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PubMed1997

Candida pericarditis: clinical profile and treatment.

BACKGROUND: Candida pericarditis is a rare medical and surgical emergency which, unless treated, leads to impaired cardiac function and death. To facilitate early diagnosis, the clinical features of this condition should be identified. METHODS: Twenty-five cases of Candida pericarditis reported in the last 30 years along with 1 new case were reviewed with regard to demographics, precipitating factors, diagnosis, treatment, and outcome. RESULTS: The syndrome occurred in immunocompromised (73%), antibiotic-treated (62%), or postpericardiotomy (54%) patients. The clinical presentation was frequently subtle and nonspecific. Nevertheless, unexplained fever, an increasing cardiac shadow on chest roentgenogram, or the development of cardiac tamponade may be suggestive. Positive culture for Candida in pericardial fluid or histologic evidence of yeast forms in pericardial tissue establishes the diagnosis. A combination of pericardiocentesis followed by operative drainage and antifungal agents is the usual treatment. Untreated, Candida pericarditis is 100% lethal, whereas prompt diagnosis and treatment lead to cure (mean follow-up, 19 months). CONCLUSIONS: Fever and evolving cardiac tamponade in immunocompromised or postpericardiotomy patients may be suggestive of Candida pericarditis; the presence of organisms in pericardial fluid is diagnostic. Pericardiocentesis followed by operative drainage and antifungal agents appears to be the treatment that is most likely to be curative.

Adenocarcinoma↗
PubMed1985

Constrictive pericarditis: assessment of current diagnostic procedures.

Constrictive pericarditis frequently poses a diagnostic challenge because of its varied manifestations. Accurate diagnosis is essential, however, because surgical decortication may yield excellent clinical results. Although new diagnostic procedures have helped the clinician to diagnose constrictive pericarditis, the initial clinical suspicion of this diagnosis must be high for appropriate interpretation of these tests. Echocardiography is useful, primarily for distinguishing various other cardiac abnormalities that may simulate constrictive pericarditis. Computed tomography is a valuable procedure for assessment of pericardial thickening. In addition, evaluation of early diastolic filling by computerized digitization in conjunction with echocardiography, angiography, and invasive hemodynamics shows promise as a diagnostic tool. Even with these new diagnostic aids, distinguishing constrictive pericarditis from restrictive cardiomyopathy may be difficult and, in some cases, may necessitate an exploratory operative procedure.

Aged↗
PubMed1975

Pericarditis in acute myocardial infarction.

In a prospective study of 300 consecutive patients who survived the first 24 h of acute myocardial infarction, pericarditis was present in 44 patients (14-7%). The only factors independently associated with pericarditis were transmural myocardial infarction, extent of myocardial damage, atrial fibrillation, and longer duration of fever. Pericarditis did not affect immediate prognosis or incidence of cardiac rupture. These findings and the high incidence of atrial fibrillation suggest that anticoagulant therapy should not be discontinued in patients with pericarditis complicating acute myocardial infarction.

Aged↗
PubMed1996

The organisms reported to cause infective myocarditis and pericarditis in England and Wales.

It is difficult to acquire an overall perspective of the range of organisms responsible for infective myocarditis or pericarditis, and their relative importance, as most studies have involved only case reports or case series of a single organism. This study analyses reports to the Communicable Disease Surveillance Centre, of the Public Health Laboratory Service. Reports where myocarditis or pericarditis was included as the main clinical features between 1990 and 1993 were studied. Between 1990 and 1993, 368 cases of myocarditis and/or pericarditis were reported to CDSC. Viruses were reported to cause 253 (69%) cases, bacteria were responsible for 49 (13%) cases, mycoplasma for 32 (9%) cases, chlamydia for 16 (4%) cases and Mycobacterium tuberculosis for nine (2%) cases. Infection with coxsackie B virus was most frequently associated with a mixed picture of myo/pericarditis, whereas influenzae virus was associated with pericarditis or myocarditis alone. This information will provide clinicians with details of the more likely pathogens responsible for these conditions.

England↗
PubMed2000

[Primary meningococcal pericarditis caused by meningococcus serogroup C].

We report the case of a 15-year-old female, with no previous medical history, who presented cardiac tamponade secondary to purulent pericarditis caused by Neisseria meningitidis serogroup C. This microorganism is the etiologic agent in 6-16% of the cases of purulent pericarditis, most in association with previous or concomitant central nervous system involvement (meningitis). Exceptionally, as in this case, the pericarditis is not accompanied by meningitis (Primary Meningococcal Pericarditis). The patient was treated with antibiotics, pericardiocentesis and steroids with excellent response. It is important to point out that meningococcal disease may present in unusual forms which may lead to diagnostic and therapeutics difficulties.

Adolescent↗
PubMed2004

[Recurrent pericarditis during meningococcal meningitis. 2 case reports].

INTRODUCTION: There is little information on the frequency, physiopathology and management of extra-cerebral manifestations of N. meningitidis meningitis. Articular, pleural and pericardial involvement is occasionally reported with a symptomatology that can be delayed with regard to the initial diagnosis. OBSERVATIONS: In two patients in whom the diagnosis of meningococcal meningitis had been confirmed, the progression was towards a recurrent pericarditis up until the 4th month after the initial episode of infection in the first case and pericarditis with tamponade and surgical draining in the second. However, the final outcome was favourable for both patients following treatment with non-steroidal anti-inflammatories (NSAIs). COMMENTS: The incidence of pericardial involvement is unknown. The distinction has to be made between purulent pericarditis, more frequent in children, and the inflammatory pericarditis that is often of late onset. The indication for surgical draining must be dominated by the clinical hemodynamic impact. The indication for NSAIs and/or acetyl-salicylic acid is not codified (doses, duration), but in the two cases reported here we would privilege NSAIs.

Adolescent↗
PubMed2002

Intrapericardial fibrinolytic therapy in purulent pericarditis.

OBJECTIVE: Purulent pericarditis is a rare disease that is being conventionally managed with intravenous antibiotics and pericardial drainage. In our study, we used intrapericardial fibrinolytic treatment together with pericardiocentesis and antibiotic therapy. We evaluated the role of intrapericardial fibrinolytic treatment in nine purulent pericarditis patients. METHODS: Six children and three adult patients with purulent pericarditis, aged between 5 and 50 years, were treated with intrapericardial fibrinolysis by streptokinase. Intrapericardial drainage catheter was placed into the subxyphoidal localization under local anaesthesia and echocardiography guidance, streptokinase was infused into the pericardial sac as the fibrinolytic agent. RESULTS: Repeat echocardiograms showed no reaccumulation of pericardial effusions, pericardial thickening or constrictions. No patients had systemic bleeding, arrhythmias, or hypotension. There was one death which was due to sepsis and congestive heart failure. CONCLUSION: We believe that early pericardial drainage and intrapericardial fibrinolysis appears to be safe and effective in the treatment of purulent pericarditis.

Adolescent↗
PubMed1997

Tuberculous pericarditis and AIDS: case reports and review.

Pericarditis is one of the most common cardiac complications in the course of HIV disease. Opportunistic infections and neoplastic processes represent the most common etiology of pericardial disease. Pericardial tuberculosis is an uncommon condition, especially in developed countries. Two cases of tuberculous pericarditis in adult patients with AIDS occurred over a 12-month period at our clinic, which prompted a literature review of the published cases of tuberculous pericarditis in AIDS. Of note is that in the first patient pericardial effusion represented the AIDS-defining illness and was an expression of a disseminated tuberculous disease. The second patient developed a fatal pericarditis due to a multiple-drug resistant Mycobacterium tuberculosis infection.

AIDS-Related Opportunistic Infections↗
PubMed1983

A controlled study of the effect of indomethacin in uremic pericarditis.

To determine the impact of indomethacin on the course of uremic pericarditis we performed a prospective, double blind study in which 24 patients with endstage chronic renal failure and pericarditis randomly received indomethacin, 25 mg four times daily, (11 patients) or a placebo (13 patients) for a 3-week period. All patients received peritoneal or hemodialysis treatment concurrently with the study drug. In contrast to the placebo, indomethacin produced an immediate and sustained reduction of fever in all but one patient. On the other hand, indomethacin had no effect on the duration of chest pain (mean days +/- SE: placebo 1.4 +/- 0.6, indomethacin 5.5 +/- 3.3), duration of pericardial friction rub (placebo 10.3 +/- 1.7, indomethacin 16.0 +/- 3.8), or on the amount of pericardial effusion. Further, indomethacin did not diminish the need for invasive surgical procedures for relief of tamponade (three of 13 placebo patients, two of 11 indomethacin patients) or result in decreased mortality rate. Death (not due to pericarditis) occurred in two patients treated with indomethacin and one patient who received the placebo. In our patients pericarditis encompassed a wide spectrum ranging from a mild illness of several days duration to a painful and debilitating disease lasting weeks and requiring surgical intervention. Although the size of our population prohibits definitive conclusions, it would appear that, except for fever, the manifestations and natural history of this illness are unaffected by indomethacin.

Adult↗
PubMed2000

Meningococcal pericarditis in a 2-year-old child: reactive or infectious?

Pericarditis is an uncommon manifestation of infection of Neisseria meningitidis. Pericarditis may be caused by direct invasion or immune-complex-mediated (reactive) inflammation. We outline the case of a two-year-old girl with probable reactive pericarditis, review the cases reported in the English literature since 1966 and discuss the pathogenesis of meningococcal pericarditis.

Child, Preschool↗
PubMed2002

Does rapid volume loading during transesophageal echocardiography differentiate constrictive pericarditis from restrictive cardiomyopathy?

BACKGROUND: Respiratory variation of the pulmonary venous (PV) peak flow velocities can be used to distinguish constrictive pericarditis (constriction) from restrictive cardiomyopathy (restriction). Rapid volume expansion has been used successfully to enhance diastolic pressure equalization in occult constriction. The effect of volume on the respiratory variation in constriction has not been studied previously. This study assessed the utility of volume in enhancing the PV respiratory variation of constriction to further separate it from restriction. METHODS: The study population consisted of 15 patients referred to the echocardiography laboratory for further evaluation of clinically suspected diastolic dysfunction. Pulsed-Doppler transesophageal echocardiography (TEE) of the left or right upper pulmonary vein and mitral inflow was performed with respiratory monitoring before and after infusion of 1 liter of normal saline over 5 to 10 minutes. The classification of patients as constriction (n = 8) or restriction (n = 7) was confirmed independently by cardiac catheterization or surgery. Peak velocities of the PV systolic and diastolic waves and the mitral inflow E were measured during inspiration and expiration. A mean of 3-6 respiratory cycles was obtained for each value before and after volume loading. The percent change from expiration to inspiration (%E) was calculated using the formula %E = expiration - inspiration / expiration. RESULTS: At baseline, patients with constrictive pericarditis can be separated reliably from those with restrictive cardiomyopathy based on a higher systolic/diastolic ratio and greater respiratory variation of their PV diastolic flow velocity. There were no complications in any patient due to volume expansion. Although the change from baseline to volume expansion was not statistically significant in either constriction or restriction, the %E of the PV diastolic wave became significantly higher in constriction than in restriction (P < 0.05). CONCLUSIONS: Rapid volume expansion is relatively safe during TEE and can be used for further separation of constrictive pericarditis from restrictive cardiomyopathy by significantly enhancing the respiratory variation of the PV diastolic flow velocity in constrictive pericarditis.

Adult↗
PubMed1998

The role of infarction-associated pericarditis on the occurrence of atrial fibrillation.

AIMS: Transient atrial fibrillation is a relatively common arrhythmia in the early phase of acute Q-wave myocardial infarction. However, the role of infarction-associated pericarditis on the genesis of atrial fibrillation is controversial. This study was designed to examine the relative importance of infarction-associated pericarditis among other clinical variables on the genesis of transient atrial fibrillation in patients with acute myocardial infarction. METHODS AND RESULTS: Three hundred and ninety-eight patients with acute Q-wave myocardial infarction were examined carefully by means of auscultation, ECG, two-dimensional echocardiography and haemodynamic measurements. The diagnosis of pericarditis was made on the basis of pericardial rub detected during the first 3 days after admission. At least 0.5 mm of PQ-segment depression from a TP segment lasting more than 24 h in both limb and precordial leads was considered diagnostic of PQ-segment depression. Atrial fibrillation was present in 76 patients (19%). Sixteen (42%) of 38 patients with PQ-segment depression had atrial fibrillation, whereas 23 (30%) of 77 patients with pericardial rub had atrial fibrillation. Based on ten clinical variables, multivariate analysis was performed to determine the important variables related to the occurrence of atrial fibrillation. PQ-segment depression (chi-square = 4.10, P < 0.05) was selected with age (chi-square = 10.52, P < 0.005), the number of left ventricular segments with advanced asynergy (chi-square = 7.73, P < 0.01) and pericardial effusion (chi-square = 7.95, P < 0.005) as important factors related to atrial fibrillation. Patients with PQ-segment depression had a significantly higher pulmonary capillary wedge pressure than those without it. CONCLUSION: Among patients with infarction-associated pericarditis, those with PQ-segment depression represent atrial involvement associated with extensive myocardial damage and hence, PQ-segment depression is one of the clinical signs related to the occurrence of atrial fibrillation in acute Q-wave myocardial infarction.

Aged↗
PubMed2000

Serum cardiac troponin I and ST-segment elevation in patients with acute pericarditis.

OBJECTIVE: ST-segment elevation in acute pericarditis is believed to be caused by superficial myocardial inflammation or epicardial injury. We used cardiac troponin I, a sensitive and specific marker of myocardial injury, to assess myocardial lesions in idiopathic acute pericarditis and its relationship to ST-segment elevation. PATIENTS AND METHODS: Sixty-nine consecutive patients (53 men, 48+/-17 years) with idiopathic acute pericarditis were included. We used an enzymoimmunoflurometric method to measure serum cardiac troponin I on admission (myocardial infarction threshold was 1.5 ng. ml(-1)). RESULTS: Cardiac troponin I was detectable in 34 patients (49%) and was beyond the 1.5 ng. ml(-1)threshold in 15 (22%). Coronary angiography performed in seven of these 15 patients was normal in all of them. ST-segment elevation was observed in 93% of the patients with cardiac troponin I >1.5 ng. ml(-1)vs 57% of those without (P<0.01). Sensitivity of ST-segment elevation to detect myocardial injury was 93% and specificity 43%. Patients with a cardiac troponin I increase higher than 1.5 ng. ml(-1)were more likely to have had a recent infection (66% vs 31%;P=0.01) and were younger (37+/-14 vs 52+/-16 years;P=0.002). There was no significant relationship with other parameters such as pericardial friction rub, fever, PR segment abnormalities, echocardiographic findings or C-reactive protein. CONCLUSION: In patients with idiopathic acute pericarditis, an increase in cardiac troponin I is frequently observed, especially in younger patients and those with a recent infection. Although ST-segment elevation does not reliably indicate myocardial injury, a significant cardiac troponin I increase is only seen in these patients.

Acute Disease↗
PubMed1977

[Pericarditis after acute myocardial infarction (author's transl)].

909 patients were treated between 1970 and 1975 in an intensive-care unit for acute myocardial infarction. 91 (10%) had associated pericarditis. In these patients the clinical course was characterised by a significantly high incidence of haemodynamically severe complications such as left and right heart failure and cardiogenic shock, as well as rhythm and conduction disturbances. High grade atrioventricular block, intraventricular conduction disturbances, ectopic and tachycardic supraventricular arrhythmias and ventricular ectopic rhythms occurred much more frequently in patients with infarct-pericarditis than in those without it. The occurrence of pericarditis indicates an extensive infarction and thus a worse prognosis. The hospital mortality of pericarditis was significantly higher (61%) than in the remaining 818 patients without it (24.4%). Anticoagulation did not increase the risk of haemopericardium.

Acute Disease↗
PubMed2005

[Bacterial pericarditis].

HISTORY AND CLINICAL FINDINGS: A 65-year-old previously healthy man was referred because of high fever, progressive dyspnea and retrosternal pain for 2 days. On admission, the patient was already in a reduced general condition, blood pressure was 120/70 mmHg, heart rate irregular at 75/min and temperature at 39.7 degrees C. Auscultation of the heart revealed distant heart sounds, murmurs were not present, but mild rales were heard over both lung bases. Jugular veins were congested. INVESTIGATIONS: ECG showed a generalized ST-segment elevation with preserved R-waves, slightly depressed PR-segment and atrial bigemini. Chest X-ray revealed an enlarged cardiac silhouette with signs of a pneumopericardium. Transthoracic echocardiography showed a circular pericardial effusion and haemodynamic impairment. Percutaneous pericardiocentesis revealed a purulent effusion with microbiological proof of pneumococci. The primary infectious focus was a maxillary sinusitis caused by pneumococci. DIAGNOSIS: Bacterial pericarditis due to by haematogenous spread of pneumococci. TREATMENT AND COURSE: Antibiotic therapy consisted of intravenous ceftriaxon and gentamicin. To rinse the pericardial space and drain the thick, purulent effusion subxiphoidal, pericardiocentesis and insertion of a drainage tube were done. Physiological saline was put into the pericardial space several times a day, drained and analysed microbiologically. In the meantime rinsing of the infected maxillary sinus was performed. Transthoracic echocardiography was done repeatedly to rule out complications of bacterial pericarditis, especially constrictive pericarditis. The pericardial tube was removed after proof of a sterile drainage 9 days after insertion. The patient was discharged after 4 weeks of hospitalization without clinical or echocardiographic signs of diastolic dysfunction. CONCLUSION: Suspected bacterial pericarditis must be treated as an emergency and confirmed or ruled out by percutaneous pericardiocentesis.

Aged↗
PubMed2006

[Recurrent autoreactive pericardial effusion. Impact of an aetiological classification of pericarditis].

HISTORY: A 36 year-old man suffered from fever, fatigue, pleurodynia and precordial discomfort. His family physician suspected febrile tracheobronchitis and treated it with ampicillin for 5 days. Because symptoms persisted an ECG was done which suggested acute myocardial infarction. The patient underwent an emergency coronary angiography which excluded coronary artery disease and aortic dissection. Pericarditis was suspected and the patient put on aspirin, 500 mg/d. Because of persisting cardiac symptoms an echocardiography was performed which revealed systolic separation between epi- and pericardium, characteristic of a small pericardial effusion after acute pericarditis. The symptoms improved after one week of treatment with diclofenac and the ECG had become normal. Two months later the patient was seen at our cardiac outpatient clinic. He had night sweats, sporadic precordial pain and severe dyspnoe. INVESTIGATIONS: Further investigations revealed tachycardia (120/min), hypotension (95/70 mm Hg), pulsus paradoxus and jugular vein sustension. Echocardiography revealed a large pericardial effusion ("swinging heart"), which explained the low voltage and the electrical alternans in the ECG. TREATMENT AND COURSE: Pericardiocentesis was carried out the same day to relieve the tamponade. It was followed by pericardioscopy and epi- as well as pericardial biopsy. 485 ml of a serous effusion were drained. Cytology and histology demonstrated a lymphocytic fibrinous pericarditis. Polymerase chain reaction (PCR) on viral and bacterial RNA and DNA of potentially cardiotropic agents remained negative. The pigtail catheter was left in place and 80 mg of gentamycin were given intrapericardially on day 1 and 2, followed by 500 mg of crystalloid triamcinolone acetate after the PCR was found to be negative. Oral treatment with 0.5 mg colchicine three times a day (off-label use) was started and maintained for 6 months. After 9 months no effusion was detected and the patient was free of symptoms. CONCLUSIONS: After exclusion of bacterial and viral pericardial infection, a high single dose of intrapericardial triamcinolone combined with long-term oral colchicine has proven to be a highly efficacious treatment of autoreactive pericarditis which will avoid relapses in most cases.

Adult↗
PubMed1990

Pericarditis: a probably overlooked complication of endoscopic variceal sclerotherapy.

Two cases of acute pericarditis following endoscopic variceal sclerotherapy (EVS) that were resolved with conservative management are described. This complication arose respectively one and three days after EVS. The possible pathogenesis is the involvement of the pericardium in an inflammatory reaction that develops in the esophageal wall and surrounding tissues. Only five cases have been previously reported in the literature; the authors suppose that this fact may be due to the mild symptoms presented by the patients, which may result in underestimation of this complication. The technical details of EVS in the seven patients with pericarditis were analyzed, but no common etiologic factor was found. The authors strongly advise regular checks for clinical and instrumental signs of acute pericarditis after every session of EVS, so that appropriate management can be undertaken in an early phase and, if necessary, further EVS sessions delayed, in order to avoid cardiac tamponade or constrictive pericarditis.

Acute Disease↗
PubMed2002

Drug induced pericarditis in a patient with chronic renal failure.

Drug induced pericarditis is reported very rarely. We presented a patient with pericarditis due to antituberculosis therapy induced pericarditis and chronic renal failure. We did not find clinical and serologic findings of pseudo-lupus clinical symptoms and pericarditis regressed in a short time with cessation of antituberculosis drugs and initiated steroid.

Antitubercular Agents↗