P136 “THERE’S NO TWO WITHOUT THREE”: A STRANGE CASE OF RECURRENT CORONARY EMBOLISM

Abstract

Abstract Background A 68 year–old woman with rheumatic heart disease underwent surgery replacement of aortic and mitral valves with mechanical prostheses 20 years ago, and since then has been in VKAs therapy. One year after the operation, she was hospitalized for ischemic stroke without relics. For detection of 2:1 block on the ECG Holter/24h a PM was implanted. After 4 years, she had an acute coronary syndrome (ACS) with VF (treated with DC–Shock). Coronary angiography (CA) showed no coronary stenosis. It was replaced PM to ICD. In 2017, she had a TIA and a mitral prosthesis dysfunction was detected from EET with hemidisk thrombosis. After CA, mitral valve replacement was performed but on the 2nd day after surgery she had an anterior STEMI caused by the occlusion of LAD. PTCA and stenting were performed. In October u.s. the patient was referred to the Emergency room for typical angina. An inferior–posterior STEMI was revealed to ECG. CA highlighted embolic occlusion of Cx and good result of prior LAD’s stenting. After multiple and ineffective attempts, invasive recanalization’s procedure was interrupted considering both patient’s high bleeding risk and embolic aetiology. Excluded prosthetic thrombosis and thrombophilic anomalies, patient was discharged in clinical stability with SAPT+ VKAs therapies. Discussion Coronary embolism (CE) represents 3% of ACS because the coronary arteries are protected from embolism thanks to their acute’s angle origin from the aorta. Embolism origin is various and it can originate from left (LAA, LVx, valvular, prosthetic structures) or right heart sections (paradoxical embolism in the case of PFO),generally during AF. In our case, prosthetic origin is the most probable embolic source as demonstrated by cerebral ischemic (TIA/stroke) and coronary events (first anterior then inferior–posterior STEMI) after valves surgery. Treatment consists of restoring antegrade flow without DES implantation, using if possible intracoronary thrombolysis or thromboaspiration. In secondary prevention, embolism sources removal and anticoagulant therapy are mandatory. In our case we recommended SAPT+VKAs with strict INR’s control (range 3.5–4). Conclusions Although CE is a rare and potentially fatal phenomenon it should be suspected in the absence of coronary atherosclerosis and in the presence of predisposing conditions such as those mentioned above. This case demonstrates that CE can occur in absence of prosthetic thrombosis with suboptimal INR control.