Aware of the evils of life-saving antidote of heparin: clues from 12-lead electrocardiogram during protamine-mediated adverse events Free

I have read the case series of Leung et al.¹ with great interest regarding the protamine sulfate-mediated adverse cardiac events in three patients after catheter ablation for atrial tachyarrhythmias. As mentioned by the authors, protamine sulfate as a life-saving antidote of heparin, particularly in cases with life-threatening bleeding events, can result in severe allergic reactions which can lead to significant morbidity and mortality. Although severe allergic reaction result in anaphylaxis due to protamine sulfate is rarely reported, mild-to-moderate allergic reactions result in flushing are more common. Thus, all the staff should be aware of and careful about the possible adverse reactions after administration of protamine suphate in such cases. As reported by the authors, all the events have occurred after administration of protamine sulfate and thus the pathophysiological mechanisms of events should be assessed around the chemical reactions due to responsible drug. Although the authors questioned and discussed all the probabilities in the article appropriately, I have a comment regarding the 12-lead electrocardiogram (ECG) of the second patient (Figure 1 of the article). When we closely evaluated the ECG, it was in pacemaker rhythm with wide QRS complex and significant ST segment elevation at both inferior derivations and all precordial leads 3 min after administration of protamine sulfate. Additionally, ST segment elevation was much more prominent and looks like thombstone appearance at precordial leads. Just after apperance of ST segment elevation, there was R-on-T wave phenomenon and subsequently non-sustained ventricular tachycardia and ventricular fibrillation. Although coronary angiography has been performed in all cases to rule out vasospasm, coronary occlusion or air embolism, it was unclear that operators have administered intracoronary nitrate or not. As authors mentioned in the article, Kounis syndrome due to protamine sulfate might be probable cause for the anaphylactic cardiovascular collapse in these patients. In type I Kounis syndrome, allergic mediators induce coronary vasospasm either with or without myocardial infarction and may cause ST segment elevation on ECG.² Thus, differentiation of cardiac output reduction either due to myocardial hypoperfusion from systemic vasodilation and leakage of plasma or from myocardial tissue due to coronary vasoconstriction and thrombosis might be challenging during anaphylactic cardiac collapse. Combination of anti-allergic, anti-ischaemic, and anti-thrombotic treatment may be beneficial in such cases. Thus, the authors may comment on discussed ECG of second patient and the ECGs of other patients and also efficacy and safety of intracoronary nitrate administration as anti-ischaemic therapy in order to exclude vasospasm in those patients with allergic reaction.

Conflict of interest: U.C.: Proctoring for Abbott, Lecturer for Medtronic.

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