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Abstract Background Myocardial work acquired by echocardiography has emerged as a novel method to evaluate myocardial function. We investigated global and segmental myocardial work in hypertension (HT) among patients with different patterns of left ventricular (LV) geometry in order to analyze the contribution of segmental myocardial work to global myocardial work. Methods and results One hundred twenty-five patients with HT were divided into 4 groups: normal geometry (NG), concentric remodeling (CR), concentric hypertrophy (CH) and eccentric hypertrophy (EH). Longitudinal strain (LS) and the following indices were obtained by echocardiography: myocardial work index (MWI), myocardial constructive work (MCW), myocardial wasted work (MWW), and myocardial work efficiency (MWE). The global longitudinal strain (GLS) decreased gradually among the groups: NG, CR, CH and EH (P

Abstract Objective Transthoracic echocardiography (TTE) is generally recognized as the top choice for detecting myocardial and cardiac cavity lesions. Sonographers mostly focus on myocardium, cardiac cavity and cardiac hemodynamics, whereas the abnormal extra-cardiac lesions are easily remain unrecognized. The aim of this study was to investigate the ultrasonic image features in abnormal extra-cardiac lesions and the value of TTE in the detection of extra-cardiac lesions. Methods 49 cases of abnormal extra-cardiac lesion detected by TTE from January 2014 to December 2019 were collected, which were confirmed by surgical pathology. The two-dimensional ultrasonic characteristics and the relationships with the cardiac and great vessels were summarized on the basis of multi-view by TTE. All patients were also examined by computed tomography (CT). Results In 49 patients with abnormal extra-cardiac lesions, 37 malignant cases and 12 benign cases were included. There were 41 cases (41/49, 86.67%) of mediastinal lesions and 8 cases (8/49, 16.33%) of lung lesions. The maximum diameter ranged from 3.2 cm to 13.66 cm, and the median diameter was about 7.4 cm, among which 29 cases (29/49, 59.18%) were larger than 5 cm. 4 cases (4/49, 8.16%) of cystic anechoic lesions were pericardial cyst. 2 cases (2/49, 4.08%) of cystic-solid echogenic lesions were teratoma. The remaining 43 cases (43/49, 87.76%) presented as solid hypoechoic or heterogeneous masses. 6 cases compressed the heart and 21 cases encroached on the heart and vessels. Diagnosis coincidence rates of TTE and CT were respectively 77.55% and 93.88%, with a statistical difference (p = 0.012). Conclusion Although the diagnostic coincidence rate of TTE is slightly lower than that of CT, TTE has certain diagnostic value for extra-cardiac lesions.

Abstract Background Cardiac remodeling is one of the major risk factors for heart failure. In patients with type 2 diabetes, sodium–glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of the first hospitalization for heart failure, possibly through glucose-independent mechanisms in part, but the underlying mechanisms remain largely unknown. This study aimed to shed light on the efficacy of dapagliflozin in reducing cardiac remodeling and potential mechanisms. Methods Sprague–Dawley (SD) rats, induced by chronic infusion of Angiotensin II (Ang II) at a dose of 520 ng/kg per minute for 4 weeks with ALZET® mini-osmotic pumps, were treated with either SGLT2 inhibitor dapagliflozin (DAPA) or vehicle alone. Echocardiography was performed to determine cardiac structure and function. Cardiac fibroblasts (CFs) were treated with Ang II (1 μM) with or without the indicated concentration (0.5, 1, 10 μM) of DAPA. The protein levels of collagen and TGF-β1/Smad signaling were measured along with body weight, and blood biochemical indexes. Results DAPA pretreatment resulted in the amelioration of left ventricular dysfunction in Ang II-infused SD rats without affecting blood glucose and blood pressure. Myocardial hypertrophy, fibrosis and increased collagen synthesis caused by Ang II infusion were significantly inhibited by DAPA pretreatment. In vitro, DAPA inhibit the Ang II-induced collagen production of CFs. Immunoblot with heart tissue homogenates from chronic Ang II-infused rats revealed that DAPA inhibited the activation of TGF-β1/Smads signaling. Conclusion DAPA ameliorates Ang II-induced cardiac remodeling by regulating the TGF-β1/Smad signaling in a non-glucose-lowering dependent manner.

Abstract Background This study is aimed at investigating myocardial multi-directional systolic deformation in hypertensive with different left ventricular ejection fraction (LVEF), and exploring its contribution to LVEF. Methods One hundred and twenty-three patients with primary hypertension (HT) were divided into group A (LVEF ≥ 55%), group B (45% ≤ LVEF

Diabetic cardiac fibrosis increases ventricular stiffness and facilitates the occurrence of diastolic dysfunction. Retinoid X receptor (RXR) plays an important role in cardiac development and has been implicated in cardiovascular diseases. In the present study, we investigated the effects of RXR agonist treatment on streptozotocin (STZ)-induced diabetic cardiomyopathy (DCM) and the underlying mechanism. Sprague-Dawley (SD) rats induced by STZ injection were treated with either RXR agonist bexarotene (Bex) or vehicle alone. Echocardiography was performed to determine cardiac structure and function. Cardiac fibroblasts (CFs) were treated with high glucose (HG) with or without the indicated concentration of Bex or the RXR ligand 9-cis-retinoic acid (9-cis-RA). The protein abundance levels were measured along with collagen, body weight (BW), blood biochemical indexes and transforming growth factor-β (TGF-β) levels. The effects of RXRα down-regulation by RXRα small interfering RNA (siRNA) were examined. The results showed that bexarotene treatment resulted in amelioration of left ventricular dysfunction by inhibiting cardiomyocyte apoptosis and myocardial fibrosis. Immunoblot with heart tissue homogenates from diabetic rats revealed that bexarotene activated liver kinase B1 (LKB1) signaling and inhibited p70 ribosomal protein S6 kinase (p70S6K). The increased collagen levels in the heart tissues of DCM rats were reduced by bexarotene treatment. Treatment of CFs with HG resulted in significantly reduced LKB1 activity and increased p70S6K activity. RXRα mediated the antagonism of 9-cis-RA on HG-induced LKB1/p70S6K activation changes in vitro. Our findings suggest that RXR agonist ameliorates STZ-induced DCM by inhibiting myocardial fibrosis via modulation of the LKB1/p70S6K signaling pathway. RXR agonists may serve as novel therapeutic agents for the treatment of DCM. [ABSTRACT FROM AUTHOR]

The article examines the clinical application of tissue doppler (TD) echocardiographic in patients with idiopathic pulmonary hypertension (HP). The presence of normal/reduced mean pulmonary capillary wedge pressure in patients with idiopathic PH can be predicted by TD imaging of the lateral mitral annulus. The improvement in right ventricular function and left ventricular filling with long-term targeted therapy are monitored.

We sought to examine the hemodynamic determinants and clinical application of the peak acceleration rate of early (Ea) diastolic velocity of the mitral annulus by tissue Doppler. Simultaneous left atrial and left ventricular (LV) catheterization and Doppler echocardiography were performed in 10 dogs. Preload was altered using volume infusion and caval occlusion, whereas myocardial lusitropic state was altered with dobutamine and esmolol. The clinical application was examined in 190 consecutive patients (55 control, 41 impaired relaxation, 46 pseudo-normal, and 48 restrictive LV filling). In addition, in 60 consecutive patients, we examined the relation between it and mean wedge pressure with simultaneous Doppler echocardiography and right heart catheterization. In canine studies, a significant positive relation was present between peak acceleration rate of Ea and transmitral pressure gradient only in the stages with normal or enhanced LV relaxation, but with no relation in the stages where the time constant of LV relaxation (τ) was ≥50 ms. Its hemodynamic determinants were τ, LV minimal pressure, and transmitral pressure gradient. In clinical studies, peak acceleration rate of Ea was significantly lower in patients with impaired LV relaxation irrespective of filling pressures (P < 0.001) and with similar accuracy to peak Ea velocity (area under the curve for septal and lateral peak acceleration rates: both 0.78) in identifying these patients. No significant relation was observed between peak acceleration rate and mean wedge pressure. Peak acceleration rate of Ea appears to be a useful index of LV relaxation hut not of filling pressures and can be applied to identify patients with impaired LV relaxation irrespective of their filling pressures. [ABSTRACT FROM AUTHOR]