Cardiac resynchronization therapy (CRT) is an important and effective therapy for end-stage heart failure. Non-response to CRT is one of the main obstacles to its application in clinical practice. There is no uniform consensus or definition of CRT "response." Clinical symptoms, ventricular remodeling indices, and cardiovascular events have been reported to be associated with nonresponders. To prevent non-response to CRT, three aspects should be thoroughly considered: preoperative patient selection, electrode implantation, and postoperative management. Preoperative selection of appropriate patients for CRT treatment is an important step in preventing non-response. Currently, the CRT inclusion criteria are mainly based on the morphology of QRS waves in deciding ventricular dyssynchrony. Echocardiography and cardiac magnetic resonance are being explored to predict nonresponse to CRT. The location of left ventricular electrode implantation is a current hot spot of research; it is important to identify the location of the latest exciting ventricular segment and avoid scars. Cardiac magnetic resonance and ultrasonic spot tracking are being progressively developed in this field. Some new techniques such as His Bundle pacing, endocardial electrodes, and novel sensors are also being investigated. Postoperative management of patients is another essential step towards preventing non-response; it mainly focuses on the treatment of the disease itself and CRT program control optimization. CRT treatment is just one part of the overall treatment of heart failure, and multidisciplinary efforts are needed to improve the overall outcome.
Objectives: To verify the accuracy of the International Warfarin Pharmacogenetics Consortium (IWPC) algorithm, identify the effects of genetic and clinical factors on warfarin stable dose, and to establish a new warfarin stable dose prediction algorithm for the elderly Han-Chinese population under the guidance of pharmacogenetics. Methods: According to the inclusion criteria, 544 non-valvular atrial fibrillation patients taking warfarin for anticoagulation treatment were enrolled. Data information of three groups including the whole population, people under 65 years old and over 65 years old were substituted into the IWPC algorithm respectively to verify its accuracy. The basic data and clinical information of 360 elderly people were collected for statistical analysis and the genotypes of VKORC1-G1639A and CYP2C9 were detected by Sanger sequencing. The new algorithm of the elder pharmacogenetics warfarin dosing was obtained by stepwise multiple regression. The determination coefficient (R2), root mean squared error (RMSE), and the proportion of the predicted value within the true value range of ±20%(20%-p) were used to evaluate the accuracy of the IWPC algorithm and the new algorithm. Results: Among the three different age groups, the warfarin stable dose predictive accuracy of IWPC algorithm was the lowest in the elderly patients above 65-year-old. In this study, the important factors influencing the stable dose of warfarin in the elderly Han-Chinese were height, weight, body surface area, serum creatinine level, amiodarone usage, CYP2C9 (*1*2, *1*3), and VKORC1 (GG/GA) genotypes. By means of stepwise multiple regression analysis, we established a new elder warfarin dosing algorithm (R 2 =0.3714) containing height, creatinine, amiodarone usage, CYP2C9 (*1*2 or *1*3), and VKORC1 (GA or GG) genotypes. The prediction accuracy and clinical availability of the Elderly algorithm was significantly better than that of IWPC algorithm verified by RMSE, R2, and (20%-p) methods.
Background Two-dimensional speckle tracking echocardiography (2D-STE) is a novel and non-invasive technique for the diagnosis of coronary artery disease (CAD). This retrospective study from a single center aimed to identify myocardial ischemia using 2D-STE in CAD patients identified by angiography. Material/Methods From March 1 to November 30, 2019, 690 patients in Beijing Hospital were enrolled. After angiography, 346 patients were diagnosed with CAD. Reduction in vessel diameter of ≥50% by stenosis in at least 1 major coronary artery or its main branch was considered CAD. Analysis of 2D-STE was performed using EchoPAC version 201. Results The global strain was significantly impaired in CAD patients ( P <0.01). Global longitudinal peak strain (GLPS) was analyzed in layers. For GLPS of the epicardium, the odds ratio (OR) was 1.297 (1.217–1.382; P =0.002), the area under the curve (AUC) was 0.727, and the cut-off value was −16.95; sensitivity and specificity were 73.7% and 63.0%, respectively. For GLPS of the middle layer, the OR was 1.260 (1.192–1.333; P <0.001), the AUC was 0.732, and the cut-off value was −20.95; sensitivity and specificity were 82.4% and 56.2%, respectively. For GLPS of the endocardium, the OR was 1.193 (1.137–1.251; P <0.001), the AUC was 0.708, and the cut-off value was −22.95; sensitivity and specificity were 82.9% and 52.9%, respectively. Conclusions The findings from this study support the clinical application of 2D-STE in patient populations with suspected myocardial ischemia due to CAD. Therefore, 2D-STE combined with ECG monitoring may have a future role for early screening of CAD patients.
Objective: Many studies showed that angiotensin II(Ang II) is a potent biologically active product of renin-angiotensin system and a key regulator of renal inflammation and fibrosis. Thymoquinone (TQ) is an herbal medicine which has been shown to have anti-inflammatory and anti-fibrosis effects in previous our studies. The aim of this study was to determine the role of TQ in Ang II-induced renal damage. Design and method: In present study, we used a model of Ang II-induced renal damage in ApoE-deficient (ApoE−/−) mice. Thirty eight-week-old male ApoE-/- mice were randomly divided into three groups: a control group, Ang II group and Ang II + TQ group. All groups mice were with different treated for 4 weeks. Blood samples were obtained from the inferior vena cava and collected in serum tubes; the blood samples were stored at minus 80°C until use. Coronal sections of kidney tissues were fixed in 10% formalin and then embedded in paraffin for histological evaluation. The kidney was stored in liquid nitrogen for immunoblotting or mRNA analysis. All data are presented as the mean ± SEM. Statistical analysis was performed using SPSS software version 23.0 (SPSS Inc., Chicago, IL, USA). Inter-group variation was measured by one-way ANOVA and subsequent Tukey's test. The minimal level of significance was P < 0.05. Results: The Ang II group showed a marked increase in CRE levels in ApoE-/- mice, but these parameters were significantly decreased in the Ang II + TQ group(Table1). There were significant pathophysiological changes (HE and Masson staining) in Ang II group mice, but the pathophysiological changes were inhibited in Ang II + TQ group(Figure1). Thymoquinone reduced Ang II-induced kidney fibrosis and inflammation in ApoE-/- mice(Figure2 and 3). Conclusions: Our data established that thymoquinone helps mitigate AngII-induced renal damage as shown by the downregulation of fibrosis expression and the suppression of inflammatory markers.
Objective: Heart failure is a complex end stage result of various cardiovascular diseases, and has a poor prognosis. Exercise training according to oxidative stress, myocardial fibrosis, inflammation pathways improve cardiac function. The aim of this study was to investigate the possible protective effects of exercise training against cardiac damage in doxorubicin (DOX)-induced heart failure in Sprague-Dawley Rats. Design and method: This study used 45 male Sprague-Dawley (SD) rats weighing 150 ± 20 g that were randomly divided into a control group (normal saline), doxorubicin (DOX) group and DOX plus exercise (DOX + E) group. Heart failure was induced experimentally by intraperitoneal injections of the cardiotoxic agent DOX. All groups received different treatment for 8 weeks. Blood samples were obtained from the inferior vena cava and collected in serum tubes; the blood samples were stored at minus 80°C until use. Heart tissues were fixed in 10% formalin and then embedded in paraffin for histological evaluation. The heart was stored in liquid nitrogen for immunoblotting or mRNA analysis. Results: Left ventricular fractional shortening and ejection fraction were higher in DOX + E group rats than in DOX group rats on an echocardiographic examination (Figure 1 and Table 1). Significant cardiac tissue damage (haematoxylin and eosin, Masson's trichrome staining) was seen in rats of the DOX group compared to those of the DOX + E group (Figure2). Exercise inhibited DOX-induced cardiac fibrosis (transforming growth factor, smooth muscle actin, collagen I, and collagen III) and oxidative stress (Nox4, p53) in an immunoblotting analysis (Figure 3 and 4). Conclusions: These results indicate that exercise training may be a potential therapeutic target for cardiac damage caused by DOX-induced heart failure.
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