Search

Abstract Aims Recently, liver fibrosis markers, such as the fibrosis‐4 index (FIB‐4), have been shown to be associated with prognosis in patients with heart failure. The fibrosis‐5 (FIB‐5) index, which assesses albumin, alkaline phosphatase, aspartate transaminase, alanine aminotransferase and platelet count, is a simple liver fibrosis marker that was reported to be superior to FIB‐4 for differentiation of liver fibrosis. This study aimed to compare the prognostic value of FIB‐4 and FIB‐5 in patients with heart failure. Methods and results The FIB‐4 and FIB‐5 scores were calculated at discharge in 906 patients hospitalized with heart failure. The patients were stratified into three groups based on their FIB‐5 scores: low (n = 303), middle (n = 301), and high (n = 302) FIB‐5 groups. The primary endpoint was a composite of cardiac death or rehospitalization for heart failure. The low FIB‐5 group was older and had larger inferior vena cava diameters and higher brain natriuretic peptide levels than the other two groups. The primary endpoint occurred in 156 (51.5%), 110 (36.5%), and 54 patients (17.9%) in the low, middle, and high FIB‐5 groups, respectively (P

Abstract Background Left atrial spontaneous echo contrast (LASEC) is common in patients with atrial fibrillation (AF), although scarce information exists on LASEC occurring in nonvalvular AF patients who have low thromboembolic risk scores. We therefore examined prevalence and determinants of LASEC under low CHADS2 or CHA2DS2-VASc scores in these patients. Methods Among 713 patients who underwent transesophageal echocardiography, 349 with a CHADS2 score

Abstract Background Tissue Doppler imaging (TDI)-derived atrial electromechanical delay (AEMD) has been reported to be useful for detecting paroxysmal atrial fibrillation (PAF). However, its usefulness remains unknown when analyzed along with patients seemingly at high-risk for AF as controls. From this standpoint, we investigated whether AEMD would be of use for identifying patients with PAF. Methods We retrospectively analyzed TDI recordings to obtain AEMD in 63 PAF patients. Thirty-three patients with multiple cardiovascular risk factors (MRFs) but without history of AF and 50 healthy individuals served as disease and healthy controls, respectively. AEMD was defined as the time-interval between the electrocardiogram P-wave and the beginning of the spectral TDI-derived A’ for the septal (septal EMD) and lateral (lateral EMD) sides of the mitral annulus. Results There was no significant difference in the left atrial volume index between PAF patients and disease controls (28 ± 9 mL/m2 vs. 27 ± 5 mL/m2). PAF patients had longer AEMD, particularly for the lateral EMD (75 ± 23 ms), compared with disease (62 ± 22 ms, P = 0.009) and healthy (54 ± 24 ms, P

Autophagic activity decreases with age via unknown mechanisms. Here the authors show that expression of the negative autophagy regulator Rubicon increases with age, that its genetic ablation improves lifespan and ameliorates a number of age-associated phenotypes in invertebrates and in mouse models.

BackgroundInfluenza virus infection (IVI) was reported to be associated with minor cardiac changes, mostly those detected on electrocardiogram with and without elevated blood markers of myocardial injury; however, the characteristics of myocardial involvement in association with IVI are poorly understood. This study used echocardiographic tissue imaging (tissue Doppler, strain, and strain rate) to evaluate changes in left atrial (LA) and left ventricular (LV) myocardial function after IVI.Methods and resultsWe examined 20 adult individuals (mean age, 43 years) at 2 and 4 weeks after diagnosis of IVI. For myocardial functional variables, we obtained LV global longitudinal strain (GLS), LV early diastolic strain rate (e'sr), LA strain, and LA stiffness (E/e'/LA strain), in addition to data on tissue Doppler (s', e', and a') and myocardial performance index. Blood markers of myocardial injury were also examined. During follow-up, there were no significant changes in global chamber function such as LV ejection fraction, E/e', and LA volume. However, significant changes in myocardial function were observed, namely, in s' (8.0 ± 1.6 cm/s to 9.3 ± 1.5 cm/s; p = 0.01), e' (10.2 ± 2.8 cm/s to 11.4 ± 3.0 cm/s; p < 0.001), e'sr (1.43 ± 0.44 1/s to 1.59 ± 0.43 1/s; p = 0.005), and LA strain (35 ± 8% to 40 ± 12%; p = 0.025), and the myocardial performance index (0.52 ± 0.20 to 0.38 ± 0.09; p = 0.009), but not in a', LA stiffness, or GLS. Cardiac troponin T and creatinine kinase isoenzyme MB were not elevated significantly at any examination.ConclusionsMyocardial dysfunction during IVI recovery appeared to be transient particularly in the absence of myocardial injury. Echocardiographic tissue imaging may be useful to detect subclinical cardiac changes in association with IVI.

We reported a 67-year-old woman in whom large atrial thrombi were found by chance during discontinuation of therapeutic anticoagulation. The patient, with a history of mitral valve replacement surgery, had stopped anticoagulation for months because of intractable gastrointestinal bleeding, during which she was found to have 3 large thrombi in the atria on transesophageal echocardiography: left atrial free-floating ball-shaped thrombus, left atrial appendage thrombus, and right atrial appendage thrombus. One month following diagnosis, she still had the free-floating thrombus despite adequate anticoagulation. Free-floating ball-shaped thrombus is a rare finding observed on echocardiography in patients with mitral valve disease and an even rarer finding in case of appendage thrombi coexisting.

Objective: Rare coexistence of disease or pathology Background: The left atrial appendage (LAA) has considerable variations in its size, shape, and spatial relationship with other cardiac structures. Absence of the LAA is a congenital cardiac condition usually identified by an imaging modality intended for other purposes. Absence of the LAA has been described in a total of 19 case reports so far; however, no cases of "hypoplastic" LAA in a real sense have ever been reported. Case Report: We herein report a case of hypoplastic, but not truly absent, LAA in a 76-year-old man scheduled for catheter ablation against atrial flutter. Preprocedural transesophageal echocardiography (TEE) performed in this patient to exclude intracardiac thrombosis failed to detect the LAA, although Doppler color-flow mapping revealed a jet signal spewed out into the main LA around where the LAA would be located. The LAA was also not detectable by routinely developed tomographic images from computed tomography (CT) angiography. Eventually, however, the multiplanar reconstruction into 3-dimensional volume rendering via the CT angiography identified a very small LAA. Those findings by TEE and CT led to a diagnosis of hypoplastic LAA. Conclusions: Hypoplastic LAA should be kept in mind when considering LAA interventions as well as anticoagulation treatment. Multiple imaging modalities are necessary to recognize morphological aberration of the LAA. [ABSTRACT FROM AUTHOR]

Objective: Rare disease. Background: Left atrial appendage (LAA) ostial stenosis is a rare cardiac condition usually identified by transesophageal echocardiography (TEE). LAA ostial stenosis can be classified into 2 types: one is idiopathic and the other is a complication after incomplete surgical LAA ligation. The former one is even rarer and only 12 cases have previously been reported. Case Report: An asymptomatic young woman was found at a medical checkup to have an abnormal jet signal in the left atrium on transthoracic echocardiography. TEE revealed that the abnormal signal originated from a narrowed orifice of the LAA. There were no other cardiac abnormalities in this woman. Unlike the previously reported cases, our case had LAA ostial stenosis detected by transthoracic echocardiography but not by TEE. Conclusions: We describe a case of anatomic narrowing of the LAA orifice in a young woman. This was a first-ever case of idiopathic LAA ostial stenosis that was detected by transthoracic echocardiography. Because of the very small number of such cases reported, it remains unknown whether anticoagulation is required to prevent intra-atrial thrombus formation. [ABSTRACT FROM AUTHOR]

Cancer invasion and metastasis are the major causes of cancer patient mortality. Various growth factors, including hepatocyte growth factor (HGF), are known to promote cancer invasion and metastasis, but the regulatory mechanisms involved are not fully understood. Here, we show that HGFpromoted migration and invasion of breast cancer cells are regulated by CUB domain-containing protein 1 (CDCP1), a transmembrane activator of SRC kinase. In metastatic human breast cancer cell line MDA-MB-231, which highly expresses the HGF receptor MET and CDCP1, we show that CDCP1 knockdown attenuated HGF-induced MET activation, followed by suppression of lamellipodia formation and cell migration/invasion. In contrast, in the low invasive/nonmetastatic breast cancer cell line T47D, which had no detectable MET and CDCP1 expression, ectopic MET expression stimulated the HGF-dependent activation of invasive activity, and concomitant CDCP1 expression activated SRC and further promoted invasive activity. In these cells, CDCP1 expression dramatically activated HGF-induced membrane remodeling, which was accompanied by activation of the small GTPase Rac1. Analysis of guanine nucleotide exchange factors revealed that ARHGEF7 was specifically required for CDCP1-dependent induction of HGF-induced invasive ability. Furthermore, immunofluorescence staining demonstrated that CDCP1 coaccumulated with ARHGEF7. Finally, we confirmed that the CDCP1-SRC axis was also crucial for HGF and ARHGEF7- RAC1 signaling in MDA-MB-231 cells. Altogether, these results demonstrate that the CDCP1-SRC-ARHGEF7-RAC1 pathway plays an important role in the HGF-induced invasion of a subset of breast cancer cells. [ABSTRACT FROM AUTHOR]