An interesting note from Gordon Ens, President of Creative Clinical Concepts and Laboratory Director of Inflammatory Markers Laboratory, Marblehead, Mass.
I recall that recently someone questioned the clinical implications of shortened closure times on the PFA-100. I have not followed it further to see if you came to any conclusions, but I was reminded of the spontaneous platelet aggregation that we observed many times over the years at Colorado Coagulation Consultants. I recall in some instances that aggregation occurred immediately on beginning to stir the platelets in the aggregometer in the absence of any aggregating reagent. It would not surprise me if such an individual would also have shortened closure times on the PFA. I wonder if they check platelet aggregation in their patient?
One patient I remember in particular. He had spontaneous aggregation, so his cardiologist put him on aspirin which only delayed the onset slightly. He then added another platelet modifying drug, which delayed the onset of spontaneous aggregation further but did not eliminate it. He than asked me if I could recommend anything else. I said you might tryRobitussin cough syrup. It was successful in eliminating spontaneous aggregation altogether but only worked for about 24 hours. I do not remember what ultimately became of the patient.
Gordon.
Gordon, I recall running an agg on that patient one time; you never needed an agonist. Do you recall what made you suggest Robitussin? Geo.
I asked the original question. My question was hypothetical,
I asked the original question. My question was hypothetical, but thanks for the interesting case. In the case of an extrememly short PFA closure time then an aggregation study would seem to be the appropriate follow-up if there was a question of hypercoagulability.