INTRODUCTION Transcatheter aortic valve implantation (TAVI) and minimally invasive aortic valve replacement (minithoracotomy and ministernotomy) have become a valuable alternative to conventional surgical treatment of severe aortic stenosis (AS) in high-risk patients. OBJECTIVESThe aim of the study was to evaluate long-term results and complications in patients with symptomatic AS treated with TAVI, surgical aortic valve replacement (SAVR), minithoracotomy, or ministernotomy. PATIENTS AND METHODSA total of 173 patients with symptomatic AS were enrolled to the study between the years 2011 and 2013. Propensity scores were calculated for TAVI and each surgical method separately. Differences in clinical outcomes between patients treated with TAVI and those treated with surgical methods were adjusted for propensity scores using a logistic regression analysis and presented as adjusted odds ratios with 95% confidence intrervals.RESULTS A median follow-up was 583.5 days (interquartile range, 298-736 days). Before aortic valve replacement (AVR), no significant differences in ejection fraction (EF) were observed between the groups. At 1 week after AVR, mean EF values were significantly higher in patients after TAVI in comparison with the other groups (TAVI, 50.2% ±13.1%; minithoracotomy, 44.1% ±13.4%; ministernotomy, 37.8% ±12.8%; SAVR, 40.3% ±12.5%; P = 0.001). There were no differences in the longest available follow-up mortality between the analyzed groups (P = 0.8). To our best knowledge, this is the first study comparing minithoracotomy, ministernotomy, and SAVR with TAVI in terms of long-term outcomes such as the longest available follow-up mortality, left ventricular (LV) function, complications after the procedure, and conduction disturbances and arrhythmias after the procedure.CONCULSIONS Patients undergoing TAVI show more beneficial long-term outcomes in comparison with patients undergoing minithoracotomy, ministernotomy, and SAVR and do not differ in terms of the longest available follow-up mortality. TAVI seems to have a more favorable effect on LV function and an increase in EF in comparison with the surgical methods.

BackgroundFibrosis of extracellular matrix (ECM) in dilated cardiomyopathy (DCM) corresponds to the myocardial over-production of various types of collagens. However, mechanism of this process is poorly understood.ObjectiveTo investigate whether enhanced metabolism of ECM occur in DCM.MethodsSeventy consecutive DCM patients (pts) (48 ± 12.1 years, EF 24.4 ± 7.4 %) and 20 healthy volunteers were studied. Based on symptoms duration, pts were divided into new-onset (n = 35, 6 months) and chronic DCM (n = 35, >6 months). Markers of collagen type I and III synthesis-procollagen type I carboxy- and amino-terminal peptides (PICP and PINP) and procollagen type III carboxy- and amino-terminal peptides (PIIICP and PIIINP), collagen 1 (col-1), ECM metabolism controlling factors—tumor growth factor beta-1 (TGF1-β), connective tissue growth factor (CTGF), and ECM degradation enzymes—matrix metalloproteinases (MMP-2, MMP-9) and their tissue inhibitor (TIMP-1) were measured in serum. All pts underwent right ventricular endomyocardial biopsy to study ECM fibrosis.ResultsThe presence of fibrosis was detected in 24 (34.3 %) pts and was more prevalent in chronic DCM [17 (48.6 %) vs. 7 (20 %), p < 0.01]. The levels of PIIINP [4.41 (2.17–6.08) vs. 3.32 (1.69–5.02) ng/ml, p < 0.001], CTGF [3.82 (0.48–23.87) vs. 2.37 (0.51–25.32) ng/ml, p < 0.01], MMP-2 [6.06 (2.72–14.8) vs. 4.43 (2.27–7.4) ng/ml, p < 0.001], MMP-9 [1.98 (0.28–9.25) vs. 1.01 (0.29–3.59) ng/ml, p < 0.002)], and TIMP-1 [15.29 (1.8–36.17) vs. 2.61 (1.65–24.09) ng/ml, p < 0.004] were significantly higher in DCM, whereas levels of col-1 [57.7 (23.1–233.4) vs. 159.4 (31.2–512.9) pg/ml, p < 0.001] were significantly lower in DCM compared to controls. There were no differences in all measured serum markers of ECM metabolism between newonset and chronic DCM and as well as fibrosis positive and negative pts. Fibrosis was weakly correlated only with the duration of DCM (r = 0.23, p < 0.05), however, not a single serum marker of fibrosis correlated with fibrosis. Neither unadjusted nor adjusted models, constructed from serum markers of ECM metabolism, predicted the probability of myocardial fibrosis.ConclusionsDynamics of ECM turnover in DCM is high, which is reflected by the increased levels CTGF and degradation enzymes. Synthesis of collagen type III prevailed over collagen type I. ECM metabolism was not different in DCM regardless of the duration of the disease and status of myocardial fibrosis. Serum markers of ECM metabolism were found not to be useful for the prediction of myocardial fibrosis in DCM.

Aims The aims of this paper were to investigate the analytical performance of the nine prognostic scales commonly used in heart failure (HF), in patients with dilated cardiomyopathy (DCM), and to develop a unique prognostic model tailored to DCM patients. Methods and results The hospital and outpatient records of 406 DCM patients were retrospectively analysed. The information on patient status was gathered after 48.2 ± 32.0 months. Tests were carried out to ascertain the prognostic accuracy in DCM using some of the most frequently applied HF prognostic scales (Barcelona Bio-Heart Failure, Candesartan in Heart Failure-Assessment of Reduction in Mortality and Morbidity, Studio della Streptochinasi nell'Infarto Miocardico-Heart Failure, Eplerenone in Mild Patients Hospitalization and Survival Study in Heart Failure, Meta-Analysis Global Group in Chronic Heart Failure, MUerte Subita en Insuficiencia Cardiaca, Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients With Heart Failure, Seattle Heart Failure Model) and one dedicated to DCM, that of Miura et al. At follow-up, 70 DCM patients (17.2%) died. Most analysed scores substantially overestimated the mortality risk, especially in survivors. The prognostic accuracy of the scales were suboptimal, varying between 60% and 80%, with the best performance from Barcelona Bio-Heart Failure and Seattle Heart Failure Model for 1-5 year mortality [areas under the receiver operating curve 0.792-0.890 (95% confidence interval 0.725-0.918) and 0.764-0.808 (95% confidence interval 0.682-0.934), respectively].Based on our accumulated data, a self-developed DCM prognostic model was constructed. The model consists of age, gender, body mass index, symptoms duration, New York Heart Association class, diabetes mellitus, prior stroke, abnormal liver function, dyslipidaemia, left bundle branch block, left ventricle end-diastolic diameter, ejection fraction, N terminal pro brain natriuretic peptide, haemoglobin, estimated glomerular filtration rate, and pharmacological and resynchronisation therapy. This newly created prognostic model outperformed the analysed HF scales. Conclusions An analysis of various HF prognostic models found them to be suboptimal for DCM patients. A self-developed DCM prognostic model showed improved performance over the nine other models studied. However, further validation of the prognostic model in different DCM populations is required.

It is unknown whether fibrosis‐associated microRNAs: miR‐21, miR‐26, miR‐29, miR‐30 and miR‐133a are linked to cardiovascular (CV) outcome. The study evaluated the levels of extracellular matrix (ECM) fibrosis and the prevalence of particular microRNAs in patients with dilated cardiomyopathy (DCM) to investigate any correlation with CV events. Methods: Seventy DCM patients (48 ± 12 years, EF 24.4 ± 7.4%) underwent right ventricular biopsy. The control group was comprised of 7 patients with CAD who underwent CABG and intraoperative biopsy. MicroRNAs were measured in blood and myocardial tissue via qPCR. The end‐point was a combination of CV death and urgent HF hospitalization at the end of 12 months. There were differential levels of circulating and myocardial miR‐26 and miR‐29 as well as myocardial miR‐133a when the DCM and CABG groups were compared. Corresponding circulating and myocardial microRNAs did not correlate with one another. There was no correlation between microRNA and ECM fibrosis. By the end of the 12‐month period of the study, CV death had occurred in 6 patients, and a further 19 patients required urgent HF hospitalization. None of the circulating microRNAs was a predictor of the combined end‐point; however, myocardial miR‐133a was an independent predictor in unadjusted models (HR 1.53; 95% CI 1.14‐2.05; P < .004) and adjusted models (HR 1.57; 95% CI 1.14‐2.17; P < .005). The best cut‐off value for the miR‐133a level for the prediction of the combined end‐point was 0.74 ΔCq, with an AUC of 0.67. The absence of a correlation between the corresponding circulating and myocardial microRNAs calls into question their cellular source. This study sheds new light on the role of microRNAs in ECM fibrosis in DCM, which warrants further exploration.