LAUSR

ecule, binds to the negatively charged heparin, and this complex is removed from circulation by the reticuloendothelial system. Usually 1–1.5 mg of protamine is used to neutralize 100 U of heparin. In our patient, almost 40 mg of IV protamine was used to reverse heparin. It is recommended that protamine should be administered rather slowly to prevent histamine release and/or nitrous oxide–mediated hypotension.4,5 Our patient developed hypotension immediately after administration of protamine. During profound hypotension, the patient also developed an ST elevation in the inferior electrocardiographic leads. An urgent cardiac catheterization revealed a significant coronary stenosis of more than 75%, which required percutaneous coronary intervention with a drug-eluting stent. We believe that the hypotension resulting from protamine administration resulted in a significantly lower perfusion distal to the coronary stenosis, resulting in an ST elevation. As soon as the blood pressure improved, the patient had complete resolution of the ST elevation. The use of protamine is increasing in various electrophysiology laboratories, especially after AF ablation. Our case highlights the importance of being aware of this immediate side effect of protamine. It is recommended that protamine should be infused slowly, and close attention should be paid to hemodynamics, especially blood pressure. We recommend splitting the dose of total protamine and giving it a few minutes apart. We do not believe that protamine caused any plaque disruption in our patient because he did not have any clot and/or total occlusion noted during cardiac catheterization. Those would be features of a plaque disruption. In our patient, it was severe hypotension caused by protamine administration in a patient with significant coronary stenosis, which resulted in transient ST elevation. CONCLUSIONS