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Introduction: According to the new European Society of Cardiology Guidelines for Heart Failure may be acute or chronic. According to the left ventricular ejection fraction (LVEF) heart failure (HF) is divided into the preserved (HFpEF, LVEF >50%), mid-range (HFmrEF, LVEF 40-49%) and reduced ejection fraction (HFrEF, LVEF <40%). Sacubitril/ valsartan is used in the treatment of HFrEF in patients who, despite of the optimal medical therapy with ACE inhibitors, beta blockers and mineralocorticoid receptor antagonist, have no symptom improvement. In the PARADIGM-HF study, its superiority was demonstrated in relation to enalapril.1,2 Case report: We present a patient with history of rheumatoid fever, mitral valvuloplasty, implanted heart electrostimulator, and multiple (20 times) hospitalizations due to acutization of chronic, dominant right-sided HF. In May 2018 he was hospitalized again at our Clinic because of acutization of dominantly right-sided HF. There was no sign of pulmonary congestion, but with elevated liver transaminases, ultrasound findings of enlarged liver and distended hepatic veins, ascites and peripheral edema. The left ventricle was borderline size, slightly reduced systolic function (LVEF 43%). The right ventricle was dilated with severe tricuspid insufficiency as a result of anulus dilatation and decreased systolic function (VCI 25 mm, TAPSE 14 mm). Value of NT-proBNP 4356 pg/ml. He was treated according to the recommendations for acute HF and after stabilization of the condition for the first time with sacubitril/valsartan. Control echocardiographic finding showed a lower volume of the right ventricle (VCI 19 mm, TAPSE 15 mm). At regular ambulatory control there was clinical improvement, the value of NT-proBNP 873 pg/ml. Conclusion: Although it has been shown that sacubitril/ valsartan in treatment of HFrEF reduces overall mortality and number of hospitalization and improve quality of life, its role in HFpEF and HFmrEF has not been investigated. The PARAGON-HF study is underway to investigate its role in comparison to valsartan in HFpEF. Our patient has fewer clinical symptoms and lowered the level of NTproBNP. [ABSTRACT FROM AUTHOR]

Background: Left ventricular non-compaction cardiomyopathy (LVNCC) can be associated with left ventricle (LV) dilation or hypertrophy, systolic or diastolic dysfunction, or both.1 Heart failure (HF) symptoms and presentations vary, and some patients may be asymptomatic. Affected individuals are at risk of left and/or right ventricular HF, embolization and malignant arrhythmias when device implantation is necessary. One study showed that LVNCC patients showed better response to resynchronization therapy. Case presentation: 36-year-old previously healthy male was admitted because of acute left ventricular failure in NYHA III/IV class. ECG showed left bundle branch block with QRS duration of 168 ms. Bedside echocardiography revealed a dilated LV (71 mm in end-diastole) with estimated ejection fraction (EF) of 26%, moderate mitral regurgitation, moderate left atrial enlargement, moderate pulmonary hypertension with indirect signs of preserved right ventricular function. Standard therapy with diuretics, ACE inhibitors, beta-blocker, mineralocorticoid receptor antagonist and prophylactic dose of enoxaparine was introduced. After initial recompenzation he suffered from an acute embolization of the right superficial femoral artery. Successful embolectomy was performed and therapeutic doses of enoxaparine were introduced with warfarin overlap. Control echocardiography revealed no residual thrombi in the LV, that showed trabeculization, but without clear echocardiographic criteria for LVNCC. Warfarin was titrated to optimal INR value, and after optimization of medical therapy he was discharged in NYHA II class and scheduled for MSCT coronary angiography and cardiac MR. Ischemic heart disease was excluded and cardiac MR confirmed LVNCC with EF of 24%. He was scheduled for CRT-D implantation under warfarin in therapeutic range. All three electrodes were implanted with optimal sensing and stimulation values and during resynchronization he had high R wave in V1 and V2 lead, with echocardiographic signs of a super-responder. After 9 months of follow-up he was in NYHA I class without loop-diuretics, and with 100% successful biventricular pacing and no ventricular ectopy detected after introduction of sacubitril/valsartan. Conclusion: Patients with LVNCC and appropriate criteria appear to be great responders to resynchronization with chances of optimal reverse remodeling. [ABSTRACT FROM AUTHOR]