CONGRESS ABSTRACT

Introduction Patent foramen ovale (PFO) can play a pathogenic role in systemic thromboembolic syndromes. Cerebral embolisms represent the most common expression (37-50%), followed by lower and upper limbs, visceral arterial circulation, and coronary circulation (7-9%). Clinical Case: A 39-year old woman who was former smoker and suffered from hypertension, accessed our Emergency Department (ED) with worsening dyspnea and bilateral edema. Symptoms started two months before after a flu-like syndrome. She also reported epigastric pain. An abdominal ultrasound revealed ascites and pleural effusion. BNP was 1600 pg/ml and TnI hs 18000, while echocardiography reported severe left ventricular dysfunction (LVEF: 30%), dilated left heart chambers, and dilated inferior vena cava with partial collapse during inspiration. She was admitted to intensive care unit. Coronary angiography showed normal coronary arteries. Cardiac MRI revealed myocardial edema and reduced perfusion at rest in the basal and mid segments of the inferolateral and inferior walls of the left ventricle (LV). LGE sequences demonstrated ischemic transmural necrosis in the basal and mid inferolateral and inferior segments of the LV with concomitant small thrombotic islands due to microvascular obstruction (MVO). A total body CT scan confirmed ascites, pleural effusions, and a hypodense area with a wedge shape (about 30 x 35 mm) in the right cerebellar region, without contrast enhancement and suggestive of ischemic sequelae. Transesophageal echocardiogram with microbubbles revealed significant passage of microbubbles from the right atrium to the left atrium after Valsalva manoeuvre which could be referred to PFO (tunnel length: 13 mm). The interatrial septum was thinned, with mild right-convex bulging at rest. Heart failure therapy was progressively optimized and LV function was still set at 35% at discharge. We decided for a wearable defibrillator and advised her to undergo percutaneous PFO closure. Five months later, the patient turned back for percutaneous PFO closure: complete resolution of her clinical symptoms were obtained as well as LV contractile function (EF: 50%). Conclusions: PFO is a challenging diagnosis which might underline and provoke different and several clinical syndromes on a thromboembolic base. Rarely, atypical locations of emboli migration might cause coronary circulation obstruction and explain some cases of MINOCA.