LUS appears a useful method to assess severity and monitor the resolution of lung congestion. At hospital admission, B-lines are strongly related to respiratory rate, which may be a key component of the sensation of dyspnea. Measurement of lung congestion at discharge provides prognostic information for patients with either HFpEF or HFrEF.

Purpose To characterize the genetic architecture of left ventricular noncompaction (LVNC) and investigate the extent to which it may represent a distinct pathology or a secondary phenotype associated with other cardiac diseases. Methods We performed rare variant association analysis with 840 LVNC cases and 125,748 gnomAD population controls, and compared results to similar analyses on dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM). Results We observed substantial genetic overlap indicating that LVNC often represents a phenotypic variation of DCM or HCM. In contrast, truncating variants in MYH7, ACTN2, and PRDM16 were uniquely associated with LVNC and may reflect a distinct LVNC etiology. In particular, MYH7 truncating variants (MYH7tv), generally considered nonpathogenic for cardiomyopathies, were 20-fold enriched in LVNC cases over controls. MYH7tv heterozygotes identified in the UK Biobank and healthy volunteer cohorts also displayed significantly greater noncompaction compared with matched controls. RYR2 exon deletions and HCN4 transmembrane variants were also enriched in LVNC, supporting prior reports of association with arrhythmogenic LVNC phenotypes. Conclusion LVNC is characterized by substantial genetic overlap with DCM/HCM but is also associated with distinct noncompaction and arrhythmia etiologies. These results will enable enhanced application of LVNC genetic testing and help to distinguish pathological from physiological noncompaction.

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Admission NGAL measurement appears a sensible tool for in-hospital WRF prediction as well as an early marker for adverse outcome during post discharge vulnerable phase.

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Myocardial infarction (MI) results in myocardial scarring which can have an impact on left ventricular (LV) stiffness and contractile function, ultimately leading to reduced LV systolic function and LV remodelling, However some concerns about the relation between scar extension and segmental wall motion contractility is not enough clear. Thus, the association between myocardial scar, LV regional and global function and LV remodeling should be investigated. We studied the relationship between scar extension, wall motion score index (WMSI), LV dimensions and systolic function in a group of patients with previous MI by cardiac magnetic resonance (CMR). 133 patients with previous (>6 month) MI were retrospectively enrolled in the study. Indexed end-systolic volume (ESVi), indexed end-diastolic volume (EDVi), LV ejection fraction (EF), stroke volume (SV), LV mass were measured using CMR. WMSI and sum scar score (SSS) were also measured following AHA\ACC criteria giving an arbitrary cut-off to distinguish larger from restricted late gadolinium enhancement (LGE) area. A total of 2261 segments were studied: regional wall motion abnormalities were present in 1032 segments (45 %) and 724 (32 %) showed presence of MI (LGE). WMSI correlated significantly with EF (r = −0.87, p < 0.0001) in all patients and in both patients with EF ≥ 40 % (r = −0.77, p < 0.0001) and EF < 40 % (r = −0.68, p < 0.0001). WMSI also correlated significantly with SSS (r = 0.57, p < 0.0001). The correlation between WMSI and SSS was more significant in patients with transmural MI (WMSI 2.1 ± 0.5 and SSS 17 ± 8; r = 0.55, p < 0.0001) than with non transmural MI (WMSI 1.6 ± 0.7 and SSS 6 ± 4; r = 0.34 and p = 0.02). A significant correlation was also found between EF and SSS (r = −0.55 and p < 0.0001) and between SSS and LV indexed volumes (EDVi; r = 0.44, p < 0.0001 and ESVi; r = 0.51, p < 0.0001). Infarct transmurality and extension as expressed as SSS assessed with cardiac MRI has an impact on global and regional systolic function. A multi-parametric score measuring WMSI scar transmurality and extension, could better identify an increased cardiac remodeling after coronary event

Gal-3 is not able to distinguish between HFrEF and HFpEF patients. However it is related to diastolic dysfunction severity and LV stiffness in HFpEF. Gal-3 demonstrates a prognostic role independently from renal dysfunction in subjects with HFpEF.

Background: Cardiorenal syndrome (CRS) is associated with increased cardiovascular morbidity and mortality; still, its biomarker pattern has been poorly evaluated so far. The aim of this study was to measure the inflammatory activation, neurohormonal status and kidney and myocardial damage in patients with CRS compared to patients with heart failure (HF) without renal impairment (RI). Methods: We analyzed 246 patients on the basis of renal function (group 1: 120 HF patients without RI; group 2: 126 CRS patients). In each group, interleukin-6, tumor necrosis factor-E, B-type natriuretic peptide (BNP), neutrophil gelatinase-associated lipocalin (NGAL), troponin T (TnT), osteoprotegerin and blood urea nitrogen (BUN) were measured. The diagnostic power of all laboratory parameters to detect CRS was evaluated by the receiver operating characteristic (ROC) curve and logistic regression analysis. Results: A significant increase in BNP [626.4 pg/ml, confidence interval (CI) 518-749 vs. 487.8 pg/ml, CI 411-578; p < 0.05], NGAL (156 ng/ml, CI 129-186 vs. 89.1 ng/ml, CI 72-109; p < 0.0001), BUN (108.9 mg/dl, CI 98-120 vs. 51 mg/dl, CI 46-55; p < 0,0001) and TnT (0.62 ng/ml, CI 0.51-0.75 vs. 0.21 ng/ml, CI 0.15-0.28; p < 0.001) was seen in CRS patients compared to HF patients without RI. ROC curve analysis showed that only NGAL, BUN, BUN/creatinine ratio and TnT can discriminate patients with CRS from patients without RI. Conclusions: In CRS patients, renal tubular damage and neurohormonal and cardiac injury activation are increased compared to patients without RI. The current biomarker pattern could be used for an early diagnosis of RI in acute and chronic HF. i 2014 S. Karger AG, Basel