 L, during which time the blood pressure was supported with inotropic agents. The next day, chest tube drainage was minimal, a transthoracic echocardiogram was unremarkable, and the patient was extubated. Shortly thereafter, the patient became hypotensive and dyspneic. TEE revealed a large loculated effusion with linear adhesions and thrombus that compressed both atria, as well as a large pleural effusion. There was marked respiratory variation in Doppler velocities across the tricuspid and mitral valves. At thoracotomy, 1 L of blood was removed from the pericardial space, bleeding at the site of aortic cannulation was sutured, and the patient made an uneventful recovery. Treatment of effusive and constrictive pericardial disease is often simple and gratifying, but frustration and unforeseen challenges await the unwary clinician. The symptoms and signs of pericardial disease, at times unmistakable (as in the patient described above), may be overshadowed by extracardiac manifestations of a systemic disorder; at other times, they are insidious and conceal their true nature. Pericardial constriction mimics hepatic cirrhosis and myocardial failure and may be virtually indistinguishable from restrictive cardiomyopathy. Another important problem is the lack of placebo-controlled trials from which appropriate therapy may be selected and of guidelines that assist in important clinical decisions; as a result, the practitioner must rely heavily on clinical judgment. Finally, therapeutic options in most cases are limited to antiinflammatory agents, drainage of pericardial fluid, and pericardiectomy. However, despite general agreement on how these measures should be applied in patients with either very mild or severe disease, there is little consensus on the management of the large number of cases encountered with clinical manifestations between …

Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy

This study assesses how the newer modalities of tissue Doppler echocardiography and color M-mode flow propagation compare with respiratory variation of Doppler flow in distinguishing between constrictive pericarditis and restrictive cardiomyopathy. We studied 30 patients referred for further evaluation of diastolic function who had a diagnosis of constrictive pericarditis or restrictive cardiomyopathy established by diagnostic tests, including clinical assessment, magnetic resonance imaging, cardiac catheterization, endomyocardial biopsy, and surgical findings. Nineteen patients had constrictive pericarditis and 11 had restrictive cardiomyopathy. We performed 2-dimensional transesophageal echocardiography combined with pulsed-wave Doppler of the pulmonary veins and mitral inflow with respiratory monitoring, tissue Doppler echocardiography of the lateral mitral annulus, and color M-mode flow propagation of left ventricular filling. Respiratory variation of the mitral inflow peak early (peak E) velocity of ≥10% predicted constrictive pericarditis with 84% sensitivity and 91% specificity and variation in the pulmonary venous peak diastolic (peak D) flow velocity of ≥18% distinguished constriction with 79% sensitivity and 91% specificity. Using tissue Doppler echocardiography, a peak early velocity of longitudinal expansion (peak E a) of ≥8.0 cm/s differentiated patients with constriction from restriction with 89% sensitivity and 100% specificity. A slope of ≥100 cm/s for the first aliasing contour in color M-mode flow propagation predicted patients with constriction with 74% sensitivity and 91% specificity. Thus, the newer methods of tissue Doppler echocardiography and color M-mode flow propagation are equivalent and complimentary with Doppler respiratory variation in distinguishing between constrictive pericarditis and restrictive cardiomyopathy. The additive role of the new methods needs to be established in difficult cases of constrictive pericarditis where respiratory variation may be absent or decreased.

Calcific constrictive pericarditis: is it still with us?

The presence of pericardial calcification on a plain radiograph strongly suggests constrictive pericarditis in patients with heart failure. However, calcific constrictive pericarditis is considered rare in the United States since tuberculosis incidence has decreased, and doubt has therefore been raised about the importance of this radiologic finding in modern cardiovascular practice. To determine the clinical and prognostic significance of pericardial calcification on radiography in patients with constrictive pericarditis. Retrospective cohort study. Tertiary referral center. A consecutive series of 135 patients (mean age +/- SD, 56 +/- 16 years) who from 1985 through 1995 had constrictive pericarditis confirmed surgically (n = 133) or by autopsy (n = 2). Patients were divided into two groups: those with pericardial calcification on chest radiography (group I) and those without (group II). Clinical and diagnostic findings were compared in both groups, and outcome was compared in 132 patients who had pericardiectomy. Pericardial calcification was seen in 36 patients (27%). The cause of constrictive pericardial disease was indeterminate in 67% of patients in group I and in 21% of patients in group II (P < 0.001). Patients in group I had had symptoms for a longer period and were more likely to have pericardial knock, larger atrial size, and atrial arrhythmia. Significantly more perioperative deaths were seen in group I, but incidence of late survival and incidence of noncalcific disease were similar in both groups. Pericardial calcification is a common finding in patients with constrictive pericarditis. It is often associated with idiopathic disease and other markers of disease chronicity and is an independent predictor of increased perioperative mortality rates.

Constrictive pericarditis: its history and current status.

The diagnosis of constrictive pericarditis remains a challenge because it is often mimicked by restrictive cardiomyopathy. The last few years have seen numerous advances in our ability to differentiate between these two conditions which often have similar physical findings and hemodynamics. This review begins with a brief history of constrictive pericarditis; this is followed by an extensive discussion of newer etiologies, and then the classical clinical history and physical examination findings are described. Radiologic, electrocardiographic, and angiographic findings are discussed. The hemodynamics of constrictive pericarditis are reviewed. Recent results of echocardiographic and echo-Doppler investigations are presented. Emphasis is placed upon the limitations of M-mode echocardiography in the diagnosis of constrictive pericarditis. The value of echocardiographic Doppler studies of mitral and tricuspid flow velocity patterns, as well as of those in the pulmonary veins and hepatic veins, is described. Nuclear ventriculograms and angiocardiograms tend to show more rapid ventricular filling in constrictive pericarditis than in restrictive cardiomyopathy. Although only a small number of patients has been studied, these evaluations seem to have merit in separating restrictive cardiomyopathy from constrictive pericarditis. The role of computed tomography scanning and magnetic resonance imaging studies of pericardial thickness in confirming the presence of constrictive pericarditis is discussed. Abnormal pericardial thickening (> 3 mm) confirms the diagnosis of constrictive pericarditis, but only if the characteristic hemodynamic pattern is present. The usefulness of endomyocardial biopsy in recognizing specific varieties of restrictive cardiomyopathy is presented.(ABSTRACT TRUNCATED AT 250 WORDS)

Constrictive pericardial disease caused by epicardial implantable cardiac defibrillator patches: Treatment by pericardial stripping and nonthoracotomy lead system implantation

Constrictive pericardial disease caused by epicardial implantable cardiac defibrillator patches: Treatment by pericardial stripping and nonthoracotomy lead system implantation

Radiation-Induced Cardiovascular Disease Including Stenosis of Coronary Ostium, Coronary and Carotid Arteries, and Aortic Valve

Clinical and necropsy findings are described in a 42-year-old man who received mediastinal irradiation (about 40 Gy) for Hodgkin's disease when he was 24 years old. He subsequently developed virtually every cardiovascular manifestation of radiation heart disease, including constrictive pericardial disease, complete occlusion of the ostium of a coronary artery, severe narrowing of the right coronary artery and of both carotid arteries, complete heart block (infranodal), hemodynamically confirmed aortic valve stenosis, and transmural right ventricular infarction.

Usefulness of dynamic hand exercise for developing maximal separation of left and right ventricular pressures at end-diastole and usefulness in distinguishing restrictive cardiomyopathy from constrictive pericardial disease

Advances in differentiating restrictive cardiomyopathy from constrictive pericarditis has been gained by examining echocardiographic measures of diastolic function. Using Doppler echocardiography, Appleton et al 1 demonstrated an increase in right ventricular (RV) size and a concomitant decrease in left ventricular (LV) size during inspiration in patients with constriction. Using these same techniques, Hatle et al 2 showed opposite changes in inflow velocity across the mitral and tricuspid valves in patients with constrictive pericarditis but not restrictive cardiomyopathy. Despite these improvements in distinguishing restrictive cardiomyopathy from constrictive pericarditis in patients at rest, there have been few studies examining the effect of dynamic maneuvers on diastole as a means of distinguishing these 2 conditions. We addressed the hemodynamic differentiation of restrictive cardiomyopathy and constrictive pericarditis by evaluating the separation of LV and RV end-diastolic pressures after physiologic maneuvers. The traditional method for developing maximal separation of RV and LV end-diastolic pressures is rapid intravenous infusion of saline solution. 3 This method allows separation of end-diastolic pressures in patients with restrictive cardiomyopathy but not constrictive pericarditis. 3,4 Most patients with these disease states have elevated diastolic pressures, and a fluid challenge is potentially unsafe. Accordingly, we tested the hypothesis that dynamic hand exercise could provide a safe alternate means of maximizing the separation of LV and RV end-diastolic pressures in patients with restrictive cardiomyopathy but not constrictive pericarditis.

Pericardial drainage: subxiphoid vs. transthoracic approach

The optimal management of effusive pericardial disease remains controversial. Subxiphoid drainage has been criticized for a high recurrence rate while transthoracic procedures (window or pericardiectomy) are more invasive operations with greater potential for morbidity. We compared subxiphoid (SX group) and transthoracic (TT group) drainage in 131 patients (age range from 1 month to 81 years) treated from 1979 to the present. The etiology of effusion included cancer (38), uremia (24), infection (27), radiation (9), and other (33) causes. The two groups had similar age and sex distribution, etiology, and fluid volume. There was no difference in the operative mortality between the two groups (SX 15%, TT 13%, p = NS). Patients undergoing thoracotomy for treatment of effusive pericardial disease had a higher incidence of respiratory complications as defined by the presence of pneumonia, pleural effusion, prolonged ventilation, and need for reintubation (SX 11%, TT 35%, p less than 0.005). This may account, in part, for the longer mean hospital stay in transthoracic group (14.4 vs. 11.4 days). Nine patients were lost to follow-up after hospital discharge. The remaining 104 hospital survivors were followed for between 1 month and 11 years (mean 34 months, cumulative of 297 patient years). Three patients in each group experienced fluid recurrence and all but one were successfully treated by needle aspiration or percutaneous catheter placement. Following discharge, no patient required reoperation for effusive or constrictive pericardial disease or died from tamponade. There were no significant differences in 5-year actuarial survival (SX 54%, TT 49%) or actuarial freedom from recurrence (SX 89%, TT 93%).(ABSTRACT TRUNCATED AT 250 WORDS)