An unusual cause of a large fibrinous pericardial effusion

The commonest cause of a large fibrinous pericardial effusion in sub-Saharan Africa is tuberculosis. There are, however, limited resources available for making a definitive diagnosis of tuberculous pericarditis. The diagnosis is largely based on clinical criteria. There is a risk of misdiagnosing lesscommon causes of large fibrinous pericardial effusions. We present a patient who had a pericardial angiosarcoma that was initially thought to be a tuberculous pericardial effusion, and discuss the challenges in making a definitive diagnosis of tuberculosis.     

Pericardial effusion with cardiac tamponade as a cardiac manifestation of duchenne muscular dystrophy

Duchenne muscular dystrophy (DMD) is the most common hereditary neuromuscular disease in children. It is an X‐linked hereditary dystrophinopathy due to the absence of dystrophin. Its onset is often in early childhood and presents with proximal distribution of weakness and a progressive course. Cardiac involvement in DMD is common, and its onset is usually after the age of 10 years. The most common cardiac manifestations are a dilated cardiomyopathy and cardiac arrhythmia. However, pericardial effusion with cardiac tamponade is a very rare cardiac complication of DMD. We report a boy with DMD who initially presented with progressive dyspnea and an enlarged cardiac silhouette on chest radiography who subsequently developed a large pericardial effusion with cardiac tamponade. Early recognition of pericardial effusion with cardiac tamponade is important for institution appropriate therapy. Muscle Nerve, 2009     

Use of an Autologous Blood Recovery System during Emergency Pericardiocentesis in the Electrophysiology Laboratory

Introduction: Emergency pericardiocentesis during electrophysiology procedures is often associated with significant aspiration of pericardial blood, requiring transfusion. We sought to assess the feasibility of urgent use of an autologous blood recovery system in the electrophysiology laboratory to autotransfuse blood aspirated from the pericardium.
Methods and Results: We retrospectively analyzed Mayo Clinic electrophysiology records for patients who had ablation procedure-related pericardial effusions requiring emergency pericardial drainage during an 8-month period. An autologous blood recovery system was used during pericardiocentesis to separate and clean packed red blood cells from the pericardial aspirate. These cells were returned acutely to the patient intravenously. The procedural safety, aspirated and autotransfused volumes, and efficacy of this approach were evaluated. During the study period, nine patients underwent pericardial drainage with autotransfusion using a cell-salvage instrument during electrophysiology procedures. The mean aspirated volume was 1,078 mL, with a mean autotransfused volume of 390 mL. For four patients, all with aspirated volumes of 1,100 mL or less, autotransfusion alone was sufficient to maintain hemodynamic stability and avoid allogeneic transfusion. One patient required surgical intervention because of ongoing pericardial bleeding. The ablation procedure was completed after aspiration in two patients. No procedural complications related to the use of the cell-salvage system occurred. 
Conclusion: Autologous blood recovery during pericardiocentesis is safe, convenient, and feasible. With early use it may decrease or eliminate the need for allogeneic blood transfusion and, in selected cases, may permit completion of the ablation procedure.     

USE OF NICOTINE, BRADYKININ AND VERATRIDINE TO ELICIT CARDIOVASCULAR CHEMOREFLEXES IN UNANAESTHETIZED RABBITS

1. We have characterized in unanaesthetized rabbits the reflex effects of injecting nicotine into the pericardial sac or left atrium on heart rate, arterial pressure, systemic vascular resistance and the amplitude and frequency of respiration. These effects were compared with those of atrial administration of nicotine and veratridine, and intrapericardial administration of veratridine and bradykinin. 2. Injection of nicotine (6.25-400 micrograms) into the pericardial sac caused dose-dependent falls of heart rate and arterial pressure, and a brief period of hypopnoea. The fall in arterial pressure was mainly due to a fall in systemic vascular resistance. The threshold dose was 25 micrograms. Near maximal falls in heart rate (108 beats/min) and arterial pressure (47 mmHg) occurred at a dose of 200-400 micrograms. The latency between injection and the onset of bradycardia was 3.0 s. 3. The effects of intrapericardial nicotine on arterial pressure and respiration were antagonized in a dose-dependent fashion by intrapericardial mecamylamine (1-100 micrograms/kg) but were unaffected by intrapericardial hyoscine methylbromide (10 micrograms/kg) or vecuronium (1-10 micrograms/kg). The haemodynamic and respiratory effects were abolished by intrapericardial procaine. The haemodynamic effects were increased, though not significantly, by sino-aortic baroreceptor denervation. In decerebrate, artificially ventilated rabbits, bilateral cervical vagotomy converted the hypotensive and bradycardic response into a slowly developing tachycardia without change in arterial pressure. 4. Left atrial injection of nicotine (6.25-100 micrograms) caused bradycardia, a rise in arterial pressure, and prolonged hyperpnoea preceded by transient hypopnoea. After sino-aortic barodenervation it caused profound falls in heart rate and arterial pressure and transient hypopnoea, which were abolished by intrapericardial procaine. 5. Intrapericardial injection of veratridine (50-100 micrograms) had no consistent effect under control conditions. After sino-aortic barodenervation it caused falls in heart rate and arterial pressure which were abolished by intrapericardial procaine. Left atrial injection of veratridine caused highly variable haemodynamic effects. 6. Intrapericardial bradykinin (2.5-25 micrograms) caused rises in both arterial pressure and heart rate. These were abolished by intrapericardial procaine. 7. We conclude that when nicotine is injected into the pericardial sac of conscious rabbits the reflex haemodynamic and respiratory effects are due to the selective activation of neuronal-type nicotinic cholinoceptors on vagal afferents that originate in the epicardium. The reflex effects of left atrial nicotine are probably due to the excitation of a combination of carotid chemoreceptors and cardiac receptors. 8. The effects of nicotine, veratridine and bradykinin that we observed in conscious rabbits were profoundly different from those reported in anaesthetized rabbits.     

Accumulation of anaphylatoxins and terminal complement complexes in inflammatory fluids

The presence of anaphylatoxins (C3a and C5a) and terminal complement complexes (TCC) in different inflammatory fluids and plasma was studied in 33 patients. Anaphylatoxins were assayed using a radioimmunoassay technique, and the terminal complement complexes were determined by an ELISA method. Patients with peritoneal (n = 14), pleural (n = 7), pericardial (n = 6) or burn bullae fluid (n = 6) were studied. High C3a and TCC concentrations were found in all these fluids. Elevated C3a and TCC concentrations in inflammatory fluids were found not only in patients with elevated plasma C3a and TCC concentrations, but also in patients with normal plasma levels. No increases in C5a concentration were observed in pleural or burn bullae fluid. In one patient with pericarditis, and in subjects with acute pancreatitis with ascites, high C5a levels were found in the fluid. However, the high TCC concentration in the fluids suggests that C5a had been formed but was probably removed by leucocytes present in the fluid.     

Cardiac manifestations of noncardiac tumors. Part I: Direct effects

Cardiac manifestations of secondary tumors of the heart may exert their effects directly by endocardial, myocardial, epicardial, or cavitary deposits (metastatic lesions), indirectly via tumor products such as in carcinoma, or mediated by therapy (chemotherapy, radiation) to treat the primary neoplasm. Part I of this review summarizes the frequency of metastatic cardiac involvement by various tumors and discusses pericardial manifestations (effusion, tamponade, constriction), one of the most common consequences of direct cardiac involvement by secondary tumors.