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Chronic constrictive pericarditis may complicate both rheumatoid arthritis and systemic lupus erythematosus. To our knowledge, however, this is the first time it has been described in a patient with dermatomyositis. This association should be kept in mind as constrictive pericarditis should be considered in the differential diagnosis of liver cirrhosis and Budd-Chiari syndrome in rheumatic diseases.
Serious complications of pneumococcal pneumonia have become uncommon with effective antibiotic treatment. Purulent pericarditis is a rare though well described complication of untreated pneumococcal sepsis. A case of untreated pneumococcal pneumonia complicated by purulent pericarditis is described. This presented as an out of hospital asystolic cardiopulmonary arrest.
A case of rheumatoid pericarditis that developed into cardiac tamponade without deterioration of rheumatoid arthritis is described. The concentration of interleukin-6 (IL-6) in pericardial fluid was notably increased compared with serum. IL-6 may be associated with progression or maintenance of rheumatoid pericarditis.
Reference tracings are of great value in the diagnosis and assessment of constrictive pericarditis. The Q-h interval in the jugular venous pulse tracing is strongly correlated with the mean right atrial pressure (r=0.91). The left ventricular ejection time, the Q-A2 interval, and the Q-h interval are independent during atrial fibrillation from the preceding diastolic filling interval. This differentiates constrictive pericarditis from valvular heart disease. Cases with haemodynamically significant constrictive epicarditis are characterized by a rapid evolution, absence of pericardial calcification and absence of an early diastolic filling sound, a dominant a wave in the jugular venous pulse tracing, and a high early diastolic ventricular pressure. The haemodynamic behaviour is similar to that found in cases with myocardial fibrosis.
Systolic time intervals (STI) were measured from simultaneously recorded phonocardiograms, carotid pulse tracings, and electrocardiograms in 11 patients with constrictive pericarditis and in 10 patients with cardiomyopathy to assess the value of STI in the differential diagnosis of the two conditions. The predicted ejection fraction was calculated from the STI. The results were compared and found significantly different in the two groups of patients. The ratio PEP/LVET and the ejection fraction were found to have greater discriminatory values and separated the two groups clearly. Measurement of STI, a simple, noninvasive bedside technique, appears to be useful in distinguishing between constrictive pericarditis and cardiomyopathy.
Ten patients with constrictive pericarditis were studied echocardiographically with specific reference to inter-ventricular septal dynamics. Abnormal movement of the interventricular septum was present in 8 patients and consisted of flattening in systole and unusual posterior motion in diastole. The aetiology of this type of movement is at present unknown but may be related to restriction of normal cardiac rotational dynamics. The interventricular septum also showed diminished degree of thickening (mean 21-2%). The amplitude of excursion was generally at the upper limit of or greater than normal. Left ventricular posterior wall amplitude of excursion was normal. Flattening of left ventricular posterior wall diastolic movement was seen in 4 patients. Right ventricular end-diastolic dimension was slightly increased (1-2 to 1-7 cm/m2) in 5 of 8 patients with abnormal septal motion, but no haemodynamic evidence of diastolic volume overload was found. Posterior pericardial thickening was noted echocardiographically when posterior calcification was present. We conclude that the most common though non-specific feature of the echocardiogram in patients with constrictive pericarditis is abnormal septal motion. Flattening of left ventricular posterior wall diastolic movement, posterior pericardial thickening, and epicardial-pericardial separation may also occur.
The case is described of an 18-year-old schoolboy who developed pericarditis during the course of meningococcal meningitis; he had evidence of a preceding chronic meningococcaemia. Good recovery followed on systemic antibiotics only. The pericarditis was probably a direct septic complication of meningococcal meningitis.
A healthy 22-year-old man developed acute varicella pericarditis, characterised by an enanthem with diagnostic rising titres of varicella zoster antibodies but without the typical exanthem. This, the third reported case of varicella pericarditis, is the first to be documented without a typical varicella eruption.
In a study of 30 consecutive patients with constrictive pericarditis diagnosed by clinical, radiological, and echocardiographic criteria 21 (70%) were found to have pulsatile hepatomegaly. The pulsations were felt clinically and confirmed by external hepatic recordings. These pulsations conformed almost identically to the jugular venous pulsations in the neck. The hepatic pulsations disappeared after successful pericardiectomy. Persistence of the hepatic pulsations was associated with poor postoperative relief suggesting that it is another useful sign in the assessment of the adequacy of pericardiectomy. Thus this poorly appreciated clinical finding appears to be present in a high proportion of patients with constrictive pericarditis.
Constrictive pericarditis developed in a 55 year old man two years after transmural myocardial infarction complicated by severe acute pericarditis. Pericardiectomy was successful. Although this very rare late complication of myocardial infarction has been reported as a sequela of frank anticoagulant induced haemopericardium, in this case there was no clinical evidence of such an association.
A 42 year old man admitted with effusive-constrictive pericarditis had diastolic dysfunction and pericardial thickening. Pericardiectomy was performed because of uncontrolled heart failure. The Epstein-Barr viral IgG antibody titre was exceptionally high. The EB viral genome was demonstrated in the resected pericardium by polymerase chain reaction and in situ hybridisation. EB viral pericarditis was diagnosed.
OBJECTIVES: Plasma hormones at rest in patients with untreated severe congestive cardiac failure are similar to those occurring during heavy exercise in healthy people. This study examines the hypothesis that the neuroendocrine effects of exercise are modified in untreated congestive cardiac failure. DESIGN: The effect of lying, standing, upright exercise, and recovery on several plasma hormones was measured in healthy controls and 2 groups of patients with severe untreated heart failure. The level of exercise was the same in all groups and low enough to be within the capacity of patients with severe failure. PATIENTS: There were 12 healthy controls, 9 patients with untreated severe congestive cardiac failure caused by myocardial disease, and 12 patients with untreated constrictive pericarditis. SETTING: A tertiary referral centre in North India. RESULTS: Heart rate, noradrenaline, renin activity, aldosterone, cortisol, growth hormone and atrial natriuretic peptide (ANP) were higher in the 2 groups of patients than in the healthy controls during both rest and exercise (P < 0.01 for both comparisons). In general, the effects of this mild degree of exercise were no greater than those of standing. The increase in heart rate during exercise was greater in the group with constrictive pericarditis than in the controls (P = 0.04) and (non-significantly) in congestive heart failure. Apart from these differences the pattern of responses to standing and exercise was similar in the three groups. CONCLUSIONS: While there was evidence of a broad neuroendocrine activation in patients with congestive cardiac failure, the only abnormal increase during exercise (of marginal significance) was found for renin activity in those with myocardial disease. In patients with untreated congestive failure, a substantially normal endocrine response to exercise was superimposed on abnormal resting concentrations.
A patient developed pulmonary infiltration, pleural effusions and pericarditis three months after starting dantrolene sodium. Peripheral blood eosinophilia and a raised ESR were present. Symptoms and signs resolved after the drug was discontinued. Dantrolene toxicity should be considered in the differential diagnosis of pneumonitis and pleuro-pericarditis.
A patient is described who developed acute pericarditis during a severe first attack of Crohn's disease. The opportunity was taken to measure levels of circulating immune complexes, both during the acute phase of the illness and during convalescence; no significant change in these levels from normal values was found. The Crohn's disease and the associated pericarditis responded to systemic corticosteroid therapy, and no relapse has occurred during 14 months of follow-up.
A girl with chickenpox is presented. She developed arthritis, pericarditis with pericardial effusion and meningism during the course of her illness. Pericarditis is an unusual complication of this disease, and in this instance was associated with characteristic electrocardiographic changes. Aspects of her case history are discussed.
Purulent pericarditis is an infrequent, but important complication of infective illnesses, in particular pneumonia, which if diagnosed early has a good prognosis. The incidence of the condition is probably increasing, particularly in the immuno-compromised group of patients. 'Classical' symptoms and signs are often absent, and a high index of awareness is required to diagnose the condition. This review deals with the epidemiology, microbiology, clinical features, treatment and prognosis of purulent pericarditis with two illustrative examples of typical cases.
Seven patients with constrictive pericarditis associated with collagen disease underwent pericardiectomy with good results in all but one. The collagen disease was confirmed as rheumatoid arthritis in five patients, but in two its nature remained obscure. In one case the illness was marked by a persistent eosinophilia and eosinophilic infiltration of the pericardium. The association of constrictive pericarditis with rheumatoid arthritis and other collagenoses is briefly discussed.
The mechanism of atrial flutter and fibrillation induced by rapid pacing in 22 dogs with 3-day-old sterile pericarditis was investigated by computerized epicardial mapping of atrial activation before and after administration of agents known to modify atrial electrophysiologic properties: procainamide, isoproterenol, and electrical stimulation of the vagosympathetic trunks. Before the administration of any of these agents, a total of 30 episodes of sustained atrial flutter (greater than 1 min duration, monomorphic; regular cycle length, 127 +/- 12 ms, mean +/- SD) was induced in 15 out of 22 dogs and 9 episodes of unstable atrial flutter (duration, less than 1 min; cycle length, 129 +/- 34 ms; monomorphic, alternating with fibrillation) were induced in the remaining 7 preparations. In the latter, administration of procainamide transformed unstable atrial flutter and atrial fibrillation to sustained atrial flutter (cycle length, 142 +/- 33 ms; n = 9 episodes). During control atrial flutter, atrial maps displayed circus movement of excitation in the right atrial free wall with faster conduction parallel to the orientation of intra-atrial myocardial bundles. Vagal stimulation changed atrial flutter to atrial fibrillation in 32 of 73 trials; this was associated with acceleration of conduction in the lower right atrium, leading to fragmentation of the major wave front. Isoproterenol produced a 6-25% increase of the atrial rate in 6 out of 14 trials of atrial flutter and induced atrial fibrillation in 4. After procainamide, the reentrant pathway was lengthened and conduction was slowed further in the right atrium. Maps obtained during unstable atrial flutter showed incomplete circuits involving the right atrium. Following procainamide infusion, the area of functional dissociation or block was enlarged and a stable circus movement pattern, which was similar to the pattern seen in control atrial flutter, was established in the right atrium. We conclude that (1) the transitions among atrial fibrillation, atrial flutter, and sinus rhythm occur between different functional states of the same circus movement substratum primarily located in the lower right atrial free wall, and (2) the anisotropic conduction properties of the right atrium may contribute to these reentrant arrhythmias and may be potentiated by acute pericarditis.