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Uremic pericarditis progressed to subacute constriction despite intensive medical treatment in two patients with concomitant metabolic stress of surgery and infection. Total pericardiectomy was successful and should be done as soon as medical measures fail to resolve the pericarditis.
A 50-yr-old man developed constrictive pericarditis following an episode of acute pericarditis. Cardiac catheterization revealed a typical early diastolic dip and plateau configuration in both the right and left ventricular pressure curves. The coronary flow velocity pattern determined using an intracoronary Doppler guidewire showed an abrupt decrease in peak velocity at early diastole and followed by plateau until late diastole, the so-called dip and plateau configuration. After a successful pericardiectomy, cardiac catheterization no longer showed the dip and plateau configuration, but the early diastolic dip in the coronary flow velocity persisted probably because of infiltration of the organic involvement into the myocardium.
Patients with advanced cystic fibrosis typically have chronic bacterial infection of the upper and lower respiratory tracts, but rarely develop extrapulmonary sites of infection. We report a case of purulent pericarditis due to Pseudomonas aeruginosa in a patient with cystic fibrosis and no other risk factors for pericarditis. This is a previously unreported complication in cystic fibrosis prior to lung transplantation.
To study the evolution of pericardial inflammation, we have developed a model of pericarditis in sheep by surgically injecting heat-killed staphylococci and Freund's adjuvant into the pericardial cavity under sterile conditions. The pericarditis evolved through the following phases: 1) inflammatory response, 2) mesothelial cell injury and desquamation, and 3) fibrotic phase. At 3-24 hr there was increased microvascular permeability, which resulted in the exudation of fluid, neutrophils, macrophages, and fibrin into the pericardial cavity and the pericardial interstitium. By 72 hr, large numbers of inflammatory cells were aggregated on the mesothelial surfaces and dispersed throughout the pericardial cavity, either as free-floating cells or located between strands of fibrin. At 6 days, fibrinolysis was apparent along the mesothelial surfaces; and newly formed collagen fibrils were deposited throughout the interstitial spaces and among the aggregated cells. These fibrils provided a matrix for the growth of new blood and lymphatic vessels into new connective tissue on both parietal and visceral pericardial surfaces. At 2 weeks, intrapericardial fibrosis had produced focal adhesions between the pericardial surfaces. At 1 month, extensive areas of the pericardial cavity were obliterated. By 9 months, there was a marked reduction in the numbers of cells and blood vessels and increased deposition of collagen and elastic fibers. The intrapericardial injection of heat-killed staphylococci and adjuvant provides a reproducible animal model to study the time course of pericardial inflammation.
The pericardial effusion in a case of rheumatoid pericarditis was studied to determine whether immune complexes and mediators of cellular immunity, represented by migration inhibitory factor (MIF), were present. MIF-like activity was detected in the pericardial fluid, but only traces of immune complexes were revealed by ultracentrifugation. The MIF-like activity was partially characterized by column fractionation and sugar inhibition tests. The role of lymphokines in the pathogenesis of this case of rheumatoid pericarditis is strongly suggested.
A 17-year-old male with systemic lupus erythematosus presented with clinical signs of severe constrictive pericarditis that was confirmed by cardiac catheterization. At surgery, a fibrous pericardium was removed, followed by complete relief of symptoms. Immunopathology of the pericardial tissue revealed deposition of IgG, IgM, and C3. A review of the literature produced only three similar cases. Although rare, constrictive pericarditis, a potentially life threatening complication, may occur in systemic lupus erythematosus presumably with an immunological basis.
Bacterial pericarditis is commonly a disease of children for which the primary treatment is surgical drainage. We report the case of a 19-yr-old patient presenting with pneumococcal pericarditis and tamponade treated successfully with intrapericardial catheter drainage and intravenous antibiotics. The technical aspects are discussed.
An 88 year old woman with streptococcal pneumonia developed purulent pericarditis and cardiac tamponade despite treatment with antibiotics. Percutaneous pericardial drainage was effected with a 6 French pigtail catheter inserted via the subxyphoid approach. Catheter drainage was continued for 7 days in conjunction with systemic antibiotics. Catheter patency was maintained with antibiotic lavage. Immediate hemodynamic improvement followed the initial pericardial drainage. Fever, leukocytosis, and sepsis resolved during the course of therapy. The patient recovered fully from the closed space bacterial infection without additional surgical drainage. There has been no recurrence of streptococcal infection and no echocardiographic evidence of recurrent pericardial effusion after 3 months of follow-up. Indwelling catheter drainage combined with antibiotics may be an effective substitute for surgical drainage in the treatment of streptococcal pericarditis.
A 38-year-old man with a history of migraine headaches with aura and one episode of ischemic stroke was found to have a patent foramen ovale (PFO). After percutaneous closure with the nickel-containing Amplatzer PFO occluder, the patient developed pericarditis, atrial fibrillation, and increased migraine headaches with aura that abated with oral prednisone. He tested positive for nickel hypersensitivity, which we conclude is the likely etiology of his pericarditis.
We report the case of a 35-year-old man with constrictive pericarditis who had a B-type natriuretic peptide (BNP) level of 129 pg/dl despite a left ventricular end diastolic pressure of 35 mmHg. We discuss a possible explanation for the relatively low BNP level given this patient's markedly elevated intracavitary pressures in the setting of constrictive pericarditis.
A 43-year-old man with idiopathic hypereosinophilic syndrome survived a relatively long term (6 1/2 years) before he succumbed to intractable heart failure. Six months before death, his chronic heart failure from restrictive cardiomyopathy was well compensated. Autopsy demonstrated severe constrictive pericarditis which was not suspected antemortem. Constrictive pericarditis as a late complication of idiopathic hypereosinophilic syndrome is discussed.
Constrictive pericarditis is a fibrotic process involving both layers of the pericardium and is known to give rise to obstruction to blood flow in the right heart. We report a patient with constrictive pericarditis who had echocardiographic features of mitral stenosis caused by a fibrocalcific mass lesion involving the mitral annulus with infiltration into the base of the posterior mitral leaflet. To our knowledge, this has not been reported in the literature.
Pneumococcal pericarditis has been an uncommon condition in recent years. This report describes the case of a 57-year-old woman with sarcoidosis who presented with cardiac tamponade due to pneumococcal pericarditis. She responded to pericardiocentesis and intravenous antibiotic therapy. At 4-month review, she remains well.
A case of the sick sinus syndrome and constrictive pericarditis with effusion (seroconstrictive pericarditis) as manifestations of lymphomatous involvement of the heart is presented. Autopsy findings documented infiltration of the sinus node by undifferentiated malignant lymphoma cells. The clinical course is described and problems with diagnosis and management of such a complication are discussed. This is one of the few cases in the literature in which an uncommon cause of conduction system disease and pericardial constriction was substantiated by electrocardiogram, angiography, and autopsy.
A patient with Aspergillus endocarditis, myocarditis and pericarditis is described. A 55-year-old man developed necrotizing fasciitis of the lower abdominal wall, pelvis and right thigh. Despite aggressive surgical débridement and antibiotic coverage, the patient died of multisystem organ failure. Autopsy revealed Aspergillus thromboulcerative endocarditis, myocarditis and pericarditis, acute necrotizing fungal bronchopneumonia and mycotic dissemination to brain, kidney and thyroid gland. A review of the literature showed that in the absence of open-heart surgery Aspergillus endocarditis and myocarditis are very uncommon.
The radiographic features of pericarditis due to Histoplasma capsulatum are described in 5 children. This diagnosis is suggested when enlargement of the cardiac silhouette is associated with pneumonia, parenchymal nodules or adenopathy. These findings are particularly significant if the patient lives or has lived in an area which is endemic for histoplasmosis. While pleural effusion is rare in primary histoplasmosis, it is frequently present in patients with histoplasma pericarditis.
The electrocardiograms of 18 out of 21 patients hospitalized between 1964 and 1972 with purulent pericarditis presented significant changes. With the exception of three cases of primary isolated pericarditis, most of the patients presented with septicemia. Staphylococcus aureus was the predominant pathogen in 16 cases. Classical electrocardiographic evolution in four phases was recorded in six cases. Draining of the pericardial effusion in the patients without pleurisy was followed by low-voltage amelioration in half of the cases. The duration of the electrocardiographic changes was shorter in patients who underwent intrapericardial treatment. One quarter of the patients suffering from myopericarditis with conduction disturbances--Block AV 1, 2 and Wenckebach's periods--had a worse prognosis.
A 43-year-old woman was hospitalized for fulminant pericarditis. During diagnostic work-up, an as yet unknown bronchial carcinoma was detected. In the pericardial exudate Legionella pneumophila serogroup 3 was demonstrated by direct fluorescent antibody technique and by culture. In a lung biopsy L. pneumophila serogroup 3 was found, too. Using an antigen-ELISA for L. pneumophila serogroup 1, antigenuria was demonstrated. In cases of pericarditis negative for common bacterial pathogens, all diagnostic tests for legionellae, e.g. culture, antigen detection in pericardial, pleural effusion and urine and antibody detection should be included in the diagnostic programme.