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PubMed2005

Coccidioidal pericarditis: a case presentation and review of the literature.

BACKGROUND: Pericardial involvement with Coccidioides immitis is an infrequent occurrence with a relatively unfavorable prognosis. METHODS: A case of coccidioidal pericarditis is presented along with a review of the medical literature on coccidioidal pericarditis to give the clinician a better understanding of the various presentations, complications and outcomes of this disease. Medline (National Library of Medicine, Bethesda) was electronically searched covering the years 1966-2003 using search words coccidioidomycosis and pericarditis. RESULTS: Sixteen patients were identified from the literature review and one new patient was added. All the patients were males with a mean age of 37.5 years. Chest pain, dyspnea and cough were the most common presenting symptoms. Five patients had evidence of pericardial tamponade, pulsus paradoxus was noted in three patients and three patients presented with pericardial constriction. One patient had Kussmaul's sign, one patient had pericardial frictional rub and another had pericardial knock. Cardiomegaly on chest x-ray was present in ten patients; EKG was noted to have low voltage in five and ST segment elevation in four patients. Delayed hypersensitivity to coccidioidal antigen was reported in nine patients and positive in eight patients. Complement fixation titers were positive in all 11 patients in whom it was assayed. Fifty-three percent of the patients with coccidioidal pericarditis died. CONCLUSION: Coccidioidal pericarditis is a rare disease entity that has a relatively unfavorable prognosis, yet many patients present with diagnostic clues to this disorder. An enhanced understanding of the clinical features of coccidioidal pericarditis may lead to improved outcomes.

Adult↗
PubMed1987

Treatment of uremic pericarditis and pericardial effusion.

Pericarditis occurred 161 times in 136 of 1,058 patients undergoing chronic dialysis during a period of 13.7 years. Cardiac tamponade occurred during 27 episodes, while pretamponade occurred in 30. Tamponade was less frequent and resolution of pericarditis without invasive intervention more frequent when pericarditis occurred within 2 weeks of initiation of chronic dialysis. Similarly, resolution with conservative therapy was more frequent with first episodes than with recurrences, and when pericarditis occurred within 3 months of initiation of chronic dialysis. The overall survival was 89.7% and was the same irrespective of the duration of dialysis or whether the pericarditis was a first episode or a recurrence. We recommend that patients with pericarditis and no hemodynamic alterations receive intensive hemodialysis, with careful hemodynamic and echocardiographic monitoring, as primary treatment. Invasive intervention is indicated if cardiac tamponade or pretamponade develops, if a pericardial effusion increases progressively in size, or if a large effusion persists after ten to 14 days of intensive dialysis. In our experience, the invasive intervention of choice is either formal pericardiectomy or subxiphoid pericardiotomy with intrapericardial steroid instillation. In our experience, pericardiocentesis has proven to be a high-risk procedure. It is reserved for emergency circumstances, and then is preferably performed in the operating room just prior to induction of anesthesia for definitive surgical drainage.

Humans↗
PubMed1976

Differential characteristics of the electrocardiogram in early repolarization and acute pericarditis.

Electrocardiographic mimicry necessitates differentiation between acute pericarditis and early repolarization. Among 96 persons, limb-lead RST deviations occurred in all 48 with pericarditis, but only 27 with early repolarization. RS-T vectors (A RS-T) in pericarditis tended to be horizontal (25 patients) and left of the T vector, A T (28 patients); in early repolarization, A RS-T was vertical in 15 subjects and right of A T (20 subjects); P less than or equal to 0.01. RS-T depression in Lead V1 was more common in pericarditis (14 vs. two); isoelectric RS-T in Lead V6 was more common in early repolarization (10 vs. one); P less than or equal to 0.01. PR segment deviations occurred in both limb and precordial leads in pericarditis; in early repolarization they were confined to either lead group. Thus, R-ST deviations in both limb and precordial leads with horizontal A RS-T to left of A T and RS-T depression in Lead V1 favor pericarditis; vertical A RS-T and isoelectric RS-T in Lead V6 favor early repolarization.

Acute Disease↗
PubMed2002

Constrictive pericarditis caused by candida glabrata in an immunocompetent patient: case report and review of literature.

Candida pericarditis is a rare disease described mostly in patients with recent cardiothoracic surgery or debilitating chronic diseases and is generally considered to be associated with high mortality. To our knowledge, we report the first case of Candida pericarditis in a healthy host who had not undergone thoracic surgery and the first documented case and cure of pericarditis caused by C. glabrata. The most probable underlying factor in the development of this pericarditis was the abdominal surgery the patient underwent to correct a gastrogastric fistula, without an intraabdominal leak, which developed 10 y after surgical gastric stapling for weight reduction. The literature on Candida pericarditis is reviewed. If Candida pericarditis is diagnosed early and treated with a combined medical and surgical approach, the prognosis today is much more favorable than that previously reported.

Adult↗
PubMed2004

Chart review for potential features of myocarditis, pericarditis, and cardiomyopathy in children and adolescents treated with clozapine.

Clozapine is known to cause cardiac side effects, including myocarditis, pericarditis, and cardiomyopathy. Prompted by a case of clozapine-related pericarditis in an adolescent, we undertook a retrospective chart review to discover whether any unrecognized cases of myocarditis, pericarditis, or cardiomyopathy were among the children, adolescents, and young adults we had treated with clozapine. The sample comprised a total of 36 patients, who were monitored regularly over a period ranging from 2.5 to 79 months. The average observation period was 7.5 months. Patients were assessed for potential indicators of myocarditis, pericarditis, or cardiomyopathy. In more than 66% of all patients, at least one of several parameters potentially indicative of pericarditis, myocarditis, or cardiomyopathy was abnormal in at least one instance during the observation period. In all cases in which abnormalities were discovered, the abnormalities were found to be unspecific for myocarditis, pericarditis, or cardiomyopathy. With the exception of the case which prompted our study, none of the patients were found to have developed any such disorder in the course of further treatment with clozapine.

Adolescent↗
PubMed1994

Anaerobic pericarditis: case report and review.

Purulent pericarditis is uncommon and is rarely caused by anaerobic bacteria. We describe a 58-year-old man with purulent pericarditis secondary to infection with Bacteroides fragilis; the most likely source for the B. fragilis infection was subsequently found to be a ruptured appendix. His pericarditis eventually resolved after drainage of purulent fluid and treatment with antibiotics directed against B. fragilis. We also review 29 cases of anaerobic pericarditis previously reported in the English-language literature (we excluded those cases due to actinomyces). In 17 cases only anaerobic bacteria were isolated, while in 13 anaerobes were isolated with a mixture of facultative and/or aerobic bacteria. The cases were secondary to a contiguous focus of infection or occurred via hematogenous seeding. Treatment of both anaerobic pericarditis and purulent pericarditis due to aerobic bacteria entails adequate drainage and appropriate antibiotic therapy, and in all cases there should be a search for the source of the organism infecting the pericardium.

Appendicitis↗
PubMed2003

Adjuvant corticosteroids for tuberculous pericarditis: promising, but not proven.

BACKGROUND: There is controversy regarding the effectiveness of corticosteroids in tuberculous pericarditis, particularly in patients who are immunocompromised by HIV. AIM: To determine the effectiveness of adjuvant corticosteroids in tuberculous pericarditis. DESIGN: Systematic review of randomized controlled trials. METHODS: We searched the Cochrane Infectious Diseases Group trials register (June 2002), the Cochrane Controlled Trials Register (Issue 2, 2002), MEDLINE (January 1966 to March 2003), EMBASE (1980 to May 2002), and the reference lists of existing reviews, for randomized and quasi-randomized controlled trials of adjuvant corticosteroids in the treatment of suspected tuberculous pericarditis. We also contacted organizations and individuals working in the field. Two reviewers independently assessed trial quality and extracted data. We used meta-analysis with a fixed effects model to calculate the summary statistics, provided there was no statistically significant heterogeneity, and expressed results as relative risk. RESULTS: Four trials with a total of 469 participants met our criteria. Three (total n = 411) tested adjuvant steroids in participants with suspected tuberculous pericarditis in the pre-HIV era. Fewer participants died in the intervention group, but the potentially large reduction in mortality was not statistically significant (relative risk RR 0.65, 95%CI 0.36-1.16, n = 350; p = 0.14). One trial with 58 patients that enrolled HIV-positive individuals also showed a promising but non-significant trend on mortality (RR 0.50, 95%CI 0.19-1.28; p = 0.15). There was no significant beneficial effect of steroids on re-accumulation of pericardial effusion or progression to constrictive pericarditis. Patients with pericardial effusion were significantly more likely to be alive with no functional impairment at 2 years following treatment. However, the effect was not sustained in a sensitivity analysis that included patients who were lost to follow-up. DISCUSSION: Steroids could have large beneficial effects on mortality and morbidity in tuberculous pericarditis, but published trials are too small to be conclusive. Large placebo-controlled trials are required, and should include sufficient numbers of HIV-positive and HIV-negative participants, and an adequate adjuvant steroid dose.

Adrenal Cortex Hormones↗
PubMed1971

Pericarditis after acute myocardial infarction.

Fifty-two (6.8%) of 779 patients admitted to a coronary monitoring unit with acute myocardial infarction developed a pericardial friction rub. A diagnosis of postmyocardial infarction syndrome was made in three of these.The course of the 52 patients with pericarditis was compared with that of a consecutive series of 100 patients without pericarditis. As a group those with pericarditis manifested a longer period of pyrexia, a greater rise in serum enzymes, and a higher incidence of major arrhythmias and of radiological pulmonary oedema. The Peel prognostic index, however, did not differ significantly in the two groups. The hospital mortality of the pericarditis group was not significantly different from that of the 727 non-pericarditis patients. No specially adverse features were found in a follow-up of the pericarditis group.Though the presence of a pericardial rub in the first few days after a myocardial infarction may be a sign of extensive myocardial damage and is associated with a relatively high incidence of ventricular fibrillation, it does not appear to influence the hospital mortality of patients treated in a monitoring unit.

Acute Disease↗
PubMed2000

Relevance of adenosine deaminase and lysozyme measurements in the diagnosis of tuberculous pericarditis.

OBJECTIVE: To assess the value of pericardial fluid adenosine deaminase (ADA) and pericardial lysozyme (Lys) as tools in diagnosing tuberculous pericarditis. METHODS: Forty-one patients (age range 17--77 years) with significant pericardial effusion were included in the study. Diagnostic pericardiocentesis and pericardial biopsy were performed while serum and pericardial fluid ADA and Lys were measured in all patients. Grouping of patients resulted as follows: group I = 7 patients with tuberculous pericarditis; group II = patients with neoplastic pericarditis; group III = 30 patients with idiopathic pericarditis. RESULTS: Pairwise multiple comparison procedures revealed a significant difference of ADA in group I versus group III (p < 0.05) but not versus group II. Furthermore, pericardial Lys in group I was higher than in groups II and III (p < 0.05). A strong correlation between pericardial ADA and Lys was found (r = 0.733, p = 0.01) for all the patients. Receiver operating curves showed a value of 72 U/l as cutoff point of pericardium ADA, with a sensitivity of 100% and a specificity of 94% in the diagnosis of tuberculous pericarditis. Similarly for pericardial Lys, a value of 6.5 microg/dl had a sensitivity and specificity of 100 and 91.17%, respectively. CONCLUSIONS: Both measurements of pericardial ADA and Lys need to be taken into account when attempting the early diagnosis of tuberculous pericarditis.

Adenosine Deaminase↗
PubMed2003

Acute pericarditis and pleural effusion complicating cytarabine chemotherapy.

BACKGROUND: Pericarditis is a rare but possibly severe complication of treatment of acute leukemia with cytarabine. CASE REPORT: We report a possibly cytarabine-induced acute pericarditis and pleuritis with a rapid onset. A patient with acute myelomonocytic leukemia developed an isolated pericarditis 3 weeks after the first course of chemotherapy with cytarabine and idarubicin. The second course of chemotherapy with cytarabine and amsacrine was started after clinical improvement; 3 days later an acute pericarditis with a large pericardial effusion accompanied by a left pleural effusion developed. A pericardio- and pleuracentesis was performed and the symptoms improved rapidly without reaccumulation of the fluid. The third course of chemotherapy with mitoxantrone and etoposide was completed without further cardiopulmonary complications. CONCLUSION: The differential diagnosis of pericarditis in the setting of chemotherapy with cytarabine should include cytarabine- induced pericarditis. The pathogenesis remains unclear, directly toxic and immunological mechanisms are suggested. Severe progression with massive pericardial effusion necessitating risky pericardiocentesis can occur and therefore a therapy with high-dose corticosteroids should be considered early.

Acute Disease↗
PubMed2004

Novel model of constrictive pericarditis associated with autoimmune heart disease in interferon-gamma-knockout mice.

BACKGROUND: Constrictive pericarditis represents a serious hemodynamic syndrome that may lead to heart failure. Studies of its pathophysiological mechanisms have been impeded by the lack of an animal model. METHODS AND RESULTS: Cardiac myosin-induced experimental autoimmune myocarditis in interferon (IFN)-gamma-knockout (KO) mice results in increased cardiac inflammation and development of severe grossly detectable pericarditis. Using in vivo pressure-volume studies, we found that the acute phase of experimental autoimmune myocarditis in IFN-gamma-KO mice was characterized by reduced left ventricular (LV) volumes compared with wild-type mice. The KO mice exhibited a classic restrictive/constrictive phenotype with decreased cardiac output, increased chamber stiffness, preserved ejection fraction, and impaired diastolic filling, characterized by reduced deceleration time and pressure tracings showing the square root sign similar to that observed in clinical cases of constrictive pericarditis. This phenotype was not associated with the severity of myocarditis but correlated with the presence of grossly detectable adhesive pericarditis present only in the KO group and characterized by increased pericardial inflammation and fibrosis. Comparison of IFN-gamma-KO and wild-type mice matched for the severity of myocardial disease further confirmed that pericarditis, and not myocarditis, was responsible for smaller LV volumes, reduced cardiac output, increased cardiac stiffness, and increased peak filling rate adjusted for end-diastolic volumes in KO mice. CONCLUSIONS: Autoimmune heart disease in IFN-gamma-KO mice results in increased pericardial inflammation and fibrosis, leading to constrictive phenotype during the acute phase of disease. It represents a novel animal model of constrictive pericarditis.

Animals↗
PubMed1982

The differential diagnosis of acute pericarditis from the normal variant: new electrocardiographic criteria.

We examined the quantitative electrocardiographic differentiation of acute pericarditis from normal variant ST-T changes. The ECGs of 19 patients with acute pericarditis were compared with those of 20 subjects with typical normal variant changes. Patients were excluded if their ECGs demonstrated conditions that markedly altered repolarization. The positive predictive values (PPV) and negative predictive values (NPV) of previously reported criteria were not high (PPV = 0.54-0.83, NPV = 0.56-0.58). In contrast, in the present study, a T-wave amplitude in lead V6 of less than or equal to 0.3 mV diagnosed acute pericarditis (p less than 0.005, PPV = 0.85, NPV = 0.85), but there was overlap of patients between the groups. The ratio of the amplitude of the onset of the ST segment to the amplitude of the T wave in that lead (ST/T ratio in V6) proved to be the most reliable discriminator. An ST/T ratio greater than or equal to 0.25 diagnosed all patients with acute pericarditis (p less than or equal to 0.005, PPV = 1.0, NPV = 1.0). The ST/T ratio greater than 0.25 in V4, V5 (both p less than 0.005, PPV = 0.87, NPV = 1.0) and I (p less than or equal to 0.005, PPV = 0.80, NPV = 0.81) were also significant discriminators. Thus, if V6 is unavailable, an ST/T ratio greater than or equal to 0.24 in V5, V4 or I is highly suggestive of acute pericarditis. An ST/T ratio greater than or equal to 0.25 in V6 discriminated the ECGs of all patients with acute pericarditis from normal variants in this study.

Acute Disease↗
PubMed1993

Electrocardiographic diagnosis of postinfarction regional pericarditis. Ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction.

BACKGROUND: The ECG recognition of diffuse pericarditis following acute myocardial infarction has been based on changes of the ST segment and, to a lesser extent, alterations of the PQ segment. No ECG criteria exist for the diagnosis of postinfarction regional pericarditis. Recently, it was observed that the T wave evolution follows an atypical pattern before fatal free wall rupture and that this pattern is due to the associated pericarditis. Therefore, this study was conducted on 200 patients with acute myocardial infarction to further elucidate the sensitivity and specificity of the atypical T wave changes in patients with regional postinfarction pericarditis without rupture and to assess the affect of lytic treatment on the rapidity and amplitude of postinfarction T wave evolution. METHODS AND RESULTS: An analysis of the clinical courses and serial ECGs of 200 consecutive patients with acute myocardial infarction was performed. Among 43 patients with postinfarction pericarditis, the pattern of T wave evolution consistently differed from the customary postinfarction pattern of T wave evolution. This unusual evolutionary course was expressed as either persistently positive T waves 48 or more hours after infarction (67%) or premature, gradual reversal of inverted T waves to positive deflections (33%). The sensitivity and specificity of these T wave alterations were 100% and 77%, respectively. The only other processes identified that caused this type of postinfarction T wave evolution were cardiopulmonary resuscitation, reinfarction, and very small infarcts. Both reperfusion, as judged by the creatine kinase-MB curve, and patency, as assessed by the angiogram, were correlated with the rapidity and depth of T wave inversion. Ninety percent of patients with reperfusion attained a maximum T wave negativity of 3 mm or more within 48 hours after the onset of chest pain in the lead that initially displayed the greatest ST segment elevation. Seventy-six percent of patients without reperfusion attained a maximum negativity of 2 mm or less within 72 hours. Thus, like the ST segment, accelerated evolution and deepening of the T wave may be noninvasive markers of reperfusion. CONCLUSIONS: First, premature reconcordancy of the ST segment and T wave after acute myocardial infarction is a sensitive, reasonably specific, and easily recognizable ECG manifestation of postinfarction regional pericarditis. Second, reperfusion is associated with accelerated evolution and deepening of the T waves following acute myocardial infarction.

Clinical Enzyme Tests↗
PubMed1994

Adenosine deaminase and carcinoembryonic antigen in pericardial effusion diagnosis, especially in suspected tuberculous pericarditis.

BACKGROUND: Adenosine deaminase (ADA) and carcinoembryonic antigen (CEA) have been measured in pleural fluid to help distinguish malignant from benign effusions, especially in tuberculous pleurisy. We investigated ADA and CEA levels in patients with moderate to large pericardial effusions of different etiologies. METHODS AND RESULTS: We performed diagnostic and therapeutic pericardiostomy with drainage and biopsy. We measured ADA and CEA levels in the pericardial fluid in 26 patients with moderate to large pericardial effusion and 19 control patients. Patients were included in a prospective protocol from August 1991 to August 1993. Patients were grouped as follows: group 1, 9 patients with tuberculous pericarditis (TP) confirmed by bacteriologic culture or histology of pericardial biopsy; group 2, 5 patients with clinically strongly suspected TP; group 3, 12 patients with malignancy (8) and acute pericarditis (4); group 4, 19 control patients without pericardial disease. We treated patients with TP with isoniazid, rifampin, and either streptomycin or ethambutol for 12 months and pyrazinamide for 2 months. We observed for symptoms and signs of recurrent pericarditis or constrictive pericarditis on follow-up. In group 1 the ADA activity was significantly higher (101 +/- 14 U/L) than that in group 3 (22 +/- 5 U/L) or that in group 4 (17 +/- 2 U/L) (P < .05). There was no significant difference between ADA activity in group 1 (101 +/- 14 U/L) and that in group 2 (100 +/- 26 U/L). With a cutoff value for ADA activity of 40 U/L, sensitivity was 93% and specificity 97% in the diagnosis of TP. In benign diseases, the CEA level was significantly lower (1.0 +/- 0.3 ng/mL) than that in malignant diseases (135.1 +/- 79.7 ng/mL) (P < .05). With a cutoff value for CEA level of 5 ng/mL, sensitivity was 75% and specificity 100% in the diagnosis of malignant pericarditis. Follow-up study (mean, 12.9, 19.8, and 11.8 months in groups 1, 2, and 3, respectively, showed no symptoms or signs of constrictive pericarditis, except for 1 patient. CONCLUSIONS: Pericardial fluid ADA and CEA are useful for the differential diagnosis of pericardial effusion of various causes. They also have great value in early diagnosis of TP, particularly when the results of other clinical and laboratory tests are negative.

Adenosine Deaminase↗
PubMed1975

Pericarditis of acute myocardial infarction.

Forty patients with acute myocardial infarction and pericarditis (AMI-P) were encountered over a three-year period. The incidence of AMI-P was 7.2 percent (40 of 554 patients). Fifty consecutive patients with acute transmural infarction without pericarditis (AMI-C) were used as a control group. There were no significant differences between the AMI-P and AMI-C groups regarding age, sex, infarct location, hospital stay or mortality. Painful symptoms of pericarditis were experienced by 37 patients (92 percent), all of whom had developed symptoms by the fourth hospital day. The pericardial friction rub lasted three days or less in 34 patients (85 percent), but an occasional rub could be heard for up to eight days. Twenty patients with AMI-P (50 percent) developed pleural effusions and/or parenchymal pulmonary infliltrates. Twenty-eight AMI-P patients (70 percent) were thought to have had congestive heart failure (CHF) on the basis of their symptoms and physical findings. Radiographic examination could confirm only 13 cases of CHF among the 28 patients in whom the diagnosis was made clinically. Glucocorticoids were given parenterally to 31 of the 37 patients (84 percent) who had symptomatic pericarditis and was felt to be effective in ameliorating painful symptoms. Followup data was obtained on 28 of the 32 surviving patients. Five patients (15 percent) had seven episodes of the postmyocardial infarction syndrome (PMIS). Pericarditis is generally a shortlived complication of acute myocardial infarction. Pleural and parenchymal pulmonary abnormalities are common and probably account for the tendency to "overdiagnose" CHF in patients with AMI-P. PMIS appears to occur more frequently in patients who have had pericarditis at the time of the acute myocardial infarction.

Administration, Oral↗
PubMed1987

Aortic dissection presenting as pericarditis.

In five patients with aortic dissection, signs and/or symptoms of pericarditis were part of the early manifestations of the aortic disease. Signs of inflammatory pericarditis were noted clinically in four patients and were found at autopsy in one. In the three nonoperated patients who died of aortic rupture leading to fatal hemopericardium, symptoms of pericarditis preceded fatal rupture of the aorta by four to five days. A fourth patient died after surgical repair of aortic dissection 35 days after the onset of pericarditis. In the fifth patient, manifestations of chronic constrictive pericardial disease occurred over a period of seven months after which old aortic dissection was first identified. In each case, the internal tear of classic aortic dissection was located in the ascending aorta. Microscopic evidence of cystic medial necrosis of the aorta was present in each case. In each of two cases, there was a congenital bicuspid aortic valve. The phenomenon observed represents acute aortic dissection in which slow penetration of blood into the pericardial space caused inflammatory pericarditis. The interval between the onset of pericarditis and rupture of the aorta may allow sufficient time for appropriate diagnosis and potentially lifesaving treatment of the aortic disease.

Adult↗
PubMed2002

Clustering of recurrent pericarditis with effusion and constriction in a family.

OBJECTIVE: To describe a cluster of cases of pericarditis in a midwestern family of German and Danish ancestry. PATIENTS AND METHODS: Retrospective review of available medical records identified 5 family members in 2 generations with confirmed diagnosis of pericarditis. RESULTS: Five family members, 3 males and 2 females, presented for medical evaluation of recurrent chest pain between 1969 and 1991. Physical examination resulted in the diagnosis of pericarditis with effusive and constrictive features. The age at presentation ranged from 8 to 46 years. Despite extensive investigations, an idiopathic etiology was assigned to each case. In follow-up, all 5 family members had recurrent episodes of chest pain, self-limiting or responsive to medical therapy, but the effusive component remained a notable feature of the syndrome. CONCLUSIONS: Diagnosis of pericarditis in 5 family members may represent the first description of familial clustering of isolated pericarditis. In addition, 3 other family members had symptoms of chest pain, but pericarditis remained undiagnosed. The aggregate history suggests autosomal dominant inheritance with incomplete penetrance.

Adult↗
PubMed2003

[Etiological diagnosis of the patients with pericarditis after pericardiectomy].

OBJECTIVE: To explore the etiological diagnosis of the patients with pericarditis after pericardiectomy to improve the clinical diagnosis. METHODS: The clinical and pathological data of 52 patients with pericarditis after pericardiectomy were a retrospective analyzed. RESULTS: Fourteen cases (26.9%) were tuberculous, 4 cases (7.7%) were cancerous and 34 cases presented as non-idiopathic changes. Of the non-idiopathic cases, 2 cases were traumatic pericarditis and 1 case was related to radiation, the cause of the other patients were of unknown. Compared with non-idiopathic group, the patients in tuberculous group had a shorter course (P < 0.01). The histories of fever, acute pericarditis, pericardial effusion and cardiac tamponade were more frequent in the tuberculous group than in the non-idiopathic group (P < 0.01-0.05). Four patients with cancerous pericarditis were all refractory pericardial effusion. CONCLUSION: Most of constrictive pericarditis are of unknown cause, but in known causes tuberculosis has a high incidence. Refractory pericardial effusion is often seen in patients with malignant tumor.

Adolescent↗