Hypothermic machine preservation (HMP) remains investigational in clinical liver transplantation. It is widely used to preserve kidneys for transplantation with improved results over static cold storage (SCS). At our center, we have used HMP in 31 adults receiving extended criteria donor (ECD) livers declined by the originating United Network for Organ Sharing region (''orphan livers''). These cases were compared to ECD SCS cases in a matched cohort study design. Livers were matched for donor age, recipient age, cold ischemic time, donor risk index and Model for EndStage Liver Disease (MELD) score. HMP was performed for 3-7 h at 4-88C using our previously published protocol. Early allograft dysfunction rates were 19% in the HMP group versus 30% in the control group (p ¼ 0.384). One-year patient survival was 84% in the HMP group versus 80% in the SCS group (p ¼ NS). Post hoc analysis revealed significantly less biliary complications in the HMP group versus the SCS group (4 vs. 13, p ¼ 0.016). Mean hospital stay was significantly shorter in the HMP group (13.64 AE 10.9 vs. 20.14 AE 11.12 days in the SCS group, p ¼ 0.001). HMP provided safe and reliable preservation in orphan livers transplanted at our center.

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Biomarkers (various laboratory biochemical markers), such as natriuretic peptides (NP), soluble ST2 receptor, copeptin, galectin-3, are widely studied in patients with chronic heart failure (CHF). The European Society of Cardiology recommends the determination of blood NP level in suspicion of HF and its use as one of the mandatory diagnostic criteria for CHF with preserved and mid-range ejection fraction. Dynamics of NP concentration may be predictor of the effectiveness of the therapy and the necessity of the titration of the dose of HF drugs. Neprilyzin destroys NP, but does not destroy their precursors, including NT-proBNP. Therefore, it is necessary to use NT-proBNP as a marker of therapeutic efficacy and prognosis when using neprilysine inhibitors (sacubitril). ST2 is a protein receptor for interleukin-33 (IL-33). The transmembrane ST2 (ST2L) binds to IL-33 and forms the IL-33/ST2L complex, which has a cardioprotective effect, prevents the development of myocardial hypertrophy, fibrosis and apoptosis. The soluble ST2 receptor (sST2) is a “trap” for IL-33 and neutralizes the protective effects of the IL-33/ST2L complex, which leads to hypertrophy and fibrosis of the myocardium, dilatation of the chambers and reduction of the contractility of the heart. It can be considered as a marker of unfavorable prognosis in heart failure, but it is not specific. Copeptin is a part of the arginine-vasopressin, or antidiuretic hormone, precursor which plays an important role in the pathogenesis of CHF. Since arginine-vasopressin has a short half-life and is unstable outside the body, copeptin is being actively investigated. Its level increases during the CHF decompensation and relates with the functional class of CHF. A combined measurement of the concentration of copeptin and NP may improve the risk stratification in CHF patients. Galectin-3 is a peptide that stimulates the activation of fibroblasts and the development of fibrosis. It increases in CHF patients and is associated with the severity of the condition, systolic and diastolic LV dysfunction and prognosis. Currently, NP are the best biomarkers that can and should be used in routine clinical practice. To prove the need for widespread use of other biomarkers, additional research is needed.

Aims Cardiomyopathies are a heterogeneous group of disorders that increase the risk for atrial fibrillation (AF). The aim of the study is to assess the prevalence of AF, anticoagulation management, and risk of stroke/transient ischaemic attack (TIA) in patients with cardiomyopathy. Methods and results Three thousand two hundred eight consecutive adult patients with cardiomyopathy (34.9% female; median age: 55.0 years) were prospectively enrolled as part of the EURObservational Research Programme Cardiomyopathy/Myocarditis Registry. At baseline, 903 (28.2%) patients had AF (29.4% dilated, 27.5% hypertrophic, 51.5% restrictive, and 14.7% arrhythmogenic right ventricular cardiomyopathy, P < 0.001). AF was associated with more advanced New York Heart Association class (P < 0.001), increased prevalence of cardiovascular risk factors and co-morbidities, and a history of stroke/TIA (P < 0.001). Oral anticoagulation was administered in 71.7% of patients with AF (vitamin K antagonist: 51.6%; direct oral anticoagulant: 20.1%). At 1 year follow-up, the incidence of cardiovascular endpoints was as follows: stroke/TIA 1.85% (AF vs. non-AF: 3.17% vs. 1.19%, P < 0.001), death from any cause 3.43% (AF vs. non-AF: 5.39% vs. 2.50%, P < 0.001), and death from heart failure 1.67% (AF vs. non-AF: 2.44% vs. 1.31%, P = 0.033). The independent predictors for stroke/TIA were as follows: AF [odds ratio (OR) 2.812, P = 0.005], history of stroke (OR 7.311, P = 0.010), and anaemia (OR 3.119, P = 0.006). Conclusions The study reveals a high prevalence and diverse distribution of AF in patients with cardiomyopathies, inadequate anticoagulation regimen, and high risk of stroke/TIA in this population.

Cardiac amyloidosis (amyloid cardiomyopathy) is a disease damage to the heart caused by extracellular amyloid deposition. In some cases, there may be local damage to the structures of the heart, for example, the atria; more often, heart damage is part of a systemic (generalized) pathology. Depending on the amyloid precursor protein, 36 types of amyloidosis are described, among which hereditary and acquired forms are distinguished. Cardiac amyloidosis is diagnosed 1) in the case of the amyloid infiltration in the myocardial bioptates or 2) in the case of non-cardiac amyloid deposition and the left ventricular wall thickening >12 mm without arterial hypertension and other reasons. The heart is most often affected in AL-, ATTR-, AA-, AANF-types of amyloidosis. Cardiac amyloidosis should be considered in patients with a heart failure with an unclear etiology, especially with preserved left ventricular ejection fraction, refractory to treatment, with proteinuria and CKD 4-5, in patients with idiopathic atrial fibrillation and conduction disturbances, in patients with left ventricular wall thickening of unclear etiology, low ECG voltage, unexplained arterial hypotension and pulmonary hypertension. Screening for cardiac amyloidosis should include non-invasive methods such as electrophoresis and immunofixation of blood and urine proteins, the free light lambda and kappa chains of immunoglobulins, 99Tc-DPD scintigraphy, genetic testing (if hereditary variants of amyloidosis are suspected), as well as a histological examination of biopsy samples stained with Congo red and polarizing microscopy.