Aggressive dual antiplatelet
therapy is associated not only with more
bleeding, impaired wound healing, and potentially more solid
cancer rates but it also causes higher
infection risks including
sepsis, and
systemic inflammatory response syndrome (SIRS). This may be especially true considering the alarming
off-label use of
prasugrel. A 65-year-old white male patient with a history of
myocardial infarction treated with
percutaneous coronary intervention and implantation of 2 bare
metal stents, was treated with off-label
clopidogrel for 4 years, including a double daily dose (150 mg) for the initial 13 months. Still on
clopidogrel, the patient was hospitalized with suspected
pneumonia. A diagnostic cardiac catheterization revealed a 60%-70% blockage of the mid left anterior descending, but there was no need for coronary intervention. At discharge,
clopidogrel 75 mg/d was switched over to off-label
prasugrel 10 mg/d on top of
aspirin (81 mg/d). On day 3 after
prasugrel was given, a football-sized
bruise appeared on the patient's lower right abdomen, but computed tomography results were unremarkable. On day 6 after administration of
prasugrel, the patient became dizzy, disoriented, confused, experienced difficulty breathing, severe
headache, weakness, intensive petechial
rash covering the entire body, and breathing difficulty requiring ventilation. Within 24 hours, the patient was unable to correctly identify his age; his eyes were pale in color to almost colorless and when hearing a sound he would turn his entire head toward the sound and he appeared to be blind. His lungs, liver, and kidneys began to show signs of failure over the next 5-9 days. Sixteen days after the administration of the first
prasugrel dose, the patient died of
sepsis complicated with SIRS. Aggressive
off-label use of
clopidogrel (double dose for 13 months, and >4 years overall duration), followed by off-label switchover to the highest daily dose (10 mg)
prasugrel may trigger
sepsis and fatal SIRS. The mechanism responsible for such harmful association is probably indirect, and involves the weakening of platelet-neutrophil-endothelial crosstalk necessary to combat
infections, and/or keep
inflammation from spreading.