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PubMed1990

Pericarditis in AIDS.

A wide variety of organisms and conditions have been reported to cause pericarditis in patients that present and die with AIDS. Although pericarditis is remarkably common in patients dying of AIDS, no consistent pattern of cause emerges. Patients with AIDS are susceptible to pericarditis as a concomitant of the terminal condition, but it seldom contributes to the patient's death. Alternatively, pericarditis (as opposed to silent pericardial effusion) as a cardinal symptom in a patient's illness is likely to have an origin that can be ascribed to organisms typically associated with infectious pericarditis in those patients who have profound cellular immunodeficiency. Thus, it is important to make the diagnosis of infectious or neoplastic pericarditis in the setting of AIDS, since control of the agent has the potential of influencing the clinical course. In the absence of signs of hemodynamic compromise or inflammation, pericardial effusion may be accepted as an accompaniment of pleural effusions or ascites in the appropriate clinical context. Invasive diagnostic measures may be reserved for those cases in which pericardial disease is a prominent feature of the symptom complex or of accompanying pleural effusion. The study of epidemiology and biology of AIDS is a rapidly changing field. Explanations of the high incidence of pericardial disease in terminal disease may emerge with broad-ranging studies of the incidence of myocarditis in AIDS as well as the relative contribution to pericardial disease of agents used in the treatment of the illness.

Acquired Immunodeficiency Syndrome↗

PubMed1987

Pericarditis in the course of acute leukemia.

Among 140 patients with acute leukemia (AL) diagnosed according to FAB criteria, pericarditis was diagnosed clinically in 5 of them. They were 2 women and 3 men with different types of AL (L2-in one, M2-in one, M3-in one and M4-in two persons). It occurred in one patient at the onset of the disease and was associated with hyperuricemia, in another one--in complete remission, in the third--during partial remission, and in remaining two patients--during induction therapy. In all patients pericarditis was manifested by fever up to 38-40 degrees C, tachycardia and pericardial friction, in 3-heart silhouettes were enlarged. The ECG revealed mainly depression of ST segments. In 1 case only ECG pattern was typical of pericarditis. Clinically the symptoms of right ventricle failure predominated in 3 and of septic shock--in 2 patients. The etiologic factors were: Pseudomonas aeruginosa 2 X, Enterobacter cloacae 1 X, tuberculosis infection 1 X and hyperuricemia and Enterobacter sepsis 1 X. Pericarditis was favourably influenced by treatment with antibiotics, cardiaca and diuretics in 4 patients. One patient died of a sepsis. In no case the patient's death was attributable to pericarditis. The results of postmortem examinations in 79 cases of AL has revealed three additional cases of pericarditis due to tuberculosis infection, Staphylococcus aureus sepsis and aspergillosis.

Adolescent↗

PubMed1995

Chylothorax associated with constrictive pericarditis in a dog.

Chylothorax was associated with constrictive pericarditis in a 6-year-old mixed-breed dog. Clinical signs included hepatomegaly, bilateral jugular pulses, muffled heart sounds, and dyspnea. Pleural effusion was identified on thoracic radiographs. Thoracentesis yielded 3 L of chylous effusion, confirmed by the cholesterol/triglyceride ratio (0.14). Echocardiography revealed a thickened pericardium, with numerous fibrin tags, which was suggestive of constrictive pericarditis. Central venous, right atrial, and right ventricular pressures were high and on right ventricular diastolic pressure tracings, the square-root sign, which is indicative of constrictive pericarditis, was evident. Exploratory thoracotomy and pericardiectomy were performed. Histopathologic findings were consistent with chronic non-suppurative pericarditis. The dog's condition improved after surgery. On reevaluation 11 months later, central venous pressure and results of physical examination and thoracic radiography were normal. On the basis of these findings, we concluded that chylothorax was caused by constrictive pericarditis in this dog. Chylothorax is often associated with disorders that have a poor prognosis, but if constrictive pericarditis can be identified as the cause of the chylothorax, exploratory thoracotomy and pericardiectomy can provide a cure.

Animals↗

PubMed1977

[Therapy of uremic pericarditis].

An uraemic pericarditis can appear as complication of a haemodialysis in different stages. At the beginning an uraemic pericarditis is still to be referred to the uncompensated retention or to adaptation processes in the cellular mineral metabolism. An uraemic pericarditis in the later course of the dialysis nearly regularly is connected with an underdialysis syndrome which can be evoked by fistula or shunt complications or by infections of different genesis (sepsis, hepatitis, virus infections). - It is reported on own experiences in the dialytic treatment of uraemic pericarditis. In the period from 1970 to 1976 among 83 patients who were in chronic dialytic treatment an uraemic pericarditis was observed in 21 cases. In 3 patients developed haemorrhagic effusions with tamponade. The longest survival time of a patient with uraemic pericarditis and acute cardiac arrest in the early stage of the dialytic treatment is up to now 5 1/2 years after transplantation of a kidney of a corpse. - The possibilities of an operative exonneration of the heart from pericarditic changes are discussed.

Chronic Disease↗

PubMed2000

Post-Myocardial Infarction Pericarditis.

Post-myocardial infarction pericarditis occurs in approximately 5% to 6% of patients who receive thrombolytic agents. It should be suspected in any patient with pleuropericardial pain. A pericardial friction rub may or may not be present. Differentiation of pericarditis from recurrent angina may be difficult, but a careful history and evaluation of serial electrocardiograms can help distinguish the two entities. Dressler's syndrome, pericarditis that occurs at least 1 week following myocardial infarction, is now exceedingly rare. Most cases of pericarditis have a benign course; however, because pericarditis is associated with larger infarcts, overall long-term mortality rate is increased. Rare complications include hemopericardium, cardiac tamponade, and constrictive pericarditis. Therapy is directed toward relief of pain, which usually responds well to nonsteroidal anti- inflammatory agents (eg, aspirin or ibuprofen).

Journal Article↗

PubMed1979

Pericarditis: differential diagnostic considerations.

A retrospective analysis of 133 patients was performed to define the factors identifying those individuals at risk for the more serious causes of pericardial disease. In 90% of the cases, the initial assessment from data obtained without pericardiocentesis or pericardiectomy proved correct. Underlying tuberculous or maligant pericarditis were the most common sources of error on initial assessment. Hemodynamic compromise exclusive of anticoagulants, roentgenographic cardiomegaly, pleural effusion, low voltage on ECG, and large pericardial effusion by echocardiography were more common (P less than .05) in tuberculous pericarditis than in acute idiopathic pericarditis. We discuss similar risk factors in patients with chronic idiopathic, rheumatologic, and uremic pericarditis. Anterior pericardiectomy is favored as the diagnostic procedure of choice in patients at risk for the more serious causes of pericarditis because of greater safety, diagnostic sensitivity, and potential therapeutic benefit.

Adult↗

PubMed1980

Unusual complications of epicardial pacemakers. Recurrent pericarditis, cardiac tamponade and pericardial constriction.

Three patients with unusual complications after insertion of an epicardial pacemaker are described. In one patient pericarditis and severe cardiac tamponade developed that required emergency pericardiocentesis 8 weeks after pacemaker insertion. No evidence of myocardial perforation was observed at operation. In another patient two unusual complications developed: (1) migration of the pulse generator from the epigastric site of implantation into the pelvis, and (2) recurrent pericarditis with occult signs of constriction. In another patient recurrent pericarditis and clinical evidence of constriction developed. All three patients required pericardiectomy. Recurrent pericarditis after insertion of an epicardial pacemaker requires careful medical follow-up because either life-threatening tamponade or chronic constrictive pericarditis may develop.

Adult↗

PubMed1990

Myocardial and endocardial involvement in tuberculous constrictive pericarditis: difficulty in biopsy distinction from endomyocardial fibrosis as a cause of restrictive heart disease.

Differentiation of constrictive pericarditis and endomyocardial fibrosis by the available diagnostic methods is difficult at present. With this in mind, we compared autopsy data in heart specimens from 8 patients of constrictive pericarditis of tuberculous origin and 6 patients with tropical endomyocardial fibrosis. Post-mortem endomyocardial biopsies were also performed from both the ventricles. Pericardial thickening and adhesions were present in all cases of constrictive pericarditis and in none of those with endomyocardial fibrosis. Interestingly, significant endocardial thickening was seen in four, and myonecrosis, lymphohistiocytic cellular infiltration and myofibrosis were observed in seven of the eight cases of constrictive pericarditis. This suggests that the tubercular insult to heart may result in involvement of all three layers with varying severity. The endomyocardial biopsy specimens from the affected areas revealed similar histopathological changes of endocardial thickening and focal myofibrosis with cellular infiltrates in patients with both constrictive pericarditis and endomyocardial fibrosis, making distinction of the two difficult. The hallmark of differentiation between these two clinical entities appears to be a diligent attempt at identification of the thickened pericardium.

Biopsy↗

PubMed1975

[Acute pericarditis. Study of 50 consecutive cases].

50 consecutive cases of pericarditis were studied. Idiopathic and viral pericarditis made up 36 p. cent of all cases. The occurrence of tuberculous or rheumatic conditions was even lower than that reported in similar series in the literature. Amongst the clinical signs of these diseases, emphasis should be placed upon the frequency of chest pain which was increased by deep inspiration in only three out of four cases. Circulatory problems associated with the pericarditis were, on the whole, minimal. However, a fall in blood pressure was seen in 6 cases and true collapse in 3 more. The electrocardiogram showed, in addition to the classical signs, sagging of the PR interval in 36 p. cent and transient atrial fibrillation in 4 cases. As far as biological tests are concerned, it should be noted that elevation of creatine phospho-kinase to levels 4 times greater than normal may be seen, creating problems with the differential diagnosis from myocardial infarction. The course was in general favourable though two deaths occurred in this series (4 p. cent), one with tuberculous pericarditis and the other with idiopathic pericarditis.

Acute Disease↗

PubMed1989

Differentiation of constrictive pericarditis and restrictive cardiomyopathy by radionuclide ventriculography.

Patterns of left ventricular diastolic filling in five patients with unoperated constrictive pericarditis, the same five patients following pericardiectomy, five patients with restrictive cardiomyopathy, and 14 healthy control subjects were studied by radionuclide ventriculography. Patients with constrictive pericarditis had more rapid peak left ventricular filling rates (mean 5.62, range 4.23 to 7.32 end-diastolic volumes [EDV] per second) compared to control subjects 3.44, range 2.62 to 4.45 EDV/sec, p less than 0.05). Heart rate-corrected first one-third and first one-half diastolic filling fractions were greater in patients with preoperative constrictive pericarditis compared to members of the restrictive cardiomyopathy and control groups p less than 0.05). Following pericardiectomy, patients with constrictive pericarditis had significant decreases in peak filling rate and corrected filling fractions, and all diastolic filling measurements were indistinguishable from those of control subjects. These noninvasively obtained data indicate that patients with preoperative constrictive pericarditis have an increased rate of left ventricular early diastolic filling compared to patients with restrictive cardiomyopathy and control subjects, and that these findings return to normal following surgical removal of the pericardium.

Adult↗

PubMed1980

Genesis of pericardial knock in constrictive pericarditis.

A pericardial knock is a common finding in constrictive pericarditis. However, its origin has been uncertain. One hypothesis suggests that it is due to sudden deceleration of ventricular filling. To validate this hypothesis, left ventriculograms, phonocardiograms and external pulse recordings were obtained in seven patients with hemodynamic and pathologic findings of constrictive pericarditis and in seven normal subjects. Left ventriculographic silhouettes were digitized and left ventricular volumes were calculated by computer at 16 ms intervals. Curves of left ventricular volume versus diastolic filling time were constructed for each patient. Pericardial knock was recognized as an early high frequency sound recorded between 90 to 120 ms after the aortic closing sound and occurring at the trough of the Y descent of the jugular venous pressure tracing. The timing of the pericardial knock in five patients with constrictive pericarditis corresponded to a sudden and premature plateau of the diastolic left ventricular volume curve representing 85 +/- 4 percent (mean +/- standard deviation) of ventricular filling. The diastolic plateau was missing in two patients with constrictive pericarditis who had no pericardial knock. In these cases, the rate of ventricular filling was faster than normal in the first 20 percent of diastole. Thus, this study related pericardial knock to an abrupt plateau inthe diastolic left ventricular volume curve, supporting the view that sudden cessatin of ventricular filling generates the pericardial knock of constrictive pericarditis. Two mechanisms are proposed by which the filling plateau may produce the knock, and it is postulated that both ventricles may participate in the knock phenomenon.

Adult↗

PubMed1993

Rate-dependent hemodynamic responses during incremental atrial pacing in chronic constrictive pericarditis before and after surgery.

Chronic constrictive pericarditis is a frequent cause of diastolic dysfunction, and results in impaired ventricular filling. Unlike in normal subjects, ventricular filling in constrictive pericarditis occurs almost entirely in the initial one third of diastole, and cardiac output is dependent predominantly on heart rate. Tachycardia impairs ventricular filling in normal subjects, but its effects in patients with constrictive pericarditis have not been studied. The effect of increasing heart rate alone with atrial pacing on the central and peripheral hemodynamics of patients with untreated chronic constrictive pericarditis before and after pericardiectomy was evaluated. Increased heart rate with atrial pacing increased cardiac output, whereas stroke volume remained unchanged up to heart rates of 140 beats/min. Further increases in heart rate resulted in reductions of cardiac output and stroke volume. There were no significant changes in ventricular filling pressures. Infusion of 300 ml of saline solution at peak pacing rates did not improve cardiac output. After successful surgical pericardiectomy, the hemodynamic effects of atrial pacing returned to normal. It is concluded that moderate tachycardia improves the hemodynamic profile of patients with constrictive pericarditis.

Adult↗

PubMed1980

Procainamide-induced lupus erythematosus pericarditis encountered during coronary bypass sugery.

Procainamide is probably the most common offending drug responsible for the drug-induced lupus erythematosus syndrome today. Pericarditis has been reported to occur in from 14 to 18 per cent of the cases of procainamide-induced lupus erythematosus, and occasional reports of massive pericardial effusion, pericardial tamponade and constrictive pericarditis have appeared in the literature. We describe a patient who presented with features of procainamide-induced lupus erythematosus without any clinical evidence of pericarditis. He underwent coronary bypass surgery 12 days after administration of the drug was stopped and was found to have a significant pericardial effusion at the time of surgery; histologic examination of pericardial tissue and pericardial fluid confirmed that the pericardial effusion was related to the procainamide-induced lupus syndrome. The incidence of pericarditis in procainamide-induced lupus erythematosus may be higher than presently accepted figures would indicate. Symptoms and signs related to procainamide-induced lupus pericarditis may cause diagnostic confusion with common postoperative bypass complications; the full implications of this disease entity to the patient undergoing coronary bypass are unknown.

Biopsy↗

PubMed1984

Predicting success of intensive dialysis in the treatment of uremic pericarditis.

To identify predictors of the success or failure of daily intensive dialysis in uremic pericarditis, a retrospective examination was made of initial clinical, laboratory, and echocardiographic data in 97 patients using univariate and multivariate statistical analysis. In this group, 67 patients showed response to intensive dialysis, and 30 patients did not (22 required surgery and eight died). By univariate analysis, nine factors correlated with intensive dialysis failure (p less than 0.10): admission temperature over 102 degrees F, rales, admission blood pressure under 100 mm Hg, jugular venous distension, peritoneal dialysis treatment only because of severe hemodynamic instability, white blood cell count over 15,000/mm3, white blood cell count left shift, large effusion by echocardiography, and both anterior and posterior effusion by echocardiography. Echocardiographic left ventricular size and function were not useful predictors of success or failure; there was no difference in response to hemodialysis in patients with pericarditis before dialysis (69 percent) versus patients with pericarditis during a maintenance program (67 percent). By discriminant analysis, a seven-variable function was constructed that divided the patients into three groups: (1) those likely to show response to intensive dialysis (48 patients, predictive value of 98 percent), (2) those with an intermediate (38 percent) chance of showing response to intensive dialysis (30 patients), and (3) those unlikely to show response to intensive dialysis (14 patients, predictive value of 100 percent). When the function was applied prospectively to 12 patients (eight with success and four with failure), all were classified correctly. Thus, discriminant analysis of patients with uremic pericarditis allows improved selection of patients with uremic pericarditis likely to have response to daily intensive dialysis and early consideration of alternative forms of treatment in patients unlikely to show response to intensive dialysis. However, the model should be validated in the particular institution where it is to be used before its application.

Echocardiography↗

PubMed1993

A fatal case of constrictive pericarditis due to a marked, selective pericardial accumulation of amyloid.

Distinguishing constrictive pericarditis from restrictive cardiomyopathy, usually due to amyloidosis, is a relatively frequent and difficult diagnostic problem. This report describes, for the first time, a patient with constrictive pericarditis caused by direct, extensive infiltration of the pericardium by amyloid, with only minimal amyloid in the myocardium, and a normal heart weight of 320 g. This patient demonstrates that amyloid may be predominantly deposited in the pericardium and actually cause constrictive pericarditis, as well as simulate its hemodynamic presentation by myocardial deposition. Given a clinical and hemodynamic presentation compatible with either constrictive or restrictive disease, an endomyocardial biopsy or other biopsy revealing amyloidosis does not necessarily rule out pericardial constriction that may be due to amyloid infiltration. The relationship between constrictive pericarditis, seen in this patient, and the other more common manifestations of amyloid heart disease, and the hemodynamic profiles of amyloid cardiomyopathy and constrictive pericarditis are reviewed.

Aged↗

PubMed1994

Diagnostic role of Doppler echocardiography in constrictive pericarditis.

OBJECTIVES: This study was conducted to assess the diagnostic role of Doppler echocardiography in constrictive pericarditis. BACKGROUND: It has been observed that patients with constrictive pericarditis have a characteristic Doppler pattern of respiratory variation in ventricular filling and central venous flow velocities. However, the observation was based on a small number of patients with known diagnosis. METHODS: We reviewed the echocardiographic features of 28 patients (21 men and 7 women; mean age +/- SD 55 +/- 15 years) with suspected constrictive pericarditis who underwent exploratory thoracotomy or pericardiectomy. RESULTS: At operation, constrictive pericarditis was diagnosed in 25 patients, restriction in 1 and normal pericardium in 2. Of the 25 patients with constriction, correct preoperative Doppler diagnosis was made in 22 (88%) and Doppler echocardiography showed restriction in 3. In two patients with a normal pericardium, Doppler features were consistent with constriction in one patient and were normal in the other. In the one patient with restriction, Doppler echocardiography showed restriction. In 19 patients with surgically proved constriction, repeat Doppler study after pericardiectomy showed normal findings in 14 and restriction in 5. Twelve of the 14 patients with normalized Doppler findings became asymptomatic, whereas all 5 with restrictive Doppler features remained symptomatic. CONCLUSIONS: Doppler echocardiography performed simultaneously with respiratory recording is highly sensitive for diagnosing constrictive pericarditis, and it appears to predict functional response to pericardiectomy.

Adult↗

PubMedDate not supplied

Radiation pericarditis and breast reconstruction: a surgical dilemma.

OBJECTIVE: To discuss a case of radiation pericarditis and the physiology of the disease, and to discuss the left thoracotomy as an effective alternative to median sternotomy for pericardiectomy in the treatment of complicated radiation pericarditis. DESIGN: A case report with accompanying discussion of the disease and literature search. SETTING: Keesler Air Force Base Medical Center, a military training facility and general surgery residency program. PARTICIPANTS: A single case report with review of literature. RESULTS: Left thoracotomy is an effective alternative to median sternotomy for the surgical treatment of radiation pericarditis, with a mild increase in pulmonary-associated complications. CONCLUSIONS: With an increase in the use of mediastinal radiation for treatment of malignant disease as well as the increase in women having reconstructive procedures of the breast, one may expect complicated cases of radiation pericarditis that may not be amenable to median sternotomy. Left thoracotomy may be an alternative to median sternotomy for pericardiectomy in cases of pericarditis complicated by cosmetic constraints.

Breast Neoplasms↗

PubMed2006

Triage and management of acute pericarditis.

The pericardium is involved in a large number of systemic disorders, and acute pericarditis may be due to several causes. The diagnosis is based on clinical criteria, and laboratory testing is not routinely recommended. Deciding on the extent of the diagnostic evaluation requires good clinical judgement based on a careful evaluation of the risk-benefit ratio, and knowledge of basic epidemiological data for the development of a rational management program. In clinical practice a probabilistic approach seems reasonable: in Western countries most cases are idiopathic or viral with a brief and benign course and an excellent response to non-steroidal anti-inflammatory drugs, thus an extensive diagnostic evaluation is not routinely necessary. On the contrary, in developing countries specific pericarditis such as tuberculous pericarditis is quite common and should be ruled out. A clinical triage is feasible on a clinical basis. Patients with pericarditis can be safely managed on an outpatient basis without a thorough diagnostic evaluation unless the patient has high risk features such as temperature >38 degrees C, a subacute onset, immunodepression, a history of recent trauma, oral anticoagulant therapy, myopericarditis, a large pericardial effusion, and cardiac tamponade. The reported diagnostic yield of extensive laboratory evaluation and pericardiocentesis is low in the absence of cardiac tamponade or suspected purulent, tuberculous, and neoplastic pericarditis. Invasive procedures should be limited mainly to patients in whom therapeutic intervention is necessary.

Acute Disease↗