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We read with interest the article "Propofol Infusion Syndrome: A Rare Complication With Potentially Fatal Results" in the June issue (2008:18–27). The authors review detailed important points of propofol infusion syndrome, which has been reported to have a high mortality, although the mechanism of this constellation of effects is opaque.1 The electrocardiogram (ECG) in case 1 of the article had a pattern characteristic of a Brugada electrocardiographic pattern (BEP)—the sharp downsloping ST elevation in V1 to V3. This pattern has been reported with propofol infusion syndrome and may be a predictor of imminent death,2 but was not discussed by the authors.
The BEP has been reported with other medications and is similar to the pattern seen with Brugada syndrome, which is associated with high mortality and sudden cardiac death and is due to a genetic myocardial sodium dysfunction.3 BEP has been reported with tricyclic antidepressant and cocaine use4,5; however, dysrhythmic death has not been more common with tricyclic-induced BEP. Recently, BEP has also been reported with propofol and was associated with a high mortality.6 Therapeutic doses of propofol are sufficient to cause this effect, and previous cases have correlated this dose-response relationship.7,8
The mechanism for the propofol-induced BEP has not be delineated. Tricyclic- and cocaine-induced BEP may be from myocardial sodium channel blockade. The sodium channel effects have not been previously correlated with propofol infusion syndrome or the coappearing BEP; however, propofol has significant neurologic and myocardial sodium channel inhibitory effects.7,8 Thus the sodium channel effects from propofol may not only induce the characteristic BEP in this and other cases, but it may also cause some of the propofol infusion syndrome cardiac manifestations. Further study on propofol infusion syndrome and its relationship to the BEP is important and may illuminate the cause of propofol infusion syndrome.
References
Brugada syndrome is a heterogenous genetic disease that predisposes to life-threatening ventricular tachyarrhythmias and sudden cardiac death.1 There are nongenetic factors that have been discussed in the literature as possible inducers of the ECG pattern resembling Brugada syndrome.1
A Brugada ECG pattern (ST-segment elevations of a coved type in leads V1 through V3) can be induced by several factors, including medications (specifically agents that have a sodium channel blocking effect), electrolyte abnormalites (hyperkalemia, hypercalcemia, hypokalemia), and disease states (fever, increased adrenergic tone).
The role of propofol in the appearance of an ECG pattern of Brugada syndrome has been described, but the pathophysiology and mechanism remains unclear. The presence of a Brugada-type ECG during infusion is an indicator of imminent malignant arrhythmia.1
Reference
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