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PubMed1994

Acute pericarditis resulting from an endocardial active fixation screw-in atrial lead.

We examined the occurrence of acute pericarditis after pacemaker implantation in 123 consecutive patients (61 males, 62 females, ages 17-87 years) in whom a newer atrial active fixation bipolar lead was inserted endocardially in the right atrium for dual chamber pacing. The atrial leads were positioned to obtain the best possible pacing and sensing thresholds, after an initial attempt was made for insertion into the right atrial appendage or medially into the right atrial septum. Six patients (4.9%) developed acute symptomatic pericarditis with effusion within 24 hours of implantation. Of these six patients, four had leads screwed into the lateral wall, and the other two had leads placed in the anterolateral wall. The lead implantation parameters between patients with pericarditis and those without did not show any significant difference in the atrial P wave amplitude (2.3 +/- 0.4 vs 2.9 +/- 0.9 mV), pacing threshold (1.1 +/- 0.2 vs 1.1 +/- 0.4 V), or resistance (524 +/- 112 vs 480 +/- 94 ohms). All symptomatic patients were treated with nonsteroidal anti-inflammatory drugs with symptoms resolving in 1-2 weeks. We conclude that: (1) a significant number of patients (4.9%) developed acute symptomatic pericarditis after insertion of this type of atrial fixation lead; (2) because of the lead design, the implantation parameters could not be taken to predict the occurrence of pericarditis; and (3) caution should be taken for the insertion of this lead into the thin atrial wall.

Acute Disease↗
PubMed1976

Usefulness of systolic time intervals in differential diagnosis of constrictive pericarditis and restrictive cardiomyopathy.

Systolic time intervals in 15 patients with constrictive pericarditis and seven patients with restrictive cardiomyopathy were compared in order to assess their value in the differential diagnosis of the two disorders. Clinical examination had failed to make the distinction. Right heart catheterization was helpful in diagnosing restriction but failed to differentiate patients with constrictive pericarditis from those with restrictive cardiomyopathy. The systolic time intervals clearly separated the two groups. The PEP/LVET was normal in all patients with constrictive pericarditis (0.34 +/- 0.01) and abnormal in all patients with restrictive cardiomyopathy (0.70 +/- 0.09, P less than 0.001). In 13 patients (five with restrictive cardiomyopathy and eight with constrictive pericarditis) the results of quantitative left ventricular angiocardiography were available. A high correlation (r=-0.90, P less than 0.01) between the PEP/LVET and the ejection fraction confirmed the validity of the PEP/LVET as a measure of left ventricular performance in these patients. Thus the systolic time intervals clearly distinguished between constrictive pericarditis and restrictive cardiomyopathy and are a reliable non-invasive technique for making the difficult differential diagnosis.

Adult↗
PubMed1989

Restrictive cardiomyopathy and constrictive pericarditis: non-invasive distinction by digitised M mode echocardiography.

It is difficult to distinguish between restrictive cardiomyopathy and constrictive pericarditis on the basis of clinical findings and simple investigation. Cardiac catheterisation has been the reference standard for diagnosis but even this does not always permit an accurate distinction. A Summagraphics digitiser and Prime 750 computer system were used to digitise the echocardiograms of 15 patients with restrictive cardiomyopathy, 10 with constrictive pericarditis and a group of 20 age and sex matched normal subjects of similar age and sex distribution. Compared with controls, patients with restrictive cardiomyopathy showed a significant reduction in the following variables (a) decreased fractional shortening, (b) decreased peak left ventricular filling and emptying rates, (c) decreased percentage posterior wall thickening, and (d) decreased peak left ventricular posterior wall thickening and thinning rates. Whereas patients with constrictive pericarditis only had significantly reduced peak left ventricular filling and posterior wall thinning rates and significantly increased posterior wall thinning rate. When patients with restrictive cardiomyopathy were compared with those with constrictive pericarditis the significant differences were: (a) decreased peak left ventricular emptying rate, (b) decreased percentage posterior wall thickening, and (c) decreased peak left ventricular posterior wall thickening and thinning rates. Digitisation of M mode echocardiograms, with particular attention to posterior wall function, may be a useful adjunct to cardiac catheterisation in distinguishing restrictive cardiomyopathy from constrictive pericarditis.

Adult↗
PubMed2002

Pericarditis due to anaerobic bacteria.

This review describes the microbiology, diagnosis and management of pericarditis due to anaerobic bacteria. The predominant anaerobes recovered from patients with pericarditis were: gram-negative bacilli (mostly of the Bacteroides fragilis group), anaerobic streptococci, Clostridium spp., Fusobacterium spp., and Bifidobacterium spp. Anaerobic bacteria can be isolated in pericarditis resulting from the following mechanisms: (1) spread from a contiguous focus of infection, either de novo or after surgery or trauma (pleuropulmonary, esophageal fistula or perforation, and odontogenic); (2) spread from a focus of infection within the heart, most commonly from endocarditis; (3) hematogenous infection, and (4) direct inoculation as a result of a penetrating injury or cardiothoracic surgery. No differences were found in the clinical diagnostic features between cases of pericarditis due to anaerobic bacteria and those due to aerobic and facultative bacteria. Anaerobic gram-negative bacilli have increased their resistance to penicillins and other antimicrobials in the last decade. Complete identification and testing for antimicrobial susceptibility and lactamase production are therefore essential for the management of infections caused by these bacteria. Treatment of pericarditis involving anaerobic bacteria includes the use of antibiotic therapy effective against these organisms.

Anti-Bacterial Agents↗
PubMed1984

Carcinoembryonic antigens in the pericardial fluid of patients with malignant pericarditis.

The diagnostic accuracy of measurement of carcinoembryonic antigen (CEA) and of analysis of the cytological characteristics of pericardial fluid was assessed in 10 patients with benign pericarditis and 7 patients with malignant pericarditis. The mean CEA levels of pericardial fluid specimens from patients with malignant pericarditis were significantly higher than those from patients with benign pericarditis. However, a high CEA level was not seen in a specimen of pericardial fluid which contained nonepithelial tumor cells. Positive cytological findings were obtained in specimens of pericardial fluid from 85.7% of the patients with malignant pericarditis. Correct diagnosis of malignancy was made by CEA assay alone or by cytological examination alone in 85.7% of the patients examined, while a combination of these methods raised the diagnostic rate to 100%.

Carcinoembryonic Antigen↗
PubMed1976

Uremic pericarditis as a cause of cardiac tamponade.

Uremic pericarditis may complicate either acute or, more commonly, chronic renal failure. When dialysis is not employed, uremic pericarditis is usually a preterminal event and is characterized by a serofibrinous exudation of an amount inadequate to cause cardiac tamponade. Nevertheless, cardiac tamponade may uncommonly be observed in nondialyzed patients. Cardiac tamponade, which may be life-threatening, is more common in dialyzed than in nondialyzed patients with chronic renal failure. The primary causes of cardiac tamponade in uremic pericarditis in order of decreasing frequency are (1) pericardial effusion, usually of the serosanguineous type, (2) massive hemorrhage into the pericardial sac and (3) collagenization of pericardial exudate. From pathologic evidence, the following forms of therapy appear appropriate to manage uremic pericarditis that has reached the stage of causing cardiac tamponade. For effusion, pericardiocentesis or parietal pericardiectomy are logical procedures. Massive hemorrhage into the pericardial sac is usually attended by clotting and requires pericardiotomy and evacuation of clot. Collagenization of exudate yields an encasing, fibrous shell over the heart and requires decortication, as is practised in classical constrictive pericarditis.

Acute Kidney Injury↗
PubMed1986

Ventricular coupling in constrictive pericarditis.

Because of the close anatomic association, the volume or pressure in one ventricle can directly influence the volume and pressure in the other ventricle. Disease states that reduce pericardial compliance should accentuate this coupling between the ventricles. We examined this hypothesis in six dogs. Constrictive pericarditis was induced by injecting an irritant mixture into the pericardial cavity. Three to 4 weeks after this injection, the hearts were removed and placed in cool cardioplegic solution. Balloons were inserted into each ventricle and the pressure and volume changes caused by increasing the contralateral ventricular volume were measured. Compared with that in a control group of four dogs, the coupling between the ventricles was significantly augmented in the group with constrictive pericarditis. All the measured changes in ventricular pressure or volume caused by increasing contralateral ventricular pressure or volume were significantly greater (p less than .05) in the group with constrictive pericarditis. The results of these experiments show increased coupling between the ventricles with constrictive pericarditis, which helps to explain some of the signs and symptoms of constrictive pericarditis.

Animals↗
PubMed1991

Electrophoretic studies on serum proteins in cows with traumatic pericarditis.

Diagnostic significance of electrophoretic findings of serum protein in cows with traumatic pericarditis was evaluated. Affected cows were classified into 3 groups according to autoptical findings: fibrinous, sero-fibrinous, and purulent types. Slight hypoprotenemia, moderate hypo-albuminemia, slight hyper-alpha globulinemia and tendency of hyper-beta globulinemia were commonly observed in the affected cows. The level of gamma globulin tended to be lower in the cows with fibrinous or sero-fibrinous, and higher in purulent pericarditis, than the level in healthy cows. In the serum protein electropherograms of the cows with fibrinous or sero-fibrinous pericarditis, there was pathognostic pattern composed of slender albumin, acute shape of alpha globulin with a broad rising accompanied by double peaks and with main peak migrating toward the albumin side, tendency of rising beta globulin fraction, and large indentation between beta and gamma fractions. These findings except for the slender albumin fraction, however, was not or poorly observed in purulent pericarditis. Electrophoretic findings were subacute inflammatory pattern with non-selective serum protein losing in fibrinous or sero-fibrinous, and chronic inflammatory pattern in purulent pericarditis.

Alpha-Globulins↗
PubMed1999

Chronic constrictive pericarditis induced by long-term bromocriptine therapy: report of two cases.

OBJECTIVE: To report two cases of chronic constrictive pericarditis that appear to be related to the intake of bromocriptine for Parkinson's disease. CASE SUMMARY: Two white men (aged 63 and 69 y) were treated with bromocriptine for four (40 mg/d) and two years (30 mg/d), respectively, with a cumulative dose intake of 58.4 and 21.9 g, respectively. The patients experienced dyspnea with bilateral lower-limb edema and pleural effusion, suggesting right cardiac dysfunction. Echocardiography, computed tomography, and cardiac catheterization results were compatible with a diagnosis of constrictive pericarditis, so pericardectomy was performed on both patients. The anatomic pathology examination showed a fibrous pericardium; cultures were sterile. In the first case, pleural effusion recurred seven months after the pericarditis; bromocriptine was suspected and treatment was discontinued. In the second case, just prior to the pericardectomy, an episode of mental confusion occurred and prompted the cessation of bromocriptine therapy. DISCUSSION: To the best of our knowledge, only one case of constrictive pericarditis induced by bromocriptine therapy has previously been described in the literature. CONCLUSIONS: Our cases call attention to a possible association between bromocriptine use in patients who have Parkinson's disease and constrictive pericarditis.

Aged↗
PubMed1983

Postoperative pericarditis following thymectomy for myasthenia gravis. A prospective study.

Eight consecutive patients who underwent thymectomy for the treatment of myasthenia gravis were evaluated prospectively for the development of postoperative pericarditis. In four of the eight patients (50 percent) pericarditis developed within 48 hours after thymectomy. All four had a three-component pericardial friction rub, two of the four patients had a new postoperative pericardial effusion by echocardiography, and in two typical ECG diffuse concave ST segment elevation and evolutionary ST and T wave changes developed. In the four patients with postoperative pericarditis, a malignant thymoma adherent to the pericardium was found in two, while two patients had a normal thymus histology with no adherence to the pericardium. Thus, postoperative pericarditis was found in both of the patients with a thymoma and in two of six patients without a thymoma. This study demonstrates that a high incidence of pericarditis occurs following thymectomy for the treatment of myasthenia gravis.

Adolescent↗
PubMed1987

Constrictive pericarditis associated with patch electrodes of the automatic implantable cardioverter-defibrillator.

A case of constrictive pericarditis intimately involving patch electrodes of the automatic implantable cardioverter-defibrillator is described. Typical clinical and hemodynamic findings for constrictive pericarditis were noted 15 months after lead installation. Additionally, chest x-ray examination revealed a severe crumpling deformity of the patch electrodes. Thoracotomy was performed and revealed marked fibrous reaction surrounding both surfaces of each patch electrode. Histologic examination revealed fibrous tissue with multinucleated giant cells, consistent with a foreign body reaction. The patient had complete resolution of signs and symptoms of constrictive pericarditis after removal of the patch electrodes and pericardial stripping. Constrictive pericarditis from implanted patch electrodes appears to be an uncommon complication of the automatic implantable cardioverter-defibrillator and should be considered in patients with one or more patch electrodes and other signs of constrictive pericarditis.

Aged↗
PubMed1975

Rheumatic valvulitis and constrictive pericarditis. Report of case.

A 13-year-old girl was admitted with congestive heart failure, edema, ascites, and jaundice. There was an apical pansystolic murmur of mitral insufficiency and marked cardiomegaly. Her venous pressure was elevated. Despite medical treatment her condition deteriorated, hepatic and renal failure as well as disseminated intravascular coagulation ensued, leading to her death. At post mortem she was found to have rheumatic mitral valvulitis and constrictive pericarditis. The pathologic picture of pericarditis was nonspecific, but in presence of a positive skin test for tuberculosis the latter is considered to be the most likely cause of the pericarditis, nevertheless, rheumatic etiology of pericarditis in this case cannot be excluded. The presence of rheumatic heart disease and cardiomegaly may have led to the exacerbation of symptoms and signs of constrictive pericarditis and severe right heart failure.

Adolescent↗
PubMed1997

Porphyria cutanea tarda with constrictive pericarditis in a family.

Two cases of familial porphyria cutanea tarda (PCT) with constrictive pericarditis are described. A 50-year-old woman and her 48-year-old younger brother were admitted because of right ventricular heart failure. Constrictive pericarditis was diagnosed by RV pressure waveform and echocardiogram. The patients were diagnosed as PCT based on clinical symptoms, histologic findings and elevated urinary excretion levels of uroporphyrin. Even to this day, over 40% of the etiology of constrictive pericarditis remains unknown. There is a possibility of overlooking porphyria cutanea tarda in constrictive pericarditis patients. This report describes the first documented cases of familial PCT with constrictive pericarditis.

Coproporphyrins↗
PubMedDate not supplied

Propylthiouracil-induced perinuclear-staining antineutrophil cytoplasmic autoantibody-positive vasculitis in conjunction with pericarditis.

OBJECTIVE: To describe a case of propylthiouracil-induced vasculitis manifesting with pericarditis. METHODS: We present the first case report of a woman with hyperthyroidism treated with propylthiouracil in whom a syndrome of pericarditis, fever, and glomerulonephritis developed. Serologic testing and immunologic studies were done, and a pericardial biopsy was performed. RESULTS: A 25-year-old woman with Graves' disease had a febrile illness and evidence of pericarditis, which was confirmed by biopsy. Serologic evaluation revealed the presence of perinuclear-staining antineutrophil cytoplasmic autoantibodies (pANCA) against myeloperoxidase (MPO). Propylthiouracil therapy was withdrawn, and she was treated with a 1-month course of prednisone, which alleviated her symptoms. A literature review revealed no prior reports of pericarditis in anti-MPO pANCA-positive vasculitis associated with propylthio- uracil therapy. CONCLUSION: Pericarditis may be the initial manifestation of drug-induced vasculitis attributable to propylthio- uracil therapy.

Adult↗
PubMed2000

Calcific constrictive pericarditis: is it still with us?

BACKGROUND: 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. OBJECTIVE: To determine the clinical and prognostic significance of pericardial calcification on radiography in patients with constrictive pericarditis. DESIGN: Retrospective cohort study. SETTING: Tertiary referral center. PATIENTS: 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). MEASUREMENTS: Clinical and diagnostic findings were compared in both groups, and outcome was compared in 132 patients who had pericardiectomy. RESULTS: 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. CONCLUSIONS: 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.

Adolescent↗
PubMed2000

Fibrinofibrous pericarditis mimicking a pericardial tumor.

Primary pericardial disease is rare in children. The clinical features usually reflect limited venous return and cardiac output. Tuberculous pericarditis is the leading cause of pericardial disease in developing nations. A definitive diagnosis in children is frequently difficult and the manifestations are protean. We report a 10-month-old girl with fibrinofibrous pericarditis that manifested as constrictive pericarditis with prolonged fever, hepatomegaly, edema, and poor appetite. Echocardiography showed a solid mass that originated from the thickened pericardium and compressed the whole heart. In contrast, computed tomography revealed pericardial thickening with fluid collection. The symptoms and signs dramatically improved after surgical pericardiectomy. Pathologic analysis confirmed the diagnosis of tuberculous fibrinofibrous pericarditis. The patient received a 1-year course of antituberculosis therapy and has remained symptom free for 2 years. We suggest that a discrepancy between echocardiography and computed tomography (CT) findings might indicate a diagnosis of fibrinofibrous pericarditis.

Diagnosis, Differential↗
PubMed2000

Constrictive pericarditis. Early experience in 12 patients in light of modern cardiology.

The last several decades have witnessed major advances in the understanding and management of constrictive pericarditis. The aim of the present study was to compare the diagnosis, treatment and outcome of constrictive pericarditis of 40 years ago to today. The study population consisted of 12 patients with a diagnosis of constrictive pericarditis who presented at the Institute of Cardiology of Beilinson Hospital, from 1961 to 1970. Their main physical findings, electrocardiographic and chest X-ray changes, and hemodynamic study results are discussed in relation to the surgical outcome of patients with constrictive pericarditis today. New noninvasive imaging modalities, such as M mode, two-dimensional and Doppler echocardiography, computed tomography and magnetic resonance imaging are presented, and their advantages and disadvantages in the diagnosis of constrictive pericarditis and its differentiation from restrictive cardiomyopathy are explained.

Adolescent↗
PubMed2000

[Efficacy of colchicine in recurrent acute idiopathic pericarditis].

Acute idiopathic pericarditis is complicated by recurrence in 15 to 30% of cases. The preventive treatment of recurrences is not well codified. Aspirin, non-steroidal anti-inflammatory drugs and corticoids are the commonest prescribed treatments. The objective of this study was to assess the value of colchicine in the prevention of recurrences of acute idiopathic pericarditis. Twenty-eight cases of recurrent acute pericarditis (2 episodes, 1 month between each episode) admitted to a department of internal medicine between 1989 and 1999 were reviewed. Analysis was concentrated on the 13 idiopathic forms. The subjects were 7 women and 6 men with an average age of 41 years (10-62) at the time of the first episode of acute pericarditis. These 13 patients were treated with colchicine (1 to 2 mg/day) after failure of conventional treatment (aspirin 13/13, NSAID 13/13, steroids 9/13 and pericardiocentesis 3/13). Ten patients were followed up regularly (6 months after starting colchicine) and were improved with respect to number, duration and intensity of their recurrences. The average duration of colchicine therapy was 17 +/- 14 months (6-48). Progressive withdrawal of NSAID and steroids was obtained in 8/10 cases. The authors conclude that colchicine is useful in the prevention of recurrence of acute pericarditis. It may be proposed as treatment of choice, especially in the idiopathic forms.

Acute Disease↗