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Introduction Prosthetic valve thrombosis (PVT) is a rare but feared complication of cardiac valve replacement which usually represents a difficult diagnostic challenge. Although PVT is not frequent in bioprosthetic valves, the advent of transcatheter heart valves and the advances in computed tomography, allowing the detection of subclinical thrombosis, have yielded growing interest in that field, specially taking into account that there is no consensus on optimal antithrombotic approach in these patients. Clinical Case A 74-year-old male with prior cardiac antecedents of aortic valve replacement (April 2010) with a bovine pericardial bioprosthesis (Mitroflow 25, Sorin group Inc.), ischemic dilated cardiomyopathy with moderately depressed left ventricle ejection fraction (33%) and carrier of VDD pacemaker due to third degree atrioventricular block was admitted to advanced heart failure unit. During routine follow-up echocardiograms, prosthetic valve presented no signs of dysfunction except slightly increased gradients (image C): max 38 mmHg (normal 95%) and dyspnea NYHA class III the patient was referred for upgrade to cardiac resynchronization therapy (CRT). Computed tomography to asses epicardial venous anatomy prior to CRT implant was performed. In addition to venous distribution, it was described a repletion defect in aortic bioprosthetic valve suggestive of leaflet thrombosis (image A). To complete the study the patient underwent a transesophageal echocardiography (TOE) revealing a swallow’s nest shaped hypoechoic occupation of non-coronary and left aortic leaflets (image B), and 3D effective orifice area of 0,9 cm2. Oral anticoagulation was started in association to previously taken acetylsalicylic acid (ASA). Control TOE was performed 3 months after diagnosis showing almost complete resolution of thrombi. During the follow-up a CRT-D was implanted, with significant response in systolic performance, reaching a LVEF of 45%. Interestingly, despite the increase in anterograde aortic flow, progressive decrease of aortic gradients (max 24 mmHg, med 15 mmHg) until normalization was found (image D). Clinical benefit was also patent, being the patient in NYHA class I at the moment. Discusion Valve thrombosis could be difficult to diagnose in the presence of left ventricle dysfunction as gradients shall remain low despite an important compromise in valve motion. We present a case of incidental diagnosis of non-obstructive leaflet thrombosis that was managed conservatively with oral anticoagulation and ASA. The descent in transaortic gradients, moreover taking into account the response to CRT increasing LVEF, indicates that gradients slightly increased or in the upper limit of normality should raise suspicion in valve dysfunction in the presence of decreased LVEF. Abstract 1645 Figure.

Background Patients with mid-range ejection fraction heart failure (HFmrEF) are a new category defined in actual guidelines. The aim of this study was to establish the prognostic value of several parameters obtained by Cardiac Magnetic Resonance (CMR) and Transthoracic Echocardiography (TTE) in patients with HFmrEF. Methods Thirty patients, defined as HFmrEF by TTE and CMR, were included between 2012-2018. Patients with structural heart disease different from Left Ventricular (LV) dysfunction were excluded. Cine sequences in CMR (SSFP) were used to obtain atrial and ventricular volumes and mass. Myocardial fibrosis was quantified by late gadolinium enhancement. TTE was used to obtain anatomical and functional parameters as LV and Right Ventricular (RV) ejection-fraction, LV and RV global longitudinal strain, and RV free-wall longitudinal strain. The primary endpoint was the combination of all-cause death or heart failure admission. The median follow-up was 1.9 (0.5-3.3) years. Results Mean age was 59.3 ± 12.4 years, and 67.9% patients were male. The aetiology of LV dysfunction was mainly ischemic (n = 16, 53.3%). Results are shown in Table1. Patients who presented the primary endpoint had a lower RV ejection-fraction by CMR and a lower absolute value of RV free-wall longitudinal strain by TTE(Figure 1). Conclusions In HFmrEF patients, worse RV function (by CMR and TTE-Speckle Tracking) may be associated with a worse prognosis. Larger studies are needed to confirm this hypothesis. Table1 All-cause death or HF admission (n = 5; 16.7%) No all-cause death of HF admission (n = 25; 83.3%) p iRVEDV (ml/m2) by CMR 65.5 ± 13.5 66.2 ± 12.3 0.906 iRVESV (ml/m2) by CMR 30.4 ± 7.5 24.4 ± 6.2 0.065 iLVEDV (ml/m2) by CMR 85.8 ± 23.7 98 ± 19.5 0.225 iLVESV (ml/m2) by CMR 47.8 ± 15.3 54.9 ± 11.7 0.246 Indexed LA Volume (ml/m2) by CMR 42.8 (36.5 - 49) 48.4 (42 - 63.5) 0.386 LVEF (%) by CMR 44.9 ± 3.3 44 ± 2.6 0.506 RVEF (%) by CMR 52.2 ± 7.2 61.7 ± 7.2 0.012 RV-FAC (%) by TTE 43.4 ± 4.4 44.7 ±7.5 0.378 TAPSE by TTE 2.1 ± 0.3 2.5 ± 0.1 0.032 LV Longitudinal Global Strain by TTE -14.3 ± 3.3 -15.5 ± 4.9 0.663 RV Longitudinal Global Strain by TTE -11.3 (-13.2 - -7.0) -19.5 (-23.7 - -10) 0.089 RV Free-Wall Longitudinal Strain by TTE -11.5 (-14.2 - -8.2) -20 (-26 - -13.7) 0.043 HF: Heart Failure; CMR: Cardio Magnetic Resonance; LV: Left Ventricle; RV: Right Ventricle; iRVEDV: Indexed RV End-Diastolic Volume; iRVESV: Indexed RV End-Systolic Volume; iLVEDV: Indexed LV End-Diastolic Volume; iLVESV: Indexed LV End-Systolic Volume; LA: Left Atrium; LVEF: LV Ejection Fraction; RVEF: RV Ejection Fraction; RV-FAC: RV Fractional Area Change; TAPSE: Tricuspid Annular Plane Systolic Excursion Abstract P816 Figure 1

Introduction Aortic stenosis (AS) is the most prevalent valve disease. It involves increased left ventricle (LV) postcharge leading to LV hypertrophy. The aim of the study was to assess the burden of LV hypertrophy and its different patterns among a large cohort of patients with severe AS. Methods Observational, multicentre and prospective study of consecutive cases. Patients with severe AS defined as aortic valve area (AVA) 95 g/m2 in females or >115 g/m2 in males. LV geometry was assessed by relative wall thickness ratio, considering a cut-off value of 0.42. A p value Results A total of 805 patients with severe AS were included, 49.7% (n = 400) of them females and 50.3% (n = 405) males. LV indexed mass was available in 665 subjects, most of them (74.9%, n = 498) presenting LV hypertrophy. Females showed higher prevalence of LV hypertrophy than males (82.7% vs. 60.5%; p Conclusions LV hypertrophy affects most of patients with severe AS. LV remodelling is different between gender, with women developing higher grade of hypertrophy despite lesser AS severity. LV hypertrophy is associated with poor prognosis echocardiographic signs (increased PSAP and indexed LAV). Differences related to LV mass Normal LV mass LV hypertrophy P value Indexed AVA (cm/m2) 0.42 ± 0.01 0.41 ± 0.01 0.52 Mean gradient (mmHg) 42 ± 0.7 36 ± 1.1 Abstract 619 Figure. Sex related LV geometry patterns

Introduction and aim Aortic stenosis (AS) represents the main valve disease, thus, addressing its epidemiology and natural history becomes crucial. The aim of the present study is to shed light in the differences appearing with age in severe AS. Methods Observational, multicentre and prospective study of consecutive cases. Patients with severe AS, defined as aortic valve area (AVA) volume (iSV) A p-value Results A total of 636 patients were included, with slight predominance of females (53.9%; n = 343). No differences were found in AVA, LVEF, end-diastolic indexed values, LV mass or LV geometry between both age groups. MG and SVi were significantly lower in people over 85, who also presented more frequently with atrial fibrillation (AF) and significant mitral (MR) and tricuspid regurgitation (TR). Flow and gradient pattern vary significantly as shown in the graphic. Conclusions In our cohort, flow and gradient pattern in severe AS varies with age, despite no differences in LV geometry. This contrasts with previously assumed, relating LF and LG to more severe concentric hypertrophy. LF and LG can be explained by AF, significant MR and TR affecting more frequently those over 85. Age-related differences in severe AS Less than 85 y.o. ≥85 y.o. p-value AVA (cm2) 0.73 (± 0.16) 0.72 (±0.18) 0.46 LVEF (%) 65 (±7.9) 64 (±7.8) 0.21 MG (mmHg) 41 (±14.2) 37 (±13) 0.04 iSV (mL/m2) 40 (±11) 36 (±11) 0.01 iLVEDV (mL/m2) 47 (±16) 45 (±16) 0.07 iLVMass (g/m2) 126 (±36) 127 (±36) 0.66 Normal geometry (%) 3.9 2.5 0.64 Concentric remodelling (%) 24.3 24.4 Concentric hypertrophy (%) 64.2 66.4 Eccentric hypertrophy (%) 7.6 6.7 AF (%) 12.3 19.3 0.04 Significant MR (%) 11.3 18.7 0.02 Significant TR (%) 50.4 65.7 Abstract 616 Figure. Age-related flow and gradient pattern

A 85 years old woman with shortness of breath and leg edema with proggresive intensity last three weeks is admited in the cardiology department. As significant comorbidities, the patient has arterial hypertension (although last months all the medication that she needed was discontinued due to tendency toward low blood pressure) and paroxysmal atrial fibrillation. As previous surgical background, the patient only refers a carpal tunnel syndrome surgery (in both sides). In the physical exam she has a blood pressure of 110/60 Hg mm, lung crackles in the lower third of both lungs and a systolic murmur in the aortic area with a very low second sound. After being admitted in the cardiology department an echocardiography was done, showing severe left ventricle hypertrophy. As seen in the image (picture A), the myocardium, showed a characteristic granular ang bright pattern. It also showed a moderate to severe aortic stenosis. Although she was in atrial fibrillation during the echocardiography, the transmitral Doppler showed signs of significantly elevated filling pressures as for example, the presence of L waves. Finally, the exam was completed with an analysis of longitudinal deformation of the left ventricle, showing a clearly depressed global longitudinal strain, with a base-apex gradient (preserved at the apex, picture D). With these findings a Tc-PYP scintigraphy was performed, showing moderate and difuse uptake of the radioactive tracer in both ventricles (as shown in the image C). To complete the diagnosis, a cardiac magnetic resonance was performed showing a subendocardial ring pattern of delayed enhancement (image B). The diagnosis of transthyretin cardiac amyloidosis was done. Cardiac amyloidosis is clearly underdiagnosed entity, and sometimes differential diagnosis is really hard. Patients with cardiac amyloidosis are not always so "typical" as in this case. In fact, even a 5% of patients with history of aortic stenosis surgery may have also a cardiac amyloidosis. Maybe the use of myocardial deformation study and nuclear imaging can be useful solving this problem. Several studies have shown that nuclear imaging may be useful in the early diagnosis of this disease, even before that with echocardiography or cardiac magnetic resonance. Besides, new sequences of cardiac magnetic resonance may be very useful solving the problem of the differential diagnosis in left ventricle hypertrophy: The extracellular volume mapping. In cardiac amyloidosis hypertrophy is due to the deposit of amiloid in extracellular space. Because of that, the extracellular space is significantly increased in comparison with almost every other cause of left ventricle hypertrophy, making this sequence very useful in differential diagnosis. CONCLUSION Transthyretin cardiac amyloidosis is a rare and very under-diagnosed disease. However these problems with the advance of cardiac imaging and the development of new treatments could change very soon. Abstract P874 Figure. Image 1

Introduction A non-invasive diagnosis of cardiac amyloidosis is a challenge, especially in cases of atypical phenotypic presentation. Differential diagnosis includes hypertrophic cardiomyopathy (HCM), hypertensive cardiomyopathy, and other infiltrative disorders. Multimodality imaging is essential to make a final diagnosis. Case We present the case of a 65 years old woman, with a personal history of resistant arterial hypertension and mild hypertensive cardiomyopathy. She was diagnosed 6 years earlier with multiple myeloma, treated with chemotherapy and allogeneic hematopoietic stem cell transplant, presenting with several relapses and in a stable situation at the moment of our first consult. The patient was referred for heart failure in context of acquired community pneumonia one month earlier. Transthoracic echocardiography showed severe asymmetric left ventricle (LV) hypertrophy (Image A), systolic anterior motion of the mitral valve and diastolic dysfunction suggestive of HCM, not present in the previous examination. Strain imaging of the LV showed a typical amyloid infiltration pattern, with lower longitudinal strain values in the base compared to the apical segments (Image D). Further characterization of the myocardial tissue established the diagnosis along with performing a cardiac magnetic nuclear imaging (MRI). It showed the presence of inferior septum severe LV hypertrophy along with extensive patchy late gadolinium enhancement (LGE) of the lateral wall involving the endocardium (Image C), with normal LV contractility. There was no pleural effusion, but a small pericardial effusion was seen (Image B). With the suspicion of infiltrative heart disease, probably amyloid with an atypical LGE pattern, an oral mucosal biopsy was performed confirming amyloid diagnosis (Images E1,E2). Heart failure treatment was continued, but clinical evolution was poor with the deceasement of the patient 3 years after diagnosis. Discussion This case represents an example of the variety of imaging patterns we can see in cardiac amyloidosis. Despite the classical pattern of cardiac amyloidosis, with concentric LV hypertrophy, up to 8% of cases may present with asymmetrical LV hypertrophy, mimicking HCM. LGE extension and pattern can shows this variability as well: global transmural or subendocardial LGE is the most common, but focal patterns (up to 6% of cases) are described. The complexity of the diagnosis in these cases require a clinical and multimodality image approach. Abstract P726 Figure. Images of the case