Coronary thrombosis after European adder bite in a patient on dual antiplatelet therapy: A case report.

INTRODUCTION: Until now very few cases of an adverse cardiovascular event have been described following European viper envenomation (Aravanis et al., 1982) (Aravanis et al., 1982) (Aravanis et al., 1982) (Aravanis et al., 1982). In fact, cardiac toxicity following snake bite is rare and primary reported from tropical and subtropical areas with only twenty-one cases of myocardial infarction reported in literature. Herein, we report a case of European viper envenomation associated with coronary artery thrombosis complicated by acute myocardial infarction and cardiac arrest.

CASE REPORT: A 62-year-old man, with a history of cardiovascular disease, on dual antiplatelet therapy with ticagrelor and acetylsalicylic acid, was admitted to the Emergency Department, after a bite, on the right hand, from a snake recognized by a herpetologist as a Vipera aspis francisciredi. At ED presentation, 2 hours after the bite, he manifested with vomiting, hypotension (90/60 mmHg) and mild oedema at the bite site. Standard electrocardiogram and troponin were normal at admission. One hour after the admission the patient developed cardiocirculatory arrest (ACC) with return of spontaneous circulation (ROSC) after cardiopolmunary resuscitation. Post ROSC-ECG showed an ST-elevation on anteroseptal and lateral leads and 1-vial of Viper Venom Antitoxin (Biomed®) was i.v. administered. During the next 3 hours three other episodes of ACC occurred, always with restoration of spontaneous circulation. Percutaneous transluminal coronary angiography showed a thrombus on the bifurcation of anterior descending coronary artery and diagonal 1 without an underlined atherosclerotic plaque. Neurologic clinical manifestations also occurred 12 hours after the bite: bilateral ptosis and facial paresthesia and a second vial of the same viper antivenom administered. The patient was discharged after 9 days of hospitalization without sequelae.

CONCLUSIONS: Our case show that cardiotoxicity is a rare but possible event after snake envenomation in Europe, even if with mechanisms remains to be studied. Vipera aspis has been known to cause primarily neurotoxic manifestations, but a coagulation factor X activator have also been isolated from its venom. Moreover, a specific serine peptidase that can target both PAR1 and PAR3, that are responsible for alternate pathways of platelet aggregation, have been characterized in the venom of a viper. Coronary thrombosis in our case could thus be secondary to a combination of prothrombotic systemic state and platelets dysfunction, in a patient with predisposing factors. Antivenom specific antidotal therapy role in preventing cardiotoxicity still need to be elucidated, but it remains the mainstay of treatment together with coronary angiography if necessary.