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Editor,—We read with interest the report by Moraeset al of a left ventricular pseudoaneurysm complicating infective pericarditis.1 We have encountered a similar complication while using streptokinase as an adjunct in the management of purulent pericarditis.2 In the absence of any previous report of this unusual complication, we had linked its occurrence to intrapericardial streptokinase.2
Our patient was an 8 year old boy who presented to us with a 20 day history of high grade fever, septic arthritis of the left knee, multiple parietal abscesses, and left sided pleuritic chest pain. Echocardiography revealed a dense pericardial exudate, and blood culture grew methicillin sensitive Staphylococcus aureus. From the fourth day onwards, the child was treated with 150 000 units of intrapericardial streptokinase twice daily. After four doses of intrapericardial streptokinase, instillation was stopped because of intrapericardial haemorrhage. However, toxaemia continued and there was evidence of organisation of the fluid. He was restarted on intrapericardial streptokinase after four days, in lower doses of 75 000 units. On the second day of restarting streptokinase, a submitral aneurysm was noted and further streptokinase was stopped. A review of video recordings showed a small intramyocardial echolucency in the submitral area on the second day of starting the first streptokinase course. The submitral pseudoaneurysm gradually increased in size and had to be closed with a polytetrafluoroethylene patch under cardiopulmonary bypass (fig 1). The aneurysm completely regressed over 13 months.
Though intramyocardial abscesses are well known in staphylococcal septicaemia, submitral aneurysm in purulent pericarditis had not been previously reported. The increased incidence of myocardial rupture in patients with acute myocardial infarction receiving streptokinase is now well documented.3 Streptokinase stimulates interstitial collagen breakdown, which may be followed by inhibition of collagen synthesis in the infarcted myocardium with increased risk of cardiac rupture.4 We thought the submitral pseudoaneurysm in our case could be causally related to the intrapericardial streptokinase, which accelerated collagen breakdown in a pre-existing myocardial abscess, or even normal myocardium. The report by Moraeset al probably absolves streptokinase treatment as a cause of the pseudoaneurysm.
It is interesting that in both the patients, the causative organism wasS aureus and the aneurysm was in the posterolateral wall of the basal left ventricle, close to the atrioventricular junction. Why the location in infective pericarditis should be the same as in the more recognised submitral left ventricular aneurysms, thought to be due to congenital weakness of the left ventricle in the atrioventricular groove region,5 is not clear.
In the report by Moraes et al, it seems that pericardial drainage was not done until three weeks after diagnosis of infective pericarditis. This seems somewhat unusual, as it is essential to evacuate completely the fluid in all forms of purulent pericarditis. It is possible that delayed resolution of septicaemia could influence the occurrence of these aneurysms, as our patient also had a long period of fever and toxaemia. Whether these aneurysms can explain some deaths in infective pericarditis, as suggested by Moraeset al, is conjectural. To us, it seems that the disease kills far more often because of uncontrolled sepsis and inadequate infected fluid removal. This should be the main focus rather than looking out for pseudoaneurysms, which may be reported once in 50 years!