P214 THE THERAPEUTIC IMPLICATIONS OF A FATAL COINCIDENCE

Abstract Background Factor VII deficiency is a rare, inherited disorder secondary to a reduction or absence of factor VII (FVII) of the coagulation pathway presenting with autosomal recessive transmission and caused by different types of mutation of the F7 gene. The clinical manifestations of the syndrome are highly variable: depending on the case, it can remain asymptomatic, or it can present with episodes of bleeding secondary to trauma and surgery, or it can manifest with potentially fatal spontaneous hemorrhages. It can be treated by long–term replacement prophylaxis, which consists of periodic infusions of FVII concentrates. Clinical case A 75–year–old woman presented to the emergency room in a soporose state. On the electrocardiogram, ST–segment elevation in the antero–septal and in AVR and septal akinesia affecting the left ventricle was shown. On admission, she presented with syncope, marked hypotension, and tonic–clonic spasm. Blood tests showed sodium levels of 112 mEq/L, secondary to the administration of high doses of Escitalopram and associated with the genesis of epileptic seizures. During the emergency coronary angiography, severe stenosis of mid–proximal IVA was seenand subsequently treated with PTCA/DES. Right before the procedure, therapy with Acetylsalicylic acid (ASA) 250 mg, Ticagrelor 180 mg, and Heparin sodium was administered 5000 IU + 5000 IU. Immediately after, severe anemia (5.9 Hb) and INR lengthening were demonstrated, with widespread skin hematomas. In the complete study of the coagulative state, an almost complete factor VII deficiency was found, which required infusion of factor VII concentrate. The subsequent course was further complicated by pre–renal acute renal failure and paroxysmal atrial fibrillation. Following the initial suspension of antiplatelet and anticoagulant therapy (OAT), it was possible to reintroduce, without loading dose, ASA and clopidogrel, preserving OAT for later phases. Discussion and Conclusions FVII deficiency, a rare hemorrhagic disorder, may represent a fatal coincidence in the context of myocardial infarction, due to the therapeutic implications of the pathology, which may lead to inevitable uncontrolled bleeding. This occurrence is difficult to predict in some cases, including the present one. It would be interesting to identify indicators that could prompt, even in an emergency setting, the suspicion of such a dangerous association.