Background Prosthetic Heart Valves are always more frequent in the clinical practice. Particularly, sometimes more than one native valve is affected and needs to be surgically treated. On the other side, replaced prosthesis could also degenerate over time, leading to worsening symptomatic heart failure. There are no many cases of combined percutaneous approach to both aortic and mitral prosthetic valve deterioration: our aim is to display a case of this complex clinical setting. Case: A 76–year–old man with previous surgical mitral and aortic valve replacement, respectively through Hancock (27 mm) and Mitroflow (21 mm), was referred to our Centre for dyspnoea on mild efforts. Echocardiography revealed severe degeneration of both prosthetic valves, with moderate mitral stenosis (mean pressure gradient – MG – 6 mmHg) and severe central regurgitation, and high transaortic pressure gradients (MG 58; peak pressure gradient – PG – 103 mmHg). Pulmonary hypertension, mild right ventricle dysfunction and reverse flow in hepatic veins were evident. Results The first intervention was Valve–in–Valve Transcatheter Aortic Valve Implantation (ViV TAVI) with CoreValve Evolut PRO+ (23 mm), followed however by recoil determining moderate aortic stenosis (MG 25, PG 47 mmHg). Hence, as both the left prosthetic valves needed treatment, we decided to plan an elective percutaneous procedure aimed to treat both of them. Aortic ViV cracking was successfully obtained through non–compliant Atlas Gold Balloon (22 mm). Then, transseptal puncture by Brockenbrough needle and SL0 dilator sheath system was used to gain access to the left atrium. Finally, after interatrial shunt pre–dilation, Edwards Sapien 3 Ultra (26 mm) was applied as Mitral ViV during rapid ventricle pacing. Echocardiography showed relevant decrease of aortic pressure gradients (MG 11, PG 19) and downgrading of mitral regurgitation from severe to mild, despite unvaried persistent moderate mitral stenosis and signs of chronic severe pulmonary hypertension. The patient was dismissed in 3 days, after adjusting medical therapy. Conclusions Dysfunction of prosthetic heart valves is challenging to be approached, particularly when involving more than one. The expertise of the Centre assumes great importance in this delicate clinical setting. More explanations are further needed to define type and timing of percutaneous intervention aimed to the treatment of multiple prosthetic valves.

Introduction In Antiphospholipid Syndrome (APS) myocardial tissue can be involved through immune–mediated or thrombotic mechanisms, giving chest pain and increase of myocardial cytolysis markers. This may occur without any signs of myocardial injury at the moment of echocardiography, coronarography and cardiac magnetic resonance (CMR). The aim is to increase the awareness about this life–threating condition.Case summary. We present the case of 26–year–old woman few days after childbirth, affected by APS in anticoagulant therapy with previous deep vein thrombosis and without any other cardiovascular risk factors. She was symptomatic for intermittent chest–epigastric pain, fever and skin livedo reticularis. Lab Tests: TnI 750 ng/L, C–reactive protein 9.6 mg/dL, D–dimer 1693 µg/L; anemia; Antithyroid Antibodies and ANA 1:160 (SSB/LA). Blood cultures and COVID test were negative.Results. Echocardiography showed normal left/right ventricular function, but minimal pericardial effusion was present. Pulmonary Angio–CT revealed small thromboembolic event, ground–glass lungs compatible with hemorrhagic alveolitis.After a few days, the patient presented increased epigastric pain, headache, vomiting up to presenting a comatose state. Thrombotic or hemorrhagic events with cerebral CT and MR were excluded. Total–body CT was negative, except for peri–splenic and recto–uterine pouches.For the increase of TnI up to 4741 ng/L, the patient underwent coronary angiography which demonstrated non–obstructive coronary arteries. The assembled Neuro–Cardio–Rheumatology team suspected a rapidly developing Catastrophic APS which was developing quickly with multi–organ and life–threatening involvement.The patient underwent 4 cycles of plasmapheresis, intravenous human IgG and corticosteroids, with rapid clinical improvement. CMR subsequently demonstrated a small transmural late enhancement area on lateral left ventricle wall.The patient was discharged from the hospital on Day 6 post–therapies.Conclusions. APS may involve more organs, including myocardial tissue with different mechanisms of damage and high mortality rate. The presented case poses a multidisciplinary challenge, because thrombotic multiorgan microangiopathy may be not always diagnosed. Imaging methods such as CMR could be optimized with adenosine stress–CMR. Clinical attention is required among women with APS, to reach early diagnosis of myocardial thrombotic microangiopathy and to establish the best effective treatment.