DEVELOPMENTAL MEDICINE FORUM BRIEF REPORT (7/25/98 )
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FREQUENCY AND SIGNIFICANCE OF CISAPRIDE-INDUCED PROLONGATION OF THE QT INTERVAL (PQTI) IN ADULTS WITH PROFOUND MENTAL RETARDATION AND GERD: A Preliminary Report.

David James MD and Philip May MD

Introduction:

We felt it to be important to identify patients at our facility who were at risk for cisapride induced dysrhythmia, because of recent reports of fatal ventricular dysrhythmias in patient receiving cisapride (see http://www.interactive.net/~pmay/D7-18-98.htm) or CLICK HERE .

Methods:

All available EKG’s from the years 1996, 1997 and 1998 from 650 residents of a large State operated ICF/MR in NJ who were currently receiving cisapride for GERD, were examined for significant prolongation of the QT interval, using a standard nomogram which corrected the QT interval for rate.

Results:

One hundred eleven of the 650 residents were currently on cisapride (17%) and of those 111 residents 30 (27%) had available EKG’s from the years 1996, 1997 and 1998 to be reviewed. Five of the 30 who had available EKG's for review (16.6%) had significantly prolonged Q-T intervals corrected for rate.

The EKG’s of the remaining twenty-five (83%) were within normal limits with respect to Q-T interval.

Discussion:

The initial consideration was to determine whether those individuals receiving cisapride for GERD ought to be taken off it immediately. All EKG’s taken in the last three years from those currently on cisapride were therefore examinined for any significantly prolonged QTI’s, in order to get a first impression of how common this problem might be and of how urgent it might be to obtain an EKG from patients receiving cisapride.

Prolonged QT interval corrected for rate was found in nearly 17% of those individuals receiving cisapride for GERD .

Review of other drugs and co-morbid conditions to identify additional increased risks for PQTI’s which would further indicate appropriate interventions, is currently in progress. If EKG's of other residents (i.e. those not on cisapride) are then similarly reviewed for any of the PQTI inducing drugs and/or co-morbid conditions and any PQTI’s are identified, a much better impression of the relative sigificance of cisapride-associated PQTI’s versus non-cisapride associated PQTI could then be made.

Thus, in conlusion, the relative risk of PQTI’s caused by co-morbid conditions and/or drugs other than cisapride versus the risk from cisapride could be much better assessed if current EKG’s from a control group of residents who are neither on cisapride nor PQTI inducing drugs nor have significant co-morbid conditions were also compared.

Finally, we believe that EKG's should be obtained in all individuals who are receiving drugs that can potentially prolong the QT interval and therefore predispose to ventricular dysrhythmia.

David James MD, Philip May MD