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Introduction Splenic abcess represents a rare complication of left-sided infective endocarditis. Unlike splenic infarction, which is a more benign condition, splenic abcess requires rapid diagnosis and treatment as its course can be fatal. We present the case of a 52- year old male, with diabetes and hypertension, admitted for shortness of breath and fever in the past two months. Clinical examination revealed respiratory distress, tachypnea, diastolic murmur on the left sternal border. Baseline laboratory investigations showed elevated inflammation markers, leukocytosis and thrombocytosis. Enterococcus faecalis was isolated from the hemocultures. Transthoracic echocardiography revealed a dilated left ventricle (LV), with preserved LV ejection fraction, with severe aortic regurgitation due to valve destruction. A large (11mm diameter) vegetation-like structure attached to the ventricular side of the right coronary cusp, protruding into the left ventricular outflow tract was identified. Further evaluation by transoesopahgeal echocardiography did not identify other lesions, except for secondary moderate mitral regurgitation, with intact mitral leaflets. Dual antibiotic therapy with Ampicilin and Gentamycin was initiated. Surgery was planned after infection control. The first three days were uneventful, with rapid resolution of fever and inflammatory markers, but on the fourth day, the patient developed severe abdominal pain, with its focal point in the left hypochondrium. Contrast abdominal CT was performed and large multiple subcapsular lesions were identified. These findings, correlated with the symptomatology, suggested embolic splenic abcess and infarction. The patient successfully underwent laparoscopic splenectomy, but soon after he developed sepsis with respiratory failure and neurological deterioration (with normal CT scan) and was admitted to the intensive care unit, where he was intubated and mechanically ventilated. Consensus after discussions between cardiology, cardiac surgery and neurology services was to immediately replace the aortic valve, given the inability to otherwise control the infection. Intraoperative images were consistent with perforation of the right coronary cusp. During hospitalization in the ICU following cardiac surgery, the patient was extubated and his neurological function markedly improved. Repeated TTE and TEE showed normal prosthetic valve function and resolution of mitral regurgitation. The patient continued to improve clinically until his discharge. Conclusions We presented a case of a rare pathogenic entity- splenic abscess and infarction- due to systemic embolization from infective aortic valve endocarditis. Multidisciplinary teamwork was required between cardiologist, intensive care specialist, neurologist, infectionist, general surgeon and cardiac surgeon. Splenectomy was performed before valve replacement, a treatment-course characteristic in the occurrence of these rare cases.

Background The presence of small mobile masses on the ventricular side of the aortic valves in the absence of valvular regurgitation and signs of systemic inflammation has been previously described as marantic endocarditis and is now referred to as nonbacterial thrombotic endocarditis (NBTE). It is thought to be associated with endothelial dysfunction and procoagulative status, as is the case of acute decompensated heart failure (HF). Case description We present a series of three male patients, with similar clinical characteristics, who were admitted for acute decompensated HF. All three patients had chronic HF, due to non-ischemic dilated cardiomyopathy with severe biventricular dysfunction, with resynchronization therapy, with elevated natriuretic peptides and previous HF hospitalizations in the past year requiring prolonged intravenous treatments. Other clinical, biological criteria for the definition of advanced HF were also met. All patients were under chronic anticoagulation treatment using a direct oral anticoagulant because of persistent atrial fibrillation. Thorough echocardiographic evaluation (both transthoracic and transoesophageal ultrasound) identified small mobile masses on the ventricular side of the aortic valves, centrally, on the line of cusp coaptation, with only minor central regurgitation. The lack of progression of valve lesion and the absence of gross signs of inflammation (no fever, normal hemoleucogram, normal CRP, repeated negative blood cultures) on serial examinations during several weeks follow-up allowed for the exclusion of infective endocarditis. In one case we also identified a left atrial appendage thrombus and presumably thrombotic masses attached to right side pacing leads. No clinically systemic embolic events were identified. Conclusion We consider this to be an incidental finding in the given subclinical prothrombotic and inflammatory predisposing milieu of advanced chronic HF and the increasing high quality echocardiography imaging. Its clinical significance is still unknown, while differential diagnosis from subacute or chronic endocarditis relies largely on clinical judgment.

Background Transcatheter valve replacement (TAVR ) is currently the optimal treatment for patients with severe aortic stenosis who are considered to have an intermediate to high operative risk for surgical intervention. Intramural hematoma secondary to balloon-expandable TAVR is a poorly reported complication with unknown outcome. Among the risk factors associated with this complication are advanced age, female gender, bulky calcifications, significant basal hypertrophy and severe prothesis oversizing. Case report We report the case of a 84 year old woman with a history of permanent atrial fibrillation, who was diagnosed with severe aortic stenosis symptomatic with heart failure NYHA class III. An important comorbidity was liver cirrhosis of viral etiology (hepatitis C virus) with secondary thrombocytopenia. Transthoracic and transoesophageal echocardiography (TEE) showed severe aortic stenosis with asymmetric calcifications, with preserved gradient (a peak velocity of 4.7 m/s, mean gradient of 63.3mmHg), mild left ventricular disfunction (ejection fraction 45%), and calculated aortic valve area of 0,9 cm2. As a frail, high risk patient, the heart team recommended transcatheter aortic valve implantation. After complete computer tomographic evaluation, a 26 mm Edwards Sapien 3 valve was implanted through a femoral approach. Intraprocedural transesophageal echocardiography showed the developement of an intramural hematoma in the aortic root (right coronary and noncoronary sinuses), associated with a small pericardial effusion. After administration of Protamine, betablockers and strict blood pressure control, no extension of the hematoma was noted. Serial TEE showed significant regression of the hematoma and of the pericardial effusion, with normal parametres of the prothesis, with a transprothetic gradient of 23 mmHg, no aortic leak, no other complications.The patient was discharged 12 days after the procedure, clinically stable. Conclusion Aortic intramural hematoma may occur during intra-TAVR procedure. Although it may have a benign course, timely recognition and adequate imaging follow-up are mandatory in order to limit the extent and prevent life-threatening complications.

Introduction Left ventricular non-compaction is a rare form of cardiomyopathy charactherized by the presence of a two layered ventricular wall- a thinner epicardial layer and an inner, non-compacted layer with prominent trabeculations associated with deep, intratrabecular recesses that communicate with left ventricle cavity. Clinical manifestations vary in severity, including symptoms of heart failure, thromboembolic events or arrhythmias. Left ventricular (LV) dysfunction leads to tethering of the mitral apparatus and is a cause for secondary significant mitral regurgitation. Case presentation We report the case of a 57 year-old female patient, diagnosed with severe mitral regurgitation one year before presentation, with severe heart failure (HF) symptoms, referred to our clinic for the surgical replacement of the mitral valve. Clinical examination revealed no signs of pulmonary or systemic congestion and systolic apical murmur. Blood tests were normal, except for the elevated BNP (552 pg/ml). Electrocardiogram showed sinus rhythm and left ventricular hypertrophy. Coronary angiogram did not identify any coronary artery lesions. Echocardiography revealed mildly dilated left ventricle, but wih proeminent trabeculations and two distinct myocardial layers with a non-compacted/compacted ratio of 2:1 in the anterior and lateral walls, diagnostic for left ventricular non-compaction cardiomyopathy. LV ejection fraction was 40% , with severe secondary mitral regurgitation due to significant antero-posterior dilation of the mitral ring, with intact mitral leaflets; mild pulmonary hypertension was present. Magnetic resonance imaging (MRI) identified a two layer antero-lateral myocardium and confirmed the echo diagnosis; there was no evidence of scarring as there was absent late gadolinium enhacement. In the absence of fibrosis on MRI or any arrhythmic events on repeated Holter ECG monitoring, the implantation of a cardiac defibrillator was deferred. Given the secondary cause for mitral regurgitation (LV dysfunction), specific HF medication with beta blocker and renin-angiotensin-aldosterone blockade was initiated and titrated to optimal doses. With medical treatment the evolution was favourable. Currently, 3 years after the initial diagnosis, 6 minutes walk test revealed good functional capacity (510 m), a BNP value of 104 pg/l, without any worsening of LV systolic function nor progression of pulmonary hypertension. Conclusion Left ventricular non-compaction cardiomyopathy is a rare cause of heart failure, but due to advances in imaging modalities and increasing awareness, its prevalence is growing. Its pathogenesis and prognosis largely remain unknown, but early and adequate initiation of neurohormonal medication may be just as essential in order to prevent complications and improve long term prognosis, as for other forms of cardiomiopathy, even in the presence of severe secondary mitral regurgitation.

Alcohol septal ablation is a percutaneous intervention for hypertrophic obstructive cardiomyopathy, aiming to relieve symptoms, as an alternative to surgical myomectomy, in optimally treated but still symptomatic patients, with high surgical risk. We present the case of 65-year-old female, with persistently elevated blood pressure, presenting with severe dyspnea and angina on exertion and frequent episodes of paroxysmal nocturnal dyspnea. Clinical examination revealed an intense left parasternal systolic murmur. Electrocardiographic findings were sinus rhythm and negative T waves in V2-V6. Transthoracic echocardiography showed a small LV cavity with severe asymmetric left ventricular hypertrophy (maximum basal interventricular septum thickness of 26 mm), with important obstruction in the left ventricular outflow tract - resting gradient 77mmHg, provoked gradient 100mmHg. TOE evaluation of the mitral valve revealed significant mitral regurgitation, with intermitent telesystolic anterior motion of the anterior mitral leaflet and also P2 scallop prolapse. Further evaluation revealed a 60% stenosis of left anterior descending (LAD) artery of second segment, 60% stenosis of the left internal carotid artery, chronic renal disease (creatinine clearance 80ml/min), and moderate pulmonary hypertension. Although surgery was initially proposed to the patient, given the high operative risk (EUROSCORE II 8.45%) for a complete surgical procedure (myomectomy, mitral valve repair and coronary bypass), we attempted a stepwise approach to alleviate her symptoms. Intensive medical treatment improved blood pressure control while angioplasty of the LAD alleviated her angina. Echo-guided alcohol ablation of the interventricular septal wall was performed. Catheter-based contrast injection of a secondary septal branch of the LAD produced a subendocardial contrast in the contact area of anterior mitral valve leaflet; subsequently, embolizing the artery, producing an isolated necrosis at this level, with equalizing the pressure curves between LV and aorta. Postintervention, initial gradients were 50mmHg at rest, 100mmHg on postextrasystolic measurement. Systolic movement of the anterior leaflet maintained a mezotelesystolic pattern. At 3-months follow-up, LVOT gradients were 27/100mmHg, without any increase in pulmonary artery pressure, but with significant improvement of dyspnea. Further risk assessment by Holter ECG monitoring identified non-sustained ventricular tachycardia, so an ICD was implanted. The modest reduction in gradient was associated with significant clinical improvement in the patient’s symptomatology. This procedure has been refined in the last years, especially with the introduction of myocardial contrast echocardiography for better localizing the area at risk of infarction and to reduce the amount of alcohol used. Alcohol septal ablation may be part of a stepwise plan to improve symptoms, with lower procedural risks as compared to classic surgery.