Background and objective: Cardiovascular magnetic resonance (CMR) - based feature tracking (FT) can detect left ventricular (LV) strain abnormalities in pulmonary hypertension (PH) patients, but little is known about the prognostic value of LV function and mechanics in PH patients. The aim of this study was to evaluate LV systolic function by conventional CMR and LV global strains by CMR-based FT analysis in precapillary PH patients, thereby defining the prognostic value of LV function and mechanics. Methods: We prospectively enrolled 43 patients with precapillary PH (mean pulmonary artery pressure (mPAP) 55.91 ± 15.87 mmHg, pulmonary arterial wedge pressure (PAWP) ≤15 mmHg) referred to CMR for PH evaluation. Using FT software, the LV global longitudinal strain (GLS) and global circumferential strain (GCS), also right ventricular (RV) GLS were analyzed. Results: Patients were classified into two groups according to survival (survival/non-survival). LV GLS was significantly reduced in the non-survival group (−12.4% [−19.0–(−7.8)] vs. −18.4% [−22.5–(−15.5)], p = 0.009). By ROC curve analysis, LV GLS > −14.2% (CI: 3.229 to 37.301, p < 0.001) was found to be robust predictor of mortality in PH patients. Univariable analysis using the Cox model showed that severely reduced LV GLS > −14.2%, with good sensitivity (77.8%) and high specificity (93.5%) indicated an increase of the risk of death by 11-fold. LV GLS significantly correlated in PH patients with RV ESVI (r = 0.322, p = 0.035), RV EF (r = 0.444, p < 0.003). Conclusions: LV systolic function and LV global longitudinal strain measurements using CMR-FT correlates with RV dysfunction and is associated with poor clinical outcomes in precapillary PH patients.

Background: Severe aortic stenosis (AS) complicated by pulmonary hypertension (PH) is associated with poor outcomes after surgical aortic valve replacement (AVR). There is still scarce information about predictors of secondary PH in this group of patients. Objectives: The aim of this study was to investigate the prognostic impact of biomarkers together with conventional Doppler echocardiographic parameters of left ventricular diastolic function on elevated pulmonary systolic pressure (PSP) in severe AS patients before surgical AVR. Methods: Sixty patients with severe isolated AS (aortic valve area <1 cm2) underwent echocardiography, N-terminal pro B-type natriuretic peptide (NT-proBNP) and growth differentiation factor-15 (GDF-15) measurements before AVR. PSP, left ventricular ejection fraction (LV EF), parameters of LV diastolic function (E/E’ ratio, mitral valve deceleration time (MV DT) and left atrial (LA) volume) were evaluated. PH was defined as an estimated PSP ≥ 45 mmHg. Results: Of the 60 patients, 21.7% with severe isolated AS had PH with PSP ≥ 45 mmHg (58.5 ± 11.2 mmHg). LV EF did not differ between groups and was not related to an elevated PSP (50 ± 8 vs. 49 ± 8%, p = 0.58). Parameters of LV diastolic dysfunction (E/E’ ratio > 14 (OR 6.00; 95% CI, 1.41–25.48; p = 0.009), MV DT ≤ 177.5 ms (OR 9.31; 95% CI, 2.06–41.14; p = 0.001), LA volume > 100 mL (OR 9.70; 95% CI, 1.92–49.03; p = 0.002)) and biomarkers (NT-proBNP > 4060 ng/L (OR 12.54; 95% CI, 2.80–55.99; p < 0.001) and GDF-15 > 3393 pg/mL (OR 18.33; 95% CI, 2.39–140.39; p = 0.001)) were significantly associated with elevated PSP in severe AS. Conclusions: Left ventricular diastolic dysfunction and elevated biomarkers levels could predict the development of pulmonary hypertension in patients with severe aortic stenosis. Elevation of biomarkers paired with worsening of LV diastolic dysfunction could help to stratify patients for earlier surgical treatment before the development of pulmonary hypertension.

Background and Objectives: The aim of this study was to clarify the tricuspid valve (TV) and right ventricular (RV) geometry and function characteristics using 3D echocardiography-based analysis and to identify echocardiographic predictors for severe tricuspid regurgitation (TR) in different etiologies of functional TR (fTR). Methods and Results: The prospective study included 128 patients (median age 64 years, 57% females): 109 patients with moderate or severe fTR (69-caused by dominant left-sided valvular pathology (LSVP), 40 due to precapillary pulmonary hypertension (PH)), and 19 healthy controls. The 2D and 3D-transthoracic echocardiography analysis included TV, right atrium, RV geometry, and functional parameters. All the RV geometry parameters as well as 3D TV parameters were increased in both fTR groups when compared to controls. Higher RV diameters, length, areas, volumes, and more impaired RV function were in PH group compared to LSVP group. PH was associated with larger leaflet tenting height, volume, and more increased indices of septal-lateral and major axis tricuspid annulus (TA) diameters. LVSP etiology was associated with higher anterior-posterior TA diameter and sphericity index. Univariate and multivariate logistic regression and ROC analyses revealed that different fTR etiologies were associated with various 2D and 3D echocardiographic parameters to predict severe TR: major axis TA diameter and TA perimeter, the leaflet tenting volume had the highest predictive value in PH group, septal-lateral systolic TA diameter-in LSVP group. The 3D TA analysis provided more reliable prediction for severe fTR. Conclusions: TV and RV geometry vary in different etiologies of functional TR. Precapillary PH is related to more severe RV remodeling and dysfunction and changes of TV geometry, when compared to LSVP group. The 3D echocardiography helps to determine echocardiographic predictors of severe TR in different fTR etiologies.

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Background and objectives: Non-invasive imaging of the heart has an important place in the diagnosis and management of pulmonary arterial hypertension (PAH). The aim of this study was to establish the thresholds of cardiac magnetic resonance imaging (CMRI)-derived biventricular deformation, function parameters, and levels of N-terminal pro brain natriuretic peptide (NT-proBNP) for the prediction of survival of pre-capillary pulmonary hypertension (PHprecap) patients. Materials and Methods: In total, 64 incident PHprecap cases, who underwent CMRI, were consecutively enrolled in a prospective cohort study. Patients underwent a systemic evaluation, including measurement of NT-proBNP, two-dimensional (2D) echocardiography, six-minute walk test (6MWT), CMRI with feature tracking (FT), and right-heart catheterization (RHC). Patients were divided into two groups according to one-year survival (survival and non-survival groups). Survival analysis was performed. Results: One-year survival was 79.6%. The distribution between age, sex, mean pulmonary artery pressure (mPAP), New York Heart Association (NYHA) functional class, and 6MWT did not differ between the groups. Survival was significantly lower in the PAH group associated with connective tissue disease (CTD-PAH), where 44% (n = 4) of patients died during the first year. Univariate analysis revealed that severely reduced right-ventricle (RV) ejection fraction (EF) <25.5%, left-ventricle global longitudinal strain (LV GLS) >−14.18%, and right pulmonary artery (RPA) relative area change (RAC) <19%, and severely increased NT-proBNP level >1738 (ng/L) indicate an increased risk of death in PHprecap patients. Conclusions: Impaired RV systolic function and LV global longitudinal strain, decrease of pulmonary artery distensibility, and CTD-PAH etiology, together with high NT-proBNP level, impair prognosis in pre-capillary PH patients. These findings are important for the risk stratification and management of pre-capillary pulmonary hypertension patients.

The rising incidence of non-ST-segment elevation myocardial infarction (NSTEMI) and associated long-term high mortality constitutes an urgent clinical issue. Unfortunately, the study of possible interventions to treat this pathology lacks a reproducible pre-clinical model. Indeed, currently adopted small and large animal models of MI mimic only full-thickness, ST-segment-elevation (STEMI) infarcts, and hence cater only for an investigation into therapeutics and interventions directed at this subset of MI. Thus, we develop an ovine model of NSTEMI by ligating the myocardial muscle at precise intervals parallel to the left anterior descending coronary artery. Upon histological and functional investigation to validate the proposed model and comparison with STEMI full ligation model, RNA-seq and proteomics show the distinctive features of post-NSTEMI tissue remodelling. Transcriptome and proteome-derived pathway analyses at acute (7 days) and late (28 days) post-NSTEMI pinpoint specific alterations in cardiac post-ischaemic extracellular matrix. Together with the rise of well-known markers of inflammation and fibrosis, NSTEMI ischaemic regions show distinctive patterns of complex galactosylated and sialylated N-glycans in cellular membranes and extracellular matrix. Identifying such changes in molecular moieties accessible to infusible and intra-myocardial injectable drugs sheds light on developing targeted pharmacological solutions to contrast adverse fibrotic remodelling.

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