VASOPRESSIN-INDUCED ST-ELEVATION MYOCARDIAL INFARCTION

Abstract

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: Vasopressin is commonly used to restore blood pressure in hyperdynamic hemodynamic states, thereby reducing catecholamine requirements. The effects of vasopressin are primarily caused by the rise in the mean arterial pressure (MAP) due to systemic vasoconstriction, which, depending on the infusion rate, can also produce notable vasoconstrictive effects on the coronary microvasculature thereby reducing coronary blood flow despite an increase in coronary perfusion pressure. Here we present an interesting case of vasopressin-induced ST-elevation myocardial infarction (STEMI) on postoperative day two of cardiac catheterization for initial STEMI. CASE PRESENTATION: A 67-year-old male with a past medical history of hypertension, hypothyroidism presented to the emergency department (ED) with the complaint of left shoulder pain. In the ED waiting room, the patient suddenly collapsed losing consciousness, and was found to be in cardiac arrest. ACLS protocol was immediately started and ROSC was achieved. An electrocardiogram (EKG) was performed which showed STEMI in the anterolateral leads. Code STEMI was activated, and the patient was taken for the cardiac catheterization where LAD stenosis was observed and stented. Post-procedure, the patient was transferred to Cardiac ICU, where an amiodarone drip was initiated for recurrent episodes of non-sustained ventricular tachycardia. The hospital course was further complicated with pneumonia leading to acute hypoxemic respiratory failure and septic shock. The patient was placed on norepinephrine and appropriate antibiotics. Vasopressin was added to reduce catecholamine requirements and to achieve a target MAP. On postoperative day two, the patient was noted to have ST elevation on the tele monitor, a twelve lead EKG confirmed anteroseptal STEMI. A left heart catheterization revealed a patent LAD stent with no new findings and recommendations were made to stop vasopressin infusion and to continue the rest of the treatment. The patient was successfully extubated to BiPAP, eventually made a slow and steady recovery, and was discharged home with follow-up appointments. DISCUSSION: It has been shown that the levels of vasopressin increase as part of the stress response, which has been shown to exert vasoconstrictive effects on the coronary arteries mainly in the non-epicardial vessels of the microcirculation. These high levels in states like myocardial infarction can lead to coronary slow phenomenon mediating ischemia-perfusion injury. CONCLUSIONS: In advanced distributive shock with accompanied cardiogenic shock state, utmost caution should be taken as the vasoconstrictor properties of vasopressin are not accompanied by positive inotropic qualities, which may depress cardiac function even further as a result of impaired coronary blood flow despite increased coronary artery perfusion pressure and in severe cases can lead to myocardial ischemia. REFERENCE #1: Nobian A, Mohamed A, Spyridopoulos I. The role of arginine vasopressin in myocardial infarction and reperfusion. Kardiol Pol. 2019 Oct 25;77(10):908–17. REFERENCE #2: Hauser B, Asfar P, Calzia E, Laporte R, Georgieff M, Radermacher P. Vasopressin in vasodilatory shock: is the heart in danger? Crit Care. 2008;12(2):132. REFERENCE #3: Asfar P, Radermacher P. Vasopressin and ischaemic heart disease: more than coronary vasoconstriction? Crit Care. 2009;13(4):169. DISCLOSURES: No relevant relationships by Mohammed Ali, source=Web Response No relevant relationships by Humayun Anjum, source=Web Response No relevant relationships by Rahul Dadhwal, source=Web Response No relevant relationships by Salim Surani, source=Web Response