Value of Echocardiography and Cardiac Magnetic resonance in assessing left ventricular function in breast and gastric cancer patients after Anthracycline Chemotherapy.

BACKGROUND: Echocardiography (ECHO) and cardiac magnetic resonance imaging (MRI) are used to observe changes in the left ventricular structure in patients with breast and gastric cancer after 6 cycles of chemotherapy. Based on the observed values, we aimed to evaluate the cardiotoxicity of anthracyclines in cancer patients and to analyze the consistency of the two examination methods in assessing left ventricular function after chemotherapy. METHODS: From January 2020 to January 2022, the data of 80 patients with malignant tumors who received anthracycline chemotherapy (breast cancer, n = 40; gastric cancer, n = 40) and 40 healthy volunteers (Control group) were retrospectively collected. Serum high-sensitivity cardiac troponin T (hs-cTnT) levels were detected by an automatic immunoassay analyzer. Left ventricular end-systolic volume (LVESV), left ventricular end-diastolic volume (LVEDV) and left ventricular ejection fraction (LVEF) were measured by cardiac MRI and 2-dimensional ECHO using the biplane Simpson's method. RESULTS: Compared with baseline values, serum high-sensitivity cardiac troponin T (hs-cTnT) levels were significantly increased in patients with breast cancer and gastric cancer after 6 cycles of chemotherapy (P < 0.05). In addition, LVEDV, LVESV and LVEF measured with MRI were higher than those detected by ECHO in cancer patients after 6 cycles of chemotherapy (P < 0.05). And the Bland-Altman plot analysis showed that LVEDV, LVESV and LVEF measured by the two examination methods were in good agreement. CONCLUSION: Breast and gastric cancer patients exhibited elevated levels of hs-cTnT after 6 cycles of chemotherapy, indicating potential cardiotoxicity. Additionally, cardiac MRI and 2-dimensional ECHO showed good agreement in assessing left ventricular function, with ECHO tending to underestimate volume measurements compared to MRI.

Different phenotype of left atrial function impairment in patients with hypertrophic cardiomyopathy and hypertension: comparison of healthy controls.

Background: The impairment of atrial function and atrial-ventricular coupling in diseases with left ventricular (LV) hypertrophy has been increasingly recognized. This study compares left atrium (LA) and right atrium (RA) function, as well as LA-LV coupling, in patients with hypertrophic cardiomyopathy (HCM) and hypertension (HTN) with preserved LV ejection fraction (EF), using cardiovascular magnetic resonance feature tracking (CMR-FT). Methods: Fifty-eight HCM patients, 44 HTN patients, and 25 healthy controls were retrospectively enrolled. LA and RA functions were compared among the three groups. LA-LV correlations were evaluated in the HCM and HTN groups. Results: LA reservoir (LA total EF, ɛs, and SRs), conduit (LA passive EF, ɛe, SRe), and booster pump (LA booster EF, ɛa, SRa) functions were significantly impaired in HCM and HTN patients compared to healthy controls (HCM vs. HTN vs. healthy controls: ɛs, 24.8 ± 9.8% vs. 31.3 ± 9.3% vs. 25.2 ± 7.2%; ɛe, 11.7 ± 6.7% vs. 16.8 ± 6.9% vs. 25.5 ± 7.5%; ɛa, 13.1 ± 5.8% vs. 14.6 ± 5.5% vs. 16.5 ± 4.5%, p < 0.05). Reservoir and conduit functions were more impaired in HCM patients compared to HTN patients (p < 0.05). LA strains demonstrated significant correlations with LV EF, LV mass index, LV MWT, global longitudinal strain parameters, and native T1 in HCM patients (p < 0.05). The only correlations in HTN were observed between LA reservoir strain (ɛs) and booster pump strain (ɛa) with LV GLS (p < 0.05). RA reservoir function (RA ɛs, SRs) and conduit function (RA ɛe, SRe) were significantly impaired in HCM and HTN patients (p < 0.05), while RA booster pump function (RA ɛa, SRa) was preserved. Conclusions: LA functions were impaired in HCM and HTN patients with preserved LV EF, with reservoir and conduit functions more affected in HCM patients. Moreover, different LA-LV couplings were apparent in two different diseases, and abnormal LA-LV coupling was emphasized in HTN. Decreased RA reservoir and conduit strains were evident in both HCM and HTN, while booster pump strain was preserved.

LncRNA AFAP1-AS1 promotes M1 polarization of macrophages and osteogenic differentiation of valve interstitial cells.

Little is known about the biological functions and underlying mechanisms of long non-coding RNA AFAP1-AS1 in degenerative calcified aortic valve disease (DCAVD). This study aims to explore whether AFAP1-AS1 regulates macrophage polarization in aortic valve calcification. Macrophage polarization and AFAP1-AS1 expression were detected in normal and calcified aortic valves of DCAVD patients. To explore the effect of AFAP1-AS1 on macrophage polarization, gain and loss of function were performed in THP-1 cells, and the percentage of M1 and M2 and the expressions of M1 and M2 markers were analyzed. Meanwhile, osteogenic differentiation was examined in valve interstitial cells (VICs). Compared with normal valves, there were more M1, less M2, and high AFAP1-AS1 expressions in calcified aortic valves, which may indicate a relationship between AFAP1-AS1 and macrophage polarization. AFAP1-AS1 overexpression promoted M1 polarization in lipopolysaccharide (LPS) and interferon gamma (IFN-γ)-treated THP-1 cells but inhibited M2 polarization, as well as augmented VIC osteogenic differentiation. On the contrary, the silence of AFAP1-AS1 could induce macrophage to M2-type and inhibit VIC osteogenic differentiation. These results elucidate that AFAP1-AS1 can promote M1 macrophages polarization to aggravate VIC osteogenic differentiation, playing a role in aortic valve calcification.

MiR-182-5p Inhibits the Proliferation of Vascular Smooth Muscle Cells Induced by ox-LDL Through Targeting PAPPA.

This study aims to analyze the expression level and correlation of miR-182-5p and its target gene PAPPA in coronary atherosclerosis (CAD).Real time PCR, ELISA, and Western blotting methods were used to detect the expression levels. Dual-luciferase reporter gene assays were used to analyze the interaction between the 3'-UTR of PAPPA and miR-182-5p.The expression level of miR-182-5p in CAD was significantly lower than that in normal population, while the content of serum PAPPA was significantly increased, and the expression level of miR-182-5p was negatively correlated with the PAPPA content. The expression level of miR-182-5p decreased, while the expression level of PAPPA increased significantly in the ox-LDL treated HA-VSMC cells. Researchers found that PAPPA could promote the activation of IGF signaling pathway in HA-VSMC cells treated by ox-LDL, further activate NF-kB, PI3K/AKT and ERK signaling pathway, and promote cell proliferation. However, miR-182-5p could inhibit the expression of PAPPA, block the activation of IGF signal pathway, and inhibit the proliferation of HA-VSMC cells induced by ox-LDL. miR-182-5p had a targeted action site in the 3'-UTR of PAPPA by bioinformatics prediction. The analysis of luciferase reporter gene further confirmed that miR-182-5p could target the 3'-UTR of PAPPA to inhibit its expression.miR-182-5p demonstrated a protective effect on atherosclerosis and may be a potential therapeutic target for atherosclerosis.

Effects of miR-23b on hypoxia-induced cardiomyocytes apoptosis.

OBJECTIVES: The aim of this study was to investigate the role of miR-23b in hypoxic cardiomyocytes and the potential mechanism. METHODS: Myocardial samples of patients with cyanotic or acyanotic congenital heart disease (CHD) were collected to evaluate miR-23b expression. Agomir or antagomir of miR-23b was transfected into H9C2 cells. MTT, LDH assay and TUNEL staining were used to determine the cell proliferation and apoptosis under hypoxic conditions. Besides, the expression levels of cleaved-caspase-3, cleaved-PARP, Bad, Bcl-2 and Bax in hypoxic H9C2 cells were determined by western blot and qRT-PCR, respectively. RESULTS: Higher miR-23b expression levels were found in the patients with cyanotic CHD compared with the patients with acyanotic CHD. In addition, the expression of miR-23b was gradually up-regulated with prolonged hypoxia time in the H9C2 cells. Using MTT and LDH assays, cell growth was significantly decreased in the agomir group than that in the agomir-negative control (NC) group, while antagomir increased the cell growth. Using TUNEL staining and flow cytometry analysis, miR-23b promoted hypoxia-induced apoptosis. The expression levels of pro-apoptotic proteins, such as cleaved-caspase-3, cleaved-PARP and Bad, were significantly increased in the agomir group, while the Bcl-2 levels and Bcl-2/Bax ratio were decreased. Opposite tendency was observed in the antagomir group. Dual luciferase reporter assay and western blot analysis confirmed that Smad3 was a direct target of miR-23b. CONCLUSION: Over-expression of miR-23b may increase cardiomyocyte apoptosis and reduce cell growth under hypoxic conditions.