The diagnostic performance of AccuFFRangio for evaluating coronary artery stenosis under different computational conditions.

Background: A computational method (AccuFFrangio) based on invasive coronary angiography (ICA) and computational fluid dynamics (CFD) to calculate fractional flow reserve (FFR) without a pressure wire has been devised to clarify the physiological significance of coronary stenosis. This study aimed to evaluate the diagnostic performance of AccuFFRangio computation under different boundary conditions and vessel reconstruction approaches. Methods: Consecutive patients with stable angina pectoris who underwent ICA and FFR assessment from 2 centers were analyzed retrospectively. Using wire-based FFR as the reference standard, the diagnostic performances of AccuFFRangio and its variations were evaluated and compared. The calculation of AccuFFRangio involves several key boundary conditions, including patient-specific aortic pressure, contrast flow velocity derived from the thrombolysis in myocardial infarction (TIMI) frame count method, and vessel reconstruction based on 2 angiographic views. We considered the following 3 variations: (I) a fixed aortic pressure [fixed pressure AccuFFRangio (pAccuFFRangio)], (II) an empirical hyperemic velocity [fixed velocity AccuFFRangio (vAccuFFRangio)], and (III) vessel reconstruction using a single angiographic view [single view AccuFFRangio (sAccuFFRangio)]. Results: A total of 230 patients with 230 vessels were included in the final analysis. The accuracy for standard AccuFFRangio, pAccuFFRangio, vAccuFFRangio, and sAccuFFRangio was 93.91%, 86.52%, 81.74%, and 83.48%, respectively; the sensitivity was 90.74%, 51.85%, 83.33%, and 46.30%, respectively; the specificity was 94.89%, 97.16%, 81.25%, and 94.89%, respectively; and the area under the receiver operating characteristic curve was 0.971, 0.928, 0.892, and 0.870, respectively. Conclusions: The comparison suggested that the overall performance of the standard AccuFFRangio was superior to other variations and had the highest accuracy among all the cases.

Functional Assessment of Coronary Artery Stenosis from Coronary Angiography and Computed Tomography: Angio-FFR vs. CT-FFR.

This study was designed to compare the diagnostic performance of angio-FFR and CT-FFR for detecting hemodynamically significant coronary stenosis. Angio-FFR and CT-FFR were measured in 110 patients (139 vessels) with stable coronary disease using invasive FFR as the reference standard. On per-patient basis, angio-FFR was highly correlated with FFR (r =0.78, p <0.001), while the correlation was moderate between CT-FFR and FFR (r =0.68, p <0.001). Diagnostic accuracy, sensitivity, and specificity for angio-FFR were 94.6%, 91.4%, and 96.0%, respectively; and those of CT-FFR were 91.8%, 91.4%, and 92%, respectively. Bland-Altman analysis showed that angio-FFR had a larger average difference and a smaller root mean squared deviation than CT-FFR compared with FFR (-0.014±0.056 vs. 0.0003±0.072). Angio-FFR had a slightly higher AUC than that of CT-FFR (0.946 vs. 0.935, p =0.750). Angio-FFR and CT-FFR computed from coronary images could be accurate and efficient computational tools for detecting lesion-specific ischemia of coronary artery stenosis. Angio-FFR and CT-FFR calculated based on the two types of images can both accurately diagnose functional ischemia of coronary stenosis. CT-FFR can act as a gatekeeper to the catheter room, assisting doctors in determining whether patients need to be screened by coronary angiography. Angio-FFR can be used in the catheter room to determine the functional significant stenosis for helping decision-making in revascularization.

Modulation of miR-382-5p reduces apoptosis of myocardial cells after acute myocardial infarction.

BACKGROUND: Acute myocardial infarction (AMI) is a severe cardiovascular condition. Blocking the apoptosis of myocardial cells may mitigate AMI. Excessive expression of Stanniocalcin-1 (STC1) plays a protective role in the heart by inhibiting myocardial cell apoptosis. Here, we looked at the mechanism by which miR-382-5p regulates STC1 and affects myocardial cell apoptosis after AMI. METHODS: An AMI mouse model with a descending anterior ligament coronary artery and an HL-1 cell model with reproducible hypoxia/reoxygenation (H/R) were established. For pathological changes in myocardial tissues, terminal deoxynucleotidyl transferase dUTP nick end labelling staining and haematoxylin and eosin staining were performed. STC1 mRNA and miR-382-5p levels were measured using quantitative real-time PCR. Protein levels of STC1 and apoptosis-related proteins were measured by western blotting. The 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide assay was used to detect cell viability, and a dual-luciferase reporter assay was carried out to verify potential targets of miR-382-5p. RESULTS: The level of miR-382-5p was raised in myocardial tissues of AMI mice and H/R-induced HL-1 cells. Compared with the control group, the myocardial tissue cells in the AMI group were disordered, with evident necrosis of myocardial cells, apoptosis and inflammatory infiltration. Interference with miR-382-5p inhibited myocardial cell apoptosis after H/R, as well as inferior lactate dehydrogenase. Also, miR-382-5p adversely regulated STC1 and the expression of STC1 was increased after transfection with miR-382-5p antagomir. Furthermore, interference with miR-382-5p reduced myocardial cell apoptosis after H/R by increasing the expression level of STC1. CONCLUSION: To summarise, our study showed an increase in miR-382-5p in myocardial tissues in the AMI mouse model. Interference with miR-382-5p reduced apoptosis of myocardial cells after AMI and the effect was achieved by increasing STC1 expression.

Troxerutin attenuates oxygen­glucose deprivation and reoxygenation­induced oxidative stress and inflammation by enhancing the PI3K/AKT/HIF­1α signaling pathway in H9C2 cardiomyocytes.

Myocardial ischemia­reperfusion (MI/R) injury is a complex pathological process that occurs when tissues are reperfused following a prolonged period of ischemia. Troxerutin has been reported to have cardioprotective functions. However, the underlying mechanism by which troxerutin protects against MI/R injury has not been fully elucidated. The aim of the present study was to explore whether troxerutin­mediated protection against oxygen­glucose deprivation/reoxygenation (OGD/R)­induced H9C2 cell injury was associated with the inhibition of oxidative stress and the inflammatory response by regulating the PI3K/AKT/hypoxia­inducible factor­1α (HIF­1α) signaling pathway. The results of the present study suggested that troxerutin pretreatment prevented the OGD/R­induced reduction in cell viability, and the increase in lactate dehydrogenase activity and apoptosis. Troxerutin reversed OGD/R­induced the inhibition of the PI3K/AKT/HIF­1α signaling pathway as demonstrated by the increased expression of PI3K and HIF­1α, and the increased ratio of phosphorylated AKT/AKT. LY294002, a selective PI3K inhibitor, inhibited the PI3K/AKT/HIF­1α signaling pathway and further attenuated the protective effect of troxerutin against OGD/R­induced H9C2 cell damage. Furthermore, small interfering (si)RNA­mediated knockdown of HIF­1α reduced troxerutin­induced protection against OGD/R injury. Troxerutin pretreatment alleviated OGD/R­induced oxidative stress, as demonstrated by the reduced generation of reactive oxygen species and malonaldehyde content, and the increased activities of superoxide dismutase and glutathione peroxidase, which were reduced by HIF­1α­siRNA. Troxerutin­induced decreases in the levels of interleukin (IL)­1ß, IL­6 and tumor necrosis factor­α in OGD/R conditions were also reduced by HIF­1α­siRNA. The results from the present study indicated that troxerutin aggravated OGD/R­induced H9C2 cell injury by inhibiting oxidative stress and the inflammatory response. The primary underlying protective mechanism of troxerutin was mediated by the activation of the PI3K/AKT/HIF­1α signaling pathway.

Copeptin level in the early prediction of cardiorenal syndrome in rats.

Copeptin (CPP) has been considered as a useful marker for prediction of prognosis in heart diseases. However, CPP has not been investigated sufficiently in cardiorenal syndrome (CRS). The present study aimed to investigate the value of CPP level in predicting CRS in rats with partial nephrectomy combined with myocardial infarction (SNX + MI). A total of 60 male Sprague-Dawley rats were used to establish the CRS model by partial nephrectomy combined with MI. The rats were randomly divided into blank control (CK), SNX, MI and CRS groups. Changes in serum and urine CPP concentrations, hemodynamics, blood pressure, and renal function were examined 1-5 weeks after modeling. The predictive values of CPP in the occurrence of CRS in rats were evaluated using receiver operating characteristic (ROC) curve. The results showed that serum CPP in the CRS group in 1-5 weeks and urine CPP in 3 weeks after modeling increased significantly compared with the CK group. Also, serum B-type natriuretic peptide (BNP) in 1 and 3 weeks and urine BNP in 4-5 weeks after modeling increased significantly. No correlation was found between serum or urine CPP, BNP and BUN levels 1 week after modeling in the CRS group. The ROC curve analysis showed that the area under the curve of CRS predicted by serum CPP at 1 week was 0.908 with 56.59 pg/ml as the cutoff point, and its diagnostic sensitivity and specificity were 87.5 and 80.0%, respectively. To conclude, SNX + MI may be used to establish CRS rat model with cardiac and renal damage. Serum CPP may serve as a specific biomarker for the early prediction of CRS.