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PubMed1980

Early diagnosis of pericarditis in acute myocardial infarction.

Pericarditis complicating acute myocardial infarction assumes increasing importance in this era of quantitating infarct size by precordial ST segment mapping. Early recognition of this complication avoids diagnostic and therapeutic errors. In this study we looked for factors that could alert to the early diagnosis of pericarditis, such as ST elevation measured within 24 hours from onset, extent of CPK, LDH, and SGOT elevation, as well as degree of pump dysfunction. ST segment elevation in millimeters on admission seemed to be one factor that was of predictive value in this condition. Pericarditis occurred in three forms: (1) within a few hours from the onset of myocardial infarction and this form seems to carry a high mortality rate; (2) a more common variety occurs within 24 to 72 hours from onset and carries a higher mortality rate than matched controls; and (3) the late syndrome of Dressler's, not observed in our series. Aside from increased incidence of heart failure, other complications of myocardial infarction and the coronary risk factors were not significantly higher in patients with pericarditis. Salicylate treatment offers immediate relief in the majority of patients.

Aspartate Aminotransferases↗
PubMed1976

Pericarditis caused by Histoplasma capsulatum.

Sixteen patients with pericarditis caused by Histoplasma capsulatum were studied. Fourteen were less than 30 years old, and no patient had an underlying illness or was receiving immunosuppressive therapy. All patients experienced a flu-like prodromal illness lasting from 2 weeks to 4 months. Pneumonitis or hilar adenopathy, or both, was found in 12; pleural effusion, uncommon in primary pulmonary histoplasmosis, was found in seven patients. Pericardial fluid, pleural fluid and bone marrow cultures yielded no growth. All patients demonstrated a fourfold or greater change in complement-fixing antibody titers. No patient had disseminated disease, and only one required treatment with ampholericin B. The illness ran a protracted course, and in six patients symptomatic pericarditis recurred. Ultimately all recovered. Ten patients were restudied 6 months to 12 years after recover. Only one patient had pericardial calcification, and none had constrictive pericarditis. This form of granulomatous pericarditis, unlike that caused by Mycobacterium tuberculosis, appears to carry a good prognosis.

Adolescent↗
PubMed1982

Constrictive pericarditis as a complication of cardiac surgery: recognition of an entity.

Among 5,207 adult patients who underwent cardiac surgery, postoperative constrictive pericarditis was recognized in 11 patients (0.2% incidence rate). Seven patients had coronary arterial bypass grafting and 4 had valve replacement; the pericardium was left open in all cases. The average interval between surgery and presentation of pericardial constriction was 82 days (range 14 to 186). M mode echocardiography revealed epicardial and pericardial thickening in 7 cases and variable degrees of posterior pericardial effusion in 5 cases. Cardiac catheterization demonstrated uniformity of diastolic pressures with a characteristic early diastolic dip and late plateau pattern. Two patients responded to medical therapy for chronic pericarditis. One patient had a limited parietal pericardiectomy followed by recurrent constrictive pericarditis that eventually stabilized with medical therapy. The other 8 patients required radical pericardiectomy. The pathophysiology of constriction after surgery is unclear. Its clinical expression involves a wide spectrum of presentation and therapeutic response. Constrictive pericarditis may be a complication of cardiac surgery in spite of an open pericardium and should be considered in postoperative patients who present with deteriorating cardiac function.

Adrenal Cortex Hormones↗
PubMed1989

Diagnosis of constrictive pericarditis by pulsed Doppler echocardiography of the hepatic vein.

The diagnostic value of hepatic venous flow patterns was evaluated for constrictive pericarditis by pulsed Doppler. A characteristic flow pattern was assumed to be associated with the well-known atrial pressure curve. Thirteen patients with constrictive pericarditis were compared to 13 control subjects and to 25 patients with right ventricular pressure overload including 13 patients with tricuspid regurgitation. The characteristic finding in constrictive pericarditis was a W-wave pattern of flow velocities in the dilated hepatic veins, with abrupt reversal of flow late in systole and diastole before the A wave (100% specificity, 68% sensitivity). This depends, however, on the absence of tricuspid regurgitation (for its systolic component) or fast sinus rhythm (for its diastolic component). Additional diagnostic markers were systolic deceleration time of forward flow (40 to 130 ms) and systolic integral of flow velocities (4.3 to -4.0 cm) (sensitivity and specificity greater than or equal to 92%). In the presence of tricuspid regurgitation, diastolic deceleration time less than 150 ms and diastolic integral of flow velocities less than 6 cm were useful diagnostic signs. If combined, these criteria had 100% sensitivity and specificity for the diagnosis. Thus, pulsed Doppler assessment of flow velocities in the hepatic vein facilitates the diagnosis of constrictive pericarditis in clinical routine, using an auxiliary site with unlimited diagnostic access to the characteristic flow velocity pattern, which reflects right atrial pressure curve and filling abnormalities.

Adolescent↗
PubMed1981

Pneumococcal pericarditis: a persisting problem in contemporary diagnosis.

We reviewed the clinical and laboratory features of six patients with pericarditis caused by Streptococcus pneumoniae who were admitted to Boston City Hospital. The diagnosis of pneumococcal pericarditis was delayed or missed entirely during life in all patients. The frequent absence of pericardial friction rubs and cardimegaly on chest roentgenograms contributed to the difficulty in recognizing this illness. Electrocardiograms and physical examinations of the heart almost always disclosed abnormalities, but they were not sufficiently specific to suggest pericarditis, and patients were often thought to have had an acute complication of arteriosclerotic heart disease. Review of the English literature since 1945 supports the recent experience in our hospital that the diagnosis of pneumococcal pericarditis may be elusive.

Adult↗
PubMed1983

Surgical treatment of pericarditis in the dialysis patient.

Eighteen patients with pericarditis complicating chronic renal failure who were unresponsive to medical therapy underwent surgical decompression of the pericardium for either pericardial tamponade [16] or constrictive pericarditis [2]. There was one perioperative death and minimal morbidity. Preoperative pericardiocentesis in nine patients afforded only temporary relief in most of the patients and caused a life-threatening pericardial tamponade in one patient. Creation of a pericardial window through a left anterior thoracotomy was the procedure of choice in patients without signs of constrictive pericarditis or posterior loculated effusions and had excellent long-term results. We recommend early surgical treatment of uremic pericarditis in all patients with hemodynamic instability, enlarging pericardial effusion, or effusion that is unresponsive to intensive medical therapy.

Adult↗
PubMed1993

Electrical current paths in acute pericarditis.

The electrocardiographic changes accompanying pericarditis consist of ST elevation in most of the leads of the 12-lead electrocardiogram. The source of this ST elevation is thought to be local inflammatory changes in the epicardium underlying the inflamed pericardium. The current from this area of ST elevation must return to some unaffected region of the heart and this should be associated with a region of ST depression. This current path from the external epicardial surface has been postulated to flow back into the endocardium through the great vessels and atria. To test this hypothesis, 18 patients with pericarditis were studied by body surface potential mapping and inverse epicardial potential distributions were computed. The resultant maps were compared to those of normal people and patients with acute anterior infraction. Epicardial maps from patients with pericarditis showed a region of current flow into the heart over the great vessels and atria in all 18 patients. This pattern was not seen in normal patients or infarction patients and was consistent with the mechanism resulting in ST elevation in pericarditis being one of current flowing from the epicardium out into the thorax and back into the heart through the great vessels and atria.

Acute Disease↗
PubMed1990

Cardiac compression in rheumatoid pericarditis.

Rheumatoid pericarditis occurs in approximately one third of rheumatoid arthritis (RA) patients. However, clinically apparent rheumatoid pericarditis is infrequent. The authors found clinical pericarditis in 12 of 960 patients admitted for RA, 5 of whom had manifestations of cardiac compression. These 5 had longer duration of RA, worse functional class, and more extraarticular features than the patients without cardiac compression. Presenting features of cardiac compression included dyspnea, edema, chest pain, and pulsus paradoxus. Treatment of patients with cardiac compression due to rheumatoid pericarditis may include a trial of systemically administered corticosteroids, but this should not delay surgical intervention for impending tamponade. Pericardiocentesis should only be performed as an emergency, life-saving procedure. It may be followed by intrapericardiac injection of corticosteroids, but this does not prevent recurrence. Longer-lasting benefit is obtained by surgical decompression. Two-year mortality in patients with cardiac compression was 100%. The literature on the subject is reviewed.

Adrenal Cortex Hormones↗
PubMed1988

Reduced diastolic left ventricular posterior wall motion in patients with constrictive pericarditis--incidence, hemodynamic and clinical correlations.

In 24 patients with constrictive pericarditis proven by cardiac catheterization, the amplitude of diastolic left ventricular posterior wall motion was evaluated by M-mode echocardiography and compared to the results of 24 healthy volunteers. The amplitude was significantly less in constrictive pericarditis patients than in normal controls (0.3 +/- 0.2 mm versus 3.9 +/- 0.4 mm) (P less than 0.001). No constrictive pericarditis patient demonstrated a higher value than 2 mm whereas none of the healthy volunteers had an amplitude less than 3 mm. In 11 of 13 constrictive pericarditis patients who underwent pericardiectomy, an increase in amplitude was observed. In 6 patients the amplitude returned to normal limits after surgery. No significant correlation between the degree of heart failure or the level of left ventricular end-diastolic pressure and the reduction of the amplitude was found. In addition, the amplitude of left ventricular diastolic posterior wall motion did not allow a clear separation between patients who could be treated medically and those requiring pericardiectomy.

Adult↗
PubMed1993

Observations of angina and myocardial infarction in constrictive pericarditis.

The common symptoms of constrictive pericarditis, i.e. dyspnea on exertion, shortness of breath and cough, relate to impairment of ventricular filling and to a progressive rise in systemic and pulmonary venous pressures. Myocardial ischemia, angina and myocardial infarction are rarely associated with this disease. We have encountered two patients with constrictive pericarditis, one presenting with angina and the other with acute anterior wall infarction. Possible etiologies of constrictive pericarditis in the first case include cardiac surgery, chronic renal failure and myocarditis; in the second case, Crohn's disease. The proposed mechanism of chest pain in the first patient was a reduced cardiac output resulting in underperfusion of the coronary arteries, although it is possible that the patient experienced angina due to the presence of severe coronary artery disease. In the second patient an anterior wall infarction and post-infarction angina were attributed to obliteration of the left anterior descending artery by constraint of a thickened pericardium. In both cases non-invasive imaging modalities were not of use in establishing the diagnosis of constrictive pericarditis. Clinical awareness and accurate hemodynamic measurements continue to play a key role in the diagnostic process.

Angina Pectoris↗
PubMed1996

Changes in the proportion of types I and III collagen in the left ventricular wall of patients with post-irradiative pericarditis.

Pericardiectomy for post-irradiative constrictive pericarditis achieves poor results because of the extensive damage to the heart and pericardium caused by ionizing radiation. The extracellular structural protein, collagen, is responsible for the functional integrity of the myocardium and allows reversible interdigitation and the transmission of force between contracting myocytes. Collagen concentration and composition were examined in the cardiac tissue of three patients undergoing pericardiectomy and post-irradiative pericarditis. Normal heart tissue was taken at autopsy from patients without cardiac disease and acted as controls. Total collagen concentration (mean(s.e.m.)) was significantly increased in the ventricular tissue of patients with post-irradiative pericarditis compared with that of the controls (119.8(16.6) versus 50.4(5.2) mg/g dry weight, P<0.01). Although there was an increase in concentration of both type I and III collagen, a disproportional increase in type I was observed. The proportion of type III collagen was lower in patients with post-irradiative pericarditis than in the control group (33(2.6)% versus 38.2(3.7)%, P<0.05). The results of the present study suggest that this marked alteration in collagen concentration and proportion may contribute to the impaired diastolic distensibility of the ventricles seen in this group of patients.

Adult↗
PubMed1993

Results of subtotal pericardiectomy for constrictive pericarditis.

The operative approach to constrictive pericarditis still remains a surgical challenge. Subtotal pericardiectomy through median sternotomy was analyzed retrospectively in a series of 84 patients operated on for chronic constrictive pericarditis at our institution between 1979 and 1989. The mean duration of symptoms prior to diagnosis was 20 +/- 6 months (1-264 months). Preoperatively, 72% of patients were in NYHA class III or IV, presented signs of right cardiac failure (88%) or anasarca (18%). Chest X-ray showed pericardial calcifications in 40% of the patients. Echocardiography revealed pericardial thickening in 62%. Among 62 patients in whom cardiac catheterization was performed, a characteristic dip-and-plateau was found in 47 patients (76%). A specific etiologic factor was identified in only 37 patients: tuberculosis (12%), recurrent acute pericarditis (9%), hemopericardium (9%), radiotherapy (5%), previous cardiac surgery (4%), bacterial infection (2%), myocardial infarction (2%) and connective tissue disease (2%). In 47 patients (55%), the constrictive pericarditis remained idiopathic. In seven patients we performed a redo-operation for previous incomplete pericardiectomy. Subtotal pericardiectomy (from phrenic nerve to phrenic nerve) was performed in 75 patients. A palliative procedure consisting of pericardial "meshing" was performed in nine patients due to an unsatisfactory cleavage plane. Cardiopulmonary bypass was used in four patients for coexistent cardiac lesions. The operative mortality was 2.3% (two patients: septicemia and pulmonary embolism). Seven patients (8.2%) developed early on-lethal complications. The probability of survival for patients discharged for the hospital was 94% at 3 years and 87% at 7 years. There were four late deaths and no reoperation for recurrent constriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiopulmonary Bypass↗
PubMed2004

Recurrent pain without objective evidence of disease in patients with previous idiopathic or viral acute pericarditis.

Recurrent pain without clinical evidence of acute pericarditis was recorded in 27 of 275 patients (9.8%; mean age 55.6 +/- 16.0 years, female/male ratio 20/7) with previous viral or idiopathic acute pericarditis. Female gender (odds ratio [OR] 4.3, 95% confidence interval [CI] 1.8 to 10.6), previous use of corticosteroids (OR 5.2, 95% CI 2.2 to 12.3), and previous recurrent pericarditis (OR 3.7, 95% CI 1.3 to 10.2) were identified as risk factors for this syndrome. After a mean follow-up of 40 months, a higher recurrence rate was recorded in these patients (33.3% vs 14.1%; p = 0.02) as well as a nonsignificant trend to a higher rate of constrictive pericarditis.

Acute Disease↗
PubMed2005

Tramadol-associated pericarditis.

Tramadol, marketed as Ultram in the United States, is as a non-scheduled narcotic analgesic based on its low abuse liability. It is indicated for the treatment of moderately severe pain; however, multiple adverse effects have been reported with its use including seizures, anaphylaxis, angioedema, bronchospasm, and serotonin syndrome. An association between tramadol and pericarditis has not been previously reported. We describe the case of an 88 year-old male who developed acute pericarditis 2 days following tramadol initiation. The temporal relationship between drug initiation and pericarditis as well as the resolution of symptoms upon drug discontinuation suggested a potential association. Although pericarditis has not been described with tramadol administration, clinicians should be aware of a possible association.

Aged↗
PubMed2004

Day-hospital treatment of acute pericarditis: a management program for outpatient therapy.

OBJECTIVES: We sought to investigate the safety and efficacy of a protocol for acute pericarditis triage and outpatient management of low-risk cases. BACKGROUND: Acute pericarditis has generally a brief and benign course after empiric treatment by non-steroidal anti-inflammatory drugs, and routine hospitalization of most patients may be unnecessary. METHODS: From January 1996 to December 2001, all consecutive cases of acute pericarditis were evaluated on a day-hospital basis. Patients without clinical poor prognostic predictors (fever >38 degrees C, subacute onset, immunodepression, trauma, oral anticoagulant therapy, myopericarditis, severe pericardial effusion, cardiac tamponade) were considered low-risk cases and assigned to outpatient treatment with high-dose oral aspirin. Patients with poor prognostic predictors or aspirin failure were hospitalized for etiology search and treatment. A clinical and echocardiographic follow-up was performed at 48 to 72 h, 7 to 10 days, 1 month, 6 months, and 1 year. RESULTS: Two hundred fifty-four out of 300 (84.7%) patients were selected as low-risk cases. Outpatient treatment was efficacious in 221 out of 254 (87%) cases. Thirty-three out of 254 patients were hospitalized because of aspirin failure. Patients treated on an out-of-hospital basis had no serious complications after a mean follow-up of 38 months (no cases of cardiac tamponade). A higher frequency of recurrences and constriction was recorded in aspirin-resistant cases than in aspirin responders (60.6% vs. 10.4% for recurrences and 9.1% vs. 0.5% for constriction, respectively; all p < 0.01). CONCLUSIONS: A protocol for acute pericarditis triage and outpatient therapy of low-risk cases is safe and efficacious and may reduce management costs.

Acute Disease↗
PubMed2006

[Recurrent delayed pericarditis after pacemaker implantation: a post-pericardiotomy-like syndrome?].

INTRODUCTION: Pacemaker implantation is a usual technique in cardiology which may be followed by acute pleural effusion and delayed unusual pericarditis. CASE REPORT: We reported the case of a 67 year-old man hospitalized for faintness. Rhythmical auricular disease was diagnosed and pacemaker was implanted without immediate complication. Though pericarditis with tamponade at the day 21 will require emergency pericardiotomy surgery. A recurrent pericarditis at day 45 was treated with anti-inflammatory drugs without relapse at the end of the treatment. DISCUSSION: Repeated delayed pericarditis after pacemaker surgery may be compared to the Dressler syndrome which occurs after myocardial infarction.

Aged↗
PubMed1995

Incidence of specific etiology and role of methods for specific etiologic diagnosis of primary acute pericarditis.

To assess the incidence of a specific etiology and the role of methods for specific etiologic diagnosis in patients with primary acute pericarditis, we studied 100 patients with primary acute pericarditis consecutively admitted to our hospital between 1991 and 1993. A general diagnostic protocol was performed in all patients, whereas only pericardiocentesis was performed in patients with clinical cardiac tamponade or an unfavorable course with anti-inflammatory drugs. Surgical drainage and pericardial biopsy was performed in patients with tamponade relapse. A specific etiology was discovered in 22 patients (22%) (neoplasms in 7, tuberculosis in 4, other infections in 3, collagen diseases in 3, thyroid disorders in 4, and dissecting aortic aneurysm in 1). The general diagnostic protocol led to a specific diagnosis in 15 patients (68% of all patients with specific acute pericarditis) and pericardiocentesis in the other 7 patients (32%). The role of a diagnostic protocol, therapeutic pericardiocentesis, and diagnostic pericardiocentesis was similar and complementary. Pericardial biopsy results were negative in the 5 patients in whom it was performed. Cardiac tamponade and an unfavorable clinical outcome were significantly (p < 0.001) associated with the finding of a specific etiology; when both features were combined, sensitivity was 86% and specificity 85%, positive predictive value 63% and negative predictive value 96%. We conclude that the specific etiology in patients with primary acute pericarditis is about 20% to 25%, and that about 90% of these specific cases can be discovered by using the described systematic diagnostic protocol only in patients with an unfavorable outcome (cardiac tamponade or poor clinical course).

Acute Disease↗
PubMed1977

Traumatic hemopericardium and chronic constrictive pericarditis.

Chronic constrictive pericarditis following traumatic hemopericardium has been reported in recent years, but it has not been reproduced experimentally in dogs. The present study attempted to produce posttraumatic constrictive pericarditis in 34 experimental animals. Hemopericardium by means of trauma to the epicardium or pericardium was produced by a sharp instrument or by the injection of autologous blood inside the pericardial sac. All animals were killed at intervals between 3 and 31 months. The animals in which hemopericardium was induced by injecting blood into the pericardial cavity showed no changes. The hemopericardium was completely resolved without noticeable residual trace. Animals having hemopericardium as a result of trauma evidenced a well-developed constrictive pericarditis that was documented clinically, hemodynamically, and histologically. These experimental findings indicate that chronic constrictive pericarditis may well be due to traumatic hemopericardium rather than to specific infection.

Animals↗